Emergency Medicical Guidelines

PREFACE
Fourth Edition
Emergency Medical Guidelines

PARTICIPATING AGENCIES
INDIAN RIVER COUNTY EMS INDIAN RIVER SHORES PUBLIC SAFETY MARTIN COUNTY FIRE RESCUE SAINT LUCIE COUNTY FIRE DISTRICT STUART FIRE RESCUE TEQUESTA FIRE RESCUE ALL COUNTY AMBULANCE AMERICAN JETS COASTAL CARE TRANSPORTATION INDIAN RIVER COMMUNITY COLLEGE INDIAN RIVER MEMORIAL MEDICAL TRANSPORT SERVICE INTENSIVE AIR AMBULANCE LIFELINE MEDICAL SERVICES
EMERGENCY MEDICAL GUIDELINES
This text book was created in its entirety with Adobe PageMaker and Adobe Photoshop in a Windows environment. Research, preparation, compilation, editing and layout of this book took approximately three years and more than 2,000 man hours. No one agency alone could have produced a book of this calibre. Each agency made a unique contribution to this book without which it would not have been a success. The Development Team would like to recognize and thank each agency director for making the commitment of resources to see this project through. Without their faith and trust to let this Project find its own way, this book would not exist. As new scientific information becomes available through basic and clinical research, recommended treatments and drug therapies undergo changes. The Development Team has done everything possible to make this book accurate, uptodate and in accord with accepted standards at the time of publication. However, the reader is advised always ii
to check product information regarding dose, contraindications before administering any drug. Caution is especially urged when using new or infrequently ordered drugs. This book is published under the Sunshine Act of Florida and is protected by applicable laws. Copies of this book may be purchased from any participating agency (subject to availability). This book may be cited as a source or used in its entirety with the permission of the Participating Agencies.
PREFACE
Preface
Imagine if you will, the public outcry that would ensue if a jumbo jet filled with passengers crashed every day in the United States. Regrettably, Americans no longer need to imagine disasters that result in the tragic loss of lives. However, each day, more people die of sudden cardiac arrest than would fill a Boeing 747. The most effective way to improve the odds of survival for sudden cardiac arrest is rapid defibrillation in the pre-hospital setting. As high quality Emergency Medical Services (EMS) developed during the 1970s, cardiac arrest survival rates increased from near nothing to about 20% in a few progressive cities. However, essentially no additional progress in survival from cardiac arrest has occurred since 1980. For children, the odds of survival remain abysmal. Less than 2% of children with pre-hospital cardiac arrest survive to leave the hospital. Trauma systems developed during the 1970s to address the inadequacy of care for victims of traffic crashes. EMS began to transport patients directly to regional trauma centers, often bypassing closer community hospitals. With the establishment of these regional trauma centers the odds of survival from motor vehicle crashes improved. This reduction in mortality from injury illustrates the value of having EMS professionals who understand how to use the emergency care resources available in each community. EMS provides out-of-hospital medical care to those with perceived urgent needs. It is a component of the overall health care system. EMS delivers care as part of a system intended to attenuate the morbidity and mortality associated with sudden illnesses and injury. The positive effects of EMS care are enhanced by linkages with other community health resources and integration within the health care system. Emergency medical service is regarded as including the full spectrum of emergency care from recognition of the emergency condition, requesting emergency medical aid, provision of pre-hospital care, through definitive care in the hospital. The vast majority of patients cared for by EMS, however, are not victims of cardiac arrest or major injury. They have illnesses or injuries that are not life threatening yet require access to medical care.
This textbook is a unique approach to EMS protocols because it is a regional approach that unifies the prehospital care across boundaries, additionally it was promulgated based upon sound research and evidence based medical care thereby affording the patient the best possible approach to field medicine available. The time for major advancement in the science and practice of EMS is here. Emergency Medical Service providers must be able to deliver state of the art care based on sound scientific knowledge. A number of us, our families, or our friends will at some point turn to local EMS providers for assistance; and we expect that they will provide us with the best care possible. These guidelines take into account the complexity of emergency care in todays environment. The emergency team is afforded great latitude in treating the patient; it is difficult if not impossible to define every medical condition into a set of rules and procedures. One thing is certain though: not all the methods that we utilize today will stay the same during your career. This project is a living breathing entity that will be revisited, re-researched and updated as new technologies, procedures and treatments become standard. You as the provider of care have an obligation to not only follow these guidelines but to seek out new information that will contribute to the amassed knowledge that represents this book; some of the best ideas come from practicing Paramedics, EMTs and educators who let us know what problems they face every day in the field. This will allow the development team to keep the guidelines on the leading edge of patient care. Our goal is a High Performance EMS system that provides the patient with care that is second to none!!
-Joseph V. Ferrara
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RATIONALE OF EMERGENCY MEDICAL GUIDELINES

FOURTH EDITION
The philosophy of the Medical Directors is to treat patients to the fullest, appropriate extent within the medical standard of care for the community. This is accomplished by focusing on the goals set forth by the American College of Emergency Physicians, the American Heart Association and other guideline setting organizations. Paramedics have the discretion to alter any treatment guideline if it is deemed inappropriate. Justification must be made in the run report and reviewed by the Medical Director. All personnel will be subject to examination of case reports. Inquiries are conducted by the Medical Director, Supervisor, Training Officer or their designee at any time during or after care is rendered. The Procedural Guidelines , Treatment Guidelines with exceptions as noted in the relevant sections are hereby authorized for use by the Emergency Medical Technicians and Paramedics in accordance with Florida Statute 401. These guidelines are intended to provide a general approach to treatment of patients by the Emergency Medical Team. It is not intended that the Emergency Medical Team blindly apply these medical guidelines to each patient. It is intended that the Emergency Medical Team use their professional and clinical judgment to determine the best course of treatment for each patient. The treatments and procedures identified as Medic Discretion are generally appropriate actions to be provided by the Emergency Medical Team without prior physician orders. The treatments and procedures identified as Physician Consult are generally appropriate actions to be provided by the Emergency Medical Team after discussion with online medical control and direct physician orders received. On-line medical control will be provided by the Emergency Department Physician at the receiving facility, or by the Emergency Department Physician of the base hospital should communications be hindered. Early contact should be made to the Emergency Department Physician whenever doubt exists as to proper management of any patient. Physicians who wish to direct the Emergency Medical Team in the care of a patient should be referred to the on-line medical control physician for issuance of orders to the Team. The Medical Directors authorize the Team Paramedic responsible for controlled substances to take them to the scene of a call. All responsibility for these controlled substances remain with the Paramedic.
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PREFACE
ACKNOWLEDGMENTS
RESEARCH TEAM
ALEX NATHANSON (TEAM COORDINATOR) PETER ALLEN MARK BENTZ KEN BRYAN JENNIFER CHAMBERS MARK CHAMPION JASON DAHL TONY DUDLEY CHUCK GORDILS CRYSTAL HAUBERT DAVID HOILMAN RICH HUNTER DAVE JACKSON LISA MCCARTY FRED NEFF STACEY NEFF BILL PETERS RICK SOSA GEORGE SUMNER KIT WORLEY CHRIS ZAMBELLO
PROJECT COORDINATORS
PRE-PRESS EDITING
JAMES CHERRY (TEAM COORDINATOR) RALPH MORRISON (TEAM COORDINATOR) CINDIE BRANDT JENNIFER CHAMBERS JOSEPH COX EDWARD HILL DENNIS LIPOFSKY DONNIE LESKO FRED NEFF TERESA RAMSEY RUSTY RAMSEY ERIC WRIGHT
JOSEPH FERRARA (EDITOR) MATT HIMES (PROJECT LEAD) CORY RICHTER (EDITOR) LAYOUT
CORY RICHTER (TEAM COORDINATOR) CHUCK GORDILS RICH HUNTER RALPH MORRISON MOETAHAR PADELLAN GEORGE SUMNER CHRIS ZAMBELLO
COVER DESIGN:
RICHARD HUNTER
REVIEWERS
PETER ALLEN BLAKE BARTHOLOMEW RICK BELLOMY BRIAN BLIZZARD CINDIE BRANDT MARC DUCOTE VINCE FELICIONE MATT FENEX CHUCK GORDILS CHRYSTAL HAUBERT DAVE HOILMAN DAVE JACKSON LISA MCCARTY ALLEN MOORE DOUG MURPHY LORI RECCA JOEY RICHTER FREDDY RODRIGUEZ GARY ROTHE JOHN TAYLOR RICK VILLARS MARK WILSON KIT WORLEY CHRIS ZAMBELLO DAVID ZARKER
CONTRIBUTING AUTHORS
PETER ALLEN CINDIE BRANDT BRIAN BLIZZARD JASON DAHL MARC DUCOTE JOSEPH FERRARA CHRYSTAL HAUBERT DAVE HOILMAN DAVID HUTTON LISA MCCARTY CHRISTIAN MONTOYA ALEX NATHANSON CORY RICHTER RICK SOSA JOHN STIPO TODD STOLFI GEORGE SUMNER JOHN TAYLOR ROBERT TEARLE DAN WOUTERS DAVID ZARKER
TECHNICAL ADVISORS
J. MICHAEL ADELBERG M.D. LILLIAN I. AVNER, D.O. MARJORIE BOWERS, ED. D. TOMAS JACOME M.D. CHI CHOU LIU, M.D. PAUL F. MARCH M.D. DR. THOMAS MATESE D.O. MICHAEL J. MATTICE M.D. ROGER J. NICOSIA D.O. HOWARD M. ROBBINS M.D. DON TANABE, M.D. P. GLENN TREMML M.D. YVETTE WIRTA-CLARKE D.O. MAUREEN ZELINKA, M.D.
SPECIAL THANKS TO: MARTIN COUNTY PROFESSIONAL FIREFIGHTERS AND PARAMEDICS IAFF LOCAL 2959
FOR HOSTING THE GUIDELINES DRAFTS ON THEIR WEBSITE
KIT WORLEY
FOR WEBSITE SUPPORT AND E-MAIL LIST SERVER
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PREFACE
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PREFACE
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Emergency Guidelines
Contents
Educational Guidelines..................................... E1
INTRODUCTION ........................................................................ E2
PATIENT PRIORITIZATION ................................................................................................ E2
GENERAL MEDICAL ................................................................ E3

ABDOMINAL AORTIC ANEURYSMS .................................................................................... E3 ABDOMINAL PAIN .......................................................................................................... E3 ALLERGIC REACTION ...................................................................................................... E6 ALTERED LEVEL OF CONSCIOUSNESS/ALCOHOLISM ........................................................... E7 ANAPHYLAXIS ................................................................................................................ E8 ASTHMA ...................................................................................................................... E10 BLOODBORNE PATHOGENS ............................................................................................ E11 CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) ............................................... E13 COMBATIVE PATIENTS .................................................................................................. E14 DIABETES MELLITUS .................................................................................................... E15 DIALYSIS ..................................................................................................................... E17 DO NOT RESUSCITATE ORDER (DNRO) ...................................................................... E18 HYPERTENSION ............................................................................................................. E18 LATEX ALLERGY .......................................................................................................... E19 OBSTETRICS/GYNECOLOGY ........................................................................................... E20 PAIN MANAGEMENT ..................................................................................................... E24 PSYCHIATRIC EMERGENCIES .......................................................................................... E25 RESTRAINTS ................................................................................................................ E27 RAPID SEQUENCE INTUBATION (RSI) ............................................................................ E29 RENAL FAILURE ........................................................................................................... E30 SEIZURES ..................................................................................................................... E31 SEPSIS ........................................................................................................................ E33 SICKLE CELL ANEMIA .................................................................................................. E34 STROKE BRAIN ATTACK ........................................................................................ E34
CARDIAC................................................................................... E37
CARDIAC ALERT .......................................................................................................... E38 ACUTE CORONARY SYNDROME ...................................................................................... E38 ASYSTOLE ................................................................................................................... E40 ATRIAL FIBRILATION .................................................................................................... E40 ATRIAL FLUTTER ......................................................................................................... E41 CARDIAC TAMPONADE ................................................................................................. E41
CARDIOGENIC SHOCK ................................................................................................... E42 CESSATION OF EFFORTS ............................................................................................... E43 CONGESTIVE HEART FAILURE ........................................................................................ E44 HEART BLOCK ............................................................................................................. E45 HEART TRANSPLANT PATIENTS ..................................................................................... E47 MYOCARDIAL INFARCTION ............................................................................................ E48 PACEMAKER & AUTOMATIC INTERNAL CARDIAC DEFIBRILLATOR ..................................... E49 PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) ............................................. E50 PREMATURE VENTRICULAR CONTRACTIONS (PVC) ........................................................ E51 PULMONARY EMBOLISM (PE) ...................................................................................... E51 PULSELESS ELECTRICAL ACTIVITY (PEA) ..................................................................... E52 SINUS BRADICARDIA ..................................................................................................... E53 TORSADES DE POINTES (TDP)..................................................................................... E54 VENTRICULAR FIBRILLATION ......................................................................................... E54 VENTRICULAR TACHYCARDIA (VT) ............................................................................... E56 WOLFFPARKINSONWHITE SYNDROME ....................................................................... E57
HAZARDOUS MATERIALS MANAGEMENT....................... E58

ORGANOPHOSPHATE INSECTICIDES ................................................................................. E58 N-METHYL CARBAMATE INSECTICIDES .......................................................................... E59
TOXICOLOGY ........................................................................... E60

COCAINE TOXICITY ...................................................................................................... E60 DESIGNER DRUGS ........................................................................................................ E61 POISONING/OVERDOSE ................................................................................................. E62
TRAUMA.................................................................................... E62
ABDOMINAL TRAUMA ................................................................................................... E63 BURNS ........................................................................................................................ E63 CHEST INJURY ............................................................................................................. E64 CRUSH INJURY ............................................................................................................. E65 DROWNING/NEAR DROWNING ....................................................................................... E66 EYE INJURIES .............................................................................................................. E67 FRACTURES ................................................................................................................. E68 HEAD INJURIES ............................................................................................................ E68 HEAT TRAUMA ............................................................................................................. E69 SCUBA ........................................................................................................................ E69 SNAKE BITE ................................................................................................................. E73 SPIDERS ...................................................................................................................... E74 TRAUMATIC BRAIN INJURY (TBI) ................................................................................. E75 WOUND CARE ............................................................................................................. E77
Procedural Guidelines ...................................... P1

AIRWAY MANAGEMENT .......................................................... P2
CAREVENT .................................................................................................................... P2 CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) ........................................................ P2 ESOPHAGEAL TRACHEAL DOUBLE LUMEN AIRWAY (COMBITUBE).................................... P3 CRICOTHYROTOMY ......................................................................................................... P4 ENDOTRACHEAL INTUBATION ........................................................................................... P6 END TIDAL CO2 DETECTOR ......................................................................................... P8 ESOPHAGEAL INTUBATION DETECTOR (EID) ................................................................... P9 ESOPHAGEAL OBTURATOR AIRWAY ................................................................................. P9 LARYNGEAL MASK AIRWAY .......................................................................................... P10 NASOGASTRIC TUBE .................................................................................................... P11 PLEURAL DECOMPRESSION ............................................................................................ P11 PULSE OXIMETRY ......................................................................................................... P12 RETROGRADE INTUBATION ............................................................................................ P13 RUSCH QUICKTRACH ................................................................................................... P14 SUCTION ...................................................................................................................... P15 VENTILATOR ................................................................................................................ P17 AUTOVENT 2000 ......................................................................................................... P17 MINIVENT ................................................................................................................. P17
CARDIAC................................................................................... P18
ALERTS CARDIAC AND STROKE ................................................................................ P18 12 LEAD EKG ........................................................................................................... P18 MARQUETTE RESPONDER 1500 .................................................................................... P19 PHYSIO CONTROL LIFEPAK 10 ..................................................................................... P21 LIFEPAK 12 ................................................................................................................. P24 ZOLL M SERIES .......................................................................................................... P27 ZOLL PD 1400 PACEMAKER/DEFIBRILLATOR ................................................................ P28 PERICARDIOCENTESIS .................................................................................................... P29 TRANSCUTANEOUS PACING ............................................................................................ P30 AUTOMATED EXTERNAL DEFIBRILLATOR ......................................................................... P30
MEDICATION AND FLUID ADMINISTRATION ................. P33

AVAILABLE ROUTES OF ADMINISTRATION ....................................................................... P33 BONE INJECTION GUN (B.I.G.) ...................................................................................... P33 BURETTE ADMINISTRATION SET ..................................................................................... P34 DOUBLE LUMEN IV CATHETER ...................................................................................... P35 DRAWING UP MEDICATIONS .......................................................................................... P35 ENDOTRACHEAL MEDICATION ADMINISTRATION .............................................................. P36 EPI-PEN AUTO INJECTOR ............................................................................................. P36
F.A.S.T. 1 INTRAOSSEOUS INFUSION SYSTEM ............................................................... P37 DRUG HANDLING ......................................................................................................... P39 INFUSAPORTS ............................................................................................................ P40 INFUSION PUMP ........................................................................................................... P41 IVAC 530 .................................................................................................................... P44 IVAC MED SYSTEM 3 ................................................................................................... P45 INTRAMUSCULAR MEDICATION ADMINISTRATION ............................................................. P46 INTRAOSSEOUS INFUSIONS ............................................................................................ P47 INTRAVENOUS CATHETER INSERTION .............................................................................. P47 INTRAVENOUS MEDICATION ADMINISTRATION .................................................................. P48 MUCOSAL ATOMIZATION DEVICE (MAD) ..................................................................... P48 NEEDLESS IV SYSTEMS ................................................................................................ P49 NERVE AGENT AUTO INJECTORS ................................................................................... P50 NITROGLYCERIN IV ...................................................................................................... P50 NITROUS OXIDE ........................................................................................................... P51 PIGGYBACK ................................................................................................................. P52 RECTAL MEDICATION ADMINISTRATION .......................................................................... P52 SALINE LOCK .............................................................................................................. P53 SUBCUTANEOUS MEDICATION ADMINISTRATION ............................................................... P53 UMBILICAL VENOUS CATHETERIZATION .......................................................................... P53
GENERAL ................................................................................. P55

BLOOD ALCOHOL SAMPLING ........................................................................................ P55 BLOOD GLUCOSE LEVEL .............................................................................................. P55 BROSELOW PEDIATRIC EMERGENCY TAPE ...................................................................... P56 COLIN BLOOD PRESSURE MONITOR ............................................................................. P57 CRITICARE 506DX2 VITALCARE VITAL SIGNS MONITOR .............................................. P57 DO NOT RESUSCITATE ORDER (DNRO) ...................................................................... P58 DOPPLER MEDISONIC ................................................................................................... P58 FOLEY CATHETERIZATION .............................................................................................. P58 MORGAN MEDIFLOW LENS ............................................................................... P59 PHLEBOTOMY .............................................................................................................. P59 PROPAQ ...................................................................................................................... P60 RADIO COMMUNICATIONS ............................................................................................. P61 RESPONDER INFLATABLE PEDIATRIC SEAT ...................................................................... P61 SUSPECTED CHILD/OTHER ABUSE .................................................................................. P62 THERMOSCAN THERMOMETER ....................................................................................... P62 TRAUMADEX ............................................................................................................. P62
IMMOBILIZATION .................................................................. P64

AMBU PERFIT ACE ....................................................................................................... P64 CERVICAL IMMOBILIZATION DEVICE (C.I.D.) ................................................................ P64
HALF BACK EXTRICATION/LIFT HARNESS ..................................................................... P64 KENDRICK EXTRICATION DEVICE (KED) ...................................................................... P65 LONG SPINE IMMOBILIZATION ....................................................................................... P66 MILLER BOARD ........................................................................................................... P68 NAJO PEDIAIRALIGN BACKBOARD ........................................................................... P69 RIGID CERVICAL COLLAR ............................................................................................ P69 PATIENT RESTRAINTS ................................................................................................... P70 PEDIATRIC PATIENT IMMOBILIZATION ............................................................................. P71 SPIDERTYPE PATIENT STRAP ....................................................................................... P71 SPLINTING ................................................................................................................... P72 STA-BLOCK HEAD IMMOBILZER .................................................................................... P73
MULTIPLE CASUALTY INCIDENTS .................................... P74

LEVEL 1 RESPONSE ..................................................................................................... P74 LEVEL 2 RESPONSE ..................................................................................................... P74 LEVEL 3 RESPONSE ..................................................................................................... P75 INTERFACILITY TRANSPORTS ......................................................................................... P77 JUMP START PEDIATRIC TRIAGE .................................................................................... P79 SIMPLE TRIAGE AND RAPID TREATMENT (START) ...................................................... P81 TRAUMATIC BRAIN INJURY ........................................................................................... P82
Treatment Guidelines ...................................... M1

GENERAL TREATMENT PRECAUTIONS .............................................................................. M2
MEDICAL .................................................................................. M3
ABDOMINAL PAIN ......................................................................................................... M3 ALLERGIC REACTIONS ................................................................................................... M3 ALTERED LEVEL OF CONSCIOUSNESS .............................................................................. M4 ASTHMA ....................................................................................................................... M5 CHRONIC OBSTRUCTIVE PULMONARY DISEASE ................................................................ M6 DIABETIC EMERGENCIES ................................................................................................ M6 DIALYSIS PROBLEMS ..................................................................................................... M7 HYPERTENSION .............................................................................................................. M7 MEDICAL SHOCK SYNDROMES ....................................................................................... M8 NAUSEA / VOMITING ...................................................................................................... M9 OBSTETRICS/GYNECOLOGY ............................................................................................ M9 PAIN MANAGEMENT .................................................................................................... M10 RAPID SEQUENCE INTUBATION ...................................................................................... M11 SEDATION ................................................................................................................... M13 SEIZURES .................................................................................................................... M14 SICKLE CELL ANEMIA ................................................................................................. M15 STROKE ...................................................................................................................... M15
CARDIAC.................................................................................... C1
ASYSTOLE ..................................................................................................................... C1 BRADYCARDIA ............................................................................................................... C2 CARDIOGENIC SHOCK ..................................................................................................... C3 CARDIOVERSION / DEFIBRILLATION .................................................................................. C3 CHEST PAIN / MYOCARDIAL INFARCTION (SUSPECTED)...................................................... C4 CONGESTIVE HEART FAILURE/PULMONARY EDEMA ........................................................... C5 PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA ............................................................. C6 PULSELESS ELECTRICAL ACTIVITY ................................................................................... C7 VENTRICULAR ECTOPY ................................................................................................... C8 VENTRICULAR FIBRILLATION / PULSELESS VTACH .......................................................... C9 VENTRICULAR TACHYCARDIA ........................................................................................ C10 WIDECOMPLEX TACHYCARDIA OF UNCERTAIN TYPE ...................................................... C11
TRAUMA / ENVIRONMENTAL ................................................ T1

BITES AND STINGS ......................................................................................................... T1 BLACK WIDOW ............................................................................................................. T1 BROWN RECLUSE .......................................................................................................... T1 MARINE INJURIES .......................................................................................................... T1 SNAKE BITE ................................................................................................................... T2 CONTRAINDICATIONS ...................................................................................................... T2 BURNS .......................................................................................................................... T2 CHEST INJURY ............................................................................................................... T3 CRUSH INJURY ............................................................................................................... T3 DROWNING/NEAR DROWNING ......................................................................................... T4 EYE INJURIES ................................................................................................................ T4 FRACTURES ................................................................................................................... T4 HEAD INJURIES .............................................................................................................. T5 HEAT TRAUMA ............................................................................................................... T5 HYPOTHERMIA ............................................................................................................... T5 LOCAL ANESTHESIA ....................................................................................................... T6 SCUBA DIVING INJURIES ................................................................................................. T6
TOXICOLOGY............................................................................. T8
OVERDOSE .................................................................................................................... T8 SPECIFIC TOXICOLOGICAL EMERGENCIES ............................................................................ T8 BENZODIAZEPINE OVERDOSE ........................................................................................... T8 NARCOTIC OVERDOSE .................................................................................................... T9 TRICYCLIC ANTIDEPRESSANT OVERDOSE (TCA) ............................................................... T9 CARBON MONOXIDE .................................................................................................... T10 COCAINE OVERDOSE .................................................................................................... T10
ECSTASY (MCMA) OVERDOSE ................................................................................... T11 GHB (GAMMA HYDROXYBUTYRATE) OVERDOSE ........................................................... T11 TOXIC CHEMICAL EXPOSURE ........................................................................................ T11 INHALED TOXINS ......................................................................................................... T12 ORGANOPHOSPHATE POISONING .................................................................................... T12
Drug Reference ................................................ D1

ACETAMINOPHEN ............................................................................................................ D2 (TYLENOL*, APAP) ..................................................................................................... D2 ACETAMINOPHEN SUPPOSITORIES ..................................................................................... D2 (RECTAL TYLENOL) ....................................................................................................... D2 ACETYLSALICYLIC ACID .................................................................................................. D3 (ASPIRIN, ASA) ............................................................................................................ D3 ADENOSINE .................................................................................................................... D3 (ADENOCARD) ................................................................................................................ D3 ALBUTEROL ................................................................................................................... D4 (PROVENTIL, VENTOLIN) ................................................................................................. D4 AMIODARONE ................................................................................................................. D4 (CORDARONE, PACERONE) .............................................................................................. D4 AMYL NITRATE .............................................................................................................. D5 ATROPINE SULFATE ......................................................................................................... D5 (AS A CARDIAC AGENT) ................................................................................................. D5 ATROPINE SULFATE ......................................................................................................... D6 (AS AN ANTIDOTE FOR POISONINGS) ............................................................................... D6 CALCIUM CHLORIDE ....................................................................................................... D6 CALCIUM GLUCONATE .................................................................................................... D7 (TAGAMET) ................................................................................................................... D7 DEXAMETHASONE ........................................................................................................... D8 (DECADRON) ................................................................................................................. D8 DIAZEPAM ..................................................................................................................... D8 (VALIUM) ...................................................................................................................... D8 DILTIAZEM ..................................................................................................................... D9 (CARDIZEM) .................................................................................................................. D9 DIPHENHYDRAMINE ......................................................................................................... D9 (BENADRYL) .................................................................................................................. D9 DOBUTAMINE ............................................................................................................... D10 (DOBUTREX) ................................................................................................................ D10 DOLASETRON MESYLATE .............................................................................................. D10 (ANZEMET) .................................................................................................................. D10 DOPAMINE ................................................................................................................... D11 (INTROPIN) .................................................................................................................. D11
EPINEPHRINE ................................................................................................................ D11 (1:1000) .................................................................................................................... D11 EPINEPHRINE ................................................................................................................ D12 (1:10,000) ................................................................................................................. D12 ETOMIDATE ................................................................................................................. D12 (AMIDATE, HYPNOMIDATE) ............................................................................................ D12 FLUMAZENIL ................................................................................................................ D13 (ROMAZICON) .............................................................................................................. D13 FUROSEMIDE ................................................................................................................ D13 (LASIX) ....................................................................................................................... D13 GLUCAGON .................................................................................................................. D14 (GLUCAGON) ............................................................................................................... D14 GLUCOSE 50% ........................................................................................................... D14 (DEXTROSE 50%) ....................................................................................................... D14 GLUCOSE ORAL .......................................................................................................... D15 (GLUTOSE) .................................................................................................................. D15 HEPARIN ...................................................................................................................... D15 HYDROMORPHONE HCL .............................................................................................. D16 (DILAUDID) .................................................................................................................. D16 IPRATROPIUM ............................................................................................................... D16 (ATROVENT) ................................................................................................................ D16 KETOROLAC ................................................................................................................ D17 (TORADOL) ................................................................................................................. D17 LABETALOL ................................................................................................................. D17 (NORMYDYNE, TRANDATE) ............................................................................................ D17 LIDOCAINE HCL ......................................................................................................... D18 (XYLOCAINE) ............................................................................................................... D18 LIDOCAINE HCL 2% WITH ......................................................................................... D18 EPINEPHRINE 1:100,000 ............................................................................................. D18 LIDOCAINE HCL TOPICAL ........................................................................................... D19 (XYLOCAINE 2% JELLY) .............................................................................................. D19 LORAZEPAM ................................................................................................................. D19 (ATIVAN) ..................................................................................................................... D19 MAGNESIUM SULFATE ................................................................................................... D20 MEHTYLPREDNISOLONE ................................................................................................. D20 (SOLU-MEDROL) ......................................................................................................... D20 MIDAZOLAM ................................................................................................................ D21 (VERSED) .................................................................................................................... D21 MORPHINE SULFATE ..................................................................................................... D21 (MS) ......................................................................................................................... D21
NALBUPHINE ................................................................................................................ D22 (NUBAIN) .................................................................................................................... D22 NALOZONE .................................................................................................................. D22 (NARCAN) ................................................................................................................... D22 NITROGLYCERINE IV .................................................................................................... D23 (TRIDIL)...................................................................................................................... D23 NITROGLYCERINE SL .................................................................................................... D23 (NITROLINGUAL) (NITROBID) (NITROSTAT) .................................................................. D23 NITROGLYCERINE TOPICAL ............................................................................................ D24 (NITRO-BID) ............................................................................................................... D24 NITROPRUSSIDE ........................................................................................................... D24 (NIPRIDE) .................................................................................................................... D24 NITROUS OXIDE ........................................................................................................... D25 (NITRONOX) ................................................................................................................ D25 OXYTOCIN ................................................................................................................... D25 (PITOCIN) .................................................................................................................... D25 PROCAINAMIDE ............................................................................................................ D26 (PRONESTYL) ............................................................................................................... D26 PROMETHAZINE ............................................................................................................ D26 (PHENERGAN) .............................................................................................................. D26 PROPOFOL .................................................................................................................. D27 (DIPRIVAN) .................................................................................................................. D27 SODIUM BICARBONATE ................................................................................................. D27 SUCCINYLCHOLINE CHLORIDE ........................................................................................ D28 (ANECTINE, QUELICIN) .................................................................................................. D28 TETRACAINE HCL....................................................................................................... D28 (PRONTOCAINE) ........................................................................................................... D28 THIAMINE .................................................................................................................... D29 (VITAMIN B-1) ............................................................................................................ D29 VASOPRESSIN .............................................................................................................. D29 (PITRESSIN) ................................................................................................................. D29 VECURONIUM BROMIDE ................................................................................................. D30 (NORCURON) ............................................................................................................... D30 VERAPAMIL .................................................................................................................. D30 (ISOPTIN OR CALAN) ................................................................................................... D30
Aeromedical...................................................... A1
EDUCATIONAL SECTION .................................................................................................. A2 THE HISTORY OF AEROMEDICAL TRANSPORT ................................................................... A2 AEROMEDICAL PROGRAM OPERATION .............................................................................. A3 AIR TRANSPORT GENERAL INFORMATION ........................................................................ A5
Haz-Mat Guidelines ......................................... H1

HAZARDOUS MATERIALS MEDICAL MANAGEMENT TREATMENT GUIDELINES ........................ H2
Appendix A ..................................................... AA1

ACLS QUICKIE ......................................................................................................... AA1
Appendix B ..................................................... AB1

GUIDE TO THE HOSPITALS IN THE OPERATING REGION ................................................... AB1
Appendix C ..................................................... AC1

TRAUMA TRANSPORT PROTOCOLS ............................................................................... AC1
Appendix D ..................................................... AD1

APGAR, RULE OF NINES, AND WONG-BAKER PAIN SCALE ....................................... AD1
Appendix E ..................................................... AE1

PREHISPITAL FIBRINOLYTIC CHECKLIST ......................................................................... AE1 CINCINATTI STROKE SCALE .......................................................................................... AE2
Appendix F ..................................................... AF1

HELICOPTER ACTIVATION CRITERIA ...............................................................................AF1
Appendix G .....................................................AG1
TASER INJURIES ...................................................................................................AG1
EDUCATIONAL GUIDELINES
Educational Guidelines
The following section entitled Educational Guidelines focuses on pharmacological and emergent procedures specific to each protocol. This new section is intended to provide a detailed explaination of the thought processes behind each treatment modality. Protocols 2005 is an extremely aggressive approach to prehospital emergency medicine. Clinicians priviledged to work within the scope of this protocol now have the opportunity for greater understanding of its content.
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INTRODUCTION
Monitor ECG: As a paramedic, one of your most important skills will be to obtain and interpret ECG rhythm strips. Subsequent treatment received by your patient will be based upon a rapid, accurate interpretation. IV: In the prehospital setting, intravenous therapy is geared toward electrolyte or fluid replacement, and for the introduction of medications directly into the vascular space. Three of the most commonly used solutions in prehospital care are lactated ringers solution, 0.9% sodium chloride (normal saline), and 5% dextrose in water (D5W). Lactated Ringers is an isotonic electrolyte solution of sodium chloride, potassium chloride, calcium chloride, and sodium lactate in water. Normal Saline is an electrolyte solution of sodium chloride in water. It is isotonic with the extracellular fluid. D5W is a hypotonic glucose solution used to keep a vein open and to supply calories necessary for cellular metabolism. While it will have an initial effect of increasing the circulatory volume, glucose molecules rapidly diffuse across the vascular membrane with a resultant free water increase. Both lactated ringers solution and normal saline are used for fluid replacement, because their administration causes an immediate expansion of the circulatory volume. However, due to movement of the electrolytes and water, twothirds of either of these solutions is lost to the interstitial space within one hour. Transport: Patients who are transported under the direction of an emergency medical service system should be taken whenever possible to the closest appropriate medical facility. The medical control physician should be the authority to designate that facility, based on the needs of the patient and the availability of services. In some cases, the patients need for special services trauma, burn, pediatric, etc. means designating a facility that is not nearby. At other times, the closest facility will be designated for stabilization of the patient while transfer is arranged. The ultimate authority for this decision, however, remains with the online medical control physician.
PATIENT PRIORITIZATION
PRIORITY ONEHIGHEST PRIORITY (IMMEDIATE/CRITICAL)
Critical conditions are those which require immediate intervention involving the following: 1. Airway, Breathing, Circulation 2. Respiratory Arrest 3. Cardiac Arrest (Trauma or Medical) 4. Massive Exsanguinating Hemorrhage 5. Open Chest or Abdominal Wounds 6. Cervical Spine and/or Severe Head Injuries
PRIORITY TWOSERIOUS (SECONDARY)

Serious conditions are potentially lifethreatening or disabling problems which, if left untreated, may result in a fatality or permanent disability. Serious conditions which need prompt attention may include: 1. Disturbances of consciousness 2. Respiratory distress 3. Cardiac dysrhythmias with diminished, rapid or irregular pulses 4.Chest pain or Abdominal pain (Medical or Trauma) 5. Active hemorrhage 6. Toxic Drug Overdose or Poisoning 7. Active seizure activity 8. Deforming injuries such as: Burns, Penetrating injuries, Fractures or other trauma 9. Cardiac or Stroke Alerts
PRIORITY THREEMINOR OR STABLE CONDITION

Conditions considered minor are those which need attention but any delay in treatment will not result in immediate harm or permanent injury to the patient Minor conditions may include: 1. Minor Fractures 2. Minor Lacerations 3. Minor Contusions 4. Falls Without Trauma 5. Minor Burns REMEMBER: A patients condition is always subject to change and may occur rapidly. Continuously monitor your patient and report appropriate information to the emergency department. Your patients condition should be the primary assessment tool in determining the priority category. MCI Triage Priorities: Please refer to the START programs field operation guidelines
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commonly seen with a ruptured aneurysm. In an obese abdomen, an AAA is even more difficult to palpate. Even in 25% of patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery. The clinician need not be afraid of properly palpating the abdomen because no evidence exists that aortic rupture can be precipitated by this maneuver. Establishing diagnosis in the field is usually difficult or impossible, but certain features of aortic aneurysm or dissection may be observed. Prehospital care should consist of assuring airway management, vigorous fluid resuscitation as indicated and obtaining useful information concerning history in order to expedite treatment on ED arrival. The prognosis is guarded in patients who suffer rupture prehospital. More than 50% do not survive to the ED; of those who do, survival rate drops by about 1% per minute. However, survival rate is good in the subset of patients who are not in severe shock and who receive timely, expert surgical intervention.
GENERAL MEDICAL ABDOMINAL AORTIC ANEURYSMS

Abdominal aortic aneurysm (AAA) is a relatively common, potentially lifethreatening condition. Ruptured AAA is the 13thleading cause of death in the US. It has a wide spectrum of presentations and should be considered in the differential diagnosis for a number of symptoms. AAA is usually the result of degeneration in the media of the arterial wall, resulting in a slow and continuous dilatation of the lumen of the vessel. Rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. Most occur in association with advanced atherosclerosis. The 3 layers comprising the normal aorta are the intima, media, and adventitia. Structural and elastic properties of major arteries are most imparted by the media, which is composed of smooth muscle cells surrounded by elastin, collagen, and proteoglycans. AAA develops following degeneration of the media due to atherosclerotic changes. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity. AAAs are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time prior to rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis. Expanding AAA causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, and pain may be a less significant symptom to the patient. Patients with a ruptured AAA may present in frank shock as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital. Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease. A history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension often is elicited. It is important to note progressive symptoms, as these should alert the clinician to the possibility of expansion with imminent rupture. Presence of a pulsatile abdominal mass is virtually diagnostic but is found in less than half of the cases. It is more
ABDOMINAL PAIN
Abdominal pain is a complex, differential diagnosis and is not appropriate to prolonged evaluation in the field. Prompt, gentle transport is indicated. The Team should consider the possible etiologies of the pain: abdominal aneurysm in the elderly, ectopic pregnancy, mesenteric embolism or thrombosis, ovarian cyst, intestinal obstruction perforated ulcer, recent trauma, spleen injury, gallbladder, distended bowel, cardiac pain in epigastrium, signs of hemorrhage. Use of pain medication is discouraged without physician consult. A prolonged transport time may be an appropriate reason for request of pain medication and/or a nasogastric tube. A 12-lead EKG is indicated for epigastric pain without evidence of gastrointestinal bleeding. Textbook descriptions of abdominal pain have severe limitations, because each individual reacts differently. Infants and children may be unable to localize their discomfort and they have many diseases not seen in adults. Obese or elderly patients tend to tolerate pain better than others, but find it difficult to localize the pain. On the other hand, hysterical patients tend to exaggerate symptoms. During physical examination, the important surgical emergencies with pain as their outstanding symptom to keep in mind are appendicitis, perforated peptic ulcer, intestinal obstruction, general peritonitis from an unknown cause, perforated diverticulitis, twisted ovarian cyst, ectopic pregnancy, a leaking abdominal aneurysm, and mesenteric embolism or thrombosis. Urgent, rather than emergency care, is the rule for most patients with biliary tract disease, pancreatitis, or renal stone. E-3
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Diagnosis and therapy of a patient with severe abdominal pain must proceed simultaneously. The cause is established by history and physical examination. The history must be detailed, and in many cases it will be sufficient to make the proper diagnosis. Certain questions are always important. Is the pain acute or chronic? Chronic complaints may be entirely functional or demand a long, careful diagnostic study. However, mild chronic discomfort localized to one area may point to an involved viscus that now is subject to a serious complication (i.e., perforated duodenal ulcer, perforated diverticulitis). Recurrent attacks of severe colic suggest the possibility of gallstones, kidney stones, or recurrent attacks of mild intestinal obstruction from a benign tumor (i.e., carcinoid). Was the onset sudden? What was the patient doing when the pain started? A sudden pain severe enough to cause fainting suggests a perforated ulcer, acute pancreatitis, or ruptured aneurysm. Similar symptoms in a woman of childbearing age may be due to a ruptured ectopic pregnancy. Symptoms of intestinal obstruction usually have a less dramatic onset; crampy pains followed by severe steady pain may mark the onset of strangulation. How long did the attack last? If the pain stopped before the physical examination, biliary or renal colic is likely. However, a perforated peptic ulcer produces severe pain at the outset, which later appears to subside but again increases in severity as peritonitis is established. How severe is the pain? This is a very important guide to the importance of the complaint; severe pain may herald serious diseases (i.e., free perforation of a viscus into the peritoneal cavity or rupture of an aortic aneurysm) or be more severe than seems warranted by the physical findings (i.e., mesenteric arterial or venous thrombosis, or embolism). Where is the pain? Location is a very important guide to the involved viscus. Epigastric pain associated with stomach, duodenum, intestine, gallbladder, or pancreas; usually with appendicitis it is the initial site of pain before the pain shifts to the right lower quadrant. Renal pain is felt over the corresponding kidney, and testicular torsion in the affected testicle. Does the pain radiate? Radiation often occurs along the distribution of the nerves of the same spinal segment (referred pain). Gallbladder pain often is felt beneath the right scapula. Left diaphragmatic irritation from blood or pus (due to a ruptured spleen or pancreatitis) can be felt in the region of the left shoulder. Renal pain radiates to the region of the pubis or vagina. In an older man, severe pain beginning in the mid back and rapidly spreading to the abdomen is characteristic of a ruptured aortic aneurysm. How is the pain described? A severe, knifelike pain, esE-4 2/15/06 pecially if it is associated with shock, indicates an emergency. Tearing pain is characteristic of a dissecting aneurysm. Appendicitis often is described as an ache. What gives the patient relief? If there have been previous attacks of somewhat similar pains, some measures may have been found to relieve it; i.e., relief by antacids suggests peptic ulcer disease. During the acute attack, if the patient attempts to relieve the pain by walking the floor, biliary colic is more likely; with peritonitis he will want to lie as quietly as possible. Are other symptoms associated with the pain? Symptoms that occurred immediately before the onset of the pain or in association with it are important. Vomiting is one of the most important. When it precedes pain and especially if it is followed shortly by diarrhea, gastroenteritis is the probable diagnosis. Vomiting results from either of 3 mechanisms: (1) severe irritation of local peritoneum or mesentery; (2) obstruction of a muscular tube (i.e., bile duct, intestine, or ureter); or (3) absorbed toxin or drug stimulation of CNS centers controlling the vomiting reflex. Severe vomiting that precedes an intense epigastric, left chest, or shoulder pain suggests an emetic perforation of the intraabdominal esophagus. Vomiting usually occurs only 1 or 2 times/hour after the onset of pain with appendicitis. In patients with acute intestinal obstruction, the lower the site of the obstruction, the more delayed is the vomiting. Shock, pallor, sweating, or fainting can also accompany abdominal pain and furnish a rough guide to the severity of the pathologic process. Past history of preceding symptoms may help localize the site of the present problem. Previous symptoms of ulcer disease, gallstone colic, or diverticular disease are especially helpful. A history of either esophageal reflux, diarrhea, constipation, jaundice, melena, hematuria, hematemesis, weight loss, mucus, or blood in the stool can help establish a diagnosis. Drug history should include details concerning drugs, both therapeutic and addictive. Some drugs (i.e., K tablets, aspirin) are highly irritating to the intestine and may lead to perforations and peritonitis. Prednisone or immunosuppressives increase the chances of perforation of some portion of the gastrointestinal tract with relatively little response in the nature of pain or leukocytosis. Anticoagulants can increase the chances of bleeding. Family history of certain diseases (i.e., gallstones) may be helpful. If the symptoms include pain, vomiting, diarrhea, and other family members have just recovered from similar attacks, gastroenteritis is a probable cause. Abdominal pain in neonates, infants, and children has numerous causes not encountered in adults. They include meconium peritonitis, intestinal obstruction from atresia, stenosis,
web, volvulus of a gut with a common mesentery, imperforate anus, enterocolitis, and others. Abdominal pain in women varies greatly in intensity. Dysmenorrhea may be trivial or disabling. Endometriosis is a common cause of pain. It often can be controlled by hormones but in other cases may require operation. An ectopic pregnancy is lifethreatening without emergency laparotomy. Intrauterine contraceptive devices may migrate into the peritoneal cavity and produce peritonitis and intestinal obstruction. The most troublesome problem that occurs in young women is pelvic inflammatory disease. Preferably it is treated with antibiotics. Tuboovarian abscesses require surgical treatment. In some instances symptoms are confined to the right lower quadrant so that there is great difficulty in determining whether the patient has pelvic inflammatory disease or appendicitis. The general physical examination must not be neglected. Blood pressure, pulse, level of consciousness, and degree of shock must be evaluated in severe cases. The center of attraction, of course, is the abdomen. Peristalsis is extremely important. Active peristalsis of normal pitch suggest a nonsurgical disease (i.e., gastroenteritis). High pitched peristalsis or borborygmi (bubbling in the bowels) in rushes suggest intestinal obstruction. Severe pain combined with an absolutely silent abdomen is an indication for immediate exploration. Tenderness, rebound tenderness, degree of distention and palpable masses are important. Particular attention should be paid to operative scars, which suggest the possibility of adhesions and intestinal obstruction, and to orifices that could be the site of external hernias. Jaundice or evidence of bleeding in subcutaneous tissues is another diagnostic sign that may be present (i.e., retroperitoneal bleeding from hemorrhagic pancreatitis or a bluish discoloration or frank ecchymosis of the costovertebral angles [Grey Turners sign} or around the umbilicus [Cullens sign}). Some relatively common diseases must be considered in the diffential diagnosis of acute abdominal pain. (1) Gastroenteritis: symptoms of colicky pain, nausea, vomiting and diarrhea may be accompanied by mild abdominal tenderness, but the tenderness never becomes localized and the disease is selflimited. Gastroenteritis is likely if family members or associates have had recent similar complaints. (2) Inflammatory bowel disease: Crohns disease can mimic acute appendicitis, and diverticulitis can produce a similar syndrome (usually in the left lower quadrant). (3) Herpes zoster: at times severe pain precedes the typical rash; this can be confusing, particularly if the nerves in the right lower quadrant are involved in a patient whose appendix has not been removed. (4) Pneumonia can lead to diffuse abdominal pain, but there is no localized abdominal tenderness. (5) Acute myocardial infarction may be accompanied by diffuse abdominal pain. (6) Drug addicts may have severe colicky pains that suggest intestinal obstruction. (7) Anticoagulants or severe coughing can lead to a hematoma of the abdominal wall or rupture of the deep epigastric artery or vein, events that are associated with local pain and tenderness. (8) Sickle cell disease may be associated with attacks of severe abdominal pain. (9) Spinal or central nervous system disease can produce pain referred to the abdomen. The most common cause is radiculitis; this pain usually is chronic rather than acute. In the past, tabetic crises were a common cause of attacks of severe abdominal pain. (10) Patients with psychogenic somatoform disorders often complain of severe attacks of abdominal pain for which no organic cause can be found. Unless the patient has a peptic ulcer, complaints of burning pains are likely to remain unexplained. (11) Typhoid fever may; be accompanied by right lower pain. If rose spots are present, this disease must be considered.
RATIONALE
The abdominal cavity is the largest cavity in the body. Abdominal pain is one of the most difficult problems in the pre-hospital setting to diagnose and treat. You will usually not be able to determine the cause in the field. Your primary goal in dealing with a patient suffering an abdominal emergency consists of detection and stabilization. This patient can deteriorate rapidly. Therefore, constant reassessment and subsequent management are appropriate. IV 0.9% Normal Saline IV access is routinely established at a KVO rate. The patient who exhibits active hemorrhage (upper or lower GI bleed, bloody stools, vomiting blood) or showing signs of impeding shock (postural hypotension) will require fluid resuscitation. This access allows for immediate delivery as needed. * Current research indicates the future of EMS leaning toward the use of a much higher concentration of normal saline as well as medications that allow for oxyhemoglobin enhancement. Nitrous Oxide (Nitronox) Analgesic gas. Use of this pain medication is preferred in abdominal pain because it provides rapid relief and is easily reversible. however, patients who present with severe abdominal pain, absent bowel sounds, and distention should not receive nitrous oxide. This medication can concentrate in pockets of obstructed bowel and possibly lead to rupture. Promethazine (Phenergan) Antiemetic/Analgesic. Phenergan may be administered for prolonged, uncontrolled vomiting. The sedative and analgesic properties of this medication may make diagnosis of abdominal pain difficult once the patient arrives at the emergency room, so its administration is given sparingly. Nasogastric Tube Insertion Is indicated for the decompression of gastric distention and poisoning or overdose cases E-5
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when transport will be lengthy or delayed. The specific homeostatic function of histamine remains unclear. Its actions, which in man are exerted primarily on the cardiovascular system, extravascular smooth muscle, and exocrine glands, appear to be mediated by two distinct receptors termed H1 and H2. In the cardiovascular system, histamine is a potent arteriol dilator that can cause extensive peripheral pooling of blood and hypotension. It also increases capillary permeability by distortion of the endothelial lining of the postcapillary venules, with widening of the gap between endothelial cells and exposure of basement membrane surfaces. This accelerates loss of plasma and plasma proteins from the vascular space and, combined with arteriolar and capillary dilation, can produce circulatory shock. Histamine also dilates cerebral vessels, which may be a factor in histamine headache. The triple response is mediated by local intracutaneous histamine release, causing (1) local erythema from vasodilation, (2) wheal due to local edema from increased capillary permeability, and (3) flare from a neuronal reflex mechanism producing a surrounding area of arteriolar vasodilation. Other smooth muscle: In man, histamine may cause severe bronchoconstriction in susceptible individuals. Histamine also stimulates gastrointestinal motility. Exocrine glands: Histamine increases salivary and bronchial gland secretions. Endocrine gland: Stimulation of catecholamine release from adrenal chromaffin cells also appears to be H1receptormediated. Sensory nerve endings: Local instillation of histamine may produce intense itching. Histamine H1 receptor antagonists (H1 blockers): The conventional antihistamines possess a substituted ethylamine sidechain (similar to that of histamine) linked to one or more cyclic groups. The similarity between the ethylamine moiety of histamine and the substituted ethylamine structure of the H1 blockers suggests that this molecular configuration is important in receptor interactions. H1 blockers appear to act by competitive inhibition; they do not significantly alter histamine production or metabolism. The H1 blockers, given orally or rectally, are usually well absorbed from the gastrointestinal tract. Onset action usually occurs within 15 to 30 minutes, with peak effects attained in 1 hour; duration of action is usually 3 to 6 hours, but some blockers act considerably longer. Antihistaminic effects of H1 blockers are noted only in the presence of increased histamine activity. They block the effects of histamine on GI tract smooth muscle, but in man the allergic reaction of the bronchial smooth muscle is not dependent primarily on histamine release and does not respond effectively to antihistamines alone. H1 blockers effectively block histamineinduced increased capillary permeability and sensory nerve stimulation, thus inhibiting the wheal, flare, pruritus, sneezing, and mucous secretion responses. However,
ALLERGIC REACTION
Much more common than anaphylactic reaction, this distressing condition responds well to immediate field treatment by the Team. Early treatment is important, and multiple drug therapies is preferred. The Team should be prepared to treat the following: multiple cardiac arrythmias, airway obstruction, marked hypertension, impending anaphylaxis. Signs and symptoms include: localized redness and swelling, urticaria (hives), tachycardia, itching, sneezing, mild wheezing, mild agitation. Review of the symptoms, their relation to the environment and to the seasonal and situational variations, their clinical course, and the family history of similar problems should yield sufficient information to classify the disease as atopic. The history is more valuable than tests in determining whether a patient is allergic, and it is inappropriate to subject the patient to extensive skin testing unless reasonable clinical evidence exists for atopy. Age of onset may be an important clue (i.e., childhood asthma is more likely to be allergic than asthma beginning after age 30). Also indicative are seasonal symptoms (i.e., correlating with specific pollen seasons), or those that appear after exposure to animals, hay, or dust, or those that develop in specific environments (i.e., at home, at work). For advising the patient, it is also helpful to investigate the effects of nonspecific contributory factors (i.e., tobacco smoke and other pollutants, cold air, exercise, alcoholic beverages, certain drugs, and life stresses). Symptomatic relief with drugs should not be neglected while the patient is being evaluated and specific control or treatment is being developed. In general, early use of glucocorticoids is appropriate for potentially disabling conditions that are selflimited and/or relatively short duration (seasonal flares of asthma; serum sickness; infiltrative lung disease; severe contact dermatitis), and prudent glucocorticoid use may be necessary when other measures are insufficient to manage chronic conditions. Histamine is widely distributed in mammalian tissue. In man, the highest concentrations are in skin, lungs, and gastrointestinal mucosa. Histamine is present mainly in the intracellular granules of mast cells, but there is also an important extramastcell pool in the gastric mucosa, with smaller amounts in the brain, heart, and other organs. The release of histamine from the mastcell storage granules can be triggered by physical tissue disruption, various chemicals (including tissue irritants, surface active agents, and polymers), and most prominently by antigenantibody interactions. E-6
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theses agents are only partially effective in reversing histamineinduced vasodilation and hypotension. In addition to blocking the effects of histamine, many antihistamines have other therapeutic uses. Pharmacologic differences among them are most apparent in their sedative, antiemetic, and other CNS effects, and in their anticholinergic, antiserotonin, and local anesthetic properties. mation (the extensive network of nuclei and interconnecting fibers found throughout much of the diencephalon, midbrain, pons, and medulla). Impaired consciousness may be brief or prolonged, mild or profound. Brief unconsciousness occurs with syncope; with a convulsive seizure, unconsciousness may last somewhat longer; and in concussion, up to 24 hours. Prolonged unconsciousness usually results from severe intracranial or metabolic disorders. Obtundation, reduced alertness, is usually combined with hypersomnia. Stupor is unresponsiveness from which the patient can be aroused only briefly and by vigorous, repeated stimulation. Coma is unarousable unresponsiveness; in deep coma, even primitive avoidance reflexes may be absent. Hypersomnia (excessively long or deep sleep from which the patient can be awakened only by energetic stimulation) and delirium and confusional states also are states of impaired consciousness. A clouded or depressed state of consciousness implies dysfunction of the cerebral hemispheres, the upper brainstem, or both. Initially, focal lesions in supratentorial structures may extensively damage both hemispheres or may produce so much swelling that the hemispheres compress the diencephalic activating system and midbrain, causing brainstem damage. Primary subtentorial (brainstem or cerebellar) lesions may compress or directly damage the reticular activating system anywhere between the level of the midpons and (by upward pressure) the diencephalon. Metabolic or infectious diseases may depress hemispheric and brainstem function by a change in blood composition or a direct toxic effect. Impaired consciousness may also be due to reduced blood flow (as in syncope or infarction) or a change in electrical activity (as in epilepsy). Either inadequate blood flow or a chemical change may alter the electrical activity. Concussion and psychologic disturbances impair consciousness without detectable structural changes in the brain. The cause of unconsciousness often is not immediately evident, and diagnosis requires an orderly approach. The airway must be patent and blood pressure supported before a detailed history or examination is undertaken. The patient may be wearing a tag or carrying a diagnostic card in his wallet. Observers or relatives should be questioned about the mode of onset or injury; ingestion of drugs, alcohol, or other toxic substances; infections, convulsions, headache, and previous illnesses (i.e., diabetes mellitus, nephritis, heart disease, hypertension). Police can help to find relatives or associates. Containers suspected of having held food, alcohol, drugs, or poisons should be examined and saved (for chemical analysis and possible legal evidence). Signs of hemorrhage, incontinence, and cranial trauma should be sought. The patient's age may be significant: epilepsy and systemic infection are frequently responsible in those less than 40 years; cardiovascular disease (especially stroke), metabolic disorders (diabetes E-7
ALTERED LEVEL OF CONSCIOUSNESS/ ALCOHOLISM

Altered level of consciousness may occur from many sources. Look for data in the patients personal effects such as: medical alert tags, wallet, purse or pill containers. The patients family or friends may provide a history. Specific questions about abnormal motor movement, food or drug ingestion, trauma and underlying diseases should be asked. Altered level of consciousness includes patients with decreased level of consciousness as well as an increased response such as the violent or irrational patient. The Glascow Coma Scale is used to help determine a decrease in level of consciousness.
Glascow Coma Scale

Infant 4 3 2 1 Eye Opening spontaneously to speech to pain no response Best Verbal Response coos,babbles obeys commands irritable cries confused cries to pain inapprop. words moans,grunts incomprehensible no response no response Best Motor Response spontaneous obeys commands localizes pain localizes pain withdraws withdraws flexion flexion extension extension no response no response Child/Adult 4 3 2 1
5 4 3 2 1 6 5 4 3 2 1
5 4 3 2 1 6 5 4 3 2 1
The alert state with normal mentation requires an intact interaction between the cognitive functions of the cerebral hemispheres and the arousal mechanisms of the reticular for-
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mellitus, hypoglycemia), and uremia are more common after 40. Physical examination should note (1) temperature; (2) skin: color, evidence of trauma or hypodermic injections (narcotics, insulin), rashes, petechiae; (3) scalp: contusions or lacerations; (4) eyes: pupil size and reaction to light, ocular palsy, corneal reflex, oculocephalic reflex (dolls eye response to head rotation), fundic signs of papilledema, vascular sclerosis, or diabetic or uremic retinitis; (5) ENT: escape of CSF or blood, scarred or bitten tongue, breath odor (alcohol, acetone, paraldehyde, bitter almonds [cyanide]); (6) respiratory pattern: hyperventilation; CheyneStokes (periodic) breathing; (7) cardiovascular signs: apical rate and rhythm, character of the pulse, blood pressure in both arms, signs of cardiac decompensation, sclerosis in peripheral vessels, cyanosis or clubbing of the fingers and toes; (8) abdomen: spasm, rigidity; (9) neurologic signs: paresis, stiff neck, reflexes, muscular twitching, convulsions. The neurologic appraisal provides the key to whether the disease is supratentorial, subtentorial, or metabolic. Breathing is CheyneStokes (periodic) with hemispheric disease and irregularly irregular with pontomedullary disease; hyperor hypoventilation occurs with metabolic disease. The pupils are small and reactive to light with hypothalamic and pontine disease or narcotic poisoning, fixed in midposition with midbrain damage or severe glutethimide overdosage, lightreactive with metabolic disorders, dilated with anoxia or 3rd nerve compression, and normally reactive with hemispheric disease or psychogenic unresponsiveness. Characteristically in supratentorial mass lesions causing stupor or coma, neurologic signs and symptoms first indicate involvement of one cerebral hemisphere. Then, because of enlargement of the mass and consequent shifts in brain tissues as a result of pressure changes, signs show progressive rostralcaudal deterioration indicating involvement first of the diencephalon and finally of the brainstem. With unconsciousness from a primary brainstem lesion, pupillary and oculomotor signs are abnormal from the start. The WernickeKorsakoff syndrome refers to the coexistence of Wernicke's encephalopathy and Korsakoff's psychosis. Acute Wernicke's encephalopathy results from a failure to ingest thiamine. Continued carbohydrate ingestion gradually exhausts thiamine stores in critical areas of the thalamus and brainstem reticular formation. The most common precipitating condition is severe alcoholism, but vitaminfree fluid intake over a period of several days or weeks (i.e., as can occur in dialysis patients, during oversights in postoperative care, or in women with hyperemesis gravidarum) can produce a similar deficiency. The result causes acute abnormalities in the dorsal and medial thalamic nuclei, the mammillary bodies and the dorsal gray matter of the brainstem, including the oculomotor, vestibular, and other cranial nerve nuclei. Symptoms and signs: Acutely ill patients develop nystagmus or partial ophthalE-8 moplegia and may become ataxic, confused, drowsy, or stuporous. Confusion may be global or of the type characteristic of Korsakoff's psychosis (see below). In addition to the partial ophthalmoplegia, clinical defects often appear in other cranial nerve functions. Severe cases show a striking elevation of peripheral pain threshold, and many develop a severe, sometimes fatal degree of autonomic insufficiency. Autonomic dysfunction may appear either in the form of sympathetic hyperactivity (i.e., delirium tremens) or hypoactivity (hypothermia, postural hypotension, and syncope). Thiamine reverses these defects. Most cases of Wernicke's encephalopathy have manifestations of nutritional deficiencies affecting other parts of the body as well. Acute Wernicke's disease is underdiagnosed and can be fatal; fully developed cases should be treated as emergencies in the hospital under close supervision. Even suspected or borderline cases should receive parenteral thiamine. Treatment consists of immediately giving 50 to 100 mg thiamine IV before administering glucosecontaining fluids. This should be followed by rehydration to restore blood volume, correction of electrolyte abnormalities, and initiation of general nutritional therapy including multivitamins. Delirium tremens often supervenes within a few days after beginning corrective treatment and abstinence from alcohol.
ANAPHYLAXIS
The phrase anaphylaxis was first coined in 1902 when a second dose of sea anemone toxin caused a dogs death. The response was the opposite of prophylaxis and this was referred to as anaphylaxis, meaning without protection. Anaphylaxis is a systemic, acute reaction caused by the release of mediators from mast cells and basophiles. More than one organ system should be involved for the reaction to be considered anaphylaxis. The most common organs involved include the cutaneous, respiratory, cardiovascular, and gastrointestinal. The term anaphylactic reaction usually refers to a type l hypersensitivity reaction with mast cell degranulation mediated by antigen binding of specific immunoglobulin E (lgE). The term anaphylaxis refers to the physiologic events that follow, due to this mechanism. A sensitizing antigen elicits an lgE antibody response in a susceptible individual. The antigenspecific lgE antibodies then bind to mast cells and basophiles. Subsequent exposure to the sensitizing antigen causes crosslinking of cell-bound lgE, resulting in mast cell (and/or basophile) degranulation. Typical examples of lgE-mediated anaphylaxis include the reactions to many drugs, insect stings, and foods. When mast cells and basophiles degranulate, histamine and newly generated leukotrienes and prostaglandins are released. The physiologic responses to these mediators include smooth muscle spasm in the bronchi and gastrointestinal tract, vasodi-
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lation, increased vascular permeability, and stimulation of sensory nerve endings. These physiologic events lead to the classic symptoms of anaphylaxis, including flushing, urticaria, pruritus, bronchospasm, and abdominal cramping with nausea, vomiting, and diarrhea. Hypotension and shock can result from intravascular volume loss, vasodilation, and myocardial dysfunction. Increased permeability can result in a shift of 50% of vascular volume to the extravascular space in a matter of minutes. Anaphylaxis is a clinical diagnosis, based on a history of acute exposure to a causative agent followed by the typical systemic manifestations. Patients often initially describe a sense of impending doom, accompanied by pruritus and flushing. This can evolve rapidly into the following symptoms, broken down by organ system: Cutaneous/ocular - urticaria, angioedema, flushing, conjunctiva pruritus, and swelling. Respiratory - nasal congestion, rhinorrhea, throat tightness, shortness of breath, cough, hoarseness. Cardiovascular - dizziness, weakness, syncope, chest pain, palpitations, hypotension. Gastrointestinal - nausea, vomiting, diarrhea, abdominal distention, cramps. Neurologic - headache and seizure (very rare). Symptoms usually begin within 5-30 minutes from the time the antigen is injected. The source of the antigen should be removed whenever possible. (e.g., stinger after bee sting). When the antigen is ingested, symptoms usually occur within 2 hours, though symptoms often can occur much faster, as with severe food allergy. In rare cases, symptoms can be delayed in onset for several hours. The oral route is less likely to cause a reaction, and the reaction usually is less severe. The longer the interval between exposures, the less likely an anaphylactic reaction will recur. The first priority should be to assess the patients respiratory and cardiac status. Severe angioedema of the tongue and lips may obstruct airflow. Laryngeal edema may present as stridor or severe air hunger. Loss of voice may also be observed. Bronchospasm, airway edema, and mucus hypersecretion may manifest as wheezing. Hypoxia can cause altered mental status. Tachycardia is a compensatory measure for intravascular volume loss. Hypotension (and resultant loss of consciousness) may be observed secondary to capillary leak, vasodilation, and hypoxic myocardial depression. Anaphylaxis is a medical emergency requiring immediate recognition and intervention. Pay close attention to the airway and secure as needed. Position the patient supine, vitalize and administer supplemental oxygen as soon as possible. The source of the antigen should be removed if possible (e.g., stinger after bee sting). Anaphylactic deaths correlate with delay in administration of epinephrine. Subcutaneous epinephrine should be administered into an unaffected extremity immediately. Epinephrine maintains the blood pressure, antagonizes the effects of the released mediators, and inhibits further release of mediators from mast cells and basophiles. Physicians sometimes are reluctant to administer epinephrine for fear of adverse effects. However, epinephrine usually is well tolerated and is life saving. The initial dose can be repeated as necessary, depending on the response. Alternate extremities when administering epinephrine. Antihistamine therapy should be considered adjunctive to epinephrine. Both an H1 and H2 blocker should be administered because studies have shown the combination to be superior to an H1 blocker alone in relieving the histaminemediated symptoms. Diphenhydramine (Benedryl) and cimetidine (Tagamet) or ranitidine (Zantac) are an appropriate combination. Cautious administration of cimetidine is recommended so as to not cause hypotension with rapid infusion. Intravenous access should be established, both for administration of adjunctive medications and for intravenous fluids to maintain blood pressure if needed. Hypotension often is the most difficult manifestation of anaphylaxis to treat. Because hypotension is due to a dramatic shift of intravascular volume, the fundamental treatment intervention (after epinephrine) is aggressive intravenous fluid administration. Brochospasm that has not responded to subcutaneous epinephrine should be treated with inhaled beta2-adrenergic agonists, such as albuterol. Corticosteroids do not have an immediate effect on anaphylaxis but should be administered early to prevent a potential late-phase reaction (biphasic anaphylaxis). In the acute setting, evidence of respiratory failure mandates endotracheal intubation. If the endotracheal tube cannot be passed because of severe laryngeal edema, tracheotomy is required.
RATIONALE
The primary medication for acute anaphylaxis is epinephrine. All other therapies are adjunctive, including fluids, antihistamines, corticosteroids, and albuterol. Dopamine may also be required to maintain blood pressure. Adrenergic agonists - Epinephrine maintains blood pressure, antagonizes effects of released mediators, and prevents further release of mediators. Antihistamines - Block the effects of released histamines at the H1 receptor, thereby treating flushing, urticarial lesions, vasodilation, and smooth muscle contraction in the bronchial tree and GI tract. The EpiPen automatic injector for adults delivers 0.3ml of E-9
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1:1,000 epinephrine (0.3mg), and the EpiPen Jr for children delivers 0.3ml of 1:2,000 epinephrine (0.15mg). The automatic injector is administered by taking off the cap and pushing the opposite end firmly into the upper lateral thigh. The needle is delivered into the thigh automatically. The patient should count to 10 before removing the pen to insure complete delivery of the medication. The patient should be instructed to obtain medical care immediately after injecting the EpiPen because additional doses of epinephrine and other therapy may be required. old because of airway responsiveness and lower levels of lung function. Two thirds of all asthma cases are diagnosed before the age of 18 years. Approximately one half of all childhood asthmatics have a decreased or disappearance of symptoms by early adulthood. The diagnosis of asthma is made more often in children and young adults and is related to high levels of physical activity. It can ob observed in any age based on level of underlying airway reactivity and the level of physical exertion. Asthma is the most common cause for hospitalization for children in the United States. A detailed medical history should address if symptoms are due to asthma, support the likelihood of asthma such as with a family history, assess the severity of asthma and identify possible precipitating factors such as exposure to various allergens, occupational exposure or medications. Common symptoms are cough, wheezing, shortness of breath with use of accessory muscles to breathe and sputum production. Specific historical factors are key in the assessment of acute asthma. Duration and precipitating factors are related to weather, animal exposure, current medications and compliance (e.g., need for medication, dose of steroids), last use of medications and the date of medication. On physical examination the clinician may find the patient with accessory muscle use, stridor, altered level of consciousness, cyanosis, an inability to speak in complete sentences and wheezing. Inspiration-expiration ratio reveals prolongation of the expiratory phase (e.g., 1:1 mild, 1:3 severe). Patients with mild acute asthma are able to lie flat. In more severe cases, the patient assumes a sitting position. As the severity increases, the patient increasingly assumes a hunched-over sitting position with the hands supporting the torso, termed the tripod position. If symptomatology becomes more severe, profuse diaphoresis occurs. The diaphoresis presents concomitantly with a rise in PCO2 and hypoventilation. In the most severe form of acute asthma, the patient may struggle for air and/or be bradypneic and be profusely diaphoretic; almost no breath sounds may be heard, and the patient is willing to lie recumbent. In children, assess supraclavicular and intercostal retractions, accessory muscle use, and nasal flaring. Some causes of acute asthma may be respiratory infections, exercise, weather, including cold and dry air, weather changes, and significant increases in humidity, air pollution, aspirin ingestion, and chemical irritants. The worst bronchospasm is usually about 4am, and the best airflow is at approximately 4pm. ED visits are decreased and mortality increased at night, possibly because of acid reflux, sinusitis, or postnasal dripping during sleep. Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. The hypoxemia of uncomplicated acute asthma is readily reversible by oxygen administration. All patients with acute asthma should have oxy-
ASTHMA
The National Asthma Education and Prevention Program Expert Panel defines asthma in the following manner: Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial responsiveness to a variety of stimuli. The pathophysiology of asthma is complex and involves 3 components, airway inflammation, intermittent airflow obstruction, and bronchial hyper responsiveness, The mechanism of inflammation in asthma may be acute, sub acute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Airflow obstruction can be caused by a variety of changes including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. The extent of reversibility of airway obstruction is based on structural changes in the airway due to longstanding inflammation. One feature of asthma is the exaggerated response to numerous stimuli. The degree of airway hyper responsiveness generally correlates with the clinical severity of asthma. The disease is believed to be mediated by either water loss from the airway, heat loss from the airway, or a combination of both. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37 degrees C. The nose is unable to condition the increased amount of air required for exercise, particularly in athletes who breathe through their mouths. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction, occurring within minutes of completing exercise. Asthma incidence is increased in the very young and very E - 10
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gen saturation measured by pulse oximetry. In children, pulse oximetry is used to grade severity of acute asthma. Oxygen saturation of 97% or above constitutes mild asthma, 92-97% constitutes moderate asthma, and less than 92% signifies severe asthma. The following is intended to be utilized as a quick reference guide only! Please refer to your departmental Bloodborne Pathogens/Infection Control Program for more indepth information on this topic. In addition, information may be obtained from the following documents; OSHA 29 CFR 1910.1030 NFPA 1581 Ryan White CARE Act Needlestick Safety and Prevention Act
RATIONALE
The goals of therapy are to maintain Sa02 greater than 92% and treat dehydration if it is clinically apparent. The mainstay of therapy for acute asthma in the pre-hospital setting is inhaled beta2-agonists. Bronchodilators Their primary action is to decrease muscle tone in both the small and large airways in the lungs, thus increasing airflow and ventilation. Ipratropium - Ipratropium is chemically related to atropine, and has anti-secretory properties and inhibits secretions from glands lining the nasal mucosa and increases the duration of bronchodilation. In controlled studies, Ipratropium demonstrated the most consistent efficacy in children and smokers. Ipratropium (Atrovent) and Albuterol (Proventil, Ventolin) When utilized together create a synergistic affect. Albuterol (Proventil, Ventolin) Is a bronchodilator utilized to reverse airway obstruction due to asthma. It has little effect on the heart rate. Epinephrine - (SQ administration or Epi-Pen)Patients who respond poorly or not at all to an inhaled beta-agonist usually respond to epinephrine subcutaneously. Alpha-agonist effects increase peripheral vascular resistance and reverse peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist activity of epinephrine produces bronchodilatation. This is the best treatment of choice if bronchospasm does not improve after 2-3 treatments with inhaled beta-2 agonists. Glucocorticoids The anti-inflammatory agent Methylprednisolne (Solu-Medrol) restores the beta2-agonist receptors in the bronchial smooth muscles and, therefore, restore the response to beta2-agonists. Glucocorticoids are indicated if response to the first or second beta2-agonist inhaler treatment is incomplete. Solu-Medrol is used for treatment of inflammatory reaction. By reversing increased capillary permeability and suppressing activity, it decreases inflammation. The onset of action of steroids is approximately 4 hours in children and 6 hours in adults.
EXPOSURE DEFINITIONS:
A contaminated needlestick injury Blood/OPIM in direct contact with the inner surface of the eye, nose, or mouth A cut with a sharp object covered with blood/OPIM Blood on intact skin is not an exposure! Bloodborne Pathogens cannot be transmitted by casual contact, food or water, sneezing, coughing, saliva, sweat, urine, stool, vomitus, or nasal secretetions unless they contain gross visible blood. Potentially infectious material is blood, semen, vaginal secretions, CSF, synovial fluid, pleural fluid, pericardial fluid, peritoneal fluid, amniotic fluid, saliva in dental procedures, any body fluid that is visibly contaminated with blood, and any unfixed human tissue or organs. Infectious Diseases: Hepatitis A Virus (HAV) Hepatitis B Virus (HBV) Hepatitis C Virus (HCV) Hepatitis D Virus (HDV) Hepatitis E Virus (HEV) HIV/AIDS TB Other infectious diseases include chicken pox, diphtheria, herpes simplex, mumps, measles, meningococcal meningitis, rubella, scabies, tetnus, influenza, chlamydia, gonorrhea, syphilis, herpes zoster, pertussis (whooping cough). HEPATITISA: Cause: Hepatitis A Virus Transmission: FecalOral (enteric); food/waterborne Incubation: 1550 days E - 11 2/15/06
BLOODBORNE PATHOGENS

Vaccine: Yes Signs/Symptoms: Jaundice, fatigue, abdominal pain, nausea, vomiting, diarrhea Prevention: Universal Precautions Vaccination where contact with virus is likely Avoid touching mouth with contaminates HEPATITIS B: Cause: Hepatitis B Virus nausea, vomiting, diarrhea Prevention: Universal Precautions Avoid touching mouth with contaminates Note: This virus is the chief cause of enteric NANB Hepatitis HIV/AIDS: Cause: Human Immunodeficiency Virus Transmission: Bloodborne, sexual contact, OPIM, perinatal, breast milk Vaccine: No Signs/Symptoms: May not be apparent for years Loss of appetite Weight loss Fever Fatigue Night Sweats Skin rash or Lesions Diarrhea Swollen lymph nodes Decreased WBCs S&S of Opportunistic infections Prevention: Universal Precautions TB: Cause: Mycobaterium Tuberculosis Transmission: Exposure to Airborne Particles Incubation: 412 weeks Vaccine: No Signs/Symptoms: Cough, hemoptysis, chest pain, fatigue, weight loss, fever hoarseness Prevention: Universal Precautions Fitted HEPA Mask Surgical or Oxygen mask for Patient Do not recirculate air, use exhaust vents Open windows Engineering and Work Practice Controls:
Transmission: Bloodborne, sexual contact, perinatal Incubation: 45 to 180 days Vaccine: Yes Signs/Symptoms: Jaundice, fatigue, abdominal pain, nausea, vomiting Prevention: Vaccination Universal Precautions HEPATITIS C: Cause: Hepatitis C Virus Transmission: Bloodborne, sexual contact, perinatal Incubation: 14 to 180 days Vaccine: No Signs/Symptoms: Jaundice, fatigue, abdominal pain, nausea, vomiting Prevention: Universal Precautions HEPATITIS D: Cause: Hepatitis D Virus Bloodborne, sexual contact
Transmission: Vaccine: No
Signs/Symptoms: Jaundice, fatigue, abdominal pain, nausea, vomiting Prevention: Universal Precautions Note: Hepatitis D requires HBV for replication HEPATITIS E: Cause: Hepatitis E Virus Transmission: FecalOral (enteric) Vaccine: No Signs/Symptoms: Jaundice, fatigue, abdominal pain, E - 12
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Handwashing, PPE, cleanliness such as physical removal of dirt and debris, disinfection with a 1:10 bleach solution, sterilization with an autoclave or chemical sterilant, biohazard waste containers, needleless devices, eating, drinking, smoking, handling contact lenses and lip balm are prohibited in the work areas where there is a reasonable potential for occupational exposure. High Risk Factors: Homosexual and Bisexual Men Heterosexuals who have contact with infected persons Multiple sexual partners Infants of mother who are infected IV Drug Users Recipients of Blood or Blood Products N.I.O.S.H. 95 Standard: It is MANDATORY that the N95 fitted masks be used in the following situations: Known or suspected TB, meningitis, mumps, measles, chicken pox, diptheria, or patients who have a blood tinged productive cough. Pathological changes in COPD occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma.
CHRONIC BRONCHITIS
Mucous gland enlargement is the histologic hallmark of chronic bronchitis. The structural changes described in the airways include atrophy, cilia abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening. The respiratory bronchioles display a inflammatory process, lumen occlusion by mucous plugging, smooth muscle hyperplasia, and distortion due to fibrosis. These changes, combined with loss of supporting alveolar attachments, cause airflow limitation by allowing airway walls to deform and narrow the airway lumen.
EMPHYSEMA
Emphysema has 3 patterns. The first type is characterized by focal destruction limited to the respiratory bronchioles and the central portions of acinuss. This form is associated with cigarette smoking and is the most severe in the upper lobes. The second type involves the entire alveolus distal to the terminal bronchiole. This type is the most severe in the lower lung zones. The third type is the least common form and involves distal airway structures, alveolar ducts, and sacs.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) / CHRONIC BRONCHITIS / EMPHYSEMA

Chronic obstructive pulmonary disease (COPD) is a devastating disorder that causes exorbitant human suffering. Currently COPD is the fourth leading cause of death in the U.S. COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema. The airflow obstruction generally is progressive, may be accompanied by airway hyper reactivity, and may be partially reversible. Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months, during each of 2 consecutive years (other causes of cough being excluded). Emphysema is defined as An abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Chronic bronchitis is defined in clinical terms and emphysema in terms of anatomic pathology.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Both emphysematous destruction and small airway inflammation often are found in combination in individual patients. When emphysema is moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the mechanism of airflow limitation. By contrast, when emphysema is mild, bronchiolar abnormalities are most responsible for the deficit in lung function. Although airflow obstruction in emphysema is virtually irreversible, bronchoconstriction due to inflammation accounts for a limited amount of reversibility. Most patients with COPD have smoked at least 20 cigarettes per day for 20 or more years before the onset of the common symptoms of cough, sputum, and dyspnea. A productive cough or an acute chest illness is common. The cough is usually worse in the mornings and produces a small amount of colorless sputum. Breathlessness is the most significant. Wheezing may occur in some patients, particularly during exertion. With disease progression, intervals between acute exacerbations become shorter; cyanosis and right heart failure may occur. Anorexia and weight loss often develop and suggest a worse prognosis. Respiratory rate increases proportional to disease severity. Use of accessory respiratory muscles and paradoxical in drawing of lower intercostal spaces is evident. In advanced E - 13 2/15/06

disease, cyanosis, elevated JVD and peripheral edema are observed. Thoracic exam reveals hyperinflation (barrel chest), wheezing, diffusely decreased breath sounds, and prolonged expiration. Coarse crackles beginning with inspiration may be heard, and wheezes frequently are heard on forced and unforced expiration. The primary cause of COPD is exposure to tobacco smoke. Smoking cessation continues to be the most important therapeutic intervention. Acute exacerbation of COPD is 1 of the major reasons for hospitals admissions in the U.S. The predictors of mortality are aging, continued smoking, accelerated decline, moderate to severe airflow obstruction, poor bronchodilator response, severe hypoxemia, presence of hypercapnia, development of cor pulmonale, and overall poor functional capacity. Solu-Medrol - is used for treatment of inflammatory reaction. By reversing increased capillary permeability and suppressing activity, it decreases inflammation. The onset of action of steroids is approximately 4 hours in children and 6 hours in adults.
COMBATIVE PATIENTS
The transport of combative and potentially combative patients can be a stressful and dangerous experience for Ground and Air Medical Crew members, threatening the safety of all EMS personnel. The following protocol is adopted to deal with this possibility; 1.Recognize potential etiologies of combative behavior and carefully evaluate each patient prior to transport. a.Head Injury or other central nervous system insult. b. History of psychotic or other psychiatric disturbances; Acute psychotic crisis. c. Hypoxia, carbon monoxide poisoning. d. Alcohol or drug intoxication, withdrawal, or overdose. e. Seizure activity, or potential for seizure activity. f. Disorientation in an elderly patient; organic brain syndrome; dementia. g. History of involvement in a violent situation; anti social personality. h.Severe claustrophobia, acrophobia (heights) or aviophobia (flying). 2. Recognize behavioral clues to potentially violent behavior. a. Posture 1. Sitting on edge of seat. b. Speech pattern 1. Rapid 2. Loud 3. Abusive 4. Overly animated 5. Shrill 6. Excessive talking 7. Emotional lability 8. Expressions of anger. c. Motor Activity 1. Clenched fists 2. Pacing 3. Tightening of jaw muscles 4. Easily startled 5. Excessive fidgeting 6. Spitting 7. Biting 3. Initiate preventative measures to reduce potentially combative patients anxiety. a. Reassure patient b. Give honest answers to questions
RATIONALE
The goals of pharmacotherapy are to reduce morbidity and prevent complications. OXYGEN - COPD commonly is associated with progressive hypoxemia. Oxygen reduces mortality rates in patients with advanced COPD because of the favorable effects on pulmonary hemodynamics. Bronchodilators - These agents act to decrease muscle tone in both small and large airways in the lungs, thereby increasing ventilation and airflow. Albuterol (Proventil, Ventolin) - Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility. Most patient will benefit from this treatment. Albuterol is also a beta-agonist for bronchospasm refractory to epinephrine. Ipratropium (Atrovent) - Chemically related to atropine. Has anti-secretory properties. When administered concurrently with albuterol creates a synergistic effect, by increasing duration of bronchodilation by albuterol. Beta Adrenergic Agonist & Antocholinergic Agent Combination - (Alupent & Atrovent) Combines the effects of the rapid onset with prolonged action. Glucocorticoids - In acute exacerbation, when administered early in treatment modalities, steroids improve symptoms and lung functions over time. The anti-inflammatory agent restores the beta2-agonist receptors in the bronchial smooth muscles and, therefore, restore the response to beta2-agonists. Glucocorticoids are indicated if response to the first or second beta2agonist inhaler treatment is incomplete. E - 14
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c. Give firm, calm direction 4. En route considerations. a. Speak softly and calmly around patients. Do not yell at patient. b. Use earplugs to reduce noise stimulation to patient. This also allows the medical crew to discuss patients condition without being overheard. c. Be respectful of patients (small) personal space. Approach patient in a slow deliberate manner. 5. Should a patient become combative, the following steps should be taken. a. Look for potential etiologies and correct 1. Hypoxia. 2. Shock. 3. Excessive environmental stimulation. b. The following physical restraints are authorized for use if (a) above does not work or apply. (apply before transport if at all possible). 1. Rayon webbing strapped across chest and legs. 2. Hard extremity restraints. (All 4 limbs) a. Restrain limbs at a comfortable angle. b. Avoid compromising circulation by restraining too tightly. Check distal extremities periodically (q 15 minute pulses). c. Do not use any padding under restraints as this may reduce efficiency. d. Protect airway from aspiration. If patient vomits turn patient on his/her side and suction as needed. c. Pharmacologic restraints may be used if physical restraints are not sufficient, or if continued combativeness may interfere with deliverance of proper medical care or may cause further harm to the patient (i.e.. ventilator patient or cervical spine injury). All pharmacologic agents are used by protocol only. Respiratory status must be carefully monitored. 1. Antipsychotics: Haldol may be used for acute psychosis, organic brain syndrome or senile dementia / disorientation. May be combined with a sedative agent for better overall effect. 2. Sedative agents; 1. Diazepam (Valium). 2. Midazolam (Versed). 3. Lorazepam (Ativan). 4. Morphine Sulfate. 3. Neuromuscular blocking agents (never give without prior sedation in a conscious patient unless its an emergency). 1. Vercuronium Bromide (Norcuron). 6. Micellaneous considerations. a. Any unconscious patient who may awaken in flight should be restrained prophylactically. b. Any patient whose physical activity will hinder the delivery of good patient care or cause further injury to him/herself should be restrained (i.e.. c spine injury). c. All pharmacologic agents that can cause respiratory depression. Respiratory status must be carefully monitored if these agents are used. Respiratory assistance and/or intubation may become necessary with sedative agents, and is mandatory with all neuromuscular blockading agents. d. All combative patients will be transported by a two (2) person (minimum) medical crew. e. If an unrestrained patient suddenly becomes combative in the air and cannot be controlled, the pilot should notify A.T.C. (Air Traffic Control), declare an emergency if needed, and land at the nearest appropriate airport. Law enforcement back up should be requested to assist in restraining after landing. f. Strong consideration should be given to restraining all intubated patients. g. All criminal patients who are accompanied by a law enforcement agent shall also be restrained with handcuffs if possible. These patients must be restrained at all times. h. Use of mechanical or pharmacologic restraints, or both, must be documented on the (PCR) Patient Care Report. i. Safety must always take first priority in all transports. If a Medical Crew Member has any doubt regarding the safety of transporting a potentially combative patient by ground or in the air, (either for the patient or themselves) they should obtain the appropriate medical or law enforcement assistance and immediately notify the receiving facility physician of their concerns.
DIABETES MELLITUS
By far one of the most common emergencies you can expect to treat will involve diabetes. Frequently complications involve ketoacidosis and hypoglycemia. Diabetes Mellitus is characterized by decreased insulin secretion by the beta cells of the islets of Langerhans in the pancreas. The complications of this disease are numerous. Glucose, also called dextrose, is a simple sugar required by the body to produce energy. Sugars, also called carbohydrates, are one of the three major food sources used by the E - 15
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body along with proteins and fats. For the body to convert glucose to energy, glucose must first be transported through the cell membrane. The rate at which glucose can enter the cell is dependent upon insulin levels. Insulin acts as a messenger. When released by the pancreas, it travels through the blood to tissues. Once reaching its destination, insulin combines with specific insulin receptors on the surface of the cell membrane, allowing glucose to enter the cell. Without insulin, the amount of glucose that can be transported into the cells is far too small to meet the bodys energy demands. Diabetes mellitus results from inadequate amounts of circulating insulin. Generally, the disease can be divided into two different categories. Type 1 diabetes, or insulin dependent diabetes, usually begins in the early years. Patients who have Type 1 diabetes must take insulin. Type 11, or noninsulin dependent diabetes, usually begins later in life and tends to be associated with obesity. Type 11 diabetes can often be controlled without using insulin and by adjusting diet. In diabetes, a drop in insulin levels is accompanied by a steady accumulation of glucose in the blood. As cells become glucose-depleted, they begin to use other sources of energy. Therefore, harmful by-products such as ketones and acids are produced. When these start to accumulate classic findings of diabetic KETOACIDOSIS appear. If allowed to continue its progression, sever metabolic acidosis occurs and coma ensues. This can result in serious brain damage or death. Ketoacidosis is often called DIABETIC COMA. The kidneys will excrete glucose in the urine taking water with it. This results in osmotic diuresis, which in turn dehydrates the patient. This is evident on examination by dry, warm skin and mucous membranes. Deep respirations begin as the body tries to compensate for the metabolic acidosis as cellular glucose-depletion continues. The onset is slow, lasting 12 to 24 hours. In its early stages, the signs and symptoms include increased thirst, excessive hunger, urination, and malaise. Diabetic ketoacidosis is characterized by nausea, vomiting, marked dehydration, tachycardia, and weakness. Coma is not uncommon. The breath may have a sweet or acetone-like character. Kussmaul respirations may also occur (deep, rapid). Ketoacidosis is often associated with infection or decreased insulin intake. It can occur in patients who fail to take their insulin or who take an inadequate amount over an extended period. Persons not previously diagnosed as diabetic will occasionally present in ketoacidosis. Hypoglycemia occurs when insulin levels are excessive. Hypoglycemia is an urgent medical emergency as a prolonged episode can result in permanent brain injury. HYPOGLYCEMIA, sometimes called INSULIN SHOCK, lies at the other end of the spectrum from diabetic ketoacidosis. Hypoglycemia can occur if a patient accidentally or intentionally takes too much insulin, eats an inadequate amount of food, drinks alcohol, overdoses, is suffering from infection, has activity changes, or becomes dehydrated. The clinical signs and symptoms of hypoglycemia are many and varied. An abnormal mental status is the most important. In the early stages of hypoglycemia, the patient may appear restless or impatient or complain of hunger. As the blood sugar falls lower, he or she may display inappropriate anger or a variety of bizarre behaviors. Physical findings may include diaphoresis and tachycardia. The patient may also experience a seizure or become comatose. In contrast to diabetic ketoacidosis, hypoglycemia can develop quickly. The glucose level at which an individual becomes symptomatic is highly variable.
RATIONALE
Treatment of hypoglycemia consists of correcting the glucose deficiency and directing further treatment to the underlying cause. The mainstay for hypoglycemia is glucose. Obtaining a blood sample for glucose check is performed in the case of infants and pediatrics as part of their baseline vital signs, an unconscious patient or any patient with altered mental status. When hypoglycemia is found and treated in the diabetic patient, the patient may awaken and not desire transport. However, transport for evaluation should always be encouraged to determine the underlying cause. Treatment should include ABCs, intravenous access, oxygen, monitoring, and repeated blood glucose readings prior to and after administration of dextrose. Thiamine may also be appropriate if alcohol abuse is suspected. The hyperglycemic patient ultimately needs insulin. Treatment by emergency personnel should be geared toward rehydration via fluid administration. Glucose Supplement - This agent is used to restore the patients serum glucose levels. Dextrose - Carbohydrate. Dextrose is absorbed , stored and utilized by tissues immediately. It provides a source of carbohydrate calories. It may aid in minimizing liver glycogen depletion and exert a protein sparing action. Thiamine - Vitamin B1. Thiamine is indicated when giving
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intravenous dextrose to individuals with suspected or reported alcohol abuse. Its actions are two fold in vitamin depletion first, to prevent sudden cardiac failure and second to allow carbohydrates to be adequately metabolized. Glucose Elevating Agent - These agents can act in the pancreas or the peripheral tissues to increase blood glucose levels. Glucagon - Pancreatic alpha cells of the islets of Langerhans produce this polypeptide hormone. Exerts effects opposite of insulin on blood glucose. Elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats. Useful when IV access is problematic. 0.9% Sodium Chloride - Crystalloid. An electrolyte solution of sodium chloride in water. IV Fluids 0.9% Normal Saline - It is utilized for fluid replacement because of its immediate expansion of the circulatory volume. Complications may arise related to the venous access devices placed for chronic dialysis. Clotting of the shunt offistula can occur spontaneously. Massive hemorrhage can also occur with separation of arteriovenous fistulas. The best method to end the hemorrhage is by direct pressure and transport to the emergency department.
RATIONALE
In an immediately life-threatening emergency, personnel may use a hemodialysis access site for IV access with the precautions noted in procedures. The site should not be used for routine IV access. IV fluids should not be administered except for cases of frank shock. When used, the preferred regimen is small bolus doses (-200ml) with reevaluation for effect between doses. Lactated Ringers should not be used because of its potassium content. Most medications used in pre-hospital care are used in the usual dosages. Contact on line medical control for direction beyond immediate life threatening issues. Adjustments may need to be made in dosage or frequency of subsequent treatments to account for changes in metabolism and excretion secondary to renal disease. Cardiac arrest may be due to hyperkalemia, treat hyperkalemia with IV calcium and bicarbonate. Consider pericardial tamponade, especially in the setting of pulse less electrical activity (PEA). Consider pericardiocentesis if tamponade is suspected. Pulmonary edema is frequent in renal failure and is usually due to volume overload. It can best be treated by hemodialysis. Nitrates are effective by all routes. Loop diuretics (Lasix) may be effective at promoting diuresis in patients with residual renal function. Toxicity is potentially increased because of delayed excretion and higher blood levels. Morphine is also useful for its vasodilating effects. ELECTROLYTE SUPPLEMENTS - These agents are used to reduce potassium levels. Hyperkalemia is the most common life-threatening emergency ion patients with ESRD, as measured by T waves on EKG. CALCIUM CHLORIDE - Fastest acting drug to treat hyperkalemia (acts within Minutes). Antagonizes membrane effects of potassium. SODIUM BICARBONATE - Redistributes extra cellular potassium into cells with 10-15 minutes.
DIALYSIS
Patients with chronic renal failure require dialysis to live. This process helps remove toxic substances from the bloodstream - a function no longer adequately provided by the kidneys. Treatment of renal failure takes on of two forms: hemodialysis or peritoneal dialysis. Hemodialysis is a medical procedure whereby waste products, normally excreted by the kidneys, are removed by a machine. Patients with renal failure must undergo dialysis two to three times a week. Many people now have home dialysis units, you may be called upon to assist them. Vascular access must exist to dialyze the patient. The two most common routes of access are external arteriovenous shunts or internal fistulae. An arteriovenous shunt is a surgical connection between the arterial and venous systems. The internal fistula is located subcutaneous and will have a bruit that can be palpated. Another method for dialysis is via the peritoneum. Complication of dialysis include hypotension, chest pain and dysrhythmias, and disequilibrium syndrome. Hypotension due to dialysis is caused by dehydration, sepsis, or blood loss. Dysrhythmias produced in response to dialysis can be caused by potassium intoxication. They may also develop from transient myocardial ischemia. The most commonly seen abnormality is PVCs. Disequilibrium syndrome is characterized by cerebral symptoms in patients with severe renal failure. It can occur before, during or immediately after hemodialysis. These patients may present with headache, lethargy, convulsions, and may even lapse into coma.
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board or to the refrigerator door. A prehospital DNRO may be revoked at any time by the patient or designated health care surrogate pursuant to section 765.104, F.S., and section 64E, F.A.C.. The original form should remain at all times in the patients home or with him when traveling, a copy of the form should be made available to the EMS provider to use when transporting the patient from his home to a health care facility. It is important to note that in order to honor a DNRO it must be the properly completed original, the copy is only for informational and charting purposes at the receiving facility. The DOH form 1896 is printed on yellow safety paper. However, you may encounter the form printed on white paper also. Both of these forms are acceptable provided they are properly completed. In some cases a patient may be wearing a white DNRO bracelet, similar to a hospital bracelet, with the EMS Star of Life repeated on the bracelet.
DO NOT RESUSCITATE ORDER (DNRO)

Legislative authority for DNROs are provided for under chapter 765, Florida Statutes Health Care Advanced Directives. A competent adult, or an incompetent adult through a health care surrogate who was previously chosen, or a proxy or guardian, has the right to be able to control decisions regarding medical care, including the withdrawal or withholding of lifeprolonging procedures. The EMS Transportation Act (chapter 401) authorizes EMS personnel to honor a prehospital Do Not Resuscitate Order (DNRO) if the order is on a Department of Health Bureau of EMS (DOH) form and is presented to EMS personnel in a manner provided by DOH rule. A properly executed DNRO must be signed by a physician who has determined that the patient is in a terminal condition or vegetative state with very little probability of recovery. EMS personnel may therefore honor a DNRO, but not a living will, because a DNRO serves as evidence that a physician has made a determination regarding the patients medical condition and that there is a mutual agreement regarding a course of treatment. A living will may be executed by a perfectly healthy person or by one diagnosed with terminal condition. It states the kind of medical care an individual wants or does not want if unable to make his own decision regarding medical care. A patients signature is required in box A on side two of DOH form 1896 if the patient is competent. The signature of the health care surrogate or court appointed guardian or proxy is required in box B on side two of the form if the patient is incapacitated or incompetent. Side one of the form must be signed by the patients attending physician. The signature of the patient on the DNRO form, or the patients health care surrogate or proxy, or guardian, if applicable, must occur in the presence of two subscribing witnesses who must also sign the form. The form must have an effective date. Once the patient or surrogate or proxy or guardian has properly completed the DNRO form, they should check the box stating This DRNO has been properly completed and sign on the designated line within the rectangular box located on the bottom half of side one of the DNRO form. Completion of this part of the form provides a convenient and rapid method for EMS personnel to determine that the form has been properly executed. The form must be accessible to EMS personnel. The original prehospital DNRO should be located at the patients bedside table, or on the back of the patients bedroom door, or taped to the patients headE - 18
HYPERTENSION
SOURCE - Brady 3rd edition Paramedic Emergency Care. Physicians Desk Reference and E-Medicine Site A hypertensive emergency is a life-threatening elevation of blood pressure. It occur in one percent or less of patients with hypertension, usually when the hypertension is poorly controlled or untreated. Furthermore, there is a greater than 90% mortality rate with people who do not take control of acute hypertensive states. A hypertensive emergency is characterized by a rapid increase in diastolic blood pressure (usually >110 mmHg) accompanied by restlessness, confusion, blurred vision, nosebleed, and nausea and vomiting. The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension. Hypertension is a related factor in other emergencies. These include such things as pulmonary edema from left ventricular failure, dissecting aortic aneurysm, toxemia of pregnancy, and cerebrovascular accident. In these cases, hypertension often results from the primary problem. Treatment should be directed at the primary problem. An important point to remember in the management of the patient with any degree of BP elevation is to treat the patient and not the number. Hypertensive emergencies occur most commonly in middle-aged patients. The peak incidence in those aged 40-50 years. Patients with a true hypertensive emergency require careful titration of IV medications for good control and a smooth reduction of their BP. Blood Pressures of systolic greater than 180 mm Hg/diastolic greater than 110 mm Hg require immediate intervention. The three major organ systems affected by high BP are the CNS, cardiovascular system, and renal system.
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Additional signs observed on exam may include seizure, stupor, coma, pulmonary edema, jugular vein distension, and peripheral edema. Labetelol should only be administered with the patient in a supine position. Symptomatic postural hypotension (incidence 58%) is likely to occur if the patient is tilted or allowed to assume the upright position with 3 hours of receiving labatalol. facturing process. Latex gloves were widely recommended to prevent transmission of blood-borne pathogens, including the HIV virus. Eight billion pairs of medical gloves were imported to the US in 1988, primarily as powdered, nonsterile examination gloves. The pressure that was placed on manufacturing companies resulted in hundreds of new, poorly regulated latex factories in tropical countries. The incidence of minor and serious allergic reactions to latex began to rise rapidly among patients and health care workers. Latex sensitazation can occur after skin or mucosal contact, peritoneal contact during surgery, and possibly inhalation of aerosolized particles with latex on their surfaces. Latex exposure is associated with 3 clinical syndromes: The first syndrome is irritant dermatitis. It is a result of mechanical disruption of the skin due to the rubbing of gloves and accounts for the majority of latex-induced local skin rashes. The second syndrome is a delayed (Type IV) hypersensitivity reaction, resulting in a typical contact dermititis. Symptoms usually develop within 24-48 hours of cutaneous or mucous membrane exposure to latex in a sensitized person. The third, most serious, and least common syndrome is immediate (Type I) hypersensitivity. Symptoms generally begin within minutes of exposure. The spectrum of clinical manifestations includes localized or generalized urticaria, rhinitis, conjunctivitis, bronchospasm, laryngospasm, hypotension, and full-blown anaphylaxis. Type I allergy has been implicated clearly in intraoperative and intraprocedure anaphylaxis, and it can be fatal without emergent treatment. Latex allergy is present in 1-5% of the general population. Latex allergy is increased in populations with chronic occupational exposure to latex. It is found in 10-30% of health care workers. The highest prevalence of latex allergy (20-68%) is found in patients with spina bifida or congenital urogenital abnormalities. Patients with spina bifida also may have a genetic predisposition for latex sensitization. Other patients with a history of multiple surgeries or other latex- exposing procedures are also at increased risk relative to the general population. Patients with cerebral palsy, mental retardation, or quadriplegia also appear to have increased risk of latex allergy, probably because of multiple medical procedures. Finally, the prevalence of latex allergy is increased in persons with allergies to avocado, banana, chestnut, kiwi, papaya, peach, or nectarine. Cross-reacting antigens have been found between these fruits and latex. Hypersensitivity symptoms may include: Pruritus of exposed skin and mucous membranes, edema, hoarseness, tearE - 19 2/15/06
RATIONALE
The BP should be lowered by up to 25% of the mean arterial pressure (MAP) over minutes to hours. Labetalol should only be administered with the patient in the supine position. BETA-BLOCKERS - These agents are used for exacerbations of hypertension. Labetalol (Trandate) - Alpha and Beta-blocker. Lowers BP, reduces incidence of myocardial infarctions and death. Because of alpha and beta blocking properties, blood pressure is reduced without reflex tachycardia, and total peripheral resistance is decreased without significant alteration in cardiac output. The onset of labetalol is within 5 minutes with a target blood pressure of 160/90. ANTIHYPERTENSIVE AGENTS - Potent agents with rapid onset. Nitroglycerin - Decreases coronary vasospasm, which increases coronary blood flow. Also induces vessel dilation, decreasing cardiac workload. LOOP DIURETICS - Potent diuretic. Primarily inhibits the re-absorbption of sodium chloride Furosamide (Lasix) - Its use in hypertension is considered when the patient takes Lasix on a regular bases or is suffering with signs and symptoms of CHF. Reinstitution of previously effective therapy in noncompliant patients may be all that is required. The administration of Lasix may avoid the administration necessity of more potent IV drugs. It may be used alone or in combination with other antihypertensive agents.
LATEX ALLERGY
Allergy to natural rubber latex is increasingly common and serious in children and adults. Latex is the milky fluid derived from the lactiferous cells of the rubber tree. It also contains a large variety of sugars, lipids, nucleic acids, and highly allergenic proteins. More than 200 polypeptides have been isolated from latex. Latex proteins vary in their allergenic potential. Protein content varies with harvest location and manu-

ing, rhinitis, respiratory distress, syncope, abdominal cramping, nausea, vomiting, diarrhea, erythema, urticaria, angioedema, hypotension, and shock. The history of latex allergy may be known or unknown. Individuals may be exposed to latex through their skin, mucous membranes, or airway (e.g., OPA, NPA, or ET tubes). Medical procedures may cause reactions in sensitized providers or patients. Common sources of latex exposure include but are not limited to tourniquets, BP cuffs, stethoscopes, catheters, IV tubing, ports, and syringes, electrode pads, and multidose vial tops. to a large number of women not having prenatal care. It is important to note the number of pregnancies (gravida) and the number of live births (para) as part of the patients history. Any woman with known obstetrical problems, previous medical history of hypertension, diabetes, preexisting heart disease or gravida 3 or greater, without prenatal care, will be considered a Priority 2 patient. Aortocaval compression syndrome can decrease cardiac output by 50%, therefore all women six months or greater gestation will be transported in lateral position until delivery is imminent.
SPONTANEOUS ABORTION
Abortion generally is defined as delivery or loss of the products of conception before the 20th week of pregnancy, but definitions vary. For this discussion, 20 week of gestation, which corresponds to a fetal weight of about 500 gm, is used as the limit for abortion. Delivery between 20 and 38 weeks is considered preterm birth. About 20 to 30% of women bleed or have cramping sometime during the first 20 weeks of pregnancy; 10 to 15% actually spontaneously abort. Since in 60% of spontaneous abortions the fetus is either absent or grossly malformed, and in 25 to 60% it has chromosomal abnormalities incompatible with life, spontaneous abortion may be a natural rejection of a maldeveloping fetus. About 85% of spontaneous abortions occur in the first trimester and tend to be related to fetal causes; those occurring in the 2nd trimester usually have maternal causes. Maternal factors that have been suggested as causes of spontaneous abortion include an incompetent, amputated, or lacerated cervix; congenital or acquired anomalies of the uterine cavity; hypothyroidism; diabetes mellitus; chronic nephritis; acute infection; use of cocaine, especially crack; and severe emotional shock. Many viruses, most notably cytomegalo, herpes, and rubella viruses, have been implicated as causes. The importance of uterine fibroids or retroversion and impaired corpus luteum function appears to have been overestimated. A relationship to physical trauma has not been substantiated. An abortion is termed either early (before 12 week of pregnancy) or late (between 12 and 20 weeks). This distinction is made because more difficulties are encountered in treating late abortions. After 12 weeks of pregnancy, the uterine cavity is obliterated and instrumentation is more likely to cause perforation. Since a definitive placenta has begun to form with a more organized and larger blood supply, bleeding is more likely. Fetal bones have also begun to form, and the long bones of the limbs may perforate the uterus during evacuation. Further, the size of a fetus at greater than 12 weeks of pregnancy makes it difficult to dilate the cervix enough to pass the fetus. Abortions may be spontaneous or induced. Spontaneous abortions occur without any instrumentation. Abortions per-
RATIONALE
Patients with known or suspected latex allergy who seek care for an unrelated medical condition or injury must be kept within a latex-safe environment to prevent serious complications. This includes all patients with spina bifida. Patients presenting with frank symptoms of Type I latex allergy are treated as any other patients with systemic allergic reactions, except they must be protected from further latex contact to avoid clinical deterioration. Major reactions in sensitized patients have been precipitated with latex medical equipment. Prehospital providers should be aware of the risk of latex allergy in patients and providers. Search for and read Medical Alert-type bracelets. Note the patients history of relevant allergies to medical devices or fruits. To rule out latex allergy that could worsen with further medical exposure, review the patients history of activities/exposures immediately preceding any systemic allergic reaction. The National Institute for Occupational Safety and Health (NIOSH) recommends wherever feasible the selection of products and implementation of work practices that reduce the risk of allergic reactions. Latex-free resuscitation equipment must be available. The Treasure Coast Guideline recommend providers carry a mobile container with complete latex free equipment. The complete suggested inventory list of supplies can be found on the following page. The receiving facility must be made aware of the need to completely avoid latex exposure to the patient during exams and procedures. Early notification is key to their preparation. The cornerstones of treatment are epinephrine and H1 antihistamines. Systemic corticosteroids and H2 blockers may be useful. See allergic reaction and or anaphylactic reaction rationales.
OBSTETRICS/GYNECOLOGY
Obstetrical emergencies are quite common in our area due E - 20
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formed to save the pregnant womans life or health are referred to as therapeutic. Spontaneous abortions may be threatened, inevitable, incomplete, or complete. Threatened abortion is any bleeding or cramping of the uterus in the first 20 weeks of pregnancy. Inevitable abortion is intolerable pain or bleeding that threatens the womans wellbeing. If part of the products of conception is passed or if the membranes are ruptured, the abortion is incomplete. If all of the products of conception are passed, the uterus has contracted toward normal size, and the cervix has closed, the abortion is complete. Missed abortion occurs when the fetus has died but has been retained in utero 4 weeks or longer. After 6 weeks, the dead fetus syndrome may develop, with disseminated intravascular coagulation and progressive hypofibrinogenemia and possible massive bleeding when delivery finally occurs. The dead fetus syndrome usually occurs only when the loss is in the 2nd trimester or later. Septic abortion develops when the contents of the uterus become infected before, during, or after an abortion. The patient is acutely ill, with symptoms and signs of infection and threatened or incomplete abortionchills, high temperature, septicemia, and peritonitis. Critically ill patients may evidence bacterial shock (septic or endotoxic shock) with vasomotor collapse, hypothermia, hypotension, oliguria or anuria, and respiratory distress. In the USA before legalization of abortion, septic abortions were often associated with induced abortions performed by untrained persons using nonsterile techniques and were commonly called criminal abortions. The incidence of septic abortion in the USA has fallen dramatically. shows signs of hemorrhage, shock, and lower abdominal peritoneal irritation that may be lateralized. Interstitial (cornual) pregnancies have a somewhat longer course, since the uterine wall provides support and delays rupture. In these cases, the uterus is usually asymmetric and somewhat tender on examination. The usual signs include cramping and spotting. Cornual pregnancies rupture between 12 and 16 weeks, and the rupture is catastrophic.
HYPEREMESIS GRAVIDARUM
Malignant nausea and vomiting to the extent that the pregnant woman becomes dehydrated and acidotic. Persistent hyperemesis gravidarum may be associated with serious liver damage. Autopsies in such cases usually show severe necrosis in the central portion of the lobules or widespread fatty degeneration similar to that seen in starvation. Hemorrhagic retinitis is a serious complication and indicates a grave prognosis: the mortality rate in such patients is 50%. Patients do not gain weight; they usually lose weight. Weight loss, dehydration, and ketosis confirm that the vomiting is extensive. Many pregnant women with morning sickness feel as though they are vomiting everything they ingest, but if they continue to gain weight and are not dehydrated, the condition is not hyperemesis gravidarum. Psychologic factors are prominent in this syndrome but do not lessen the danger. Patients should be evaluated for unsuspected liver disease, kidney infection, pancreatitis, intestinal obstruction, gastrointestinal tract lesions, and intracranial lesions, since these conditions can cause vomiting.
ECTOPIC PREGNANCY
Pregnancy in which implantation occurs outside the endometrium and endometrial cavity; i.e., in the cervix, uterine tube, ovary, or the abdominal or pelvic cavity. The incidence, 1/ 100 to 1/200 diagnosed pregnancies, is rising and is higher in nonwhites. Its likelihood increases with previous tubal disease, ectopic pregnancy (10 to 25%), or induced abortion. Intrauterine devices do not prevent ectopic pregnancies. The most common site of ectopic implantation is somewhere in a uterine tube. In many cases (50%), tubal implantation is caused by a previous tubal infection. The death rate for ectopic pregnancy has been falling, but much less rapidly than for maternal mortality in general. In the USA, it is estimated at 1/826. Untreated ectopic pregnancy is usually fatal. In ectopic pregnancy, spotting and cramping pain usually begin shortly after the first missed menstrual period. The symptoms are similar to those of threatened abortion. Gradual hemorrhage from the tube causes pain and pressure, but rapid hemorrhage results in hypotension or shock. Physical examination
HIGH RISK PREGNANCY

Pregnancy in which the mother, fetus, or newborn is or will be at increased risk for morbidity or mortality before or after delivery. All pregnancies should be evaluated to determine whether there are or will be risk factors. Classifying pregnancies as high risk is an effective way to ensure extra attention to patients who need medical care the most. The incidence of high risk pregnancy varies according to population. Perinatal mortality in the USA occurs in 17/1000 deliveries. Slightly greater than 50% of these deaths are stillbirths and the remainder occur in neonates up to the 28th day of life. Most perinatal deaths not directly due to congenital anomalies are associated with prematurity often accompanied by abnormal presentation, abruptio placentae, multiple Pregnancies, preeclampsia and eclampsia, placenta previa, or polyhydramnios. Risk factors can be categorized as inherent, or present before conception, and antepartum, or occurring after conception. E - 21
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PREGNANCY INDUCED HYPERTENSION

Pregnancy induced hypertension is occurs when patients who are normotensive, develop a blood pressure of 140/90 mmHg or greater in pregnancy. Keep in mind that during pregnancy the blood pressure will drop, therefore 130/80 mmHg may be hypertensive for the patient. Preeclampsia is defined as development of hypertension with albuminuria or edema between the 20th week of pregnancy and the end of the first week postpartum. Preeclampsia will present with some or all of the following signs/symptoms: hypertension, abnormal weight gain, edema, headache, epigastric pain, protein in the urine and less frequently visual disturbances. If this condition is allowed to progress eclampsia will follow. Preeclampsia develops in 5% of pregnant women, usually in primigravidas and women with preexisting hypertension or vascular disease. If untreated, preeclampsia characteristically smolders for a variable length of time and suddenly progresses to eclampsia. Criteria for Treatment: Headache, visual disturbances, hyperflexia all constitute a medical emergency. Diagnosis of eclampsia or hypertension induced by pregnancy. Systolic blood pressure greater than 140 mm Hg or a rise of 30 mm Hg above previous readings (prenatal) Diastolic blood pressure greater than 90 mm Hg or a rise of 15 mm Hg above previous readings (prenatal) NOTE: Blood pressures should be taken during resting state and not during contractions. Any pregnant woman who develops a blood pressure of 140/90 mm Hg, edema of the face or hands, or albuminuria of greater than or = 1+ or whose blood pressure rises by 30 mm Hg systolic or 15 mm Hg diastolic (even though it does not reach levels above 140/90) must be considered to have preeclampsia. Mild preeclampsia develops as borderline hypertension, unresponsive edema, or albuminuria. Patients with a blood pressure of 150/110 or with marked edema or albuminuria are considered to have severe preeclampsia. All routine laboratory tests (CBC, urinalysis, electrolyte levels, uric acid concentration, prothrombin time, and partial thromboplastin time) should be obtained and any abnormalities corrected. BUN and creatinine levels should also be obtained to rule out unsuspected kidney disease. Eclampsia is defined as the occurrence of grand mal seizures with severe preeclampsia and may occur anywhere from the fifth month of pregnancy to the end of the first week after delivery. Signs of impending eclampsia in a severely pre E - 22
eclampsic patient include: headache, visual pain, hyper reflexia, irritability, pedal edema or abdominal pain. Eclampsia: Coma and/or convulsive seizures in the same time period, without other etiology. The etiology of preeclampsia and eclampsia is unknown. Eclampsia develops in one out of two hundred preeclamptic patients and is usually fatal if untreated. A major complication of preeclampsia is abruptio placentae, apparently caused by vascular disease. Low dose aspirin therapy has been tried as a preventive measure in highrisk patients; however, the data on results are mixed, and this therapy should probably be considered experimental. Delivery is the primary treatment for eclampsia. Magnesium sulfate should be administered before a visual pelvic exam of a patient with eclampsia accompanied by any of the warning signs due to the possible induction of a seizure in the patient. In addition, patients who must be transferred for definitive care should have magnesium sulfate before transportation. Both magnesium sulfate should be administered prophylactically if the patient is in labor, since the disease process inevitably worsens at the time of delivery. Patients with eclampsia or severe preeclampsia should be transported rapidly but without the use of light or sirens due to the possibility of inducing a seizure.
NORMAL LABOR
Labor consists of a series of rhythmic, progressive contractions of the uterus that cause effacement and dilation of the uterine cervix. The stimulus for labor is unknown. Circulating oxytocin secreted by the posterior pituitary gland may initiate labor, but no direct evidence supports this thesis. Labor usually begins within 2 weeks (before or after) of the estimated date of confinement. In a first pregnancy, labor usually lasts a maximum of 12 to 14 hours; succeeding labors are shorter, averaging 6 to 8 hours. During labor, contractions increase in duration, intensity, and frequency. A latent phase, with irregular contractions of varying intensity that apparently ripen or soften the cervix, usually precedes actual labor. This latent phase may be intermittent over several days or may last only a few hours. Bloody show (a small amount of blood with mucous discharge from the cervix) may precede the onset of labor by as much as 72 hours. Occasionally, the amniotic and chorionic sac (the membranes) ruptures before labor begins, and amniotic fluid leaks through the cervix and vagina. When a patients membranes rupture, she should contact her physician immediately. About 80 to 90% of patients with ruptured membranes go into labor spontaneously within 24 hours. If the patient does not and if the fetus is at term, labor is usually induced because of risk of infection.
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Various abnormalities of both 1st and 2nd stages of labor (problems of fetal distress, abnormal presentations, disproportions between fetus and maternal pelvis, bleeding disorders, infection, or premature labor) require special investigation; correction of the problems if feasible; and possible use of forceps, vacuum extractor, or cesarean section delivery by the delivering physician. Implantation of the placenta over or near the internal os of the cervix. The placenta may cover the internal os completely (total previa) or partially (partial previa), or it may encroach on the internal os (low implantation or marginal previa). Placenta previa occurs in one out of two hundred deliveries, usually in multiparas or in patients with abnormalities of the uterus, such as fibroids, that inhibit normal implantation. Sudden, painless vaginal bleeding begins late in pregnancy when the lower uterine segment begins to thin and lengthen and is followed by painless, massive, bright red bleeding. Placenta previa frequently cannot be distinguished from abruptio placentae by clinical findings. PROLAPSED CORD This condition refers to the situation in which the umbilical cord comes out of the vagina before the baby during delivery. The baby is thereby in great danger of suffocation, since the cord is compressed against the birth canal by the babys head, which cuts off the supply of oxygenated blood from the placenta. Do not attempt to push to cord back into the vagina. Administer high flow oxygen. Place the mother in a knee chest position or in a supine position the hips elevated and gently attempt to push the baby back up into the vagina to relieve pressure from the cord. UTERINEINVERSION This conditions occurs when the uterus turns inside out after delivery. It is commonly caused by pulling on the umbilical cord while waiting on the placenta to deliver or from attempts to expel the placenta when the uterus is relaxed. Profound shock usually accompanies this condition. Treat per the hypotension guideline. One attempt at replacing the uterus may be made. To replace the uterus, push the fundus with the palm of the hand toward the vagina, if the attempt is unsuccessful cover the uterus with towels moistened in saline and transport the patient immediately. UTERINERUPTURE This condition most often occurs at the onset of labor or can be caused by trauma. Preexisting conditions such as previous uterine surgeries can predispose a patient to this condition. Patients often report tearing sensation or constant area of specific pain, nausea or shock. Vaginal bleeding may be minimal. Noticeable contractions will cease and the uterus will be hard. Treat for shock and place in the shock position with the uterus displaced to the left. PROBLEMS WITH THE THIRD STAGE OF LABOR Maternal hemorrhage must be prevented during the 3rd stage. Ordinarily, 400 to 500 mL of blood is lost during delivery; if the loss is greater, the reasons must be sought. Possible sources of bleeding include uterine atony, vaginal or cervical E - 23 2/15/06
PROBLEMS WITH THE SECOND STAGE OF LABOR/THIRD TRIMESTER BLEEDING

BREECH PRESENTATION The feet or buttocks present before the babys head. Allow the buttocks and trunk of the baby to clear spontaneously. Once the legs are clear, the baby should be supported with hand and arm of the medic. If head does not deliver within two or three minutes, place gloved hand into vagina with palm towards babys face. Form a V with the fingers on either side of the babys nose and push vaginal wall away until delivery of head is possible or until the receiving facility has taken over patient care. LIMB PRESENTATION The presentation of an arm or leg through the vagina is an indication for immediate transport to the hospital. This condition requires rotation of the fetus within the uterus prior to delivery and can not be handled in the field. Maintain a high buttocks position to prevent further presentation and transport immediately. PLACENTAABRUPTIO Placenta abruptio is premature separation of the placenta from the uterine wall. Separation can be either complete or partial, therefore blood loss may appear to be very small or could be massive. All degrees of placental separation, from a few millimeters to complete detachment, may occur. Complete separation almost always results in death of the fetus. Several factors may predispose a patient to this condition, such as pregnancy induced hypertension, preexisting hypertension, para of greater than one, abdominal trauma, or an extremely short umbilical cord. Symptoms may include vaginal bleeding associated with pain, signs of shock and hypotension. The cause is unknown. Abruptio placentae develops in 0.4 to 3.5% of all deliveries. Retroplacental bleeding occurs, and the blood may pass behind the membranes and through the cervix (external hemorrhage) or may be retained behind the placenta (concealed hemorrhage). Symptoms and signs depend on the degree of separation and blood loss. In severe cases, they include vaginal bleeding, a tender and tightly contracted uterus, evidence of fetal cardiac distress or death, and maternal shock. Abruptio placentae may be confused with placenta previa. PLACENTAPREVIA

lacerations, or retained portions of the placenta. If the uterus does not contract, hemorrhage will occur, since the primary mechanism for hemostasis within the uterus is contraction of myometrium. When the placenta has dropped into the lower uterine segment and presents at the cervix, the corpus may be depressed toward the pelvis to help push the placenta into the vagina. However, the uterus can be inverted if this procedure is done incorrectly, especially if traction is applied on the cord before the placenta is completely separated. ply acknowledging the patients pain and concerns. Paramedics are constantly challenged by having to move patients to stretchers from awkward positions. The application of splints, traction and backboards can create tremendous discomfort for your patients. Comfort and compassion are mainstays of medical care and their importance cannot be overemphasized. Some patients perceive and verbalize pain differently, and the paramedic must be attuned to the need for pain management even in the patient who does not verbalize pain. Maintaining awareness of some patients drug-seeking behavior is also required in evaluating the need from pain control.
PAIN MANAGEMENT
Pain is the number one reason patients seek medical attention. Furthermore, patients have the right to pain control. Establishing pain levels will become the fourth vital sign. Pain and anxiety are common side effects associated with both acute and chronic medical and trauma patients. Analgesia is used to minimize pain, ensure cooperation and comfort as well as reduce complications. EMS clinicians must meet the patients needs for pain control with the judicious use of medications. The perception, interpretation and vocalization of pain vary considerably between patients. The medications used for moderate to severe pain control carry the potential for respiratory depression. DEFINITION Analgesia is defined as a reduced state of awareness of painful stimuli and sensation, created by medications that allow patients to tolerate unpleasant situations while maintaining adequate respiratory function. Paramedics must continue to monitor and assess patients during pain control and be prepared to intervene in the event of a complication. Proper pain medication can decrease heart rate, respiratory rate, anxiety and blood pressure.
POTENTIAL FOR COMPLICATIONS

Complications can occur in the pre-hospital environment as a result of over-sedation, airway obstruction, vasovagal episodes, hypoventilation, aspiration, hypoxemia, hypercarbia, hypotension or a reaction to the medication(s) in use. Elderly and pediatric patients in particular are at increased risk during analgesia. Patients who are currently taking sedative or opioids may also be at a greater risk for over-sedation.
PREMEDICATION PATIENT ASSESSMENT

All patients receiving intravenous pain medication require a rapid pre-medication evaluation to determine relative risk versus benefit, to identify problems related to preexisting medical conditions such as the presence of any abdominal pain, a difficult airway, and to recognize patient or parental concerns related to treatment. A brief history, review of current medications and allergies, as well as an assessment of cardiopulmonary status at the time of treatment are necessary to adequately provide for the safety of the patient. Determining the patients state of anxiety or pain prior to and after the administration of medication is critical. Monitoring the patients mental status is one of the most valuable indicators of the efforts of pain management. Pre-medication vital signs, including blood pressure, hear rate, SpO2, respiratory rate, EKG and temperature are documented. The use of pain medication requires continuous intravenous access until patient care is transferred to the emergency department. The paramedic must have good access to the intravenous line and medication port throughout on-scene time transport.
UNDERSTANDING THE PATIENTS NEEDS

Meeting the patients needs for pain control can improve patient care and satisfaction during an encounter with emergency pre-hospital clinicians. In addition to the usual stresses of life, chronic pain patients are plagued by the unknowns associated with their pain and the long-term consequences of pain, including a reduction in normal activities. Unrelieved acute and or moderate to severe chronic pain and poor symptom control can lead to anxiety and irritability, as well as a restricted social life, family issues, relationship issues, sleep deprivation, work issues, loss of self-esteem, and mood disturbances or depression. Between 50% and 70% of patients with chronic pain have either secondary depression or anxiety. Maximize non-pharmacological methods of pain control prior to administering medications. These methods can include transport in the position of comfort, padding with pillows and blankets at the point of contact, ice packs, and simE - 24
PAIN CONTROL
Opiates administered intravenously provide primary analgesia. Opiates require careful titration to patient needs, with continued monitoring. Opiates are administered slowly and in small increments with adequate time for the sedative effects of the injected dose to be apparent before additional medication is given. The synergistic potential of benzodiazepines and narcotics or antiemetics is significant for respiratory depression.
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Opiate and benzodiazepine antagonists, such as naloxone and flumazenil respectively, should be part of any sedation and pain medication array; however, these medications do not instantaneously reverse the respiratory depression that may be produced in pain control. The paramedic must be prepared to immediately support the patients airway, ventilation and oxygenation until sedation is reversed or eliminated. tion, but may mask impaired respiration or ventilation. Opioids depress all phases of respiratory activity to some extent. Respiratory depression becomes significant when intervention is needed. Opioids interfere with carbon dioxide chemoreceptors in the medulla by retention of carbon dioxide. The increase in carbon dioxide levels does not stimulate an increase in respiratory rate, and the patient may rely upon the less sensitive oxygen-driven, respiration-regulation mechanism. Respiratory depression may occur when the pain is relieved and is no longer a stimulant. The inherent limitations of and over-reliance on pulse oximetry as monitors of respiration have become evident with reports of unrecognized hypercarbia and delayed recognition of respiratory depression. While pulse oximetry is usually an excellent and noninvasive technology for monitoring oxygen saturation, its use for purposes of detecting ventilatory depression and/or apnea has limitations. Patients at risk for respiratory depression, whether because of illness or pharmacological intervention, are typically given supplemental oxygen and thus maintain adequate oxygenation despite inadequate ventilation, leading to significantly delayed recognition of hypercarbia. Pulse oximeters do not detect apnea. Capnography however, in the intubated patient is an excellent monitor for adequacy of ventilation. Anxiety relief via pain control using pharmacological agents are critical elements to improving patient comfort both mentally and physically, as well as outcome, particularly from the patients point of view. The patient record should document any clinical or technical problems during administration of medications, along with any significant patient events such as nausea and vomiting, respiratory distress, vagal or anaphylactic reaction or diaphoresis, as well as any intervention taken by the paramedic. The paramedics ability to use, interpret and act upon the data derived from the patient assessment and monitoring technology will help ensure a positive outcome for the patient. Promoting patient comfort and reducing or eliminating pain are the responsibilities of all pre-hospital clinicians, while at the same time ensuring patient safety.
NARCOTICS
Narcotics are divided into several classes, which include naturally occurring, semi-synthetic opioids and synthetic opioids (nalbuphine). The potency and duration of action between different classes varies widely. Fixed doses of analgesic may not meet the individual patients needs in terms of pain management. Sufficient time between doses is necessary in order to observe the effects of the agent and prevent and/or treat respiratory depression.
NARCOTIC ANTAGONISTS
Narcotic Antagonists include naloxone hydrochloride (Narcan), which is primarily used to antagonize respiratory depression and central nervous system depression secondary to narcotic overdose. Onset of action is usually within 2 minutes, and the duration of action is about 20-60 minutes. Repeat boluses may be required to maintain adequate blood levels until the opioid agonist is eliminated. This narcotic antagonist can precipitate acute withdrawal symptoms in opioid-dependant or addicted patients. Symptoms of withdrawal include agitation, hypertension, sweating and irritability.
MONITORING
Using additional personnel for monitoring does not replace continuous clinical evaluation and assessment prior to and during the administration of analgesic and antiemetics. While the risk of adverse events is low, patients should be assessed prior to administration of analgesics to establish a baseline of vital signs and level of mentation. Adverse reactions increase in frequency with the complexity of the patients illness or injury and the level of sedation. Patient observation and monitoring before, during and after the administration minimizes complications. The paramedic must be diligent in recognizing early signs of distress and implement appropriate supportive or resuscitative measures.
PSYCHIATRIC EMERGENCIES
Psychiatric emergencies stem from a wide range of disorders, including acute anxiety, depression, psychosis, and drug and alcohol abuse. When dealing with a patient experiencing a psychiatric emergency, the Teams priorities include providing for medical and psychiatric evaluation and managing aggression. Keep these guidelines in mind:
RESPIRATION MONITORING
The primary cause of morbidity with pain control medications is drug-induced respiratory depression. Monitoring of respiration, ventilation and oxygenation reduces the risk of negative outcomes associated with pain control. Hands-on monitoring should detect early signs of patient distress before compromises to vital functions occur. Supplemental oxygen administration may reduce the risk of oxygen de-satura-
GENERAL GUIDELINES
To help the patient regain their sense of selfcontrol, act E - 25
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with decisiveness and compassion. Attempt to establish rapport with the patient to gain their trust and cooperation. Speak to the patient firmly but calmly, in a nonthreatening way. Assure safety of patient and others by removing any items they could use to harm themselves or others. Obtain background information to help determine nature and severity of problem. Find out what events led to this condition, if a specific incident triggered it, who brought patient to hospital, why patient wants help now, and what patient expects from this visit. Assist with diagnostic tests to help determine if an underlying physical condition is causing the psychiatric emergency. A patient with an organic problem (usually the result of metabolic or neurologic disorder) may be disoriented or confused and have recent, sudden memory loss and decreased sensory perceptions. Perform a mental status examination. Assess patients level of consciousness, motor activity, and orientation to time, place and person. Then assess their mood (their predominant emotion); affect (flat, normal, or increased); association (normal, loose or illogical); intellect (slow, normal or bright); memory (poor or good); thought processes (normal, confused, delusionary, or hallucinatory); insight and judgment; abstract thinking; and thought content (obsessive, compulsive, suicidal, preoccupied, repetitive, phobic). Assess patients anxiety level, and determine if their judgment and insight are impaired by an acute anxiety attack. Signs and symptoms of such an attack may include hyperactivity, dry mouth, fidgeting, sensation of chest pressure, choking sensation, inability to swallow, sense of impending danger, hyperventilation, sweaty palms, tachycardia, tremors, profuse sweating, and urinary frequency. To decrease patients anxiety, provide emotional support and calmly direct the patient toward reality. Encourage the patient to express their concerns and to identify source of their anxiety. Help the patient set priorities, but allow the patient some control of situation. personal history of previous suicide attempts, mental illness, debilitating physical illness, substance abuse, or death of loved ones increases the suicide risk. When in doubt, arrange for psychiatric consultation and/or hospital admission for observation. Provide suicide patient with psychologically and physically protective environment, and establish rapport with the patient. Keep in mind that suicidal thoughts represent an attempt to solve a problem. Try to find out what the patient thinks their problem is. Typical problems include job situation, interpersonal relationships, mental or physical illness, alcohol or drug abuse, financial problems, or loss of a loved one. Try to involve their family or friends in this planning process, if possible. If hes unsure of their alternatives, or if he has no alternatives, arrange for hospitalization and obtain psychiatric consultation.
DEALING WITH THE VIOLENT PATIENT

The violent patient may take their anger out on the team, as the primary caregiver. The Teams response can calm the patient and help the patient cope, or it can make the patient even more angry and violent. Follow these guidelines to make sure the Teams interactions are helpful and appropriate. If the Team fears the patient may cause bodily harm, call for help to subdue and restrain the patient, and give medications, as ordered. Verbal abuse frequently precedes violent behavior. If patient complains vehemently, listen carefully, giving the patient the Teams undivided attention and maintaining eye contact. If their anger seems out of proportion to the situation, ask who or what hes really angry with. Agree with the real aspects of their anger (such as waiting a long line to see a doctor). Empathize with the patient about their situation and ask the patient for suggestion to help improve it. Review their complaints and restate what hes said to try to identify their real concerns. He may be demonstrating the behavior to obtain something he wants; in this situation, point out to the patient that their anger is only making it more difficult for the team and others to help the patient. Let the patient know that the Team members are people, not an impersonal target, and that their behaviors upsetting the team. Remain calm and speak softly. Be aware of both verbal and nonverbal communication as facial expressions, tone of voice, or gestures can provoke a patients anger. Closely observe their body language, and monitor personal body language for signs of hostility. Keep stance as relaxed and neutral as possible.
DEALING WITH THE SUICIDAL PATIENT

The suicidal patient typically has severe depression and low selfesteem and directs their anger inward. Typical signs and symptoms include feelings of worthlessness, hopelessness, helplessness, or confusion; insomnia and fatigue, gastrointestinal complaints; decreased physical activity; indifference; and history of past suicide attempt. Keep these points in mind when dealing with a suicidal patient: Attempt to determine the patients suicide potential. Is this a gesturea way to manipulate othersor is it a real attempt at suicide? How upset or disturbed is the patient? If he attempted suicide, did he choose a suicide method that was likely to succeed? When assessing for suicide potential, remember that widowed, divorced and single persons have a higher risk than married persons, and that a family history of suicide and a E - 26
DEALING WITH THE ACUTE PSYCHOTIC PATIENT

Acute psychotic reaction, such as schizophrenic and paranoid episodes, represent disorders of mood or thinking in which
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the patient loses contact with reality. Their thought processes, affective responses, and interpersonal dealings deteriorate until they can no longer cope with the activities of daily life. A patient having a schizophrenic episode typically has delusions; auditory hallucinations; combative, assaultive, withdrawn, or catatonic behavior; poor associations; bizarre gestures; and disordered thinking. A patient suffering from paranoia (a type of schizophrenia) may have the following signs and symptoms, in addition to those described above; feelings of uniqueness or grandiosity; restlessness and agitation; obsessive thoughts; and projective delusions. Their delusional system typically includes persecution feelings or excessive religious statements, with false beliefs based on grossly exaggerated aspects of their life. He typically believes that others are out to get him. When dealing with an acute psychotic patient, place the patient in a quiet room, and avoid arguing with the patient. If hes violent or potentially violent, apply restraints. Remove their clothing or any object that may conceal a weapon, and place the patient in a hospital gown. Then intervene as follows: to restrict a patients movement, activity, or access to their body. Patients generally have a right to be free from restraints unless restraint is necessary to treat their medical symptoms or to prevent patients from harming themselves or others. Restraining a patient raises serious concerns, such as infringement on patient autonomy, limits on freedom of movement, claims of battery, and risk of physical and/or psychological injury resulting from restraints. Therefore, before using restraints, clinicians must carefully weigh the benefits of the restraint against the risks of the restraint, and you should always consider whether alternatives to restraint are available. Every effort should be made to utilize the least restrictive method of restraint. Situations arise in which restraints are not only appropriate and necessary, but also in which failure to use a restraint could result in injury to the patient or others. Restraints may be used in response to dangerous behavior, to protect patients and as part of approved protocol. Examples of these situations include the following: Patients with invasive catheters, lines or tubes Patients who are violent or could inflict potential harm to self or others due to an impaired psychological state Allow assessment of disoriented and uncooperative patients or those under the influence of alcohol or drugs Facilitate medically necessary procedures (ie, gastric lavage) in uncooperative patients Prevent elopement while patients are being evaluated and transported for potential suicidal or homicidal behavior Protect disoriented patients from falls off stretchers and backboards Patients with brain pathologies or injury At the discretion of the flight crew to ensure flight safety All prisoners Whenever restraints are employed, their use must be consistent with federal and state laws and most importantly, sound clinical judgement. Monitoring must be performed by direct observation of and interaction with the patient. It should include a determination regarding the patients well-being as well as an on-going evaluation of the continued need for restraints upon arrival at the receiving facility. Documentation in the medical record should include clinical justification of the necessity for restraints and measures taken to protect the patients rights, dignity, and well-being (ie, monitoring, reassessment, attention to patients needs).
FOR A PATIENT WITH A SCHIZOPHRENIC REACTION:

Determine if patient has been previously hospitalized and if hes recently stopped taking major tranquilizers. Speak to the patient firmly to assure the patient that the Team is in control of the environment. Use simple, concrete language and brief sentences, avoiding words or phrases that patient might misinterpret. Obtain psychiatric consultation and arrange for hospital admission, as appropriate. Give medications, as ordered; if the Team gives phenothiazine, observe for postural hypotension and pseudoparkinsonian effects.
FOR A PATIENT WHOS PARANOID:

Avoid any physical or psychological threats or challenges. Move slowly and quietly, and sit or stand on patients level to avoid appearance of power. Avoid closed doors or blocked doorways so that he doesnt feel cornered. If possible, let the patient stand near a door thats slightly ajar. Remain calm and authoritative, and use simple, concrete expressions as the Team talks to the patient. Dont try to convince the patient their delusions are wrong. Instead, let the patient verbalize distorted or illogical thinking, but avoid validating their false beliefs.
RESTRAINTS
Restraints are any physical or pharmacological means used
ONCE RESTRAINED, ALWAYS RESTRAINED

If at any time a patient requires physical restraint, the patient should remain restrained in some manner until delivE - 27 2/15/06

ered to the emergency department. Do not allow the patient to bargain with you, or talk you into release of restraints. Remember, A COOPERATIVE PATIENT WILL COOPERATE WITH RESTRAINTS. Patients may have injuries that result from being restrained. Most injuries are minor and include abrasions and bruises. However, more serious injuries can occur if restraints are inappropriately applied or the patient is not adequately monitored.
STANDARDS
When restraints are necessary, practitoners must determine the most appropriate and least restrictive device that allows the patient to retain as much dignity as possible. For example, the following physical restraints are appropriate for the following situations: Posey vests or sheet roles to prevent disoriented patients from climbing off stretchers. Side rails are not considered restraints by themselves. Soft wrist restraints to protect confused patients from extubating themselves Limb restraints (ie, upper, lower, 4-point, opposites, soft, leather) to restrain violent patients To ensure flight safety
ALLOWANCE OF OPTIONS
It is vitally important and therapeutic for all patients to be given as many options as possible. Giving patients choices and options helps them to begin regaining a sense of selfcontrol, a sense of normalcy. Emergency situations inflict an extremely frightening and threatening sense of loss of control upon the patients who experience them. This recognition of the need to allow options, to restore a patients sense of selfcontrol, however, does not change the fact that restraint is going to occur. Once a clinician recognizes the need for restraint, restraint must be employed. Restraint application is not a patient option. As soon as possible, begin to allow patients as much control as you are comfortable with allowing. In example I need to make sure youre safe and secure. Would you prefer to be sitting up or lying down? Would you care for another blanket? Which arm would you prefer that I use for your IV? The secret to offering patients options is this; as long as it does not matter what the patient chooses, offer them the option. The fact that restraint will occur does not change. But, to improve the patients condition and encourage cooperation, the patient should be given as many opportunities as possible to exercise some sense of control over the situation.
USE OF LEATHER RESTRAINTS

Leather restraints in the pre-hospital setting are obsolete and their use is strongly discouraged. They are bulky and slow to apply They cannot be effectively anchored to afford a true medical restraint. They present a cross-contamination problem due to the material in which they are constructed. If not periodically cleaned and treated, they become brittle and can break under stress.(When was the last time you cleaned and treated your leather restraints?) They are frightening to both patients, family and onlookers. They must be a non-locking variety to facilitate quick release. They can create injuries because they are not soft and padded. Agencies currently utilizing leather restraints are encouraged to research and acquire soft, disposable posey or Velcro type limb restraints as a superior alternative. A team of several members working together (ie, police, firefighters, ems personnel) may be the best way to restrain a violent patient. Appearance of a team may convince a patient to permit application of restraints without resistance. Ideally, each team member is responsible for immobilizing one extremity. This team approach minimizes risk of injury to the patient and the crew. Although physical restraints generally are the first method employed when restraints are necessary, pharmacological restraints may be used as an alternative or adjunct to physical restraints. E - 28
COMPLICATIONS
Complications from pharmacological sedation are more numerous than from physical restraints. Uncooperative patients often provide inadequate histories, which presents increased possibility for allergic reactions. Oversedation could lead to loss of gag reflex, compromising the patients ability to protect the airway. A patient who vomits while in 4- point restraints risks choking and aspiration. Pulse oximetry is helpful in measuring such patients. Patients who are being restrained after an overdose pose particular problems because the ingested substances often are unknown. Sedation could lead to drug interactions with adverse effects. Use caution whenever caring for patients in restraints. Personnel injuries can occur from violent behavior, such as biting, scratching, spitting, and kicking. At all times, full PPE will enhance personnel protection. Be on the lookout for patients with concealed weapons or dangerous objects (ie, needles).
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CHEMICAL RESTRAINTS
Chemical restraints are any medications used for the purpose of restraining patients involuntarily to prevent them from harming themselves or personnel. The intent of such medications is sedation for the duration contact until the patient arrives at the emergency department. ADVANTAGES OF CHEMICAL RESTRAINTS Control violent behavior and patient agitation May reduce need for physical restraints DISADVANTAGES OF CHEMICAL RESTRAINTS May result in complications, such as respiratory depression and loss of gag reflex Limit mental status assessment and neurologic examination during sedation
Adverse effects include interactions with other

s3edatives, which commonly result in respiratory depression and loss of gag reflex, exacerbation of glaucoma, and paradoxical reactions.
PRECAUTIONS Patient dosing is very variable. More medication

may be administered if inadequate sedation results after initial dose. Monitor for respiratory depression and loss of gag reflex
AGENTS
Benzodiazepines Lorazepam (Ativan) is commonly used to sedate elderly patients and has a wide safety margin. Respiratory depression and loss of gag reflex usually do not result if recommended doses are used. Duration of action is long. Adult dose is 1-4mg IV, IO, IM, or intranasal titrated to effect Onset of action is 5-10 minutes Duration of action 4-8 hours Adverse effects include exacerbation of glaucoma, respiratory and gag reflex, depression (especially when combined with other sedatives or narcotics), and fetal damage. Midazolam (Versed) is commonly used for rapid sedation in emergency settings because of its rapid onset and brief duration of action. Adult IVP dose is 5mg under 60 years of age (may repeat once), 2.5mg over 60 years of age (may repeat once) initially over 2 minutes. Allowing 2 or more minutes to evaluate response; titrate slowly. Can be given IV, IO, IM or intranasal. Onset of action is 1-5 minutes Duration of action is 30-60 minutes Diazepam (Valium) is widely used for sedation, treatment of agitation secondary to alcohol withdrawal and treatment of seizures. It has a high therapeutic-to-toxic ratio. Respiratory depression and impaired gag reflex are rare when used alone. Adult dose is 2-10mg IV, IO, IM, or intranasal titrated to effect. Onset of action is 1-5 minutes Duration of action is 30-60 minutes
Chemical restraints can be an effective adjunct or replacement for physical restraints. Appropriate use of restraints promotes patient and crew safety. Health care professionals can incur liability from inappropriate use of restraints and for failure to use restraints to protect a patient; each situation in which use of restraints is considered must be evaluated carefully.
RAPID SEQUENCE INTUBATION (RSI)

Rapid Sequence Induction (RSI), is the use of specialized medications to facilitate intubation and to provide for muscle relaxation. In the past these medications have been reserved for use by anesthesiologists in the operating room, but recently have become accepted for use in the prehospital setting for an aid in intubation. Neuromuscular blockade is useful for a number of situations encountered in the prehospital setting. It will enable ventilation of patients who cannot be ventilated because of coughing or resisting ventilation attempts. Oxygen consumption is reduced, shivering may be prevented, and chest wall compliance may be increased through the use of muscle relaxants. When an airway cannot be secured by other means, neuromusclar blockade allows a patient to be more readily intubated. Occasionally a patient may need to be given a muscle relaxant in order to prevent nerve damage during transport.
CARE FOR THE PARALYZED PATIENT

It is of paramount importance to remember a patient that has been given a paralytic is not unconscious, just paralyzed. They can hear and see everything going on around them. Therefore adequate sedation and analgesia must be given. Some signs of inadequate sedation or analgesia would be: 1. Hypertension 2. Tachycardia 3. Lacrimation 4. Diaphoresis 5. Ventricular dysrhymias E - 29
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6. Bronchospasm 7. Increased pulmonary secretions. PARALYZED PATIENTS REQUIRE FULL VENTILATIONS, VENTILATOR DISCONNECTS OR MECHANICAL FAILURES CAN BE FATAL. setting is vecuronium bromide (Norcuron). Vecuronium bromide has a duration of 3060 minutes and generally requires redosing every 2040 minutes. There are no hemodynamic effects when used in clinical doses. One of the most life threatening side effects of neuromuscular blockade is Acute Malignant Hyperthermia. This is a rapid rise in body temperature that can reach life a threatening level. The condition is believed to be due to the decrease in calcium uptake by the sarcoplasmic reticulum resulting in increased intracellular calcium levels and the acceleration of aerobic and anaerobic cellular metabolic processes. The result of this increase in metabolism is excessive heat, carbon dioxide, and lactic acid. Patient will present with unexplained tachycardia, cyanosis, or tachypnea. Remember: MALIGNANT HYPERTHERMIA PRODUCES HYPOXEMIA, SEVERE RESPIRATORY AND METABOLIC ACIDOSIS, AND HYPERKALEMIA. There are a number of factors that may potentiate neuromuscular blockade. Acidosis, both respiratory and metabolic, electrolyte imbalances, preexisting neuromuscular disease, and drugs are just a few of these factors.
Be sure to protect pressure points even during a short transport. Beware not to cause joint dislocations when moving or handling the patients. Since paralyzed patients cannot swallow or cough, be sure you keep the pharynx and trachea clear of secretions. History and physical assessment may be lost when the patient is paralyzed. This may be an important factor in patients with a changing neurologic status.
PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION / BLOCKADE

A wave of depolarization reaches the motor nerve terminal. In the presence of calcium, the acetylcholine vesicles bind to the membrane and empty their contents into the synaptic cleft. Acetylcholine traverses the synaptic cleft and binds with receptors on the motor endplate causing a small endplate potential. If enough of these endplate potentials occur, a wave of depolarization is set up in the muscle membrane, calcium is then released and muscle contraction occurs. There are two types of muscle relaxants, depolarizing and nondepolarizing. With depolarizing neuromuscular blockade the medication binds to the acetylcholine receptors and creates a wave of depolarization that manifests itself as muscle fasciculation. This medication remains bound to the receptor and prevents subsequent binding of acetylcholine and neuromuscular blockade results. Whereas nondepolarizing muscle relaxants competitively antagonize acetylcholine and prevent depolarization of the muscle membrane. No fasciculation is seen when nondepolarizing agents are used.
RENAL FAILURE
Chronic renal failure (CRF) requiring dialysis or transplantation is known as end stage renal disease (ESRD). Patients with ESRD commonly present with problems related to the metabolic complications of their renal disease or dialysis. It is important to remember these patients may also suffer from medical problems unrelated to their renal condition. Medical direction via telemetry is always advised for treatment modalities other than immediate dialysis complications. Almost all major organ systems are affected by renal failure. Signs and symptoms of renal failure are due to overt metabolic derangements resulting from inability of failed kidneys to regulate electrolyte, fluid, and acid-base balance; they also are due to accumulation of toxic products of amino acid metabolism in the serum. Volume overload, a common cardiovascular complication of renal failure, occurs when salt and water intake exceeds losses and excretion. The most common cause of sudden death in patients with ESRD is hyperkalemia, (potassium) this is often encountered in patients who have missed dialysis. It may also be due to diatary indiscretion. Hyperkalemia is usually asymptomatic. An EKG may be helpful in diagnosis. Severely peaked T waves may be seen. Hypocalcemia is also potentially life threatening and re-
COMMONLY USED MUSCLE RELAXANTS

The most common depolarizing agent used today is succinycholine chloride (Anectine). Succinycholine chloride is rapidly metabolized and normal neuromuscular transmission is restored in 510 minutes. Prolonged blockade (2030 minutes) may occur in the presence of liver disease, starvation, pregnancy, and in patients with abnormally low pseudocholinesterase. Severe hyperkalemia and cardiac arrest has been reported in patients with major burns, trauma, closed head injuries, and a variety of neuromuscular diseases. Succinycholine chloride has also been associated with increased intracrainial pressure and increased intraoccular pressure. Increased intragastric pressure with regurgitation may also occur. There are many nondepolarizing agents in use today, but the most commonly used one in the prehospital E - 30
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sults from loss of vitamin D and increased parathyroid hormone levels. This may cause weakness and life-threatening dysrhythmias. Acidosis may also be present as shortness of breath due to the work of breathing from compensatory hyperpnea. toxin, lead, alcohol, cocaine), cerebral hypoxia (Adams Stokes syndrome, carotid sinus hypersensitivity, anesthesia, carbon monoxide poisoning, breathholding), expanding brain lesions (neoplasm, intracranial hemorrhage, subdural hematoma in infancy), brain defects (congenital, developmental), cerebral edema (hypertensive encephalopathy, eclampsia), cerebral trauma (skull fracture, birth injury), anaphylaxis (foreign serum or drug allergy), and cerebral infarct or hemorrhage. Convulsions may also occur as a withdrawal symptom after chronic use of alcohol, hypnotics, or tranquilizers. Hysterical patients occasionally simulate convulsive attacks. The seizures are transient in many of these conditions and do not recur once the illness ends. However, convulsions may recur at intervals for years or indefinitely if there is a permanent lesion or scar in the CNS, in which case a diagnosis of epilepsy is made. Convulsive seizures result from a generalized disturbance in cerebral function. In some instances, a small focus of dysfunctional tissue in the cerebrum discharges abnormally in response to endogenous or exogenous stimuli, and spread of the discharge to other portions of the cerebrum results in convulsive phenomena and loss of consciousness. In primary generalized epilepsy, the seizures are generalized from the outset, beginning as a diffuse abnormal discharge affecting all cerebral cortical areas simultaneously. Given a sufficient stimulus (i.e., convulsant drugs, hypoxia, hypoglycemia), even the normal brain can discharge in a diffusely synchronous fashion and produce a seizure. In susceptible persons, seizures may occasionally be precipitated by exogenous factors (sound, light, cutaneous stimulation). Epileptic seizures can be classified according to several different criteria. Partial seizures begin focally with a specific sensory, motor, or psychic aberration that reflects the affected part of the cerebral hemisphere where the seizure originates. Auras (focal manifestations that immediately precede complex or generalized seizures) reflect where the seizure begins. Sometimes a focal lesion of one part of a hemisphere activates the entire cerebrum bilaterally so rapidly that it produces a generalized grand mal seizure before any focal sign appears. Generalized seizures usually affect both consciousness and motor function from the outset. The seizure itself frequently has a genetic or metabolic cause. Seizures affect about 2% of the population; chronically recurring seizures (epilepsy) are perhaps 1/4 that frequent. Most patients have only 1 type of seizure; about 30% have 2 or more types. About 90% experience grand mal seizures, either alone (60%) or with other seizures (30%). Absence (petit mal) attacks occur in about 25% (4% alone, 21% with others). Psychomotor attacks occur in 18% (6% alone, 12% with others). E - 31 2/15/06
SEIZURES
The swift termination of seizure will protect patients from anoxic conditions conducive to brain injury. Careful recording of appearance and duration are vital. The Team should consider the following: alcoholic history, history of seizures, drugs present at scene, tracks in arms, cocaine in nose, fever, or head injury. Epilepsy: A recurrent paroxysmal disorder of cerebral function characterized by sudden, brief attacks of altered consciousness, motor activity, sensory phenomena, or inappropriate behavior caused by abnormal excessive discharge of cerebral neurons. Convulsive seizures, the most common form of attacks, begin with loss of consciousness and motor control, and tonic or clonic jerking of all extremities, but any recurrent seizure pattern may be termed epilepsy. Epilepsy is classed etiologically as symptomatic or idiopathic: Symptomatic implies that a probable cause has been identified that at times permits a specific course of therapy to eliminate that cause; idiopathic means that no obvious cause can be found, which is the case in about 75% of young adults and a smaller percentage of children under age 3. Epilepsy due to a microscopic scar in the brain resulting from birth trauma or other injury may be misclassified during life as idiopathic but show evidence of a causative lesion at autopsy or surgery for epilepsy. Unexplained, predominantly inherited neuronal abnormalities probably underlie most idiopathic cases. Idiopathic epilepsy generally begins between ages 2 and 14. Seizures before age 2 are usually related to developmental defects, birth injuries, or a metabolic disease affecting the brain; those beginning after age 25 are usually secondary to cerebral trauma, tumors, or other organic brain disease. Focal brain diseases can cause seizures at any age. Seizures may be associated with a variety of cerebral or systemic disorders, as a result of a focal or generalized disturbance of cortical function. These include hyperpyrexia (acute infection, heat stroke), CNS infections (meningitis, AIDS, encephalitis, brain abscess, neurosyphilis, rabies, tetanus, falciparum malaria, toxoplasmosis, cysticercosis of the brain), metabolic disturbances (hypoglycemia, hypoparathyroidism, phenylketonuria), convulsive or toxic agents (camphor, chloraquine, pentylenetetrazol, strychnine, picro-

Simple partial (focal, local) seizures begin with specific motor, sensory, or psychomotor focal phenomena without loss of consciousness. Isolated epileptic auras are simple partial seizures with a single sensory symptom (often olfactory) preceding a complex or generalized seizure. In Jacksonian seizures (focal motor symptoms begin in one hand or foot and then march up the extremity, or spread similarly from a corner of the mouth), the dysfunction may remain localized or may spread to other parts of the brain, with consequent loss of consciousness and generalized convulsive movements. Complex partial (psychomotor) seizures are characterized by a variety of patterns of onset. In most instances, the patient has a 1 to 2 minute loss of contact with the surroundings. The patient at first may stagger, perform automatic purposeless movements, and utter unintelligible sounds. He does not understand what is said and may resist aid. Mental confusion continues for another 1 or 2 minutes after the attack is apparently over. Psychomotor attacks may develop at any age and are usually associated with structural pathology (i.e., mesial temporal sclerosis, lowgrade astrocytomas). Status psychomotor epilepsy may occur, in which affected subjects act in a slow, bewildered, and sometimes confused state for hours or, rarely, days. Complex partial seizures of temporal lobe origin are not characterized by unprovoked aggressive behavior. If restrained, however, such a patient occasionally may lash out at the person restricting his movement, as may a patient in a postictal confused state after a generalized seizure. No satisfactory evidence suggests that premeditated or unprovoked aggression can ever be attributed to attacks of temporal lobe epilepsy. Patients with temporal lobe epilepsy experience a higher incidence of interictal psychiatric disorders than does the normal population. Selection factors in evaluation make exact figures difficult to be sure of, but some studies show as many as 33% of patients with temporal lobe epilepsy having substantial psychologic difficulties, with up to 10% showing symptoms of schizophrenia or depressive psychoses. Generalized seizures can be minor or major in their motor manifestations. Generalized seizures may be primarily generalized (bilateral cerebral cortical involvement at onset), or secondarily generalized (local cortical onset with subsequent bilateral spread). Absence (petit mal) attacks are brief, primarily generalized seizures manifested by a 10 to 30 second loss of consciousness, with eye or muscle flutterings at a rate of three per second, and with or without loss of muscle tone. The patient suddenly stops any activity in which he is engaged and resumes it after the attack. Petit mal seizures are genetically determined and occur predominantly in children: they never begin after age 20. The attacks are likely to occur several or many times a day, often when the patient is sitting quietly. E - 32 2/15/06 They are infrequent during exercise. Between seizures, patients are normal. Infantile spasms (salaam seizures) are primarily generalized seizures characterized by sudden flexion of the arms, forward flexion of the trunk, and extension of the legs. The attacks last only a few seconds but may be repeated many times a day. They are restricted to the first 3 years of life, often to be replaced by other forms of attacks. Brain damage is usually evident. Tonicclonic (grand mal) seizures occasionally begin with a partial aura of epigastric discomfort, followed by an outcry; the seizure continues with loss of consciousness; falling; and tonic, then clonic, contractions of the muscles of the extremities, trunk, and head. Urinary and fecal incontinence may occur. The attack usually lasts 2 to 5 minutes. It may be preceded by a prodromal mood change, and may be followed by a postictal state, with deep sleep, headache, muscle soreness or, at times, focal motor or sensory phenomena. The attacks may appear at any age. Akinetic seizures are brief, primarily generalized seizures seen in children and characterized by complete loss of muscle tone and consciousness. The child falls or pitches to the ground, so that attacks carry the risk of serious trauma, particularly head injury. Febrile seizures-A fever is the elevation of the body temperature above the normal temperature (0.5-1.0 degree higher for rectal temperatures) for that person. In other words, fever is essentially a resetting of the hypothalamic thermostat. The body develops a fever when pathogens enter and cause infection which in turn stimulates the production of pyrogens. Pyrogens are any substances that cause fever. They reset the hypothalamic thermostat to a higher level. Metabolism is therefore increased, producing a fever. The increased body temperature wards off infection by making the body a less hospitable environment for the invading organism. The hypothalamic thermostat will rest to normal when pyrogen production stops or when pathogens end their attack on the body. The Physicians Desk Reference (PDR) does not specify a temperature for which an antipyretic (Tylenol) should be administered. Therefore, physician consult should be made to discuss each patients condition. Altered mental status frequently accompanies fever. With that in mind oral administration may be inappropriate. Additional cooling may be obtained by removing all extra clothing and allowing the patient to lose heat to the environment by convection. Further cooling may be inappropriate and are generally not recommended as these can drop the bodys core temperature too much. The cooling will induce shivering and additional heat production. Febrile seizures are the most common type of seizures observed in the pediatric group. Febrile seizures are usually be-
nign but can cause considerable parental anxiety. In the US between 2% - 4% of children have febrile seizures by their fifth birthday. About one third of these patients have at least one recurrence. Febrile seizures are divided into 2 types, simple febrile seizures (which are generalized and lasts <15 mins) and complex febrile seizures (which are prolonged, recur more than once in 24 h, or are focal). Complex febrile seizures may indicate a more serious disease process, such as meningitis, abscess, or encephalitis. Viral illnesses are the predominant cause of febrile seizures. Interestingly, there is no data to support the theory that a rapid rise in temperature is a cause of the type of seizure. The presence of 2 of the following risk factors increase the probability of the first febrile seizure: family history, high temperature, parental report of developmental delay, perinatal illness requiring hospitalization following delivery, and day care attendance. Patients with all 4 of the following risk factors have a greater than 70% chance of recurrence: young at the time of first febrile seizure, relatively low fever at the time of seizure, family history of a febrile seizure in the first degree, and brief duration between onset and initial seizure. Patients with no risk factors have less than a 20 % chance of recurrence. In status epilepticus, motor, sensory, or psychic seizures follow one another with no intervening periods of consciousness. Grand mal status epilepticus may persist for hours or days and may be fatal. It may occur spontaneously or result from too rapid withdrawal of anticonvulsants. Partial continuous epilepsy is a form of rare focal (usually hand or face) motor seizures in which the attacks recur at intervals of a few seconds or minutes, lasting from days to weeks at a time. The history should include an eyewitness account of a typical attack and information on the frequency of seizures and the longest and shortest intervals between attacks. A history of prior trauma (i.e., cranial injury producing unconsciousness, birth trauma), infection (i.e., meningitis, encephalitis, pertussis), or toxic episodes (i.e., excessive alcohol or drug consumption and its relation to seizures) must be sought and evaluated. A family history of convulsions or neurologic disorders is significant. Fever and stiff neck accompanying convulsions of recent onset should suggest meningitis or subarachnoid hemorrhage. Focal cerebral symptoms and signs in association with seizures suggest brain tumor, cerebrovascular disease, or residual traumatic abnormalities. Grand mal seizures, particularly in an adult, always require a diagnostic search for an unsuspected focal lesion. Most patients with epilepsy are normal between attacks, although overuse of anticonvulsants can dull alertness. Progressive mental deterioration is usually related to an accompanying neurologic disease that itself caused the seizures; only rarely do seizures per se impair mental abilities. The outlook is better when no brain lesion is demonstrable. About 70% of noninstitutionalized patients with epilepsy are mentally normal, 20% show a slight reduction in intellect, and 10% have a moderate to pronounced impairment.
RATIONALE
If, upon arrival, a patient is actively seizing, prompt administration of anticonvulsants may be necessary. Regardless of the clinical manifestations of generalized seizure, aggressive supportive care and rapid termination of electrical seizure activity are the goals. Care is individualized to the patient. For example, nasopharyngeal airway placement is sufficient for some patients, particularly if the seizures are stopped and the patient is awake. For other patients, endotracheal intubation is necessary. At times, rapid sequence induction, with neuromuscular paralysis is needed. Benzodiazepines These agents are employed commonly as the first drug for treatment of seizure. Lorazepam, when available, is thought to be the most effective and has a longer seizure half-life than diazepam. Lorazepam (Ativan) Sedative hypnotic with short onset of effects and relatively long half-life. Depresses all levels of CNS. Diazapam (Diastat, Valium) Depresses all levels of CNS. Individualize doses and increases cautiously to avoid adverse effects. Anesthetics These agents stabilize the neuronal membrane so the neron is less permeable to ions. This prevents the initiation and transmission of nerve impulses, thereby producing the local anesthetic effects. Lidocaine consistently terminates status epilepticus, but controlled studies are lacking. Furthermore, lidocaine toxicity may cause seizures. Propofol (Diprivan) Has general anesthetic properties when administered IV. Growing anecdotal reports of the use in refractory status epilepticus have been promising.
SEPSIS
Sepsis is a bacterial infection of the bloodstream. It usually occurs as a complication of an infection at another site such as pneumonia, an ear infection, or a urinary tract infection. Meningitis is frequently associated with sepsis. The mortality rate in sepsis is about 16-20%. In septic shock the rate rises to about 45%. Septic shock may develop due to the release of deadly toxins by the bacteria causing the infection. These toxins cause peripheral vasodilatation, leading to a drop in blood pressure E - 33
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and decrease in tissue perfusion. Sepsis can rapidly be fatal if not promptly identified and treated. Suspect sepsis in patients who become ill or who have been ill for several days, especially if accompanied by fever, lethargy, irritability, or shock. Initial management of the septic patient includes the standard primary and secondary assessment. In addition to the previously mentioned findings, other signs and symptoms of sepsis include vomiting and diarrhea, nonspecific respiratory distress. Septic shock may include a very ill appearance, altered mental status, tachycardia, capillary refill greater than 2 seconds, hyperventilation and cool and clammy skin. Sepsis is a very serious condition that can deteriorate quickly. It must be promptly recognized and treated appropriately. The goal is to prevent the development of septic shock. from patient to patient; most have mild jaundice with bilirubin levels of 2 to 4 mg/dL. Anemia may be exacerbated in children by acute sequestration of sickled cells in the spleen. More common is the aplastic crisis in both children and adults occurring when marrow red blood cell production slows during acute infections (especially viral). The vasoocclusive lesion, which appears due to an abnormal red blood cell membrane, results in cellular adherence to endothelium and subsequent obstruction. Long bone pain (i.e., pretibial) is a common clinical complaint; in children severe pain in the hands and feet (i.e., hand+foot syndrome) is both common and typical. Episodes of arthralgia with fever may occur, and avascular necrosis of the femoral head is common. Chronic punchedout ulcers about the ankles are a recurrent problem. Episodes of severe abdominal pain with vomiting may simulate severe abdominal disorders; such painful crises are usually associated with back and joint pain. Hemiplegia, cranial nerve palsies, and other neurologic disturbances may result from occlusion of major intracranial vessels. Infections, particularly pneumococcal, are common, especially in early childhood and are associated with a high mortality rate. Progressive decreases in lung and kidney function may be seen in older patients. Priapism is a serious complication most commonly seen in the young adult. Patients may be poorly developed and often have a relatively short trunk with long extremities and a tower shaped skull. Hepatosplenomegaly is common in children, but because of repeated infarctions and subsequent fibrosis, the spleen in adults is rarely palpable. The heart is usually enlarged, with a prominent pulmonary conus. Heart murmurs may simulate rheumatic or congenital heart disease. Cholelithiasis is common.
SICKLE CELL ANEMIA

Vasoocclusive crisis result from the occlusion of a vessel by masses of sickled red cells. Pain is the principle manifestation, and this represents the most common type of crisis. The symptom complex varies with the occlusion. Hepatic, pulmonary, or central nervous system involvement can, of course, also occur, each with its own symptomatology. Keep in mind patients with sickle cell disorder have a high incidence of life threatening disorders and at a young age. Take them seriously! Sickle cell anemia is a chronic hemolytic anemia occurring almost exclusively in blacks and characterized by sickle shaped red blood cells due to homozygous inheritance of Hb S. Homozygotes have sickle cell anemia (about 0.3% of blacks in the USA); heterozygotes (8 to 13% of blacks) are not anemic, but the sickling trait (sicklemia) can be demonstrated in vitro. In Hb S, valine is substituted for glutamic acid in the sixth amino acid of the betachain. This decreases its electrical charge, and it moves more slowly toward the anode than Hb A on electrophoresis. DeoxyHb S is much less soluble than deoxyHb A; it forms a semisolid gel of rodlike tactoids that cause red blood cells to sickle at sites of low PO2. Distorted, inflexible red blood cells plug small arterioles and capillaries, which leads to occlusion and infarction. Because sickled red blood cells are too fragile to withstand the mechanical trauma of circulation, hemolysis occurs after they enter the circulation. In homozygotes, clinical manifestations are due to both anemia and vasoocclusive events resulting in tissue ischemia and infarction. Anemia is usually severe but highly variable E - 34
HEMOGLOBIN SC DISEASE
Since 10% of blacks carry the Hb S trait, the incidence of the heterozygous SC combination is much greater than that of the homozygous Hb C disease. Many cases of anemia in patients with sicklemia may present undetected examples of the SC combination. The anemia in Hb SC disease is like that of Hb C disease but milder; some patients even have normal Hb levels. Most symptoms are those of sickle cell anemia, but they are usually less frequent and less severe. However, gross hematuria, retinal hemorrhages, and a septic necrosis of the femoral head are common. Stained blood smears show target cells and a rare sickle cell.
STROKE BRAIN ATTACK

STROKE ALERT:
Stroke as a medical emergency: Brain Attack In the past, patients with possible symptoms of ischemic
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Cincinnati PreHospital Stroke Scale (CPSS)

Facial Droop Normal Abnormal Arm Drift Normal Abnormal Abnormal Speech Normal Abnormal Have the patient show teeth or smile Both sides of face move normally One side of face does not move as well as the other side Patient closes eyes and holds both arms straight out for 10 seconds. Both arms move the same or both arms do not move at all (Other findings, such as grip strength, may be helpful) One arm does not move or arm drifts down compared with the other Have the patient say You cant teach an old dog new tricks Patient uses correct words with no slurring Patient slurs words, uses wrong words, or is unable to speak
Interpretation: If any of these 3 signs fall into the Abnormal category, the probability of a stroke is 72%.
stroke were seldom regarded as highpriority cases because only supportive care was available once they entered the health care system. With the recent US FDA approval of tissue plasminogen activator (tPA) for stroke, response to stroke must change dramatically. Today, tPA must be administered within 3 hours of onset and the emerging neuroprotective therapies must also be given within a limited time frame. The National Stroke Association (NSA) is spearheading an aggressive national campaign to educate members of the general public and health care community about the facts that stroke is a medical emergency and that delays in presentation may result in irreversible but preventable disability (Time is Brain). The team (EMS) plays a critical role in the prehospital management of stroke patients. The team should look for the most common signs of stroke, including unilateral weakness or numbness, unilateral facial droop, dysarthria, and expressive or receptive aphasia. The team should be alert to the possibility of stroke in patients who have fallen, have altered mental status, have had a seizure, are unresponsive or appear confused. The team should also remember that the signs and symptoms of hypoglycemia, brain abscess or tumor, and epidural or subdural trauma often resemble those of stroke. In response to these diagnostic challenges, a brief stroke scale that can be used in the prehospital setting has now been developed (Cincinnati Prehospital Stroke Exam). It includes a check for unilateral arm weakness, facial droop, and speech abnormalities. If the medical history and physical findings suggest that a patient has had a stroke and the onset of signs and symptoms can be identified as having started within 3 hours, a Stroke Alert should be called and appropriate treatment regimens initiated. The goals of the team management of patients with suspected stroke include rapid identification of
the stroke, support of vital functions, rapid transport of the victim to the receiving facility and prearrival notification of the receiving facility. The team members must be effectively trained in the recognition and treatment of stroke. Stroke is characterized by the sudden loss of circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Also called cerebrovascular accident, or stroke syndrome, stroke is a nonspecific term encompassing a group of causes, including thrombosis, embolism, and hemorrhage. Strokes currently are classified as either hemorrhagic or ischemic. Acute ischemic stroke refers to strokes caused by thrombosis or embolism and accounts for 75% of all strokes. They are the result of complete occlusion of a cerebral artery caused by cerebral thrombosis or embolism. Hemorrhagic strokes are caused by cerebral artery rupture with bleeding into the surface of the brain (subarachnoid) or bleeding in to the tissue of the brain (intracerebral). Hemorrhagic strokes can be fatal at onset. Ischemic strokes rarely lead to death within the first hour. No historical feature distinguishes the two, although nausea, vomiting, headache, and change in level of consciousness are more common in hemorrhagic strokes. EMS plays an important role in the initial evaluation and treatment of patients with acute ischemic stroke. Therefore, your understanding of its pathophysiology, clinical presentation, and evaluation is essential. Furthermore, rapid recognition and transport within the preestablished three hour window is critical to the delivery of thrombolitics and the outcome. Stroke is the third leading cause of death and disability in the US. Although stroke often is considered a disease of the E - 35
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elderly, 25% of strokes occur in persons younger than 65 years of age. Stroke should be considered in any patient presenting with an acute neurologic deficit or altered level of consciousness. Common symptoms of stroke include abrupt onset of hemiparesis, visual deficits, ataxia, vertigo, aphasia, hyperthermia, and/or hypertension. These symptoms are more likely to occur in combination. Multiple factors contribute to delays in seeking care for symptoms of stroke. Many strokes occur while patients are sleeping and are not discovered until the patient awakes. Strokes leave some patients too incapacitated to call for help. Occasionally, strokes go unrecognized by patients or their caregivers. skilled and efficient at each point. Fibrinolytic therapy offers the opportunity to limit neurological insult and improve outcome in ischemic stroke patients. Furthermore, patients treated with fibrinolytic therapy are more likely to be discharged home and less likely to be discharged to a rehabilitative or chronic care facility. Fibrinolytic therapy is costeffective and results in sustained improvement in quality of life. For these reasons, intravenous fibrinolytic therapy should be considered for all patients presenting to the hospital within three hours of the onset of symptoms consistent with acute ischemic stroke. EMS personnel can identify stroke patients with reasonable sensitivity and specificity. Once the diagnosis of stroke is suspected, time in the field should be minimized and the patient prepared for immediate transport to a stroke center or hospital. Prearrival notification (Stroke Alert) to the receiving facility shortens the time to definitive hospitalbased evaluation and intervention for patients with stroke. The Stroke Alert is based on answering Yes to three basic questions: 1. The patient is at least 18 years of age 2. Signs and symptoms of a stroke are present based on the findings of the CPSS 3. The Onset of signs and symptoms has been within three hours. (The onset of symptoms is viewed as the beginning of the stroke and the eligibility for fibrinolytic therapy ends three hours from that time.) EMS systems should communicate the results of the stroke scale or stroke screen, the GCS, and the estimated time of symptoms onset to the receiving hospital during encode before arrival. The receiving facility should have a written plan to initiate therapy as quickly as possible by activation of the stroke teams and mobilization of necessary resources such as CT scan.
Patients with a decreased level of consciousness should be a assessed to ensure that they are able to protect their airway. With the availability of thrombolytic therapy for acute ischemic strokes in selected patients, you must be able to perform a brief, but accurate, neurologic examination on patients with suspected stroke syndromes. The Treasure Coast Guidelines participants have selected the Cincinnati PreHospital Stroke Scale (CPSS) as the mechanism to determine this information. EMS personnel will attempt to elicit any of 3 major physical findings suggestive of stroke: facial droop, arm drift, and abnormal speech. The goals of the neurologic examination include: 1. Confirming the presence of a stroke. 2. Distinguishing stroke from stroke mimics. 3. Establishing a neurologic baseline should the patients condition improve or deteriorate. TIAs precede nearly 30% of ischemic strokes. If left untreated, one third of all TIAs lead to ischemic stroke. 20% occurring within the first month, and 50% within the first year. Management of the stroke patient can be remembered by use of the mnemonic of the 7 Ds: Detection Dispatch Delivery Door Data Decision Drug Delay may occur at any of these points of management, so response to and management of the stroke victim must be E - 36
RATIONALE
The goal of acute stroke management is rapid and efficient care. Assessment of the ABCs, vital signs including blood glucose levels, temperature, and stroke scale evaluation should be performed urgently. Care should be taken to accomplish any subsequent treatment rapidly. Priority dispatch with prompt EMS response, stroke recognition, rapid transport and notification to the receiving facility are keys in accomplishing these goals. Cincinnati PreHospital Stroke Scale (CPSS) Is quick and simplistic. If any of the 3 signs are abnormal, the probability of a stroke is 72%.
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Oxygen Low Flow unless hypoxic (Sa02<90%) or inability to protect airway requires oral tracheal intubation (OTI). Transport Position Transporting the patient with the head at a 30 inclined angle may reduce blood pressure and reduce the need for more aggressive measures. ALL MEDICATIONIS GIVEN IN THE PRESENCE OF A STROKE MUST BE PHYSICIAN CONSULT. THE FOLLOWING MEDICATIONS ARE NOT ROUTINELY GIVEN IN A STROKE: (These Medications are for the specific indications discussed.) Labetalol (Trandate) Antihypertensive. Reserved for patients with markedly elevated blood pressures. In candidates for fibrinolytic therapy, strict control of blood pressure is required to reduce potential for bleeding. Fibrinolytic therapy is not recommended for systolic blood pressures of > 185 mmHg, or a diastolic blood pressure of > 110 mmHG. Therefore, the target blood pressure is <185/110 or MAP > 130mmHG. In stroke management, lowering cerebral perfusion pressure below this can lead to worsening of the stroke causing underperfusion of the ischemic penumbra. Valium (Diazepam) or Ativan (Lorazepam) Benzodiazepine/Anticonvulsant. Recurrent seizures can worsen stroke and should be controlled. Propholactic administration is not indicated. Lorazepam, which has a shorter halflife, may be superior. Acetaminophen (Tylenol) Antipyretic. Reduces fever by acting directly on hypothalamic heatregulating centers. Hyperthermia accelerates ischemic neuronal injury and can increase morbidity. Evidence suggests that mild brain hypothermia is neuroprotective. Rectal administration may be required in the stroke patient. BGL Check and Dextrose 50% Carbohydrates. Reverses the effect of hypoglycemia. Not only can both hypoglycemia and hyperglycemia produce symptoms that closely mimic stroke, both can also aggravate ongoing neuronal ischemia. Administration of glucose in hypoglycemia produces profound and prompt movement. common home medications helps in effective assessment and treatment. It is provided to help the reader feel more comfortable in handling cardiac medication problems that arise in the field. Also included is a list of the more common drugs in each class the EMS providers will frequently find among their patients prescription. ACE INHIBITORS Ace inhibitors relax blood vessels and help reduce blood pressure. They also make it easier for the heart to pump, thereby assisting in the relief of congestive heart failure and hypertension. Commonly prescribed Ace Inhibitors Benazepril (Lotensin) Enalapril (Vasotec) Lisinopril (Prinivil, Zestril) Ramipril (Altace) BETABLOCKERS The overall effect is to decrease myocardial excitability, cardiac workload, and oxygen consumption. Beta blockers also have what is referred to as a membrane-stabilizing effect that, in part, is responsible for their antiarrhythmic capabilities. In the field it is important to be aware of the fact that patient use of beta blockers can sometimes alter the bodys normal response to certain medical conditions. For example, patients in the early stage of shock, hypovolemia would normally be expected to have a rapid heart rate. Beta blocker use may modify this anticipated response by maintaining the heart rate in the normal range. They are utilized to manage hypertension, angina, SVT, atrial fibrillation, atrial flutter, and migraine headaches. COMMONLYPRESCRIBED BETABLOCKERS Acebutolol (Sectral) betaxolol (Kerlone) carteolol (Cartrol) Metoprolol (Lopressor) penbutolol (Levatol) sotalol (Beatpace) CALCIUM CHANNEL BLOCKERS The effect is dilation and relaxation of cardiac and systemic arteries; decreased peripheral vascular resistance, after load and blood pressure, and inhibited coronary artery spasms. They are utilized for the treatment of hypertension, angina, and tachyarrhythmias. Commonly Prescribed Calcium Channel Blockers Amlodipine (Norvasc) Diltiazem (Cardizem, Dilacor) bepridil (Vascor) Felodipine (Plendil) E - 37 2/15/06 atenolol (Tenormin) Bisoprolol (Zebeta) labetalol (Normodyne) nadolol (Corgard) Propanolol (Inderal) timolol (Blocadren) Captopril (Capoten) Fosinopril (Monopril) Quinapril (Accupril) Spirapril (Renormax)
Note: the generic names of all ACE Inhibitors ends in pril
Note: The generic names of all beta blockers end in lol
CARDIAC
UNDERSTANDING ACE INHIBITORS, BETA BLOCKERS, CALCIUM CHANNEL BLOCKERS AND DIGITALIS TOXICITY
In this section, some of the more commonly encountered classes of cardiac medications are listed, along with a brief explanation of how they work. The basic knowledge of thee

isradipine (DynaCirc) nicardipine (Cardene) Nifedipine (Adalat, Procardia) verapamil (Calan, Isoptin) CHOLESTEROL LOWERING AGENTS Also known as an antilipid agent, these drugs work by inhibiting the hepatic enzyme that is essential to cholesterol synthesis. They are commonly prescribed for patients who have already been diagnosed with cardiovascular disease, have had an MI, or have other significant cardiac risk factors. They are indicated to reduce total cholesterol and low-density lipids. (LDL) Commonly Prescribed Cholesterol- Lowering Agents Cerivastatin (Baycol) colestipol (Colestid) gemfibrozil (Lopid) Cholestyramine (Questran) Fluvastatin (Mevacor) Pravacol
CARDIAC ALERT
PURPOSE OF PROGRAM:
To help the team rapidly identify acute coronary syndrome patients with the appropriate assessment tools. To classify patients as qualifying or nonqualifying for cardiac alert criteria. To prenotify the receiving facility so they can make sure their resources are ready for the patient. The acute coronary syndromes: Time is Muscle Current management of AMI contrasts dramatically with the expectant waiting and retrospective diagnosis of a decade ago. The reperfusion ERA has been ushered in by the recent formulation of thrombolytic agents that can dissolve acute coronary thrombosis and by the development of percutaneous transluminal coronary angioplasty (PTCA), which can reopen blocked vessels. Now the emergency triage and treatment of patients with acute coronary syndromes changes the immediate course of the AMI and alters longterm prognosis. Early diagnosis and treatment of AMI significantly reduces mortality. Early reperfusion decreases infarct size and improves left ventricular function. The National Heart Attack Alert Program has published a series of important recommendations for the rapid identification and management of patients with AMI. This cardiac alert program is reflective of those recommendations. Because myocardial salvage is timedependent, with most benefit in the first few hours, a sense of urgency is mandatory. The team can significantly improve the doortoneedle time. The interval between arrival of the patient at the ED and the delivery of a thrombolytic agent, prehospital 12lead ECGS and a chest pain check list lead to more rapid prehospital and hospital care, including thrombolysis.
CARDIAC GLYCOSIDESAND DIGITALISTOXICITY Digitalis, the principal drug in the cardiac glycoside class, is one of the oldest medications known to humans. For hundreds of years it had been used in the treatment of congestive heart failure. Digitalis and the related cardiac glycosides increase the force (inotropic effect) of the myocardial contraction. When given to patients in congestive heart failure, it significantly increases the stroke volume, thus increasing the cardiac output. It also decreases AV node conduction, thus slowing the heart rate. It has also proved effective in the management of patients with atrial fibrillation and atrial flutter. In these patients rapid atrial rates produce accelerated ventricular rates, which can be reduced by digitalis therapy. Several digitalis preparations are available. These include the following: Digitoxin, it is the longest acting cardiac glycoside. Digoxin (Lanoxin) it is the most commonly prescribed Ouabain has a rapid rate of onset and relatively short duration of effect Desanoside (Cedilanid D) is the most rapidly acting digitalis preparation Cardiac Glycosides have profound effects on cardiac function and rhythm. The therapeutic index (therapeutic dose/toxic dose) is low, which means that the possibility of digitalis toxicity should always be considered in patients with this medication. Signs of digitalis toxicity include cardiac arrhythmias (PVCs, PSVT with 2; 1 block, and so on) nausea, vomiting, headache. Visual disturbances (yellow vision), and drowsiness. Almost any arrhythmia can be associated with digitalis toxicity. It is a potent and potentially toxic drug. Digitalis toxicity is potentiated in patients with hypokalemia, hypomagnesemia, and hypercalcemia. E - 38
ACUTE CORONARY SYNDROME

Initial diagnosis of acute coronary syndrome is based almost entirely on history, risk factors, and, to a lesser extent, ECG. The symptoms are due to myocardial ischemia, which has an underlying cause of an imbalance between supply and demand for myocardial oxygen. Myocardial ischemia most often develops as a result of reduced blood supply, due to atherosclerotic plaques, to a portion of the myocardium. The plaques initially allow sufficient blood flow to match myocardial demand. These areas of narrowing may become clinically significant and precipitate angina when myocardial demand increases. Angina that is reproduced by exercise, eating, and/or stress and is subse-
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quently relieved with rest and without recent change in frequency or severity of activity necessary to produce symptoms is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombi form. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina. Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI). Angina becomes progressively more common, as does the underlying cardiac disease responsible, with increasing age. Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It usually is described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand. Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort. Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalent symptoms. Patients may complain of the following: palpitations, pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm. Exertional dyspnea that resolves with pain or rest. Diaphoresis, nausea, and decreased exercise tolerance. Patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, lightheadedness, and nausea. Stable angina involves episodic pain lasting 515 minutes, provoked on exertion and relieved by rest or nitroglycerin. Unstable angina patients have increased risk for advance cardiac events, such as MI or death. Three clinically distinct forms exist, as follows: Newonset exertional angina, angina of increased frequency or duration or refractory to nitroglycerin, and angina at rest. Atherosclerotic plaque disease is the predominant cause. Coronary artery vasospasm is less common. Alternative causes of angina include ventricular hypertrophy due to hypertension, embolic occlusion of the coronary arteries, hypoxia, as in acute pulmonary disorders, cocaine and amphetamine use, underlying coronary artery disease, and inflammation of epicardial arteries. The immediate goal of emergency care is rapid identification of patients with AMI, and exclusion of alternative causes of nonischemic chest pain.
RATIONALE
The goals of treatment are to preserve patency of the coronary artery, augment blood flow through stenotic lesions, reduce myocardial oxygen demand thereby preventing major adverse cardiac events. All patients should receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive aggressive medical intervention until signs of ischemia, as determined by symptoms and ECG resolve. Therapeutic benefit was seen for up to 12 hours but was the greatest when fibrinolytics were administered in the first 3 hours. Hence the cardiac alert criteria. Prehospital 12 lead ECG improves prehospital diagnosis, reduces hospitalbased time to treatment, identifies patients requiring reperfusion, contributes to mortality reduction and facilitates triage to cardiac centers with interventional facilities. DRUG CATEGORY: Oxygen Evidence suggests that breathing supplemental oxygen may limit the size of ischemic myocardial injury. DRUG CATEGORY: Anti-platelet agents These inhibit cyclooxygenase, which in turn produces thromboxane A2, a potent platelet activator. Anti-platelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes and fatal myocardial infarctions. Aspirin Early administration of aspirin in patients with AMI may reduce cardiac mortality. After plaque rupture or erosion, a layer of platelets covers the surface of the plaque. Fibrinogen crosslinks platelets, and the coagulation system is further activated by thrombin generation. At this stage the thrombus is plateletrich. Therapy with antiplatelet agents is most effective at this time. Heparin When Heparin is used in the presence of aspirin a reduction in mortality as well as a reduction in reinfarction has been seen. To reduce the incidence of increased intercrainial hemorrhage a lower dose of heparin is now recommended. DRUG CATEGORY: Nitrates These agents oppose coronary artery spasm and reduce myocardial oxygen demand by reducing both preload and afterload. Nitroglycerin (All forms) Causes relaxation of the vascular smooth muscle, causing a decrease in blood pressure. DRUG CATEGORY: Analgesics These agents reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction. Morphine Sulfate Drug of choice (DOC) for narcotic analgesia because of its reliable and predictable effects, safety E - 39
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profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly titrated until desired effect is obtained. DRUG CATEGORY: Anticoagulants These agents are used to prevent recurrence of clot after a spontaneous fibrinolysis Heparin Augments activity of antithrombin and prevents conversion of fibrinogen to fibrin. Heparin does not actively dissolve but is able to inhibit further thrombogenesis. Parasympathetic influences during cardiopulmonary arrest have not been studied fully, and the clinical benefits of atropine have yet to be confirmed. Highdose epinephrine may improve the hemodynamics of CPR, thereby increasing the rate of return to spontaneous circulation; however, it has not been demonstrated to influence the final clinical outcome. Therefore, these doses no longer are recommended for children or adults. DRUG CATEGORY: Anticholinergic agents The goal in using these agents is to improve conduction through the AV node by reducing vagal tone via receptor blockade. Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. Epinephrine (Adrenaline) Considered the single most useful drug in cardiac arrest. Used to increase coronary and cerebral blood flow during CPR. May enhance automaticity during asystole. Termination of efforts A number of studies over the past decade observe consistantly that 1% of patients transported with continuing CPR survive to hospital discharge. It is now considered an unethical act to transport an arrest victim proven refractory to proper BLS and ACLS care.
ASYSTOLE
Asystole is cardiac standstill with no cardiac output and no ventricular depolarization; it eventually occurs in all dying patients. Asystole can be primary or secondary. Primary asystole occurs when the hearts electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (i.e., sclerosis) of the sinoartial (SA) node or atrioventricular (AV) conducting system. Primary asystole usually is preceded by a bradydysrhythmia due to sinus arrest or complete heart block or both. It develops when cellular metabolic functions are no longer intact and an electrical impulse cannot be generated. Secondary asystole occurs when factors outside of the hearts electrical system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia or acidosis. Asystole is associated with poor outcome regardless of its initial cause. Resuscitation is likely to be successful only if it is secondary to an event than can be corrected immediately. Prevalence of asystole as the presenting cardiac rhythm is lower in adults (25%56%) than in children (90%95%). Immediate diagnosis of asystole requires the recognition of full cardiac arrest and a confirmed flatline rhythm in 2 perpendicular leads. If the rhythm is truly asystole and has been present for more than several seconds, the patient will be unconscious and unresponsive. A few agonal breaths may be noted, but detectable heart sounds and palpable peripheral pulses are absent. Examples of common conditions that can result in secondary asystole include suffocation, near drowning, stroke, massive pulmonary embolus, hyperkalemia, hypothermia, and sedativehypnotic or narcotic overdoses leading to respiratory failure. Hypothermia is a special circumstance, since asystole can be tolerated for a longer period of time under such conditions and can be reversed with rapid rewarming while cardiopulmonary resuscitation (CPR) is being performed.
ATRIAL FIBRILATION
Atrial fibrillation (AF) is a rhythm disturbance of the atria that results in irregular, chaotic, ventricular waveforms varying from bradyarrhythmia to tachyarrhythmia. Multiple re entrant waveforms within the atria bombard the atrioventricular (AV) node, which becomes relatively refractive to conduction due to the frequency of upstream electrical activity. AF occurs in 3 distinct clinical circumstances: As a primary arrhythmia in the absence of identifiable structural heart disease. As a secondary arrhythmia in the absence of structural heart disease, but in the presence of a systemic abnormality that predisposes the individual to the arrhythmia. As a secondary arrhythmia associated with cardiac disease that affects the atria. Pertinent physical findings are limited to the cardiovascular system or, if embolization has occurred, the brain and/or peripheral vasculature. These include the following: Irregular pulse, with or without tachycardia, is described classically as the irregularly irregular rhythm. Hypotension and poor perfusion due to a decrease in atrial filling pressures and decrease in stroke volume. Signs of embolization, including transient ischemic attacks (TIAs) and cerebrovascular accidents (CVAs) may be identified. Congestive heart failure (CHF) Patients at the highest risk include those with longstanding hypertension, valvular heart disease (rheumatic), left ven-
RATIONALE
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tricular hypertrophy, coronary artery disease, or diabetes. CHF for any reason is a noted contributor to this disorder. Other causes may include: AMI, pulmonary embolism, cardiomyopathy, sick sinus syndrome, hyperthyroidism, ethanol use, cardiothoracic surgery, and use of overthecounter herbs such (i.e., ephedra, ginseng) have been noted in some patients with new onset AF. When considering drug therapy for AF, remember the treatment caveat, Electrical cardioversion is the preferred modality in the patient whose condition is unstable. fibrillation (AF), which occurs in as many as 3% of certain populations. For the most part, morbidity and mortality are due to complications of rate (e.g., syncope, congestive heart failure (CHF). In patients who suffer from flutter of the atria, the risk of embolic occurrences approaches that of atrial fibrillation (AF). A patient may present with a history of palpitations, fatigue or poor exercise tolerance, dyspnea, angina, or syncope. Pertinent physical findings are limited to the cardiovascular system. If embolization has occurred from intermittent AF, findings are related to brain and/or syncope. Tachycardia may or may not be present, depending on the degree of AV block that may be associated with the flutter activity. The rate may be regular or slightly irregular. Hypotension is possible but normal blood pressure is observed more commonly. CHF may be found and is usually be left ventricular dysfunction. Patients at the highest risk include those with long standing hypertension, valvular heart disease (rheumatic), left ventricular hypertrophy, coronary, coronary artery disease with or without depressed left ventricular function, or diabetes. Additionally, CHF for any reason is a noted contributor to this disorder. Additional causes include: postoperative revascularization, digitalis toxicity and pulmonary embolism. In cases of typical flutter, EKG reveals identically recurring regular saw tooth flutter waves. Flutter waves often are visualized best in leads II, III, AVF, or VI.. Flutter and fibrillation often coexist with alternating patterns (e.g., fib-flutter) in the same tracing. If the patient is unstable (e.g., hypotension, poor perfusion), synchronized cardioversion is commonly the initial treatment of choice. Cardioversion often requires low energies (<50J). If the electrical shock results in atrial fibrillation, shock at a higher energy level is used is used to restore normal sinus rhythm (NSR). To slow the ventricular response, dilitiazem may be the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves. These drugs generally do not convert to NSR. If the flutter cannot be cardioverted, terminated by pacing, or slowed by the drugs mentioned, IV amiodarone has been shown to slow the ventricular rate and is considered as effective as digoxin.
RATIONALE
Rate control is the goal of medication in atrial flutter. When considering drug therapy for atrial flutter/fibrillation, electrical cardioversion is the preferred modality in the patient whose condition is unstable. Delivered energy should be syncronized with the QRS complex to reduce the possibility of inducing VF, which can occur when a shock hits the relative refractory portion of the cardiac cycle. Synchronized directcurrent (DC) cardioversion is commonly the initial treatment of choice for the symptomatic patient. Cardioversion often requires low energeies. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore normal sinus rhythm (NSR). To slow the ventricular response, diltiazem is the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves. This drug generally does not convert atrial flutter to NSR. DRUG CATEGORY: Calcium Channel Blocker These agents reduce the rate of AV nodal conduction and control ventricular response. Diltiazem (Cardizem) is the DOC during depolarization. Inhibits calcium ion from entering slow channels or voltage sensitive areas of vascular smooth muscle and myocardium.
ATRIAL FLUTTER
Atrial flutter is a rhythm disturbance of the atria that results in regular tachycardia ventricular waveforms. Atrial rates in atrial flutter are 240-400 beats per minutes. The QRS complexes are uniform in shape, but irregular in rate. P waves may have saw-tooth configurations. Multiple re-entrant or primarily generated (ectopic) atrial waveforms bombard the atrioventricular (AV) node. The most common form of atrial flutter involve a reentrant circuit that encircles the tricuspid annulus of the right atrium. Less commonly, atrial scars or atrial infarction may be the cause. Atrial flutter is less common than atrial
CARDIAC TAMPONADE
Pericarditis and cardiac tamponade are clinical problems involving the potential space surrounding the heart or pericardium. Pericarditis is one cause of fluid accumulation in this potential space; cardiac tamponade is the hemodynamic reE - 41
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sult of the fluid accumulation. As the volume of pericardial fluid increases, the capacity of the atria and ventricles to fill is mechanically compromised, leading to reduced stroke volume and tamponade physiology. The pericardium (pericardial complex) consists of an outer fibrous layer and an inner serous layer. The fibrous pericardium is a flaskshaped, tough outer sac with attachments to the diaphragm, sternum, and costal cartilage. The serous layer is thin and is adjacent to the surface of the heart. The pericardium serves as a protective barrier from the spread of infection or inflammation from adjacent structures. The potential space produced by these layers contains approximately 20cc of fluid with electrolyte and protein profiles similar to plasma. Approximately 120cc of additional fluid can accumulate in the pericardium without an increase in pressure. Further fluid accumulation can result in marked increase in pericardial pressure, eliciting decreased cardiac output and hypotension (cardiac tamponade). The rapidity of fluid accumulation influences the hemodynamic effect. The early diagnosis of significant pericardial and cardiac injuries can prevent morbidity and enhance survival. Traumatic tamponade may present with acute dyspnea or altered mental status. Medical cardiac arrest patients may have a history of illness associated with the pericardium, particularly endstage renal disease, severe infection, routine cardiac surgery and radiation therapy. Cardiac tamponade is influenced by volume and rate of accumulation. On physical exam a patient may present with jugular vein distention, hypotension, and muffled heart sounds (Becks triad). Hypotension and tachycardia without elevated jugular vein distension if associated hemorrhage is outside the pericardial sac. Pulses paradoxus is measured by careful auscultation with a blood pressure cuff. The first BP reading is recorded at the point when beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle. A difference of more than 10 mm Hg defines pulses paradoxus. Cyanosis, varying degrees of consciousness may also be observed prior to cardiac arrest. Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires aggressive resuscitation. Hemopericardium is the most common feature of penetrating cardiac injuries. In acute massive hemopericardium, there is sufficient time for defibrillation to occur. The hemopericardium organizes and may partially clot, resulting in a pericardial hematoma. Potential causes of cardiac perforation include central line placement, pacemaker insertion, cardiac catheterization, and sternal bone marrow biopsies. A tamponade delay of hours to days has occurred secondary to catheter misplacement. E - 42 2/15/06 Cardiac arrest patients who present with traumatic injury or medical history as described require immediate treatment of the increase in pericardial pressure with pericardiocentesis. Removing as little as 3050ml may produce dramatic hemodynamic improvement. The pericardium may have the potential of accumulating as much as 2,000 ml of fluid over time. For penetrating injuries, traumatic arrest, pulseless electrical activity (PEA), and asystole, the prognosis depends heavily upon the rapid identification of the potential for tamponade.
CARDIOGENIC SHOCK
Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state with inadequate perfusion to the tissues. It most commonly occurs in association with, and as a direct result of, acute ischemic damage to the myocardium. The most common initiating event in cardiogenic shock is acute myocardial infarction (AMI). Dead myocardium does not contract, and once more than 40% of the myocardium is involved, cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilation, and ultimately, univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. Mortality rates for medically treated patients with AMI and cardiogenic shock exceed 70%. Most patients with cardiogenic shock have an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (i.e., chest pain, shortness of breath, diaphoresis, nausea and vomiting). Patients experiencing cardiogenic shock also may present with pulmonary edema and presyncopal or syncopal symptoms. Physical exam often reveals that the patient is in the middle of an AMI. Patients are in frank distress, are profoundly diaphoretic, and have severe shortness of breath and chest pain. Neck examination may reveal jugular vein distention, which may be prominent. This finding is evidence of right ventricular failure. With increasing ventricular dysfunction, florid pulmonary edema and severe hypotension may develop. Auscultation of the chest may reveal varying degrees of congestive heart failure. Prehospital care is aimed at minimizing ischemia and shock.
RATIONALE
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Early hemodynamic stabilization is beneficial and reduces mortality. DRUG CATEGORY: Vasopressors These drugs aug-
ment both coronary and cerebral blood flow present during the lowflow state associated with shock. Sympathomimetic amines with both alphaadrenergic abd betaadrenergic effects are indicated. Dopamine is the drug of choice to improve cardiac contractility. Dopamine (Intropin) stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and meseneric vasodilation. Higher doses cause cardiac stimulation and renal vasodilation. reassess patient status. The responsible clinician should stop the resuscitative effort when he or she determines with a high degree of certainty that the arrest victim will not respond to further ACLS efforts. No reliable criteria are available to determine neurological outcome during cardiac arrest.
TRAUMATIC CARDIAC ARREST

Treatment of patients in cardiopulmonary arrest varies as to the mechanism of the injury and whether or not they exhibit any signs of life (pulse, respirations, or reflexes) on initial evaluation. Generally, trauma patients who are found with no signs of life in the field have suffered overwhelming cardiovascular or CNS injuries, which are not amenable to surgical treatment under any circumstances. The survival rate on these patients is essentially zero and attempts at resuscitation are futile. Patients suffering traumatic cardiopulmonary arrest after treatment has begun should be Diverted to the closest facility. Due to the rapid response from providers to scenes, many traumatic arrest patients are not yet in asystole, but present on exam to be in Pulseless Electrical Activity (PEA). In this case the provider should follow protocol and attempt to address all of the physiologic causes of PEA while enroute to the emergency department. These patients should also be diverted to the closest facility.
CESSATION OF EFFORTS
Patients in cardiac arrest exhibiting asystole have a dismal rate of survival usually as low as 1 or 2 people out of 100 cardiac arrests. As with PEA, the only hope for resuscitation of a person in asystole is to identify and treat a reversible cause. The asystole protocol outlines an approach that focuses on not starting and when to stop. Field personnel will not be required to transport every victim of cardiac arrest to the hospital emergency department. However, transportation with continuing CPR and ALS interventions is justified if there are interventions available in the ED that cannot be performed in the field (such as central core re-warming equipment) or field interventions (such as tracheal intubation) that where unsuccessful in the field, or patients who do not have a valid state of Florida DNRO. For nontraumatic cardiac arrest solid evidence confirms that ACLS care in the ED offers no advantage over ACLS care in the field. Children are a special case. A pulse may be difficult to find without a Doppler. In any case, you should be especially aggressive in attempting to resuscitate children with no palpable pulse. Pregnant mothers and the newly born will also be conditions in which we will continue maximum efforts including transport. Likewise, it is inappropriate for personnel to apply routine stopping rules without thinking about their particular situation. Cessation of efforts in the pre-hospital setting, following system-specific criteria and under direct medical control will be standard practice in your EMS system. Healthcare professionals must understand the patient, the arrest features, and the system factors that have prognostic importance for resuscitation. These include time to CPR, time to defibrillation, pre-arrest state, and initial arrest rhythm. None of these factors alone or in combination is clearly predictive of outcome. The most important factor associated with poor outcome is time of resuscitation efforts. The chance of discharge from the hospital alive and neurologically intact diminishes as resuscitation time increase. Clinicians must constantly
RATIONALE
Not starting & Stopping Resuscitation One goal unique to CPR is the reversal of clinical death, an outcome achieved in only a minority of patients. However, the performance of CPR, may conflict with the patients own desires and requests or may not be in his or her best interest. Resuscitative efforts may be inappropriate if goals of patient care cannot be achieved. Each decision must be made for the individual, with compassion, based on ethical principles and available scientific information. Medical treatment is futile if its purpose cannot be achieved. The 2 major determinants of medical futility are length of life and quality of life. An intervention that cannot establish any increase in length or quality of life is futile. In resuscitation a qualitative definition of futility must include low chance of survival and low quality of life afterward. Key factors are the underlying disease before cardiac arrest and expected state of health after resuscitation. A careful balance of the patients prognosis for both length of life and quality of life will determine whether CPR is appropriate. CPR is inappropriate when survival is not expected or if the patient is expected to survive without the ability to communicate. The framework for decisions about futility can be best achieved by a social consensus. Discussion and debate among E - 43
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healthcare professionals and the public are encouraged so as to reach a consensus based on values of society. Healthcare workers are not obligated to provide treatment when there is scientific and social consensus that such treatment is ineffective. Some examples are CPR for patients with signs of irreversible death, such as rigor mortis, decapitation, dependent lividity, or decomposition. Quantitative futility implies that survival is not expected after CPR under given circumstances. Scientific evaluation has shown that there are no clear criteria to predict the futility of CPR accurately. Therefore, it is recommended that all patients in cardiac arrest receive resuscitation unless: The patient has a valid Florida DNRO order. The patient has signs of irreversible death: rigor mortis, decapitation, or dependent lividity. No physiological benefit can be expected because the vital functions have deteriorated despite maximal therapy. Specific newly born conditions that may be set forth by your individual agency. Traumatic injury resulting in asystole. Furthermore, a number of studies over the past decade observe consistently that < 1% of patients transported with continuing CPR survive to hospital discharge. The new ACLS asystole algorithm recognizes that some people in asystole can be resuscitated, and therefore it presents recommendations to follow for resuscitation. It also recognizes that when people have died, the heart monitor displays a flat line, or asystole. Therefore, the new algorithm contains notes about what to do if asystole persists, that is when the patient is dead. nating weak and strong pulse indicative of depressed left ventricle), skin may be diaphoretic, cold, gray, and cyanotic, wheezing or rales may be heard on auscultation. A variety of cardiac diseases cause CHF and pulmonary edema. The most common cause of heart failure is coronary artery disease, which is secondary to loss of left ventricular muscle, ongoing ischemia, or decreased diastolic ventricular compliance. Longterm prognosis is variable. Mortality rates from 10% in patients with mild symptoms to 50% with advanced, progressive symptoms.
RATIONALE
The goal of pharmacotherapy is to maintain adequate blood pressure and perfusion to essential organs. The use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Continuous positive airway pressure (CPAP) ventilation therapy has demonstrated decreased need for intubation rates when utilized. CPAP splints the airways open with positive pressure which will increase the surface area for gas exchange at the alveolar/capillary membrane and will reduce atelectasis from the washout affect of surfactant. The outcome should produce increased lung volume, improve oxygenation and reduce the work of breathing. Former mainstays used to decrease preload such as alternating tournaquets and phelbotomy with removal of 500 cc of blood have been replaced with newer more promising therapies such as intravenous nitroglycerin. DRUG CATEGORY: Diuretics Firstline therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium chloride reabsorption in the ascending loop of Henle. Furosemide (Lasix) Administration of this loop diuretic IV will allow for both superior potency and higher peak concentration. Because diffentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach often is employed, particularly as both may cause bronchospasm. Aerosolized beta2agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function. Albuterol has been shown to be successful in this setting. Steroids have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension. DRUG CATEGORY: Nitrates Reduce myocardial oxygen demand by lowering preload and afterload. IV Nitroglycerin is the therapy of choice for afterload re-
CONGESTIVE HEART FAILURE

Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to maintain the circulation of blood adequately. The most severe manifestation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung. CHF can be categorized as forward or backward ventricular failure. Backward failure is secondary to elevated systemic venous pressure, while left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. CHF is the leading diagnosis among hospitalized patients older than 65 years. Findings such as peripheral edema, jugular venous distention, and tachycardia are highly predictive of CHF. Some additional findings may include: tachypnea, use of accessory muscles of respiration, hypertension, pulsus alternans (alterE - 44
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duction. SL and nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. Similar to SL, nitrosprays onset is 13 minutes with a halflife of 5 minutes. Topical nitrate therapy is reasonable in a patient presenting with classic CHF. However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred since it is easier to monitor hemodynamics and absorption, particularly in the diaphoretic patient. Oral nitrates, due to delayed absorption, have little role in the acute presentations of CHF. DRUG CATEGORY: Analgesics Morphine IV is an excellent adjunct in acute therapy. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload. Also causes arterial dilation, which reduces systemic vascular resistance (SVR) and increases cardiac output. DRUG CATEGORY: Inotropic agents In the hypotensive patient presenting with CHF, dopamine is the agent usually employed. Hemodynamic effects depend on the dose. Lower produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses. Dopamine is a positive inotropic agent at 210 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg cause vasoconstriction, which increases afterload. For these reasons, dopamine is reserved to be used with caution in patients whose blood pressure requires maintainance to continue the administeration of IV nitrates. following are the most common causes of firstdegree heart block: Intrinsic AV nodal disease, enhanced vagal tone, AMI, particularly inferior wall AMI, myocarditis, electrolyte disturbances, and drugs such as calcium channel blockers, beta blockers, and digitalis. These drugs increase the refractory time of the AV node, thereby slowing AV conduction. Patients with firstdegree heart block occasionally may progress to a highergrade block, often with accompanying hemodynamic instability. This occurs primarily in patients with AMI or myocarditis; however, it may also be drug related, especially in the setting of an acute overdose. Seconddegree heart block or seconddegree atrioventricular (AV) block refers to a disorder of the cardiac conduction system in which some P waves fail to conduct to the ventricle and to generate a QRS complex. Seconddegree AV block comprises 2 types, Mobitz I and Mobitz II. Mobitz I AV block, or Wenckebach block, is characterized by progressive prolongation of the PR interval causing progressive RR interval shortening until a P wave fails to conduct to the ventricle. Mobitz II AV block is characterized by sudden unexpected blocked P waves without variation or prolongation of the PR interval. Mobitz II most commonly is caused by AMI (anterior or inferior). Mobitz I (Wenckebach) block is caused by conduction delay in the AV node in 72% of patients and by conduction delay in the HisPurkinje system in the other 28%. A narrow QRS complex may be due to AV nodal or infranodal conduction delay. It can be caused by AMI, vagal stimulation or enhanced vagal tone, or toxicity relating to digitalis, beta blockers, or calcium channel blockers. Mobitz II block carries a high risk of progression to complete heart block, often with associated cardiovascular collapse. Both Mobitz I and Mobitz II blocks may present in the same way. Most are asymptomatic, with Mobitz II more likely to present with dizziness, lightheadedness, or syncope. Patients may have symptoms of myocardial ischemia or myocarditis. Patients may also have symptoms of myocardial ischemia or a history of organic heart disease. Patients may have an irregular heart rate, and often accompanying bradycardia, but the examination is otherwise generally unremarkable. Symptomatic patients may have signs of hypoperfusion, including hypotension and altered mental status. Patients with concomitant myocardial infarction (MI) may exhibit signs related to AMI. Seconddegree heart block requires no specific prehospital therapy, unless the patient is symptomatic from a resulting E - 45 2/15/06
HEART BLOCK
Firstdegree heart block, or firstdegree atrioventricular (AV) block, is a condition that results in prolongation of the PR interval on electrocardiogram (ECG) to > 0.02 seconds. The PR interval is defined as the time from the initial deflection of the P wave from the baseline to the beginning of the QRS complex. Electrophysiological studies have shown that firstdegree heart block may be due to conduction delay in the AV node, in the HisPurkinje system, or a combination of the two. AV nodal dysfunction accounts for the majority of cases. However, in the HisPurkinje system is the most likely cause. Morbidity and mortality rates from heart disease appear to be unaffected by the presence of firstdegree block. No specific therapy is required by the clinician. However, patients with concomitant AMI should receive appropriate therapy Firstdegree heart block is generally an incidental finding noted on ECG without any particular associated signs. The

bradycardia. Follow standard advanced cardiac life support (ACLS) guidelines in Bradycardic patients. Use caution in administering atropine to a patient with suspected AMI, because atropine has been reported to precipitate ventricular tachycardia or ventricular fibrillation in seconddegree blocks. Furthermore, atropine is much less likely to be successful in Mobitz II block. Transcutaneous pacing in the symptomatic patient is always appropriate. Because new onset Mobitz II patients have a propensity for progression to complete heart block, consider applying pacing pads to patients even if they are asymptomatic during prehospital care and transport. Thirddegree heart block, also referred to as thirddegree atrioventricular (AV) block or complete heart, is a disorder of the cardiac conduction system with complete absence of AV conduction. No P waves conduct to the ventricle, and AV dissociation is complete. The ventricular escape mechanism may originate anywhere from the AV node to the bundle branchPurkinje system. Not all patients with AV dissociation have complete heart block. For example, patients with accelerated junctional rhythms that are faster than their native sinus rates have AV dissociation but not complete heart block, because no AV conduction disorder is present. Thirddegree heart block is caused by conduction block at the level of the AV node, the His bundle, or the bundle branchPurkinje system. Block below the His bundle accounts for the majority o cases (approximately 61%). Patients with complete heart block frequently are hemodynamically unstable. This may lead to cardiovascular collapse, syncope, and death. Symptoms are more likely to be minimal in patients with narrow complex escape rhythms. Most commonly, patients are profoundly symptomatic, especially when the escape rhythm is wide and slow. Symptoms may include the following: syncope, confusion, sudden death, or associated AMI symptoms. Patients may have a prior history of organic heart disease or be on medications that affect AV nodal conduction. These would include betablockers, calcium channel blockers and digitalis glycorides. The physical examination will be notable for bradycardia, which may be profound. Symptomatic patients will have signs of hypoperfusion, including the follow: Hypotension, altered mental status, lethargy, and congestive heart failure. In patients with concomitant AMI, signs of acute myocardial infarction may be evident on examination. Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. The rhythm is regularized because of the junctional escape rhythm. Thirddegree heart block may be congenital or acquired. Acute inferior wall MI, drug intoxication, metabolic disturbances and cardiomyopathies are some causes for this condition. E - 46 Prehospital treatment consists of rapid transport, transcutaneous pacing with the symptomatic patient, oxygen administration, IV access and avoidance of maneuvers likely to increase vagal tone (i.e., Valsalva, painful stimuli). Atropine can be administered (cautiously, if acute MI is the underlying cause) but is likely to be ineffective unless the escape QRS complex is narrow. Vagolysis leads to unopposed sympathetic stimulation, causing increased ventricular irritability and, potentially, ventricular tachycardia (VT)/ ventricular fibrillation (VF) when atropine is administered in suspected AMI.
RATIONALE
Firstdegree AV block alone does not require treatment. The possibility of progression to higher degrees of block is always present and should be the primary concern. Careful monitoring is essential. The goal is to improve conduction through the AV node by reducing vagal tone via atropineinduced receptor blockade. This is effective only if the site of the block is the AV node. For patients with infranodal seconddegree heart block, atropine generally is ineffective. Atropine may in fact enhance the block or precipitate third degree AV block. Similarly, seconddegree AV block of the Mobitz 1 (Wenckebach) variety does not require therapy in the absence of hemodynamically significant slowing of the ventricular rate. If treatment is required, atropine should be tried first. TCP may be necessary if atropine is not effective or if hemodynamically significant slowing is recurrent. When seconddegree AV block of the Mobitz type 11 variety is associated with infarction, it carries a significant risk of progression to complete heart block. Therefore, its presence is an indication for TCP. The prognosis for patients who develop complete heart block is poor because of its usual association with extensive myocardial injury. There is little to suggest that pacing will markedly change outcome. The reestablishment of sequential atrioventricular contraction maybe of some value in these patients. If clinicians are concerned about the use of atropine in higherlevel blocks, remember that transcutaneous pacing (TCP)is a class 1 intervention and is ALWAYS appropriate. DRUG CATEGORY: Anticholinergic Drug therapy in seconddegree heart block is aimed at vagolysis. Atropine is the only currently available agent. Atropine enhances sinus node automaticity. In addition, blocks the effects of acetycholine at the AV node, thereby decreasing refractory time and speeding conduction through the AV node. Insufficient doses may cause paradoxical effects, further slowing the heart rate. Drug therapy in thirddegree heart block is aimed at
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vagolysis, with atropine being the only currently available agent. Catecholamines have only a limited role. DRUG CATEGORY: Vagolytics The goal is to improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. This is effective only if the site of the block is within the AV node. For patients with infranodal block, this therapy is ineffective. Atropine enhances sinus node automaticity and blocks effects of acetylcholine at the AV node, thereby decreasing refractory time and speeding conduction through the AV node. Insufficient doses may cause paradoxical effects, further slowing the heart rate. DRUG CATEGORY: Catecholamines These agents improve hemodynamics by acting via betaadrenergic receptor stimulation to increase the heart rate and contractility and via alphaadrenergic receptor stimulation to increase systemic vascular resistance. Dopamine in low doses 25mcg/kg/min, acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilation in these beds. In midrange doses (515mcg/kg/ min), acts on betaadrenergic receptors to increase heart rate and contractility. In high doses (1520mcg/kg/min), acts on alphaadrenergic receptors to increase systemic vascular resistance and raise BP. Epinephrine stimulates betaadrenergic receptors, predominatly by increasing heart rate, cardiac contractility, and cardiac output; alphaadrenergic receptors are stimulated to a lesser degree, causing systemic vasoconstriction and increased BP. Heart transplantation involves excision of the recipients heart above the atrioventricular valves and replacement with the donor heart. The donor heart is resected at the atria and, most commonly, is placed into the recipient at the level of the atria and at the base of the aorta and pulmonary artery. The graft includes the sinus node so that a sinus rhythm is possible after transplantation; however, some patients need lifelong pacing. Because the transplanted heart is denervated, it can respond to cardiovascular influences by humoral mechanisms but not by sympathetic or parasympathetic nerve stimulation. Extremely rarely, myocardial ischemia in the denervated heart results in chest pain. Graft rejection is controlled through an immunosuppressant regimen. A longterm immunosuppression usually is maintained with cyclosporine, azathioprine, and prednisone. The most common problems in the heart transplant recipient that may be observed are graft rejection, infection, and renal dysfunction. The latter may lead to volume overload and hypertension. Acute rejection is cell mediated and results in myocardial dysfunction in more severe cases. The heart transplant recipient averages perhaps 12 rejection episodes per year; most rejection episodes are minor and are treated with steroids and adjustments in immunosuppressant dosages. Chronic rejection involves progressive coronary artery stenosis over the course of years and terminates in myocardial ischemia with its attendant consequences. Heart transplant recipients may present to the emergency worker with any complaint observed in the general population. Vigilance must be maintained to detect rejection and infection, because these conditions may have subtle presentations. Acute cellmediated rejection is most common in the first 3 months following transplant and decreases in frequency with time. Symptoms of mild rejection are nonspecific and may include lowgrade fever, fatigue, malaise, and decreased exercise tolerance. Moderately severe rejection may include hemodynamic compromise presenting with myocardial dysfunction. Symptoms associated with infection may be masked because of the immunosuppressant regimen. Fever may be low grade or absent. Acute rejection is not associated with specific physical findings. Mild rejection may have no physical findings and must be diagnosed by endomyocardial biopsy. Patients with moderately severe to severe rejection may present with hypotension, tachycardia, decreased heart sounds, and signs of decreased peripheral perfusion such as distal cyanosis. An ECG is indicated in all but minor complaints. A major E - 47 2/15/06
HEART TRANSPLANT PATIENTS

Heart transplantation has become an accepted and definitive therapy for endstage heart failure. With advances in surgical technique and immunosuppression, survival rate following transplantation significantly exceeds that following medical therapy. Approximately 2400 transplantations are performed annually, and 4000 patients are awaiting transplantation. Chances are good that the clinician will encounter patients who have undergone heart transplantation. In patients with advanced heart failure, survival rate following transplantation exceeds that following medical therapy. The oneyear survival rate is approximately 85% in experienced centers, and the 5year survival rate exceeds 65%. The most common cause of death is infection, and acute rejection is the second most common cause.

goal of the emergency worker is to evaluate for evidence of infection or rejection in patients who present with compatible symptoms. Fluid resuscitation in patients presenting with hemodynamic compromise should be approached carefully, be aggressive only if evidence of hypovolemia exists. Over resuscitation can lead to worsening of right ventricular failure. patients once they arrive at the ED.
RATIONALE
The main goal of treatment are rapid identification of candidates for thrombolysis, coronary reperfusion via thrombolytic therapy, or percutaneous transluminal angioplasty and preservation of coronary artery patency and the myocardium. Performing 12 lead V4R RV dysfunction and acute infarction are very dependant on maintenance of RV filling pressures to maintain cardiac output. Therefore, intravenous volume loading of up to 1 to 2L is appropriate to achieve this objective. DRUG CATEGORY: Antithrombotic agents These agents prevent the formation of thrombus associated with myocardial infarction and inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortaility by reducing the risk of fatal myocardial infarctions, fatal strokes, and vascular death. Aspirin is administered as soon as possible. Aspirin inhibits cyclooxygenase, which produces thromboxane A2, a potent platelet activator. Early administration has been shown to reduce 35day mortality rate by 23% compared to a placebo. There is an added mortality benefit when used in combination with thrombolytics. Heparin augments activity of antithrombin lll and prevents conversion of fibrinogen to fibrin. Does not actively lyse preformed clot, but it is able to inhibit further thrombogenesis after thrombolysis. Prevents reaccumulation of clot after spontaneous fibrinolysis. DRUG CATEGORY: Vasodilators Opposes coronary artery spasm, which augments coronary blood flow and reduces cardiac work by decreasing preload and afterload. It is effective in the management of symptoms in AMI but may reduce the mortality rate only slightly. Nitroglycerin can be administered sublingually by tablet or spray, topically, or IV. In the setting of AMI, topical administration is less desirable route because of unpredictable absorption and onset of clinical effects. Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in blood pressure. DRUG CATEGORY: Analgesics Reduce pain, which decreases sympathetic stress. May provide some preload reduction. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience chest discomfort resulting from a myocardial infarction. Morphine is the DOC for analgesia because of its reliable
MYOCARDIAL INFARCTION
Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. The most common cause of AMI is narrowing of the epicardial blood vessels due to plaque. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 46 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality. AMI is the leading cause of morbidity and mortality in the United States. Chest pain, usually across the anterior precordium, is described as tightness, pressure, or squeezing. Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is affected more frequently than the right arm. The patient may also report nausea and/or abdominal pain often associated in inferior wall infarcts. CHF, anxiety, lightheadedness, syncope, cough. The clinician may also observe diaphoresis and wheezing. Hypertension may precipitate AMI, or it may reflect elevated catecholamines do to anxiety or pain. Hypotension indicates ventricular dysfunction due to ischemia. It usually indicates a large infarct and may be observed with right ventricular infarct. The predominant cause of myocardial infarction is a rupture of an atherosclerotic plaque with subsequent spasm and clot formation. The risk factors associated with plaque formation include: age, being male older than 70 years, smoking, high cholesterol and/or triglycerides, poorly controlled hypertension, Type A personality, a family history, and sedentary lifestyle. Significant STsegment changes in the ECG are indicative of a high probability for AMI however; normal or nonspecific findings do not exclude the possibility of AMI. Performing fibrinolytic screening in the prehospital setting is intended to speed up the administration of thrombolytic agents to eligible E - 48
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and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used; commonly titrated until a desired effect is obtained. amplitude and pulse width. Signal amplitude is measured in electrical units of volts or milliamperes. Pulse width is a measure of output duration and is measured in milliseconds. For proper permanent pacer operation, signal amplitude and width are set high enough to reliably achieve capture of the myocardium, yet low enough to prolong battery life. Pulse generators can be set to a fixedrate (asynchronous) or demand (synchronous) mode. In the fixedrate mode, an impulse is produced at a set rate and has no relationship to the patients intrinsic cardiac activity. This mode carries a small but inherent danger of producing lethal dysrhythmias should the impulse coincide with the vulnerable period of the T wave. In the demand mode, the sensing circuit searches for an intrinsic depolarization potential. If this is absent, a pacing response is generated. Patients should carry a card with them providing information about their particular model. This information is crucial when communicating with the cardiologist or ED about a pacer problem. Most pacemaker generators, however, have an x ray code that can be seen on a standard chest xray. Placing a magnet over a permanent pacemaker causes sensing to be inhibited by closing an internal read switch. This temporarily reprograms the pacer into the asynchronous mode, where pacing is initiated at a set rate. The application of a magnet can determine if the pacers battery needs to be replaced. Major pacemaker complications include failure to output, failure to capture, and failure to sense correctly. Failure to output occurs when no pacing spike is present despite an indication to pace. This may be due to battery failure, lead fracture, and a break in lead insulation, oversensing, poor lead connection at the takeoff from the pacer, and crosstalk (i.e., a phenomenon seen when atrial output is sensed by a ventricular lead in a dualchamber pacer).
PACEMAKER & AUTOMATIC INTERNAL CARDIAC DEFIBRILLATOR

Among the myriad of patients emergency workers evaluate daily are those with pacemakers and implantable cardioverterdefibrillators (ICDs). Although numerous issues may arise with these devices, emergency workers must understand their common problems in order to manage them effectively. Permanent pacemakers are devices that provide electrical stimuli to cause cardiac contraction during periods when intrinsic cardiac electrical activity is inappropriately slow or absent. They function by sensing intrinsic cardiac electric potentials. If these potentials are too infrequent or absent, electric impulses are transmitted to the heart, thereby stimulating myocardial contraction. An ICD is a specialized device designed to directly treat a cardiac tachydysrhythmia. If a patient has a ventricular ICD and the device senses a ventricular rate that exceeds the programmed cutoff rate of the ICD, the device performs cardioversion/defibrillation. Alternately, the device, if so programmed, may attempt to pace rapidly for a number of pulses, usually around 10, to attempt pacetermination of the ventricular tachycardia. Note that newer devices are a combination of ICD and pacemaker in one unit. These combination ICD/pacemakers are implanted in patients who require both devices. Pacing systems consist of a pulse generator and pacing leads. With permanent systems, endocardial leads are inserted into the venous system, usually via the subclavian, axillary, or cephalic vein, and advanced to the right ventricle and/or atrium. The pulse generator is placed subcutaneously or submuscularly and connected to the leads. Pulse generators contain, among other things, a battery, an output circuit, a sensing circuit, and a timing circuit. The battery most commonly used in permanent pacers is a lithiumiodide type and has a life span of 58 years. Pacemaker energy output is dependent upon the signal
RATIONALE
Failure to capture occurs when either an atrial or a ventricular complex does not follow a pacing spike. This may be due to lead failure, lead dislodgement, a break in insulation, an elevated pacing threshold, myocardial infarction at the tip, certain drugs, metabolic abnormalities (i.e., hyperkalemia, acidosis, alkalosis), cardiac perforation, poor lead connection at the takeoff from the generator, and improper amplitude or pulse width settings. Management of pacer capture complications is the same as for output complications, with extra consideration given to treating metabolic abnormalities and potential myocardial infarction. Oversensing occur when a pacer incorrectly senses elecE - 49
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trical activity and is inhibited from correctly pacing. This may be due to muscular activity, particularly oversensing of the diaphragm or pectoralis muscles, electromagnetic interference, or lead insulation breakage. Undersensing occurs when a pacer incorrectly misses intrinsic depolarization and paces despite intrinsic activity. This may be due to poor lead positioning, lead dislodgment, magnet application, low battery states, or myocardial infarction. Management is similar to that for other types of failures. A final category of pacer failures is termed operative. This includes malfunction due to mechanical factors, such as pneumothorax, pericarditis, infection, skin erosion, hematoma, lead dislodgement, and venous thrombosis. Treatment depends on the etiology. Major ICD complications include operative failure, sensing and/or pacing failures, inappropriate cardioversion, ineffective cardioversion/defibrillation, and device deactivation. Operative failures are identical to those found in regular pacemakers. Inappropriate cardioversion is most frequent complication associated with ICDs. This should be considered if a patient presents in atrial fibrillation or if a patient has received multiple shocks in rapid succession without premonitory symptoms. Use of a magnet over the ICD inhibits further shocks. It does not however, inhibit bradycardic pacing should the patient require it. If the magnet is left on for approximately 30 seconds, the ICD is disabled and a continuous tone is generated. involves abnormalities in impulse formation and conduction pathways. It is helpful to characterize SVT by comparing the RP interval to the PR interval. Long RP tachycardias result when atrial activity precedes the QRS complex. In short RP tachycardias, atrial activity occurs simultaneously with or shortly after ventricle excitation. In short RP tachycardias, the P wave is found within the QRS complex or shortly after the QRS complex. The most common cause of PSVT is AV nodal reentrant tachycardia (AVNRT). AVNRT is diagnosed in 50 60% of patients who present with regular narrow QRS tachyarrhythmia. The heart rate is 120150 bpm and typically is quite regular. It is important to note that AVNRT does not involve the ventricles as part of the reentry circuit. Atrioventricular reentrant tachycardia (AVRT) is the second most common form of PSVT. AVRT is the result of 2 or more conducting pathways: the AV node and 1 or more bypass tracts. In a normal heart, only a single route of conduction is present. Conduction begins at the sinus node, progresses to the AV node, then to the bundle of His and the bundles branches. In AVRT, however, 1 or more accessory pathways connect the atria and the ventricles. The accessory pathways may conduct impulses anterogradely, retrogradely or both. When impulses travel down the accessory pathway in an anterograde manner, ventricular preexcitation results. This produces a short PR interval and a delta wave as seen in WolffParkinsonWhite. PSVT may start suddenly and last for seconds or days. Patients may present with mild or severe cardiopulmonary complaints depending on their hemodynamic reserve as well as their heart rate, the duration of the PSVT, and coexisting diseases. PSVT can result in heart failure, pulmonary edema, myocardial ischemia, and/or myocardial infarction secondary to increased heart rate in patients with poor left ventricle function. In fact, one study found that one third of patients with SVT experienced syncope, required cardioversion, or had an episode of sudden death. Incessant SVT can cause tachycardiainduced cardiomyopathy. Palpitations and dizziness are the most common symptoms reported by patients with SVT. Chest discomfort may be secondary to rapid heart rate, and it frequently subsides with the termination of the tachycardia. A 12 lead ECG allows classification of the tachyarrhythmia, and it may allow a precise diagnosis. P waves may not be visible; when present, they may be normal or abnormal depending on the mechanism of atrial depolarization. Following termination of the tachycardia, an ECG should be obtained during sinus rhythm to screen for WPW syndrome. Patients. Patients with WPW syndrome may be at risk for cardiac arrest if they develop AF or atrial flutter in the presence of a rapidly conducting accessory pathway. Extremely rapid ventricular rates during AF or atrial flutter can cause deterioration to ventricular fibrillation. In the absence of manifest preexcitation (i.e., WPW), the risk of sudden death with PSVT is extremely
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)

Paroxysmal supraventricular tachycardia (PSVT) is episodic with an abrupt onset and termination. Depending on the site of origin of the dysrhythmia, SVT may be classified as an atrial or atrioventricular tachyarrhythmia. Supraventricular tachycardia (SVT), a common clinical condition, is any tachyarrhythmia that requires only atrial and/or atrioventricular (AV) nodal tissue for its initiation and maintenance. It usually is a narrow complex tachycardia that has a regular, rapid rhythm; exceptions include atrial fibrillation (AF) and multifocal atrial tachycardia (MAT). Aberrant conduction during SVT results in a wide complex tachycardia. SVT occurs in all age groups, and treatment can be challenging. studies have determined that the pathophysiology of SVT E - 50
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low. Patients who are hemodynamically unstable should be resuscitated immediately with cardioversion. The majority of the patients who present with PSVT have AVNRT or AVRT. These arrhythmias depend on AV nodal conduction and therefore can be terminated by transiently blocking AV nodal conduction. 90% of tachycardia due to AVNRT or AVRT can be terminated with Adenosine. thetic properties may also help to suppress ventricular ectopy during an AMI. The net effect is to decrease firing of ectopic foci and allow a normal rhythm to reassert itself. Lidocaine seems to be more effective during AMI. The toxictotherapeutic balance is delicate. The routine use of Lidocaine is no longer recommended. Procainamide may also be used to treat PVCs. It may be effective when Lidocaine has not achieved suppression. It increases the refractory period of the atria and the ventricles. Myocardial excitability is reduced by causing an increase in the threshold for excitation and inhibition of ectopic pacemaker activity.
RATIONALE
The goals of pharmacotherapy are to correct arrhythmia, prevent complications, and reduce morbidity. DRUG CATAGORY: Antiarrhythmic agents These drugs can be used to treat or prevent arrhythmia. Adenosine (Adenocard) is a firstline medical treatment for termination of PSVT. It is a shortacting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. It is effective in terminating both AVNRT and AVRT. More than 90% of patients convert to sinus rhythm with adenosine 12mg. As a result of its short halflife, adenosine is best administered in an antecubital vein as an IV bolus followed by a rapid saline infusion. DRUG CATAGORY: Calcium Channel Blocker This drug decreases conduction velocity and prolongs the refractory period. Diltiazem (Cardizem) Decreases conduction velocity in the AV node. It also increases the refractory period via blockade of calcium influx. This, in turn, stops the reentrant phenomenon.
PULMONARY EMBOLISM (PE)

Pulmonary embolism (PE) is an extremely common and highly lethal condition that is a leading cause of death in all age groups. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. Unfortunately, the diagnosis is missed far more often than it is made, because PE often causes only vague and nonspecific symptoms. Pulmonary thromboembolism is not a disease in and if itself. Rather, it is an oftenfatal complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually with the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. Under pathological conditions, microthrombi may escape the normal fibrinolytic system to grow and propagate. PE occurs when these clots break loose and embolize to block pulmonary blood vessels. Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. Current techniques allow us to demonstrate PE in 6080% of these patients, even though about half have no clinical symptoms to suggest PE. Thrombus in the popliteal segment of the femoral vein (the segment behind the knee) is the cause of PE in more than 60% of cases. The belief that calf vein deep vein thrombosis (DVT) is only a minor threat is outdated and inaccurate. DVT of the calf is a significant source of PE and often causes severe morbidity or death. In fact, one third of the cases of massive PE have their only identified source in the veins of the calf. PE is the third most common cause of death in the US. Massive PE is one of the most common causes of unexpected death, being second only to coronary artery disease as a cause E - 51
PREMATURE VENTRICULAR CONTRACTIONS (PVC)

Therapy for complex ventricular ectopy depends on the setting and the underlying cause. In drug toxicity specific therapies are available. With electrolyte imbalances, correction of abnormalities is therapeutic. Lidocaine is the DOC in the setting of complex ectopy in the periMI period if the patient is symptomatic, yet no firm evidence supports this practice. DRUG CATEGORY Antiarrhythmics These agents alter the electrophysiologic mechanisms responsible for PVCs. Lidocaine stabilizes cell membranes and blunts action potential. Furthermore, lidocaine shortens repolarization. Lidocaine suppresses ventricular arrhythmias predominatly by decreasing automaticity by reducing the slope of diastolic depolarization as seen in the QRS complex. Its local anes-
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tients are classified as having pseudoPEA. True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity. PEA is most frequently the end result of a major cardiac insult and commonly is caused by respiratory failure with hypoxia. Situations that cause sudden changes in preload or afterload (i.e., massive pulmonary embolus) often result in PEA. The initial insult weakens cardiac contractions, and this situation is exacerbated by worsening acidosis, hypoxia, and increasing vagal tone. Further compromise of the inotropic state of cardiac muscle leads to inadequate mechanical activity, even though electrical activity is present. This event creates a vicious cycle, causing degeneration of the rhythm and subsequent death of the patient. PEA is caused by the inability of cardiac muscle to generate a sufficient force despite an electrical depolarization. This form of electromechanical decoupling may be the final result of many factors. PEA is always caused by a profound global cardiac insult (i.e., severe prolonged hypoxia, acidosis). Hypoxia secondary to respiratory failure is probably the most common cause of PEA. The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. Rapid initiation of advanced cardiac life support (ACLS) is paramount. The initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly reversed. For this reason, PEA is considered a rhythm of survival. PEA is classified on the basis of etiology. Some common causes are: respiratory arrest, cardiac tamponade, massive myocardial infarction, cardiac rupture, tension pneumothorax, and severe CHF. In preload and afterload changes: severe hypovolemia, massive pulmonary embolus and sepsis may be the cause. In metabolic changes: hyperkalemia, hypothermia, drug ingestion (TCA, digitalis, calcium channel blockers). Postdefibrillation PEA is characterized by the presence of organized electrical activity, occurring immediately after electrical cardioversion and in the absence of palpable pulse. This condition may result in PEA in as many as 60% of patients. Postdefibrillation PEA may be a marker for a better prognosis than if ventricular fibrillation continues. A spontaneous return of pulse is likely, and cardiopulmonary resuscitation (CPR) should be continued for as long as 1 minute to allow for spontaneous recovery. Reversible causes should be sought out and corrected immediately. This may include chest decompression, pericardiocentesis, volume infusion, rewarming, or sodium bicarbonate administration.
of sudden unexpected natural death at any age. Most clinicians do not appreciate the extent of the problem, because the diagnosis is unsuspected until autopsy in approximately 80% of cases. Symptoms that should provoke a suspicion of PE must include chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, hemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax. The classic triad of signs and symptoms of PE are hemoptysis, dyspnea and chest pain. Many patients with PE are initially completely asymptomatic, and most of those who do have symptoms have an atypical presentation. Patients with PE often present with primary or isolated complaints of seizure, syncope, abdominal pain, high fever, productive cough, newonset atrial fibrillation, disseminated intravascular coagulation, or any of a host of other signs and symptoms. The most important clinically identifiable risk markers for DVT and PE are a prior history of the same, recent surgery or pregnancy, prolonged immobilization, or underlying malignancy. The most important thing that can be done in the prehospital setting is to transport the patient to a hospital. As long as no reliable method is available of making a clinical diagnosis of PE without diagnostic tests, treating PE in a meaningful way in the field will remain difficult. In the hospital, fibrinolytic therapy has been the standard of care for all patients with massive or unstable PE since the 1970s. Oxygen should always be started in the prehospital phase, and an IV line should be placed if it can be accomplished rapidly without delaying transport. Fluid loading should be avoided unless the patients hemodynamic condition is deteriorating rapidly, because IV fluids may worsen the patients condition. Without invasive testing or trial and surveillance, the clinician cannot know weather additional preload will help or hurt a heart that is failing already because of high outflow pressures from pulmonary vascular obstruction.
PULSELESS ELECTRICAL ACTIVITY (PEA)

Pulseless electrical activity (PEA) is a clinical condition characterized by loss of palpable pulse in the presence of recordable cardiac electrical activity. PEA is also referred to as electromechanical dissociation (EMD). PEA may result various etiologies and has a spectrum of manifestation. Patients may present with recordable aortic pressures and absent peripheral pulses from weak cardiac contractions or severe peripheral vascular disease. These paE - 52
RATIONALE
The goals of pharmacotherapy are to reduce morbidity and
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prevent complications. Identifying all possible causes and attempting to correct them is of the upmost importance to the survivibility of this rhythm. Bradycardic TCP May be beneficial early on because a healthy myocardium exists and only a temporarily disturbed cardiac conduction system stands between survival and death. Fluid Resusitation Hypovolemia is the most common cause of electrical activity without measurable blood pressure. Through prompt recognition and fluid challenge, many causes of hypovolemia can be corrected. DRUG CATEGORY: Inotropic agents Increases the central aortic pressure and counter myocardial depression. Main therapeutic effects are cardiac stimulation, bronchial smooth muscle relaxation, and dilation of skeletal muscle vasculature. Epinephrine (Adrenalin) has alphaagonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilation, systemic hypotension, and vascular permeability. Betaagonist effects of epinephrine include bronchodilation, chronotropic cardiac activity, and positive inotropic effects. DRUG CATEGORY: Anticholinergic agents Improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. Atropine is used for treatment of bradyarrhythmias. It works to increase heart rate through vagolytic effects, causing an increase in cardiac output. DRUG CATEGORY: Alkalinizing agents Useful in alkalinization of urine. Routine administration is discouraged because it worsens intracellular and intracerebral acidosis and is not proven to benefit mortality. Sodium Bicarbonate is used only when a patient is diagnosed with bicarbonateresponsive acidosis, hyperkalemia, TCA, or phenobarbital overdose, or a long arrest interval in the intubated patient Routine use is not recommended. ranial pressure. Sinus bradycardia also may be caused by the sick sinus syndrome, which involves a dysfunction in the ability of the sinus mode to generate or transmit an action potential to the atria. This is the most common cause of symptomatic sinus bradycardia. Sick sinus syndrome includes a variety of disorders and pathologic processes that are grouped within one loosely defined clinical syndrome. The syndrome includes signs and symptoms related to cerebral hypoperfusion, in associated with sinus bradycardia, sinus arrest, sinoatrial (SA) block, carotid hypersensitivity, or alternating episodes of bradycardia and tachycardia. Sick sinus syndrome occurs most commonly in elderly patients with concomitant cardiovascular disease and follows an unpredictable course. Cardiac auscultation and palpation of peripheral pulses reveal a slow, regular heart rate. The physical examination is generally nonspecific, although it may reveal the following signs: decreased level of consciousness, cyanosis, peripheral edema, pulmonary vascular congestion, dyspnea, and poor perfusion. Emergency care should first rapidly ensure the stability of the patients condition. This is followed by an investigation into the underlying cause of the bradycardia. Unstable patients may require immediate endotracheal intubation and transcutaneous pacing. In sick sinus syndrome, atropine may aide patients transiently, most ultimately require placement of a pacemaker. In patients with hypothermia who have confirmed sinus bradycardia with a pulse, atropine and pacing usually are not recommended because of myocardial irritability. Rewarming and supportive measures are the mainstays of therapy.
RATIONALE
Drug treatment for sinus bradycardia usually is not indicated for asymptomatic patients. In symptomatic patients, underlying electrlyte or acidbase disorders or hypoxia should be corrected. IV atropine may provide temporary improvement in symptomatic patients, although its use should be balanced by an appreciation of the increase in myocardial oxygen demand this agent causes. Although in the past, isoproterenol was used quite commonly in patients with bradycardia; further appreciation of its substanial risks has deminished its role. Temporary pacing is recommended in symptomatic patients who are unresponsive or only temporarily responsive to atropine, or in whom atropine therapy is contraindicated. Transcutaneous pacing, where available, is the initial procedure of choice. DRUG CATEGORY: Anticholinergics These agents are indicated when symptoms of hypoperfusion exist. They are thought to work centrally by suppressing conduction in the E - 53
SINUS BRADICARDIA
Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats/minute or less. However, few patients actually become symptomatic until their heart rate drops to less than 50 beats/minute. The pathophysiology of sinus bradycardia is dependant upon the underlying cause. Other causes of sinus bradycardia are related to increased vagal tone. Physiologic causes of increased vagal tone include bradycardia seen in athletes. Pathologic causes include, but are not limited to, inferior wall MI, toxic or environmental exposure, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intrac-
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vastibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous systerm. Atropine is used to increase heart rate through vagolytic effects, causing increase in cardiac output. drive pacing may be necessary at a rate of up to 140 bpm to control the rhythm in a patient with torsade who is in extremis. Magnesium sulfate is the firstline therapy in the treatment of torsade de pointes.
VENTRICULAR FIBRILLATION TORSADES DE POINTES (TDP)

Torsades de pointes (TDP), often referred to as torsade, is an uncommon variant of ventricular tachycardia (VT). The underlying etiology and management of torsade are, in general, quite different from those of garden variety VT. The management of torsade with group lA antidysrhythmic drugs can have disastrous consequences. Differentiating between these entities, therefore, is clinically important. Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. The original report described regular variation of the morphology of the QRS vector from positive to negative and back again. This was symbolically termed torsade de pointes, or twisting of the point about the isoelectric axis, because it reminded the original authors of the torsade de pointes movement in ballet. Torsade usually occurs in bursts that are not sustained; thus, the rhythm strip usually shows the patients baseline QT prolongation. In the US, 300,000 sudden cardiac deaths occur per year. TDP probably accounts for fewer than 5%. Prolongation of the QT interval may be congenital, and is associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation. The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents. The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. Since procainamide increases the likelihood of polymorphous VT developing, it generally should not be used in combination with another agent that prolongs the QT interval, such as amiodarone. Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines, tricyclic antidepressants, lithium, and chemotherapeutic agents. Other associated risk factors include a history of resuscitated arrest, congenital deafness, and a family history of sudden death. The prehospital provider should institute immediate advanced cardiac life support (ACLS) protocol for VT. OverE - 54 2/15/06 Ventricular fibrillation (VF) is a pulseless arrhythmia with irregular and chaotic electrical activity and ventricular contraction in which the heart immediately loses its ability to function as a pump. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD). VF usually develops secondary to an area of myocardial ischemia with a lowered fibrillation threshold. VF can be initiated in ischemic heart disease when a premature ventricular contraction (PVC) overcomes a lowered fibrillation threshold. Fibrillation is caused by simultaneous presence of abnormal irregular beats, conduction disturbances creating abnormal electrical propagation of the action potential, and reentry. An oftendescribed RonT extrasystole phenomenon may account for many VF cases. Propagation to the whole myocardium implies that the initial fibrillation reached sufficient critical mass. In the absence of ischemic heart disease, VF may occur secondary to antiarrhythmic drugs, prolonged QT syndromes, preexcitation syndromes, and systemic hypoxemia. Ventricular tachycardia (VT) often precedes onset of VF in these cases; VT degenerates into VF. VF has been described as the initial rhythm in almost 70% of outofhospital arrests. Cardiovascular diseases cause 12 million deaths in the world each year and are the primary causes of death in the US. Although VF seldom is listed as the cause of death, it is thought to be responsible for more than 400,000 SCD cases in the US annually. Untreated, VF causes loss of oxygen to vital organ systems and brain death in minutes. VF often occurs without forewarning. Chest pain, dyspnea, fatigue, palpitations, syncope and a possible increase in heart rate, presence of PVCs or period of VT may occur immediately preceding acute cardiac arrest. Physical findings in VF reveal no pulse or respiration, unconsciousness and wide and chaotic QRS complexes on the cardiac monitor. VF is the major electrical mechanism for cardiac arrest. Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to VF that occur outside the hospital. Interventions that impact survival and outcome of resuscitation include: early recognition of an arrest, early activation of EMS, and early access to trained personnel capable of performing CPR, defibrillation, and ACLS.
Automated external defibrillators (AEDs) have revolutionized prehospital VF management because they have eliminated the need for rhythmrecognition training. AEDs identify VF more rapidly than manual defibrillation techniques, are 92 100% specific for VF, and require less time to achieve defibrillation. Their use has resulted in increased survival rates and improved prognosis for patients in VF arrest. However, AEDs should not be used during emergency transport because patient movement creates the risk of inadvertent defibrillation. Bystander CPR reportedly plays a significant role in prolonging the period (up to 12 min) in which VF may respond to a defibrillator. CPR may increase the number of patients in VF who benefit from defibrillation by response personnel. Lack of response to standard defibrillation algorithms is challenging. In refractory VF additional medications such as magnesium and/or procainamide may be effective (class IIb). In postresuscitative care, antiarrhythmics used successfully should be continued and control any hemodynamic instability. Postdefibrillation arrhythmias (mainly atrioventricular AV blocks) have been reported in up to 24% of patients. The incidence is related to the amount of energy used for defibrillation. Always check for complication (i.e., aspiration pneumonia, CPRrelated injuries), and establish the need for emergent interventions. Automated implantable defibrillators (AICDs) are used for patients at high risk for recurrent VF. Studies indicate patients with VF arrest who receive AICDs have improved longterm survival rates compared to those receiving only medications. AICD effectively provides early defibrillation. Prognosis for survivors of VF strongly depends on the time elapsed between onset and medical intervention. Early defibrillation often makes the difference between longterm disability and functional recovery. Postresuscitation death and disability after successful resuscitation directly correlate with the amount of CNS damaged during the event. Without intervention, by 46 minutes after onset of VF, prognosis is poor. Few survive when VF lasts more than 8 minutes without intervention. tive is to interfere with all reentrant arrhythmia and allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker. Biphasic waveform defibrillation shocks (repeated at < or = 200j) have equivalent or higher success for eventual termination of VF than monophasic defibrillators that increase the current (200, 300, 360j) with successive escalating shocks. The medication administration treatment goals are to electrically terminate VF so that an organized electrical rhythm follows and restores cardiac output. Success rates significantly decrease as the duration of ischemia increases. Drug therapy may consist of sympathomimetics, antiarrhythmics, atropine, and electrolytes. Recent American Heart Association (AHA) and ACLS recommendations promote amiodarone as superior to the conventional use of Lidocaine. Controversy surrounds the issue of Lidocaine vs Amiodarone because providers have expressed reluctance to accept the recommendations. They point out that while Amiodarone has been shown to improve the chance of a patient in VF to regain a pulse, the rate of survival out of the hospital is not increased in patients who receive Amiodarone. In addition, the difficulty in drawing up and storing this medication and the cost of administration of amidodarone has been restrictive, forcing certain institutions and prehospital provider authorities to opt to ignore the ACLS updated recommendations pertaining to the use of Amiodarone. DRUG CATEGORY: Sympathomimetics/ Vasopressors Augment both coronary and cerebral blood flow present during low flow states associated with CPR. Vasopressin was recently considered equivalent to epinephrine, the single most useful drug in cardiac arrest. It is a Class 11B drug by ACLS criteria, with fewer negative myocardial effects. This means that fair to good evidence supports its use in humans. Since it lasts longer than epinephrine, vasopressin is used only once in pulseless VT and VF. Consenses exists to follow it with standard use of epinephrine after 5 minutes from the administration of vasopressin if no response/ return of spontaneous circulation. Epinephrine is considered the most useful drug in cardiac arrest. DRUG CATEGORY: Antiarrhythmics Alter electrophysiologic mechanisms responsible for arrhythmia. Lidocaine is a class 1B antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Lidocaine is the DOC for VF refractory to defibrillation and epinephrine. Amiodarone May inhibit AV conduction and sinus node function. Amiodarone prolongs action potential and refracE - 55
RATIONALE
Automated external defibrillators (AEDs) have revolutionized VF management because they have eliminated the need for rhythmrecognition training. AEDs identify VF more rapidly than manual defibrillation techniques, and are 92100% specific for VF, and require less time to achieve defibrillation. Their use has resulted in increased survival rates and improved prognoses for patients in VF arrest. Electrical external defibrillation remains the most successful treatment of VF. A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objec-
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tory period in the myocardium and inhibits adrenergic stimulation. Procainamide increases the refractory period of the atria and ventricles. Myocardiac excitibility is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. Procainamide may be effective when lidocaine is not. However, its role in VF is limited due to the time it takes procainamide to reach therapeutic levels when administered IV. DRUG CATEGORY: Electrolytes Are considered therapeutic alternatives for refractory VF. Patients with presistant or recurrent VF following antiarrhythmic administration should be assessed for underlying electrolyte abnormalities as a a cause for their refractory dysrhythmia. Among electrolyte abnormalities associated with VF are hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicardbonate are used in VF secondary to other medications. Magnesium sulfate acts as an antiarrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VF caused by hyperkalemia. Deficiency in magnesium sulfate is associated with cardiac death and can precipitate refractory VF. Magnesium supplementation is used to treat torsades de pointes, known or suspected hypomagnesemia, or severe refractory VF. Sodium bicarbonate is used only when the patient is diagnosed with bicarbonateresponsive acidosis, hyperkalemia, tricyclic antidepressant, or Phenobarbital overdose. Routine use is not recommended. Calcium chloride is also useful in the treatment of hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. It moderates nerve and muscle performance by regulating the action potential excitation threshold. rate greater than 100 beats per minute (usually 150200), wide QRS complexes (>120ms), presence of atrioventricular (AV) dissociation, and fusion beats. Ventricular tachycardia may develop without hemodynamic deterioration, yet it often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation (VF). VT usually is a consequence of structural heart disease, with breakdown of normal conduction patterns, increased automaticity (which tends to favor ectopic foci), and activation of reentrant pathways in the ventricular conduction system. Electrolyte and sympathomimetics may increase the likelihood of VT in the susceptible heart. A distinctive variant of VT is torsade de pointes, with its unusual shiftingaxis QRS complexes that appear as if the heart is rotating upon an axis. It typically occurs from drugs or conditions that prolong the QT interval (i.e., type 1a antiarrhythmics and hypomagnesemia). Arrhythmia may occur with or without either myocardial ischemia or infarction. VT is one of the most frequently observed dysrhythmias. VT can produce congestive heart failure and hemodynamic compromise, yet the principal morbidity comes from its tendency to degenerate spontaneously into VF. This degeneration also is the usual source of mortality in VT. Most patients present to the emergency worker with symptoms of either ischemic heart disease or hemodynamic compromise resulting from poor perfusion. Symptoms may include chest pain, palpitations, anxiety and diaphoresis. Physical findings usually reflect the degree of hemodynamic instability such as symptoms of CHF (dyspnea, hypoxemia, rales, and jugular vein distention), hypotension and an altered mental status. VT is generally a symptom of coronary artery disease (CAD) or structural heart disease. VT can be triggered by electrolyte deficiencies and the use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine) may stimulate VT in vulnerable hearts. Emergency workers must determine if the VT is stable or unstable. Unstable VT is characterized by symptoms of insufficient oxygen delivery such as chest pain, dyspnea, hypotension, or altered level of consciousness, indicating rate and stroke volume are not providing adequate cardiac output. Stable VT patients do not experience symptoms of hemodynamic decompensation. Unlike other dysrhythmias, VT tends to deteriorate into unstable states and more malignant dysrhythmias. Consider all patients with VT to have active myocardial ischemia, which should be sought and treated aggressively. If treated rapidly, VT generally has a favorable shortterm outcome. Longterm prognosis depends upon the underlying
VENTRICULAR TACHYCARDIA (VT)

Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute and wide QRS complexes. VT may be monomorphic (typically regular rhythm originating from a single focus with identical QRS complexes) or polymorphic (may be irregular rhythm, with varying QRS complexes). Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration; a longer duration is considered VT. No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT including a E - 56
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cardiac disease. can destabilize hemodynamic status. IV amiodarone may be better tolerated than procainamide. Proarrhythmias (torsades de pointes)are serious tachyarrhythmias or bradyarrhythmias seemingly generated by antiarrhythmic agents. With this in mind, the clinician should never use more than 1 agent unless absolutely necessary. In most patients, when an appropriate dose of a single antiarrhythmic medication fails to terminate an arrhythmia, turning to electrical cardioversion rather than a second antiarrhythmic medication is now exceptable. DRUG CATEGORY: Electrolytes This agent is considered a therapeutic alternatives for refractory VT. It can be used secondary to antiarrythmics and is reserved for treating the patient who presents with torsades de pointes. Magnesium Sulfate is the DOC for torsades de pointes. Procainamide is contraindicated because of its QT prolongation potential. Polymorphic VT of the torsade de pointes type should be treated immediately because of the frequent transition to unstable VT. This arrhythmia will recur and seldom remains stable. Lidocaince may be utilized, however torsades may be drug induced (proarrhythmic) or the result of an underlying magnesium deficiency. In these instances, magnesium sulfate, although an electrolyte, acts as an antiarrhythmic.
RATIONALE
The primary objective is to establish whether a widecomplex tachycardia is stable or unstable, thereby answering the question is the patients clinical presentation so severe that immediate electrical cardioversion is required or can the patient be managed adequately with pharmacological agents. Unstable VT is treated with immediate synchronized cardioversion, followed by expeditious airway management as needed, supplemental oxygen, vascular access, and antiarrhythmic therapy. Most patients respond to low levels of electrical energy. However, failure to synchronize the shock with the patients QRS may precipitate VF. ECG is the diagnostic modality of choice for confirming that the patients tachycardia is VT. Simultaneous 3channel recordings and 12lead tracings are more helpful than rhythm strips to analyze this dysrhythmia. Furthermore, ECG should be obtained before, during pharmacological interventions and after conversion to a regular rhythm. DRUG CATEGORY: Antiarrhythmics Mainstay treatments for clinically stable VT are antiarrhythmic drugs. These agents alter the electrophysiologic mechanisms responsible for arrhythmia. Lidocaine will more effectively suppress ventricular arrhythmias associated with acute myocardial ischemia and infarction once they occur. The net effect is to decrease firing of ectopic foci to allow a normal rhythm to reassert itself. Lidocaine is appropriate for stable, monomorphic or polymorphic VT. However, it is a second choice. Other drugs are preferred over lidocaine in each VT scenario. Although lidocaine can be administered rapidly with minimal effect on blood pressure, studies suggest that it is relatively ineffective for termination of VT and less effective against VT than IV procainamide. Procainamide is another antiarrhythmic agent known to effective in treating a broad variety of arrhythmias. Procainamide slows down phase 4 (diastolic) depolarization, decreases automaticity, and slows intraventricular conduction. In the stable VT setting, if this drug is selected by the clinician, blood pressure monitoring for hypotension is critical. This drug can also be expected to reach therapeutic levels slightly slower than Lidocaine. DRUG CATEGORY: Vasopressor Augment both coronary and cerebral blood flow present during low flow states. Amiodarone has not been studied specifically for the termination of hemodynamically stable VT, but it is effective in treating hemodynamically unstable VT and VF. Both procainamide and amiodarone have vasodilatory effects which
WOLFFPARKINSONWHITE SYNDROME
Preexcitation is defined as, if in relation to atrial events, the whole or some part of the ventricular muscle is activated earlier by the impulse originating from the atrium than would be expected if the impulse reached the ventricles by way of the normal specific conduction system only. Of the various preexcitation syndromes, the most common is Wolff ParkinsonWhite (WPW) syndrome. Emergency workers should be familiar with this syndrome and the proper treatment of its associated arrhythmias to avoid unnecessary morbidity and mortality. In some patients a conduction pathway bypasses the AV node. Such a conduction pathway is called an accessory bypass tract. In a few patients who have downward conduction through this pathway, there is the potential for extremely rapid ventricular responses during AF with degeneration to VF. Digitalis, verapamil, diltiazem, adenosine, and possibly intravenous blockers can cause a paradoxical increase in ventricular response rates in these patients with WPW. If patients are clinically unstable, synchronized electrical cardioversion is always indicated. Antiarrhythmic agents that have direct effects on accessory pathway conduction and reE - 57
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fractoriness (such as Procainamide or amiodarone) are more likely to slow ventricular response during preexcited AF or atrial flutter as well as convert the arrhythmia to sinus rhythm. Accessory connections between the atrium and ventricle are the result of embryonic development of myocardial tissue bridging the fibrous tissue that separates the 2 chambers. Although dozens of locations for bypass tracts can exist in preexcitation, the most common bypass tract is an accessory atrioventricular (AV) pathway. This is the anomaly seen in WPW. Death from WPW occurs secondary to the associated arrhythmias or from mistreatment of these arrhythmias with inappropriate medications. Men are affected 6070% more than women. Typically, those affected are young, otherwise healthy individuals. Patients may present with anything from mild chest discomfort or palpitations to severe cardiopulmonary distress or arrest. Patients commonly present with heart rates in the 250 beat per minute range, often associated with hypotension. WPW has no specific examination features except for those that may accompany the arrhythmias. On physical examination, the patient may be cool, diaphoretic, and hypotensive. Rales are common, as the high heart rate causes diastolic heart failure. with adenosine. In normal hearts, an individual is protected from exceptionally high rates by the relatively long refractory period of the AV node. In patients with WPW, however, the accessory pathway often has a much shorter anterograde refractory period, allowing for much faster transmission of impulses and correspondingly higher rates. In addition, sympathetic discharge secondary to hypotension may lead to further shortening of the refractory period and subsequent increases in the ventricular rate. If the rate becomes too high, VF may result. AF through an accessory pathway appears as a bizarre, widecomplex, irregular tachycardia on ECG, with rates often in the 250 bpm or higher. Therapy in the prehospital setting depends upon the patients degree of stability and the specific arrhythmia. Always treat arrhythmias associated with WPW with caution. The basic treatment principle in WPW AF is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. If AF were treated in the conventional manner by drugs that prolong the refractory period of the AV node (i.e., calcium channel blockers, betablockers, dioxin), the rate of transmission through the accessory pathway likely would increase, with a corresponding increase in ventricular rate. This could have disastrous consequences, possibly causing the arrhythmia to deteriorate into VF. Focus on breaking the cyclical transmission of impulses. This is best accomplished by temporarily prolonging the refractory period of the AV node with drugs such as adenosine. Patients with WPW have an excellent prognosis when treated with ablation of the accessory pathway.
Generic
Amitriptyline Imipramine Desipramine Nortriptyline Doxepin Protriptyline Maprotiline
Trade Names
Elavil, Endep, Triavil, Etrafon, Limbitrol Tofranil, Imavate, Presamine, Janimine, SkPramine, Berkomine Norpramine, Pertofrane Aventyl, Pamelor Sinequan, Adapin, Curatin Vivactil Ludiomil
The classic ECG morphology of WPW is described as a shortened PR interval, a widened QRS complex, and a delta wave. In reality, however, morphology depends directly upon the degree of preexcitation. Atrial fibrillation (AF) in patients with WPW is very common and has an incidence of 1138%. It also is the deadliest arrhythmia for these patients because of the possibility of deterioration into ventricular fibrillation Differential diagnosis includes ventricular tachycardia (VT), which is regular (unless it is torsade de pointes) or PSVT with aberrancy. Consider any regular widecomplex tachycardia to be VT until proven otherwise. However, as in narrow complex tachycardias, a stable patient initially may be treated E - 58
HAZARDOUS MATERIALS MANAGEMENT ORGANOPHOSPHATE INSECTICIDES

Organophosphates are used in agriculture, in the home, in gardens, and in veterinary practice. All apparently share a common mechanism of cholinesterase inhibition and can
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cause similar symptoms. Because they share this mechanism, exposure to the same organophosphate by multiple routes or to multiple organophosphates by multiple routes can lead to serious additive toxicity. It is important to understand, however, that there is a wide range of toxicity in these agents and wide variation in cutaneous absorption, making specific identification and management quite important. Sufficient muscular fasciculations and weakness are often observed as to require respiratory support; respiratory arrest can occur suddenly. Likewise, bronchorrhea and bronchospasm may often impede efforts at adequate oxygenation of the patient. Bronchospasm and bronchorrhea can occur, producing tightness in the chest, wheezing, productive cough, and pulmonary edema. A life threatening severity of poisoning is signified by loss of consciousness, incontinence, convulsions, and respiratory depression. The primary cause of death is respiratory failure, and there usually is a secondary cardiovascular component. The classic cardiovascular sign is bradycardia which can progress to sinus arrest. However, this may be superseded by tachycardia and hypertension from nicotinic (sympathetic ganglia) stimulation. Toxic myocardiopathy has been a prominent feature of some severe organophosphate poisonings. Some of the most commonly reported early symptoms include headache, nausea, dizziness, and hypersecretion, the latter of which is manifested by sweating, salivation, lacrimation, and rhinorrhea. Muscle twitching, weakness, tremor, incoordination, vomiting, abdominal cramps, and diarrhea all signal worsening of the poisoned state. Miosis is often a helpful diagnostic sign and the patient may report blurred and/or dark vision. Anxiety and restlessness are prominent, as are a few reports of choreaform movements. Psychiatric symptoms including depression, memory loss, and confusion have been reported. Toxic psychosis, manifested as confusion or bizarre behavior, has been misdiagnosed as alcohol intoxication. Children will often present with a slightly different clinical picture than adults. Some of the typical cholinergic signs of bradycardia, muscular fasciculations, lacrimation, and sweating were less common. Seizures (22%-25%) and mental status changes including lethargy and coma (54%-96%) were common. In comparison, only 2-3% of adults present with seizures. Other common presenting signs in children include flaccid muscle weakness, miosis, and excessive salivation. In one study, 80% of cases were transferred with the wrong preliminary diagnosis. In a second study, 88% of the parents initially denied any exposure history.
TOXICOLOGY
Organophosphates poison insects and mammals primarily by phosphorylation of the acetylcholinesterase enzyme (AChE) at nerve endings. The result is a loss of available AChE so that the effector organ becomes overstimulated by the excess acetylcholine (ACh, the impulse-transmitting substance) in the nerve ending. The enzyme is critical to normal control of nerve impulse transmission from nerve fibers to smooth and skeletal muscle cells, glandular cells, and autonomic ganglia, as well as within the central nervous system (CNS). Some critical proportion of the tissue enzyme mass must be inactivated by phosphorylation before symptoms and signs of poisoning become manifest. At sufficient dosage, loss of enzyme function allows accumulation of ACh peripherally at cholinergic neuroeffector junctions (muscarinic effects), skeletal nerve-muscle junctions, and autonomic ganglia (nicotinic effects), as well as centrally. At cholinergic nerve junctions with smooth muscle and gland cells, high ACh concentration causes muscle contraction and secretion, respectively. At skeletal muscle junctions, excess ACh may be excitatory (cause muscle twitching), but may also weaken or paralyze the cell by depolarizing the end-plate. In the CNS, high ACh concentrations cause sensory and behavioral disturbances, incoordination, depressed motor function, and respiratory depression. Increased pulmonary secretions coupled with respiratory failure are the usual causes of death from organophosphate poisoning. Recovery depends ultimately on generation of new enzyme in all critical tissues. SIGNS AND SYMPTOMS OF POISONING: Symptoms of acute organophosphate poisoning develop during or after exposure, within minutes to hours, depending on the method of contact. Exposure by inhalation results in the fastest appearance of toxic symptoms, followed Symptoms of acute organophosphate poisoning develop during or after exposure, within minutes to hours, depending on the method of contact. Exposure by inhalation results in the fastest appearance of toxic symptoms, followed by the gastrointestinal route and finally the dermal route. All signs and symptoms are cholinergic in nature and affect muscarinic, nicotinic, and central nervous system receptors. The critical symptoms in management are the respiratory symptoms.
N-METHYL CARBAMATE INSECTICIDES

N-Methyl carbamate insecticides are widely used in homes, gardens, and agriculture. They share with organophosphates the capacity to inhibit cholinesterase enzymes E - 59
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and therefore share similar symptomatology during acute and chronic exposures. Likewise, exposure can occur by several routes in the same individual due to multiple uses, and there is likely to be additive toxicity with simultaneous exposure to organophosphates. However, due to the somewhat different affinity for cholinesterases, as compared to organophosphates, these poisonings are often somewhat easier to treat. tinic effects including hypertension and cardiorespiratory depression. Dyspnea, bronchospasm, and bronchorrhea with eventual pulmonary edema are other serious signs. Recent information indicates that children and adults differ in their clinical presentation. Children are more likely than adults to present with the CNS symptoms above. While children can still develop the classic muscarinic signs, the absence of them does not exclude the possibility of carbamate poisoning in the presence of CNS depression. Malaise, muscle weakness, dizziness, and sweating are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain, and diarrhea are often prominent. Miosis with blurred vision, incoordination, muscle twitching, and slurred speech are reported.
TOXICOLOGY
The N-methyl carbamate esters cause reversible carbamylation of the acetylcholinesterase enzyme, allowing accumulation of acetylcholine, the neuromediator substance, at parasympathetic neuroeffector junctions (muscarinic effects), at skeletal muscle myoneural junctions and autonomic ganglia (nicotinic effects), and in the brain (CNS effects). The carbamyl-acetylcholinesterase combination dissociates more readily than the phosphoryl-acetylcholinesterase complex produced by organophosphate compounds. This lability has several important consequences: (1) it tends to limit the duration of N-methyl carbamate poisonings, (2) it accounts for the greater span between symptom producing and lethal doses than in most organophosphate compounds, and (3) it frequently invalidates the measurement of blood cholinesterase activity as a diagnostic index of poisoning. N-methyl carbamates are absorbed by inhalation and ingestion and somewhat by skin penetration, although the latter tends to be the less toxic route. At cholinergic nerve junctions with smooth muscle and gland cells, high acetylcholine concentration causes muscle contraction and secretion, respectively. At skeletal muscle junctions, excess acetylcholine may be excitatory (cause muscle twitching), but may also weaken or paralyze the cell by depolarizing the end-plate. In the brain, elevated acetylcholine concentrations may cause sensory and behavioral disturbances, incoordination, and depressed motor function (rarely seizures), even though the N-methyl carbamates do not penetrate the central nervous system very efficiently. Respiratory depression combined with pulmonary edema is the usual cause of death from poisoning by N-methyl carbamate compounds. SIGNS AND SYMPTOMS OF POISONING: As with organophosphate poisoning, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue AchE is reversible, and carbamates are more rapidly metabolized. Bradycardia and seizures are less common than in organophosphate poisonings. The primary manifestations of serious toxicity are central nervous system depression, as manifested by coma, seizures, and hypotonicity, and nicoE - 60
TOXICOLOGY COCAINE TOXICITY

Pharmacology Cocaine stimulates the central nervous system primarily by blocking the reuptake of norepinephrine and secondarily by marked release of norepinephrine.
PATHOPHYSIOLOGY
Dysrhythmias Tachdysrhythmias cause the most acute cocaine related nontraumatic deaths. Ischemic chest pain / myocardial infarction Risk of an AMI is increased by a factor of 24 during the first 60 minutes after cocaine use. Neurological Seizures Agitated Delirium A common presentation in patients who die of cocaine overdoses. Manifests itself as bizarre and violent behavior. Aggression, combativeness, hyperactivity, extreme paranoia, unexpected strength, and incoherent shouting. Above behavior is often followed by cardiopulmonary arrest. Hyperthermia and physical restraint of the patient are exacerbating factors in persons who die from agitated delirium. Physical Presentation Altered mental status New onset seizures Hypertension*** Tachycardia*** Chest pain
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Myocardial ischemia / infarction Shortness of breath Epistaxis Psychiatric illness ***Note: Once considered classic presentations, but not always seen, especially in chronic users. Drowsiness Deep sedation Respiratory distress Amnesia
KETAMINE
(Special K, Kay, Jet) Ketamine is commonly sold at dance clubs for its hallucinogenic effects, or mixed with other Designer Drugs for snorting, swallowing, or injecting. Since Ketamine is an anesthetic used to induce deep sleep for surgery, an overdose could result in coma or death. SIGNS AND SYMPTOMS Low doses Lack of coordination Dizziness Pleasant or unpleasant hallucinations Nausea and vomiting Increased salivation Slurred speech Side to side or up and down eye movements Mood swings from quiet to violent High doses Stiff contorted muscles Sweating Hypertension Hyperthermia Amnesia Uncontrollable muscle and tongue movements Respiratory arrest
DESIGNER DRUGS
This informal classification of illicit drugs presents the team with somewhat unique patient presentations, the following provides some backround information on some of the more common designer drugs
ECSTASY
(MDMA, ADAM, XTC, X) Ecstasy is a hallucinogenic amphetamine commonly bought in rave clubs. It is available in pill, capsules, or powder form. Ecstasy is a mind altering drug with speed effects and is commonly mixed with depressants. The normal dose is close to the toxic levels. Deaths are usually due to seizures or extremely high fever. SIGNS AND SYMPTOMS Seizure Hyperthermia Hypertension Hallucinations Agitation Irregular heartbeat Tachycardia Stroke Jaw clenching (the reason many ravers carry blow pops or pacifier) Muscle spasms Dilated pupils Sweaty
NEXUS
(STP, TOONIES) Nexus is another hallucinogenic amphetamine and produces similar effects SIGNS AND SYMPTOMS Anxiety Panic reactions
ROHYPNOL
(roofies, rophies, ropies, ruffies, roche, Flunitrazepam) Flunitrazepam (Rohypnol) is a prescription medication in other parts of the world, but is illegal in the United States. It is a benzodiazepine like Valium, but considered about 10 times stronger. Rohypnol is particularly dangerous when combined with other depressants such as alcohol. Popular at rave dances as well as used in date rape cases. frequently cocaine users will use Rohypnol to come down and it is used it enhance poor quality heroin. SIGNS AND SYMPTOMS CNS depressant
INHALANTS
Many inhalants may be present at rave dances. They include: Volatile solvents Airplane glue Correction fluids Degreasers Gasoline Lighter fluid Paint thinners Spot removers Aerosols Air fresheners Cooking spray E - 61
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Asthma inhalers Deodorants Hair spray Spray paint Volatile Nitrates Amyl nitrate Butyl nitrate Isobutly nitrate IN SUDDEN SNIFFING DEATH SYNDROME (SSDS) AVOID THE USE OF EPINEPHRINE (if possible). MONITOR FLUIDS creased level of consciousness, administration of Sodium Bicarbonate 50 mEq followed by a Sodium Bicarbonate infusion of 1 amp in 500cc 0.9% NaCl to run at 50 cc/hr. Keeping the patient in an alkalotic state decreases the incidence of ventricular fibrillation. A 12 lead EKG should also be done enroute to the emergency room.
COMMON TRICYCLIC ANTIDEPRESSANTS: SIGNS AND SYMPTOMS OF TCA OVERDOSE:

CNS (early) CNS (late) confusion, agitation, hallucinations hyperactive reflexes, positive Babinski, rapid onset of coma, seizures
GAMMA HYDROXY BUTYRATE

(GHB, fall, scoop, liquid x, goop, Georgia Home Boy) This compound was initially used by body builders to stimulate muscle growth. In recent years it has become a popular recreational drug among dance clubs. GHB is synthesized from a chemical used to clean electrical circuit boards. It is available in both liquid powder forms. Often used in combination with other drugs, such as ecstasy, it is odorless and tasteless. GHB effects can be felt within 5 to 20 minutes after ingestion and the high lasts about 1.5 to 3 hours. Because it is odorless and tasteless it can be slipped into someones drink undetected. SIGNS AND SYMPTOMS CNS depression Nausea Respiratory depression Seizures
Anticholinergic: flushing, dry mouth, dilated pupils Cardiovascular: QRS greater than 0.12 sec, bundle branch block, AV blocks, sinus tach, PVCs, ventricular bigeminy, V tach, Vfib, bradycardia, cardiac arrest, hypotension, pulmonary edema Worldwide, greater than 9 million natural and synthetic chemicals have been identified; fortunately, fewer than 3000 cause greater than 95% of accidental and deliberate poisonings. Identifying a poison and accurately assessing its potential toxicity are critical. Poisoning should be considered in the differential diagnosis of any unexplained symptoms or signs, especially in children less than 5. Similarly, in the young adult, any disparity between expected history and clinical findings should suggest poisoning. Recently, poisonings among the elderly (especially medication mixups), among hospitalized patients (drug errors), among workers exposed to occupational chemicals, and as a result of environmental pollution have been increasingly recognized. Often the type and speed of onset of the total clinical picture will confirm or refute a suspicion of poisoning. Occasionally, the absence of a specific finding will be as important as its presence. Any pertinent history should be secured and the person and premises inspected for traces of drugs; i.e., imprint identifications on solid medication forms, alcohol, etc, particularly for the unconscious patient. Specific antidotes: While not numerous, specific antidotes are remarkably effective; i.e., naloxone in opioid overdoses, atropine in organophosphate encounters, methylene blue for methemoglobinemia, acetylcysteine for acetaminophen, Digibind for digoxin. A poison center should be contacted to determine if new specific antidotes have been developed, particularly for new drugs. Inhaled poison: The patient should be removed from the contaminated environment, his respiration supported, and other personnel protected from contamination.
POISONING/OVERDOSE
A relatively small percentage of the cases of poisoning and drug overdose are actually lifethreatening situations when the Team arrives. Calm management of suspected poisonings include securing evidence from the scene and careful initial assessment of the patient. Suicidal patients should not be allowed to refuse care without law enforcement present to accept responsibility. Be alert for possible violent acts. Prompt consultation with the emergency room is appropriate. The Team should give special attention to neurological findings such as: level of consciousness., pupils, eye movement, gag reflex and response to pain.
TRICYCLIC ANTIDEPRESSANTS (TCA)

Tricyclic antidepressant overdose is probably the most common serious drug overdose encountered today. It represents an true medical emergency and is associated with approximately 20 % mortality rate. The tricyclic antidepressants remain a major cause of toxic death in the U.S. The standard of care for significant TCA overdoses includes a rapid assessment, aggressive airway management in the patient with deE - 62
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Skin and eye contamination: Contaminated clothing (including shoes and socks) should be removed. The skin should be thoroughly washed and the eyes flushed with water. around visualization and palpation of all areas of the abdomen. This does not preclude that standard traumatic primary surveys should not be completed. In fact, this is just a small part of the overall assessment of any trauma patient. After the removal of all clothing in the region, the entire abdominal region needs to be visually assessed and manually palpated. Consideration should be given during clothing removal for the maintenance of legal evidence if it is needed (i.e., GSWs, stabbings, etc.). Following the standards put forth by BTLS International, the acronym DCAPBLS TIC can be followed (deformity contusionabrasionspenetrationsburnslacerations swellingtendernessinstabilitycrepitus). One also must remember that any signs of intraabdominal trauma seen in the pre hospital setting, typically indicates a significant underlying injury since abdominal injuries typically do not manifest themselves early. Abdominal distention or tenderness is considered to be an indication for immediate transport following a traumatic incident. Although auscultation and percussion of the abdomen are nice to complete during assessment, time should not be wasted in the prehospital setting since the benefits of such are minimal. Management of the abdominal trauma patient typically revolves around the standards impressed upon us throughout our careers, ABCs (Airway Breathing Circulation). After the maintenance of each of these has been achieved and assured, treatment of abdominal injuries can be addressed as part of the circulation assessment. Treatments should reflect a minimal onscene time, as rapid transport of the patient to an awaiting OR is imperative. IVs should be considered en route to the ER and only run at a rate conducive to maintaining a systolic B/p of 90100 mmHg. Other standard shock treatments should also be included during the transport. Since specific injury diagnosis is practically impossible in the prehospital setting, early recognition of a possible problem is the key to the proper management of the abdominal trauma victim. Rapid transport of all suspected abdominal injuries is imperative when you consider that no other area of the body is capable of readily hiding such large quantities of blood. Quick recognition and rapid treatments en route help to keep us ahead of the game, especially when considering that patients with serious intraabdominal injuries can easily deteriorate rapidly and often without warning.
TRAUMA ABDOMINAL TRAUMA

Abdominal trauma is typically a difficult at best situation to assess especially in the prehospital setting. As with any traumatic incident, injury is delineated into two categories; blunt trauma and penetrating trauma. Penetrating trauma is obviously easy to recognize, as the integrity of the abdominal wall has been breeched. Blunt trauma on the other hand, can be subtle, which allows for the prehospital provider to possibly miss underlying injuries. Whether the mechanism of injury is blunt or penetrating, the two most life threatening problems associated with abdominal trauma are hemorrhage and infection. The key to proper management of the abdominal trauma patient is rapid assessment and recognition, and proper shock management. Assessment of the traumatic abdomen causes us to remember our anatomy of the three regions within the abdomen; thoracic abdomen, true abdomen, and retroperitoneal abdomen. Each region houses both solid and hollow organs within which represent different injury patterns accordingly. The thoracic abdomen is considered to encompass all the organs which reside in the abdomen, yet are still protected anteriorly by the inferior portion of the rib cage (i.e. spleen, liver, gallbladder, stomach). Special consideration must be given, as rapid hemorrhage is very possible with injuries here. Even minor lacerations to liver or spleen can cause significant blood loss, resulting in a shocky patient. The true abdomen encompasses the large and small intestines, and the bladder. One also must incorporate the anatomy of the female patient since the true abdomen also holds the ovaries, uterus, and fallopian tubes. Injury to these organs typically cause infection, peritonitis, and occasionally shock (especially in females due to the vascularity of the uterus ). Finally, the retroperitoneal region lies posterior to both the thoracic and true abdomens. This region is the most difficult to assess due to its location anatomically. Organs located within this region include; kidneys, pancreas, abdominal aorta, and the inferior vena cava. Each of these present a large opportunity for massive hemorrhage with the possibility of no obvious changes to the region, so it is imperative that other signs and symptoms of shock are observed for. Proper assessment of the abdomen typically revolves
BURNS
Each year approximately 2 million people are burned in the United States resulting in approximately 12,000 deaths. As a result, many of the survivors of these incidents are unfortunately severely disabled and/or disfigured. Burns are classified by the cause, and, more importantly, severity, or degrees, E - 63
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which depends upon the depth of the burn. Each burn creates a unique set of management problems while at the same time, each burn management case will follow the same treatment modalities. Burns are typically classified into one of the following causes: flame, electrical, chemical, radiation, steam, or scald. The skin, the largest organ in the human body, is the predominant reference made when talking about burns. However, its importance in temperature regulation, environmental protections, and other homeostatic functions is unsurpassed. Unfortunately, even though the skin is often the only place you actually see the effects of burns, it is the underlying structures, organs, and vessels which are the ultimate considerations treating a burn patient. The skin is divided into two layers: the epidermis, the thin outer layer seen on the surface, and the dermis, the thick connective tissue layer located just beneath the epidermis. Burns degrees are based upon the amount of tissue involvement as it pertains to the skin. Firstdegree burns typically involve just the outer regions of the epidermis and are commonly recognized by their red, painful skin, which usually heals within 3 to 6 days following the incident. Second degree burns (commonly referred to as partial thickness burns) involve deeper regions of the skin including all of the epidermis and typically just the outer regions of the dermal layer. Seconddegree burns are commonly seen as red, blistered skin that is very painful to touch and will typically heal within 2 to 4 weeks after the exposure. Finally, thirddegree burns, which are considered the most dangerous. These are referred to as fullthickness burns due to the fact that all layers of the skin, including the underlying subcutaneous tissues and muscle layers are commonly involved in the burndamaged area. Thirddegree burns are commonly characterized by the whitegray, leathery, charred skin that is void of pain due to the complete destruction of the nerve endings located within that region of the skin. Third degree burns do not heal naturally due to the complete destruction of all the skin cells located within the area and long term treatment typically includes skin grafts. Assessment of the burn patient encompasses the size and location of the affected area, as well as the cause of the burn itself, and, most importantly, the safety of the crew and patient. Scene safety must always be in the forefront of everyones thoughts when on any trauma call. Assessment of the burn patient follows the ABCs as we have all been taught, although special consideration must be made with regards to airway control. Inhalation burns, which account for more than half of all burn deaths, commonly cause E - 64 2/15/06 edema and swelling to the upper airways. This ultimately leads to the closing off of the airway. Early recognition of such a possibility must be considered and acted upon prior to the complete closure of the airway. Aggressive airway management will ultimately determine the viability of your patient. Determining the cause of the burn is also of great importance. Although flame exposure, chemical, and scald burns are easily recognizable on the surface, electrical burns may only manifest themselves as a small dot or circle on the skin, yet the damage created from the burn can be staggeringly more severe. One also must also consider the size of the affected area. The common Rules of Nine chart allows prehospital providers to approximate the percentage area affected by the burns, but this does not account for the possible areas affected when considering an electrical burn. One must believe that all areas between an entranceburn and an exitburn are also affected. This can drastically increase the size of your burn. One must also note the area affected by the burns. Face, hands, feet, genitals, and major joints are areas that require special attention by properly trained burn specialists. Special considerations for chemical burns are required, in such that even though you may have an easily recognizable outer burn area, you have to determine whether or not the skin has absorbed the chemical agent and is now possibly circulating it systemically. Management of the burn patient depends upon the cause and region of the burn. As a prehospital provider, you must realize that burn patients do not typically die rapidly from the burns themselves, rather, they die from the secondary conditions related to the burns (i.e. airway obstruction secondary to edema from an inhalation burn). Management should place the greatest emphasis on airway management and the removal of the patient from the source of the burn. Cooling of the burn site should be limited as to prevent the accidental causing of hypothermia or localized vasoconstriction. This would decrease the blood flow to an already damaged region. The longterm prognosis of the patient is increased when recognition for rapid transport is made. To minimize infection and other longterm considerations for the patient, pay attention to wound care. Remember, the most important thing you can do for your burn patient is airway management.
CHEST INJURY
Chest injury is often a deceptive diagnosis without the availability of Xrays. Any chest wall injury associated with difficulty breathing should be considered serious until proven otherwise. Chest injuries are the second leading cause of trauma related deaths each year. A thorough assessment is
essential, as missed injuries can lead to impaired ventilation causing hypoxia, hypercarbia, and acidosis. The major types of chest injury are listed below. Rib Fractures, Flail chest, Pulmonary contusion Pneumothorax (open and closed), Tension Pneumothorax and hemothorax, Myocardial Contusion, Pericardial tamponade, Aortic, tracheal, and bronchial rupture, Traumatic asphyxia, Penetration and compromise of the diaphragm. The above can be caused by a variety of trauma: Motor Vehicle accidents, falls, sports injuries, crush injuries, stab wounds, and gunshot wounds. The goal in the treatment of these injuries is to maintain the patients ability to oxygenate blood passing through the lungs. Provide supplemental High Flow Oxygen, do a thorough assessment, and treat the injury following the appropriate procedural guideline. Chest injury may be penetrating or blunt. Penetrating injuries are caused by forces distributed over a small area as in gunshot wound, stabbing, or falls onto sharp objects. With penetrating trauma, any structure or organ in the chest cavity may be injured. With blunt trauma, the forces are distributed over a larger area, and many injuries occur from deceleration, bursting, and shearing forces. Conditions such as pneumothorax, pericardial tamponade, flail chest, pulmonary contusion, and aortic rupture should be suspected in blunt trauma or when the mechanism of injury involves rapid deceleration. Symptoms The symptoms of chest trauma include; shortness of breath, tachypnea, and chest pain. The pain is usually pleuritic, pain upon movement of the chest wall during respiration. The patient will usually try to splint the chest wall thereby limiting the movement during respiration. Conditions such as pneumothorax, and vascular injuries might not produce any symptoms initially. Repeat assessment is essential. Signs The evaluation of the chest should include observation, palpation, and auscultation. Signs to observe include, cyanosis, bruises, lacerations, puncture wounds, jugular vein distention, tracheal deviation, subcutaneous emphysema, and asymmetrical chest rise. The neck and chest should be palpated for the presence of tenderness, bony crepitus, subcutaneous emphysema, and an unstable chest segment. The chest should be auscultated for equal lung sounds, volume of inspiration, and diminished or absent breath sounds on one or both sides of the chest. Signs and Symptoms of Specific Injuries Rib Fractures: Pain on inspiration, local tenderness, bony crepitus. Flail Chest: Paradoxical Chest movement, pain, crepitus, hypoxia. Pulmonary Contusion: Usually seen with flail segment, pain, hypoventilation, hypoxia. Pneumothorax: Unequal lung sounds, difficulty breathing, tachypnea, pleuritic chest pain. Open Pneumothorax: Pain, difficulty breathing, bubbling sound as air moves in and out of the pleural space through the defect. Tension Pneumothorax: Pain, difficulty breathing, jugular vein distention, tracheal deviation, absent or diminished lung sounds, cyanosis, tachycardia, narrow pulse pressure. Hemothorax: Tachypnea, decreased breath sounds, dullness to percussion, clinical signs of Shock, difficulty breathing. Myocardial Contusion: May have no signs and symptoms other than chest pain from striking object. Arrhythmias are to be treated by ACLS protocol be alert to mechanism of injury. Pericardial Tamponade: Tachycardia, jugular vein distention, narrow pulse pressure, Pulsus Paridoxus (can be determined by noting the radial pulse diminish or even disappear with inspiration), muffled heart sounds. Aortic Rupture: Clinical signs of Shock, unequal pulses between the arms and the lower torso. (Radial and Femoral Pulses) Tracheal/Bronchial Rupture: Severe dyspnea, hemoptysis, subcutaneous emphysema. Traumatic Asphyxiation: Bluish discoloration to face and neck, jugular vein distention, conjunctival hemorrhage, difficulty breathing. Diaphragmatic Rupture: Difficult to diagnose, decreased breath sounds particularly over the left chest, sometimes bowel sounds may be heard in the left chest. If a considerable amount of abdominal contents is displaced into the chest, the abdomen may have a hollow or empty appearance. In summary serious injury to the chest can disrupt ventilation and also cause profound circulatory compromise. Maintaining the ABCs as well as quick assessment and intervention for field treatable injuries (i.e.. Tension Pneumo, Pericardial Tamponade, Sucking Chest wound, Flail Chest) can be lifesaving. Interventions should be done enroute to the hospital if possible, as on scene times should be kept to a minimum for these trauma patients. E - 65 2/15/06

neck, and upper chest, but not below the nipple line. Associated injuries may require intubation and mechanical ventilation. All survivors in a large series were extricated within fifteen minutes of intrapment. Patients who survive for more than an hour will uniformly do well with 90+% chance of survival without sequelae or complications.
CRUSH INJURY
Crush injuries and their secondary metabolic complications are relatively uncommon, but are a significant form of trauma. The three major syndromes associated with crushing injuries are: Crush Syndrome Compartment Syndrome Traumatic Asphyxia These complex and often devastating injuries are among the most challenging types of trauma encountered by pre hospital care providers. Early recognition and prompt therapy are essential to achieving a favorable outcome, whereas delays in diagnosis and treatment may result in permanent and severe disability.
DROWNING/NEAR DROWNING
Bystander CPR may be in progress. The Team should prepare for abdominal distention with vomiting. Focus on airway management and hyperventilation, with compressions if appropriate. A significant amount of drowning victims develop marked laryngospasm with airway occlusion. The Team should consider the following: head or spinal injury, aspiration of fluid, lung sounds, down time and water temperature. Neardrowning victims, because of aspiration or laryngospasm, usually sustain significant hypoxemia, with the consequent danger of respiratory failure and hypercapnia. Acute reflex laryngospasm may result in asphyxia without aspiration of water. Aspiration of fluid and particulate matter may cause chemical pneumonitis, damaging cells lining the alveoli, and may impair alveolar secretion of surfactant, resulting in patchy atelectasis. The perfusion of nonaerated, atelectatic areas of the lungs leads to intrapulmonary shunting of blood and aggravates hypoxemia; the more fluid aspirated, the greater the surfactant loss, atelectasis, and hypoxemia. Aspiration of large quantities of water may cause sizable areas of atelectasis, resulting in stiff noncompliant lungs and respiratory failure. Respiratory acidosis with hypercapnia and hypoxemia can occur. A concomitant metabolic acidosis may also result from tissue hypoxia. Hypoxemia and tissue hypoxia often result in pulmonary edema and even cerebral edema. The mammalian diving reflex in cold water allows survival after long periods of submersion. The diving reflex, first identified in seagoing mammals, slows the heartbeat and constricts the peripheral arteries, shunting oxygenated blood away from the extremities and the gut to the heart and brain. In cold water, the O2 needs of the tissues are reduced, extending the possible time of survival. Respiratory insufficiency is more critical than changes in electrolytes and blood volume, which vary in magnitude depending on the type and volume of aspirated fluid. Sea water may cause a mild elevation of sodium and Cl, but the levels are rarely lifethreatening. By contrast, aspirating large quantities of fresh water can cause a sudden increase in blood volume, profound electrolyte imbalance, and hemolysis. Victims may succumb to the effects of these changes asphyxia and possibly ventricular fibrillation at the scene of the tragedy. Cardiac arrest, usually preceded by fibrillation, causes
CRUSH SYNDROME:
Following extrication, the patient frequently feels relatively little or no pain, and may have few physical complaints. Instead, emotional complaints dominate the history, as might be expected from a patient trapped or buried for hours. Multiple skin lacerations and tears are common when a direct pressure trauma occurs, such as when a car runs over an extremity. If crush syndrome develops and is untreated, Hypovolemic shock and hyperkalemia occur, followed by acidosis and acute renal failure secondary to myoglobin released from damaged tissue.
COMPARTMENT SYNDROME:
Compartment syndrome is caused by higher than normal pressure within a closed space, usually a muscle compartment. It occurs secondary to either a decrease in compartment size or an increase in compartment contents. The pathophysiology of compartment syndrome essentially results from too much volume in too little space leading to too much pressure. As perfusion is impaired, ischemia and tissue edema occur and are followed by more swelling. Tissue ischemia is followed by tissue necrosis. Muscle death may result in myoglobinuria, acidosis, and renal failure as well as amputation of the involved extremity, sepsis, or sepsis, or death.
TRAUMATIC ASPHYXIA:
Traumatic asphyxia, usually resulting from injuries that cause direct chest compression are rare. The exact pathology of this syndrome is unknownone hypothesis is that blood forced out of the right atrium by the crushing force moves through the innominate and jugular veins toward the head. The clinical syndrome includes subjuctival and subcutaneous hemorrhages, bluish discoloration of the face, neck, and pronounced facial edema. Peleckiae is evident at the face, E - 66
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many of the deaths attributed to drowning. However, current belief is that the pulmonary edema following near drowning is a direct result of hypoxemia and analogous to pulmonary edema of high altitude, i.e., noncardiogenic pulmonary edema. Time should not be wasted in attempts to drain water from the lungs in a freshwater victim, because the hypotonic fluid passes rapidly into the circulation. Sea water, being hypertonic, draws plasma into the lung, and the Trendelenburg position may promote drainage. Hospitalization is mandatory for all victims. Resuscitation should continue during transport, regardless of the patients condition. Consciousness is not synonymous with recovery, since delayed death from hypoxia can occur. iris, cataract, dislocated lens, glaucoma, vitreous hemorrhage, orbitalfloor fractures, retinal hemorrhage or detachment, and rupture of the eyeball may result. Emergency treatment may be needed before care by a specialist. It consists of alleviating pain and applying protective dressings. Traumatized lids should never be opened forcibly, since this could aggravate the injury. Rarely, after a laceration of the globe, the uninjured, contralateral eye becomes inflamed (sympathetic ophthalmia) and may lose vision to the point of blindness. Anterior chamber hemorrhage (traumatic hyphema) following blunt injury is potentially serious and requires attention by an ophthalmologist. It may be followed by recurrent bleeding, glaucoma, and bloodstaining of the cornea. Although initially retinal detachment may be localized, without treatment the entire retina may detach. Rhegmatogenous detachment implies a break through and through in the retina and is seen more frequently in myopia, after cataract surgery, or following ocular trauma. Non rhegmatogenous detachments can be produced by vitreoretinal traction (i.e. proliferative retinopathy of diabetes or sickle cell disease) or by transudation of fluid into the subretinal space (i.e., severe uveitis, especially in Vogt KoyanagiHarada disease, or primary or metastatic choroidal tumors). Retinal detachment is painless. Premonitory symptoms may include dark or irregular vitreous floaters, flashes of light, or blurred vision. As the detachment progresses, the patient notices a curtain or veil in the field of vision. If the macula is involved, central visual acuity fails drastically. Any patient with a suspected or established retinal detachment should be seen, on an urgent basis, by an ophthalmologist. Direct ophthalmoscopy may show retinal irregularities and a bullous retinal elevation with darkened blood vessels. Indirect ophthalmoscopy, including scleral depression, is necessary to detect peripheral breaks and detachment. If a vitreous hemorrhage obscures the fundus, especially in myopia, postcataract extraction, or eye injury, retinal detachment should be suspected and ultrasonography performed. Subconjunctival hemorrhages may develop at any age, usually following minor trauma, straining, sneezing, or coughing; rarely, they occur spontaneously. They alarm the patient but are of no pathologic significance except when associated with blood dyscrasias, which is rare. They occur as gross extravasations of blood beneath the conjunctiva and are absorbed spontaneously, usually within two weeks with treatment. Vitreous hemorrhages, extravasations of blood into the vitreous, produce a black reflex on ophthalmoscopy. They may E - 67 2/15/06
EYE INJURIES
The three principal types of eye injuries encountered by the Team are due to blunt and penetrating trauma, burns and foreign bodies (including chemicals). Chemical injury generally requires the fastest action to avoid permanent damage. Most of the field treatment of eye injuries involves only superficial care, since the majority of problems must be handled in the hospital by an opthamologist. Sudden loss of vision in one eye can be caused by thrombosis or occlusion of the retinal artery. Acute glaucoma produces pain, headache, nausea and haloes around the eye. Treatment is patching. Retinal detachment causes vision loss, flashing lights, and dark spots. Treatment is transport in supine position and patch both eyes. Trauma to the eye or adjacent structures requires meticulous examination to determine the extent of injury. Vision, range of extraocular motion, depth of anterior chamber, location of lid and conjunctival lacerations and of foreign bodies, and presence of anterior chamber or vitreous hemorrhage or cataract should be determined and recorded in detail for protection of patient, physician, and in industrial cases, employer. 1. Conjunctival and corneal foreign body injuries are the most common eye injuries. Seemingly minor trauma can be serious if ocular penetration is unrecognized or if secondary infection follows a corneal abrasion. 2. Intraoccular foreign body injuries require immediate emergency treatment, and the foreign body that has penetrated the eye must be removed by an ophthalmic surgeon. A patch and a metal shield are placed over the eye to avoid inadvertent pressure that could extrude ocular contents through the penetration site. The patient should not receive anything by mouth in preparation for urgent surgery. Trauma to the globe may severely damage internal structures. Hemorrhage into the anterior chamber, laceration of the

occur in such conditions as diabetic retinopathy or hypertension or may result from trauma, retinal neovascularization, or retinal tears. Retinal hemorrhages are flameshaped in the superficial nerve fiber layer, as in hypertension or venous occlusion, or round (dot and blot) in the deeper layers, as in diabetes mellitus or septic infarctions. Retinal hemorrhages are always significant, reflecting vascular disease that usually is systemic. Seeing floaters (spots) before one or both eyes is a frequent adult complaint. Floaters are usually most noticeable against a white homogeneous background and seem to move slowly. They result from contraction of the vitreous gel and its separation from the surface of the retina. Since the vitreous gel is denser where it attaches to the optic nerve, floaters are usually more apparent in this area. Though floaters usually are without significance, in a small number of patients they may indicate a tear in the retina. They are more prevalent in highly myopic and older persons, tending to become less noticeable with time. A minute vitreous hemorrhage may appear as a brown or red floater. Retinal detachments may be preceded by a shower of sparksor lightning flashes and may be accompanied by a shower of floaters. Only after the retina actually separates from its underlying structure (the retinal pigment epithelium) does a curtain of visual loss move across the visual field. Abnormal visual intolerance to light is common in lightly pigmented persons. Usually it is without significance and may be relieved by wearing dark glasses. It is an important, but nondiagnostic, symptom in keratitis, uveitis, acute glaucoma, and traumatic corneal epithelial abrasions. Ocular pain is important and, unless due to an obvious local cause such as a foreign body, acute lid infection, or injury, demands investigation (i.e., for uveitis, especially iridocyclitis, or glaucoma). Sinusitis occasionally causes referred eye pain. A blind spot in the field of vision is a negative scotoma. Frequently it is not noticed by the patient unless it involves central vision and interferes significantly with visual acuity. Negative scotomas noticed by the patient usually are due to hemorrhage or choroiditis. A scotoma found in the same visual field area in each eye is usually a quadrantic or hemianoptic defect resulting from a lesion in the optic pathways. A positive scotoma, perceived as a light spot or scintillating flashes, represents a response to abnormal stimulation of some portion of the visual system; i.e., as in the migraine syndrome. as simple injuries (splinting, elevation and ice). Treat long bone fractures, hip, pelvic or spinal injuries as major trauma. When the patients condition and time permits, the Team should establish IV and EKG monitoring prior to moving patient. The Team should consider the following: shock, assessment of painful areas, sensation and circulation tested before and after splinting and/or manipulation. Any complaint of paresthesia, weakness of motor function, diving or body surfing injuries should be treated as a spinal injury. Assess long bone fractures noting pulse and sensation. If a fractured limb is ischemic or cannot be stabilized because of deformity, apply gentle traction along the long axis of the limb to reduce and stabilize the fracture. Recheck and record neurovascular status after each movement of limb. Use of PASG is indicated for suspected pelvic fractures.
HEAD INJURIES
Significant head injuries, which have associated findings of disturbed consciousness, abnormal CNS exam, or significant signs of head and neck trauma, produce some of the most critical injuries attended. Assuming greater severity of injury is prudent. Treat every significant head injury as neck injury too. The Team should consider the following: CSF leaks, seizure activity, check mouth, drugs at scene, focal findings in neurological exam or CheyneStokes respirations. Nasotracheal intubation is contraindicated with severe facial injuries. Head injury causes more deaths and disability than any other neurologic cause before age 50 and is the leading cause of death in men and boys less than 35 years old. Mortality in severe injury approaches 50% and is only little reduced by treatment. Damage results from skull penetration or from rapid brain acceleration or deceleration, which injures tissue at the point of impact, at its opposite pole (contrecoup), and also diffusely within the frontal and temporal lobes. Nerve tissue, blood vessels, and meninges are sheared, torn, and ruptured, resulting in neural disruption, intra and extracerebral ischemia or hemorrhage, and cerebral edema. Hemorrhage or edema acts as an expanding intracranial lesion, causing focal neurologic deficits or increased intracranial swelling and pressure that can lead to fatal herniation of brain tissue through the tentorium or foramen magnum. Skull fractures may lacerate meningeal arteries or large venous sinuses, producing epidural or subdural hematoma. Fractures, especially at the skull base, can also lacerate the meninges, causing CSF leakage through the nose (rhinorrhea) or ear (otorrhea), or ingress of bacteria or air into the cranial vault. Infectious organisms may reach the meninges via cryptic fractures, especially when they involve the paranasal sinuses. Few head injuries occur in isolation, and most cases require simultaneous attention to other seriously traumatized parts of the body.
FRACTURES
The handling of fractures may dramatically alter prognosis of the injury. Minor or small bone fractures should be treated E - 68
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Concussion is characterized by transient posttraumatic loss of consciousness unaccompanied by gross structural lesions in the brain or leaving serious neurologic residua. Although unconscious, the patient with concussion rarely is deeply unresponsive. Pupillary reactions and other signs of brainstem function are intact; extensor plantar responses may be present, but not hemiplegia or decerebrate postural responses to noxious stimulation. Cerebral contusion and lacerations constitute more severe injuries. Depending on severity, they often are accompanied by severe surface wounds and by fractures located at the base of the skull or having depressed bone fragments. Hemiplegia or other focal signs of cortical dysfunction are common. More severe injuries may cause severe brain edema, producing decorticate rigidity (arms flexed and adducted; legs and often trunk extended), or decerebrate rigidity (jaws clenched, neck retracted, all limbs extended) is common. Coma, hemiplegia, uni or bilaterally dilated and unreactive pupils, and respiratory irregularity may result from internal brain herniation and require immediate therapy. Increased intracranial pressure, producing compression or distortion of the brainstem, sometimes produces a rising blood pressure coupled with a slowing of the pulse and respiration. The cerebral hemispheres and underlying diencephalon generally are more exposed and susceptible to the effects of nonpenetrating trauma than is the brainstem. Signs of primary brainstem injury (coma, irregular breathing, fixation of the pupils to light, loss of oculovestibular reflexes, or diffuse motor flaccidity) almost always imply severe injury and a poor prognosis. Since severe head injuries frequently are accompanied by thoracic damage, the neurologic problems often are complicated by pulmonary edema (some of which is neurogenic), hypoxia, and an unstable circulation. Damage to the cervical spine can cause fatal respiratory paralysis or permanent quadriplegia from cord injury. Acute subdural or intracerebral hematomas are common in severe head injury and, together with severe brain edema, account for most fatal cases. All 3 conditions can cause transtentorial herniation with signs of progressive rostralcaudal neurologic deterioration: deepening coma, widening pulse pressure, midposition or dilated and fixed pupils, spastic hemiplegia with hyperreflexia, quadrispasticity, decorticate rigidity, or decerebrate rigidity. Epidural hematomas most often have a temporal location (middle meningeal artery). Symptoms (increasing headache, deterioration of consciousness, motor dysfunction, and pupillary changes) may develop within minutes or hours after injury, often following a lucid interval of relative neurologic normalcy. An epidural hematoma is less common than subdural hematoma, but important, because rapid brain compression and shifting can cause fatal or permanent neurologic deficits if not promptly evacuated. Temporal fracture lines suggest the diagnosis but may not be present. Chronic subdural hematoma may not produce symptoms until some weeks after trauma. Although diagnosis in early cases (2 to 4 weeks after trauma) may be suggested by a clinical course of delayed neurologic deterioration, later diagnosis can be difficult because of the time lapse between the injury and the onset of symptoms and signs. Subdural hematomas are more common in alcoholics and patients over age 50, and the head injury may have been relatively trivial, even forgotten. Increasing daily headache, fluctuating drowsiness or confusion, and mild to moderate hemiparesis are typical. In infants, chronic subdural hematomas can cause enlarging head circumference, suggesting hydrocephalus. Post traumatic epilepsy, with seizures beginning as late as several years after trauma, follows about 10% of severe closed head injuries and 40% of penetrating head wounds. The worst form of severe head injury is that which causes nearcomplete damage to forebrain functions but spares the brainstem. Survivors exist in a chronic vegetative state, which, with assiduous nursing, can last for many years. Few patients recover from the vegetative state when it lasts as long as 3 months after injury and almost none after 6 months.
HEAT TRAUMA
Exposure injuries include heat cramps, heat exhaustion and heat stroke. These can occur from exposure or/and dehydration. Heat cramps are characterized by extreme cramping, nausea & vomiting, sweating and flushed skin. Heat exhaustion is characterized by confusion, hypotension, cool/moist skin. Heat stroke is characterized by dry, red skin, shock, decreased level of consciousness or coma. Exposure to high ambient temperature may lead either to excessive fluid loss and hypovolemic shock (heat exhaustion) or to failure of heat loss mechanisms and dangerous hyperpyrexia (heatstroke). Prolonged exposure (greater than 2 to 3 weeks) and excessive sweating, especially if accompanied by vomiting or diarrhea, lead to dehydration; sodium, potassium, and magnesium depletion; and hypovolemia. High ambient humidity, by decreasing the cooling effect of sweating, and prolonged strenuous exertion with increased heat production by muscle increase the risk of heat illness. Age, obesity, chronic alcoholism, debility, and many drugs (i.e., anticholinergics, antihistamines, phenothiazines, numerous psychotropic drugs, alcohol, and cocaine) increase susceptibility to heat illness, particularly heatstroke. Though stemming from the same cause, heatstroke and heat exhaustion are sharply different. E - 69
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within the first three hours, some almost immediately. Symptoms usually get progressively more painful though they will often be relieved with oxygen. This relief is shortlived and will return even worse when oxygen is removed. Divers will often minimize the symptoms, especially if they begin to go away with oxygen. Sprains and strains dont get better with oxygen. Dive injuries do. Below is a list of the most common barotraumatic injuries.
SCUBA
Diving barotraumas can present with a variety of manifestations, from ear or mouth pain and headaches to major joint pain, paralysis, coma, and death. As a result of the wide variety of presentations, these disorders must be considered in any patient who recently has been exposed to a significant change in barometric pressure. The 3 major manifestations of barotraumas include sinus or middle ear effects, decompression sickness (DCS), and arterial gas embolism. Pathophysiology: Injuries caused by ambient pressure changes during ascent and descent are generally governed by Boyles and Henrys Laws of physics. If air is trapped, as occurs in breath holding during rapid ascent, it expands with great force against the walls of that space (reverse squeeze). During rapid ascent, incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. In addition, when nitrogen in a divers air tank dissolves in the divers fatty tissues or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. This occurs slowly and gradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream to the lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidly and forms gas bubbles.
ARTERIAL GAS EMBOLISM (AGE)

Many of the following injuries have similar causes. When at depth, a diver is at a greater residual pressure. As the diver ascends and the ambient pressure decreases air trapped in a flexible space will expand . An arterial gas embolism occurs when air becomes trapped in the divers lungs, either through breathholding or alveolar disfunction. As the diver ascends, ambient pressure decreases and the pressure within the lungs increases until an injury occurs within the lung itself and the gas is forced through the alveolar wall and into the bloodstream and surrounding tissues. Gas bubbles may lodge in many areas including the coronary arteries, spinal cord or cerebral circulation. Gas embolism may present with symptoms similar to DCS or a stroke. Onset is usually rapid, either immediately or within a few minutes.
BAROTRAUMA
Prehospital care should consist of assessing the ABCs and correcting any immediate lifethreatening conditions while maintaining adequate oxygenation and perfusion. Patients should be placed on highflow oxygen and have large bore venous access with isotonic fluid infusion to maintain blood pressure and pulse. Supine is the only currently acceptable transport position. Perform endotracheal intubation on a patient who has an unstable airway or has persistent hypoxia despite breathing 100% oxygen. End tidal CO2 detection and sa02 monitoring are essential. Needle decompression of the chest is indicated for suspected tension pneumothorax. 12 lead interpretation is appropriate in suspected AGE. Continuous intravenous hydration to maintain adequate blood pressure. Obtaining a blood glucose level and drawing Prothrombin time (PT), activated partial thromoplastin time (aPTT) blue top blood tubes would be clinically helpful prior to hydration. Consideration for relative hypothermia and passive re warming is always appropriate for these patients who may be in shock. Make every attempt to transport the divers gear with the patient. This can be vital in interpreting the cause of the inci-
SCUBA DIVING INJURIES

Scuba divers are susceptible to many types of injuries. These injuries range from minor traumas, lacerations, bites or stings to a variety of barotraumatic injuries and even carbon monoxide poisoning. General trauma, bites, stings, allergic reactions and the like are treated like any other injury and are discussed elsewhere in these guidelines. The purpose of this information is to familiarize the team with the pathophysiology and treatment of barotraumatic injuries, those injuries that are particular to the scuba diver and caused by increased pressure while underwater. The team should always be stay alert to the possibilities of multiple injuries in the diver. The goal of treatment is early recognition of the possibility of a diving injury and prompt notification of emergency room. This will allow the hospital ample time to prepare specialized equipment and recall specialized personnel. The team must also be aware that often divers ignore symptoms or pass them off as muscle sprains or strains. If the diver has breathed compressed air underwater, even in shallow water, and is experiencing any related symptoms, including but not limited to: pain, neurologic deficit, SOB or altered LOC the patient must be assumed to have experienced a barotraumatic injury, and should be treated as such until that assumption can be ruled out. Ninetyfive percent of diving injuries present symptoms E - 70
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dent. Obtaining a small water sample to be transported with the patient can be advantageous in rapidly identifying the need for specific antibiotics and facilitating their administration. Sinus & Middle ear squeeze Symptomatic therapy with decongestants, both oral and nasal, is indicated. Aspirin may also be appropriate. Pain control should be instituted with nonsteroidal anti inflammatory drugs (NSAIDs) or narcotic analgesic medications. Decompression sickness type I These patients should receive highflow oxygen via a nonrebreather mask BVM. Intravenous access with administration of isotonic fluids (normal saline or lactated ringers) to maintain urine output at 12ml/kg/hr. This is considered normal output. These patients should also receive aspirin 324650mg for antiplatelet effects as well as pain control. If a patients medical condition continues to deteriorate, he or she is then classified as having type II DCS. Decompression sickness type II All of the interventions for type 1 are appropriate for type II DCS. These patients need recompression therapy to resolve their symptoms. The most appropriate management is to transfer to the nearest hyper baric chamber. Arterial gas embolism These patients can have mild symptoms from a small embolism that may improve with the therapy for type 1 DCS, including highflow oxygen, liberal intravenous hydration, and aspirin. Patients with severe AGE (i.e., unstable blood pressure, respirations, or neurologic status) require immediate recompression therapy in a hyper baric chamber. Consultations: Consult a specialist at a recompression chamber for any patient with type 11 DCS or an unstable AGE. The recompression chamber specialist must be contacted prior to transfer to determine chamber availability and the appropriateness of hyper baric oxygen (HBO) therapy. A complete list of recompression chambers is available from the Divers Alert Network (DAN) by phone 24 hours a day at (919) 6848111 or (919) 6844DAN (4326). Their US web site is http://www.diversalertnetwork.org. An important issue to consider is time vs distance to the HBO chamber. This frequently is accomplished by air. Helicopter transport necessitates the pilot maintain altitude at less than 1000 feet. The primary medications in treatment of dysbaric injuries are oxygen, isotonic fluids, antiinflammatory medications, decongestants, and analgesics. Medical management techniques utilizing the triad of 100% oxygen, aggressive rehydration, andomedications to alleviate and reverse the inflammatory process that is chiefly responsible for the progression of DCS. CNS cases treated with the protocol during transport were improved or asymptomatic upon arrival at the HBO chamber 72% of the time.
DECOMPRESSION SICKNESS (BENDS, DCS)

DCS usually results from the formation of gas bubbles, which can travel to any part of the body, accounting for many disorders. A gas bubble forming in the back or joints can cause paresthesias (tingling), neuropraxia, or paralysis. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli. DCS is classified into 2 types. Type 1 is milder, not life threatening, and characterized by pain in the joints and muscles and lymph node swelling. The most common symptom is joint pain, which begins mildly and worsens over time and with movement. Type II DCS is serious and life threatening. Manifestations may include respiratory, circulatory, and most commonly, peripheral nerve and/or CNS compromise. Arterial gas embolism (AGE) is the most dangerous manifestation of type II DCS. It occurs after a rapid ascent, when a gas bubble forms in the arterial blood supply and travels to the brain, heart, or lungs. This is immediately life threatening and can occur even after ascent from relatively shallow depths. DCS of the CNS is clinically similar to AGE; since the treatment of either requires recompression, differentiating between them is not of great importance. Clinical History: Patients present with a history of diving, generally within 24 hours o the onset of symptoms. A physical exam should be tailored to the patients history. Signs and symptoms that appear during or following a dive are pressure related until proven otherwise by a diagnostic or therapeutic recompression. Sinus squeeze Patients generally present with complaints of facial or E - 71
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oral pain, nausea, vertigo, or headache. Other important information to gather includes any history of recent upper respiratory infections, allergies rhinitis, sinus polyps, sinus surgeries, and whether the pain worsened during the descent or ascent. Middle ear squeeze Patients often have a history of sudden vertigo, nausea, tinnitus, ear pain, deafness, or headache. They may have a history of previous diving ear injuries or a history of previous or current ear infection. Decompression sickness type I patients often have a history of recent diving followed by a flight home. They may complain of slowly progressing pain or numbness in their limbs or back. Patients present with joint, muscle, or back pain that worsens over time. The pain worsens with motion but is always present. Pain may range from mild t9 severe (the bends). This occurs in the majority (7085%) of patients. The shoulder is the most commonly affected joint. Patients may have a history of previous decompression illness and multiple dives in the same day and frequently have not followed the dive tables closely. Divers should be questioned as to the method of computing bottom and ascent times with safety stops. This information should be recorded as part of the medical record. Decompression sickness type II Type II usually presents sooner than type I. Pain is reported in only about 30% of cases. Patients may present with shortness of breath (chokes), chest pain, severe headache, altered mental status, and shock. They also may complain of dizziness or weakness. Patients may rapidly deteriorate without emergent intervention. Essential history to ascertain includes time since dive ended, the dive profile, when the symptoms began, and prior medical history. The dive profile consists of prior dives that day, depth of dive, bottom time, decompression stop depth, and length of stop. Inquires should be made specifically about previous decompression ~ injuries, pulmonary related problems, injuries or surgeries. Arterial gas embolism (AGE) AGE usually presents with a history of a diver ascending very rapidly, often from fairly shallow depths, and suddenly screaming and losing consciousness. These patients often die before reaching medical facilities. Obtaining a history from these patients can be difficult E - 72 2/15/06 because they often present with altered mental status or in shock. Other injuries similar to AGE & occurring on rapid ascent Mediastinal emphysema gas is forced into the media stinum Pericardial emphysema gas is forced into the pericardium and presents as pericardial tamponade. Pneumothorax gas becomes trapped within the pleural space. Witnesses often report that divers experience a sudden or immediate loss of consciousness or collapse, usually within minutes of surfacing. Causes: The causes of DCS are related to predisposing medical or genetic factors, and to diver error. Examples of diver errors include multiple daily dives, poor adherence to the dive tables, breath holding (most common), rapid ascent and or flying or traveling to high altitudes within 24 hours after diving.
MEDIASTINAL EMPHYSEMA
Injury occurs similar to an AGE however the gas is forced into the mediastinum. As the diver ascends the trapped air expands, compressing the heart, lungs and great vessels. As with AGE the onset of symptoms is usually rapid.
NITROGEN NARCOSIS (RAPTURE OF THE DEEP)

Nitrogen Narcosis is caused by an oversaturation of nitrogen in the bloodstream through an unknown process. It results in a narcotic effect on the diver which may greatly affect his/her judgement. All signs and symptoms will disappear as the diver ascends to a shallower depth. The danger is that the diver will do something foolish while under the effect of nitrogen narcosis and suffer a more serious injury. Altered level of consciousness at the surface is not Nitrogen Narcosis.
OXYGEN TOXICITY
Oxygen toxicity has rarely been seen in the past when dealing with recreational divers diving within accepted limits (less than 130 ft). However, with the acceptance of Enriched Air Nitrox (EAN) as a breathing gas there is a greater chance of oxygen toxicity. EAN is essentially air with an increased O2 percentage. 32% and 36% O2 are common mixes. With the increase in oxygen the percentage of nitrogen decreases, resulting in an increased bottom time. There is a tradeoff here and that is increased risk of oxygen toxicity. The increased partial pressure of O2 at depth combined with the increased percentage of O2 results in oxygen toxicity at shallower depths
than before. Depending on the mixture oxygen toxicity can occur in water between 90 and 100 ft. The diver will experience a seizure and can obviously have a variety of complications depending on how the proximity of other divers and how quick they react. Once on the surface this diver should be treated as any neardrowning/dive accident. The diver who is now at a normal ambient pressure will no longer be suffering from oxygen toxicity and may be treated accordingly.
Copperhead (N. FL.) Cottonmouth Coral Snakes Identification of the snake, either dead or alive, is important in order to determine whether it is harmless or venomous. If the snake is not available, a reliable observer may have seen the snake well enough to identify it or describe it sufficiently. If the snake is venomous, it must be determined whether it is a pit viper or coral snake, and in the case of the former, whether it is a copperhead, cottonmouth or rattlesnake. There are three additional characteristics of pit vipers that aid in distinguishing them from harmless snakes. First, they have vertical pupils. Most harmless snakes have round pupils, although some venomous snakes also have round pupils. Obviously, identification of this characteristic should be undertaken carefully. Second, a pit vipers head is generally triangular in shape or, more precisely, is shaped like an arrowhead. Harmless snakes have oval or egg shaped heads. A final distinction between pit vipers and harmless snakes lies in the pattern of plates on the snakes underside. On a snakes ventral side, somewhat caudad, are whitish, seemingly loose scales called the anal plates. In venomous snakes, scales are arranged in a single row from the anal plate to a point approximately a third of the distance away from the tip of the tail. In most harmless snakes, the scales are arranged in double rows from the anal plate to the tip of the tail. The coral snake is a relatively small, shy snake with a rather distinct pattern of red and black bands that are wider than the interspaced yellow rings. This has given rise to the following mnemonic rhyme: Red on yellow, kill a fellowcoral snake. Red on black, venom lackharmless snake. The more plentiful species, the eastern coral snake, has a black snout with the previously described coloration of the body. They need greater leverage to puncture the skin and a longer period to inject their venom. Coral snake venom has a blocking action on acetylcholine receptor sites. The early signs of a coral snake bite are slurred speech, dilated pupils, dysphagia, and myalgia. Frequently symptoms are not evident until 212 hours after the bite. Death results from respiratory arrest secondary to CNS inhibition, as well as weakness and possible paralysis of respiratory muscles. The size and type of the snake govern the type, quantity, and quality of venom available. The condition of the snake is also important. A hungry, disturbed, and alert snake is deadlier. The angle of bite is significant, and so is its depth and the duration of the time of penetration of one or more fangs. The size of the victim is important, children and infants being more vulnerable. The condition of the victim will seriously affect the outcome. Hypertension, diabetes, advanced E - 73
PERICARDIAL EMPHYSEMA
Injury occurs similar to an AGE, however the gas is forced into the pericardium. As the diver ascends the trapped air expands, restricting the pumping action of the heart. This condition is similar to pericardial tamponade. Pericardiocentesis is the treatment of choice. As with AGE the onset of symptoms is usually rapid.
PNEUMOTHORAX
Injury occurs similar to an AGE however the gas becomes trapped within the pleural space. If this occurs at depth, a simple pneumothorax may become a tension pneumothorax as the air expands while ascending.
SUBCUTANEOUS PNEUMOTHORAX
Injury occurs similar to an AGE, however the gas escapes under the skin, usually around the neck and collarbones. Palpation of the area can produce the effect of Rice Crispies under the skin. While certainly a cause for concern this injury is seldom lifethreatening. However, the prudent team will keep close watch on the divers airway as a compromise is possible. While there are a number of different injuries that can occur from breathing compressed gas at depth, the treatment is fairly standard. Each injury is treated according to the Diving Accident Guidelines (see treatment section) and the patient is monitored for complications. A thorough history should be taken including number of dives, length and depth of dives and time on surface between dives. Ideally this patient should be transported to an emergency room that has a recompression chamber on site. Early transport and physician consult regarding the nature of the injury is critical.
SNAKE BITE
Although the annual mortality from venomous snakebites is unknown, it is believed to be somewhere between 50 and 100. Venomous snakes located in our area are: Pit Vipers Eastern Diamond Back Pygmy
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age, debility, or coagulation disorders are aggravated by a venomous snakebite. Individuals with bleeding tendencies, such as hemophilia, or those on anticoagulant therapy, with active peptic ulcers, or with open wounds are susceptible to bleeding secondary to envenomation. Women who are menstruating will bleed excessively after a pit viper bite. Women who have endometriosis may bleed excessively and develop severe pain. Cases of abortion in pregnant women who have been bitten by pit vipers have been reported. The location of the bite is of great importance. Venomous snakebites on the head and trunk are from two to three times more dangerous than those on the extremities. Venomous bites on the upper extremities are more serious than those on the lower extremities. Incidental penetration of fangs and injection of venom into a blood vessel is usually catastrophic. After identifying whether the snake is venomous or harmless, quickly examine the pattern of the snakebite on the victim. It is safe to assume that the bite is venomous if one or two fang marks are present. Rarely three or four marks may be present, according to the number of fangs. Absence of fang marks is presumptive of evidence of a harmless snakebite or an unsuccessful attempt by the pit viper without penetration. Fang marks separated by 15 mm or more indicate a bite by a very large snake, while those separated by less than 8 mm point to a smaller snake. A coral snake bite may present an atypical pattern. If the offending snake cannot be identified, the symptoms and signs are the only remaining criteria of severity. The signs and symptoms are divided into hemopathic, neurotoxic, and systemic manifestations. dominate with coral and cobra bites.
SYSTEMIC EFFECTS
General systemic signs and symptoms of venomous snakebite include elevation or depression of the temperature, nausea, vomiting, diarrhea, pain, and restlessness. The pathogenesis of the bradycardia is obscure. Renal failure from acute tubular necrosis of bilateral cortical necrosis has been reported
SPIDERS
With the exception of 2 small groups, all spiders are venomous. Fortunately, the fangs of most species are too short or fragile to penetrate the skin. Nevertheless, at least 60 species in the USA have been implicated in bites on humans. Species that are dangerous include the widow spiders, Latrodectus mactans and related species; the brown or violin spider, Loxosceles reclusa (sometimes called the brown recluse) and related species; the jumping spiders, greater than Phidippus species; the tarantulas, Rheostica and Pamphobeteus species; the trapdoor spiders, Bothriocyrtum and Ummidia species; the socalled banana spiders, Phoneutria and Cupiennius sallei, Lycosa (wolf spider), and Heteropoda; the crab spider, Misumenoides aleatorius; the running spiders, Liocranoides and Chiracanthium; the orbweavers, Neoscona vertebrata, Araneus species, and Argiope aurantia (orange argiope); the running or gnaphosid spiders, Drassodes; the green lynx spider, Peucetia viridans; and the combfooted or false black widow, Steatoda grossa. Pamphobeteus, Cupiennius, and Phoneutria are not native to the USA but may be brought into the country on produce or other materials. The incidence of spider bites in the USA is unknown. Fewer than 3 fatalities/year occur in the USA, usually in children. Only a few spider venoms have been studied in any detail. Black widow venom consists chiefly of proteins, a few of which are enzymatic. The lethal fraction appears to be a peptide that markedly affects neuromuscular transmission. Brown or violin spider venom consists of at least 10 or 12 proteins. Its enzyme activity is greater than that of Latrodectus venom, but no fraction of Loxosceles venom has been isolated that produces the entire sequence of events that give rise to the unusual necrotic lesion characteristic of Loxosceles bites. Polymorphonuclear leukocyte infiltration plays a major role in the poisoning, but the mechanism is not understood. Tarantula venom contains approximately 12 proteins, of which at least one affects cardiovascular function; however, it is highly unlikely that the bite of one tarantula would produce a harmful cardiac effect in a human. Tarantulas native to the USA are not considered dangerous.
HEMOPATHIC MANIFESTATIONS
Swelling, edema, ecchymosis, extravasation of blood, and bleeding from kidneys, lungs, peritoneum, rectum, and vagina may occur owing to endothelial damage of small vessels and lymphatic channels. Changes in red blood cells and their ability to transport oxygen may result in bleeding, drop in hemoglobin, and tissue anoxia leading to necrosis. There may be local bleeding from areas such as the endometrium or urinary tract or bleeding from pathological foci, such as peptic ulcers, because of impaired coagulation mechanisms. While hemopathic and systemic signs, including swelling, edema, and pain predominate with pit viper bites, neurologic signs may also occur.
NEUROTOXIC MANIFESTATIONS
The effects of neurotoxins A and B on the central nervous system are manifested by dysphagia, convulsions, and psychotic behavior. The myoneural junction is also affected by neurotoxin B, which results in locomotor disturbances, manifested by weakness of the muscles, fasciculation, paresthesias, and in very extreme cases, paralysis. Neurologic signs preE - 74
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Widow spiders: A Latrodectus bite usually gives rise to a sharp pinpricklike pain, followed by a dull, sometimes numbing pain in the affected extremity, and by cramping pain and some muscular rigidity in the abdomen or the shoulders, back, and chest. Associated manifestations may include restlessness, anxiety, sweating, headache, dizziness, ptosis, eyelid edema, skin rash and pruritus, respiratory distress, nausea, vomiting, salivation, weakness, and increased skin temperature over the affected area. Brown or violin spiders: A Loxosceles bite may cause little or no immediate pain, but some localized pain develops within an hour or so. The bite area becomes erythematous and ecchymotic and may itch. There may also be generalized pruritus. A bleb forms, often surrounded by either an irregular ecchymotic area or a more targetlike lesion. The lesion may appear as a bulls eye; the central bleb becomes larger, fills with blood, ruptures, and leaves an ulcer over which a black eschar forms and eventually sloughs, leaving a large tissue defect, which may include muscle. Pain can be severe and involve the entire injured area. Systemic symptoms and signs may develop, including nausea and vomiting, malaise, chills, sweats, hemolysis, thrombocytopenia, and kidney failure; death is a rare sequela. Far more common than spider bites are flea, bedbug, tick, mite, and biting fly bites; these are often mistaken for spider bites. Some arthropod bites may give rise to bullous lesions that rupture and ulcerate, resembling those produced by the violin and certain other spiders. Numerous reports of necrotic or gangrenous arachnidism attributed to Loxosceles reclusa, particularly in areas where this species is not found, are probably caused by spiders other than Loxosceles or more probably by other arthropods. If possible capture and identify the offending animal. Some cases of socalled brown recluse bites are misdiagnoses of epidermal necrolysis, erythema chronicum migrans, erythema nodosum, Lyells syndrome, chronic herpes simplex, etc. abilities result in a significant loss of productivity and income potential. The cost to society is more than $30 billion annually. Thus, neurotrauma is a serious health problem that mandates continuing efforts in the areas of prevention and treatment. During the past two decades, understanding of the pathophysiology of TBI has increased remarkably. One central concept is now known; All neurological damage does not occur at the moment of impact (primary injury), but rather evolves over the ensuing minutes, hours, and days. This secondary brain injury can result in increased mortality and more disabling injuries. Emergency Medical Services (EMS) providers are often the first health care providers for patients with TBI. TBI treatment often begins in the field by EMS providers who have varied skills, backgrounds, and qualifications. They continue this care en route to the hospital. Thus, prehospital assessment and treatment is the first critical link in providing appropriate care for individuals with severe brain injury. Over the past thirty years, EMS providers have developed sophisticated systems for delivering emergency medical care to patients. The initial impetus for this development was the need to deliver such lifesaving interventions as cardiac defibrillation. Treating trauma patients in the field, especially the head injured patient, has lagged behind prehospital advancements in medical and general trauma management. Only in the past five to ten years has any attempt been made to evaluate the care provided to trauma victims in the field. EMS providers must be familiar with the complex presentation of severe TBI patients. Early recognition of the initial signs and symptoms of TBI has a significant impact on the outcome of these patients. In addition to initial treatment, EMS providers must know about interventions aimed at minimizing secondary injury. Specifically, EMS providers must aggressively assess and treat hypoxemia and hypotension. All recommendations in these guidelines are supported by the best available scientific evidence. These guidelines cover three main areas: Assessment Triage, Prehospital Treatment, and Hospital Transport Decisions.
TRAUMATIC BRAIN INJURY (TBI)

Traumatic brain injury (TBI) is a leading cause of death and disability in children and adults in their most productive years. An estimated 1.6 million head injuries occur every year in the United States. Approximately 800,000 of the injured receive emergency department or other outpatient care, and approximately 270,000 are admitted to the hospital. Every year, approximately 52,000 deaths occur from TBI, and an estimated 70,000 to 90,000 people are left with permanent neurological disabilities. TBI has a devastating effect on the lives of the injured individuals and their families due to the fact that dis-
ASSESSMENT TRIAGE:
OXYGENATIONAND BLOOD PRESSURE: Early post injury episodes of hypotension or hypoxemia greatly increase morbidity and mortality from severe head injury. At present, the precise definitions of hypotension and hypoxemia are unclear in these patients. However, ample Class II evidence exists regarding hypotension, defined in these studies as a single observation of an SBP<90 mm Hg, or hypoxemia, defined in these studies as apnea or cyanosis in the field
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or an arterial oxygen saturation <90%. The evidence indicates that these values must be avoided, if possible, or rapidly corrected in severe head injury patients. Strong Class II evidence suggests that raising the blood pressure in hypotensive, severe head injury patients improves outcome in proportion to the efficacy of the resuscitation. GLASGOW COMA SCALE SCORE : Teasdale and Jennett developed the Glasgow Coma Scale in 1974 as an objective measure of the level of consciousness after head trauma. It has since become the most widely used clinical measure of the severity of traumatic brain injury (TBI). The GCS permits a repetitive and moderately reliable standardized method of reporting and recording ongoing neurologic evaluations. Limited prehospital GCS data indicate that initial field GCS scores between 3 and 5, as well as lack of improvement or deterioration of GCS score of two points or more from the field to the emergency department, have significant value as predictors of poor patient outcome. GCS scoring should occur after hypoxemia and hypotension are corrected and the patient has been resuscitated. The GCS score should be measured preferably prior to administering sedative or paralytic agents, or after these drugs have been metabolized. PUPILS : Examining the pupils is a standard component of the neurologic examination that is particularly important in evaluating patients with traumatic brain injury. The examination consists of assessing pupil size, symmetry, and reactivity to light. The initial pupil examination, along with the GCS score, establishes the baseline against which all subsequent neurologic evaluations are compared. Abnormalities found in the pupil examination are helpful in generating a differential diagnosis and in directing diagnostic testing and therapeutic interventions. Specifically, an unconscious TBI patient with a unilaterally dilated pupil or with bilaterally fixed and dilated pupils is presumed to have cerebral herniation and require emergent interventions to lower the ICP. Pupils are generally round and roughly equal in diameter. Inequality in pupil size of less than 1mm is common and has no pathologic significance. Pupillary constriction to light is mediated through the parasympathetic nervous system via the third cranial nerve. Destruction of the third nerve parasympathetic brainstem pathway results in a dilated pupil that is fixed to light. Therefore, the pupillary light reflex is an indirect measure of herniation or brainstem injury. Dilation and fixation of one pupil signifies herniation, whereas bilaterally dilated and fixed pupils are consistent with brainstem injury. However, hypoxemia, hypotension, and hypothermia are also associated with dilated pupil size and abnormal reactivity, making it necessary to resuscitate and stabilize the patient before assessing pupillary function. The pupil size and light reflex should be assessed and documented for each eye; and the duration of pupillary dilaE - 76 2/15/06 tion and fixation should also be documented.
PREHOSPITAL TREATMENT OF TBI

AIRWAY, VENTILATION AND OXYGENATION: Class III evidence indicates that all severe TBI patients treated in the field should receive supplemental oxygen to maximize arterial oxygen saturation. If pulse oximetry is available, the oxygen saturation should be maintained at a minimum of 90% or greater. A patent airway should be ensured and endotracheal intubation performed for patients with a GCS score less than 9 or those who are unable to maintain or protect their airway. The evidence indicates that routine hyperventilation should not be performed. If ventilatory assistance after endotracheal intubation is provided, a respiratory rate of 10 breaths per minute (bpm) for adults, 1520 bpm for children, and 20 bpm for infants should be maintained. After correction of hypoxemia or hypotension, if the patient shows obvious signs of cerebral herniation, such as extensor posturing or pupillary asymmetry or nonreactivity, hyperventilate the patient at a rate of 20 bpm for adults, 30 bpm for children, and 35 bpm for infants. This hyperventilation may be performed as a temporizing measure until the patient arrives at the hospital when blood gas analysis will guide the ventilation rate. FLUID RESUSCITATION: The principle issue concerning prehospital fluid resuscitation with TBI centers around preventing and/or rapidly treating shock. Hypotension produces a significant secondary brain injury that substantially worsens outcome. A single episode of hypotension has been shown to double mortality. Perhaps even more important is maintaining cerebral perfusion pressure and delivering oxygen to the injured brain. Fluid resuscitation in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possible. In adult trauma, hypotension is usually defined as systolic blood pressure <90mm Hg. In children, hypotension is usually defined as SBP less than the fifth percentile for the age. Hypotension can, therefore, be defined as a SBP<65 mm Hg (age 01 year), <75mmHg (age 25 years), <80mmHg (age 612 years), and <90mmHg (age 1316 years) in pediatric severe TBI patients. Fluid therapy is utilized to support cardiovascular performance in an effort to maintain adequate cerebral perfusion pressure and limit secondary brain injury. The most common used resuscitation fluid for trauma patients in the prehospital setting is isotonic crystalloid solution. It is administered in quantities necessary to support blood pressure in the normal range. Inadequate fluid volumes or underresuscitation can precipitate sudden hypotension and should be avoided. No studies prove the efficacy of mannitol in the prehospital setting.
0 SUMMARY Preservation of cerebral perfusion and oxygenation are the first priorities in managing patients with TBI. Patients who exhibit signs of cerebral herniation during field management and transport should be initially treated with hyperventilation as defined. The role of mannitol in treating herniation is yet to determined, and currently it is not recommended in these guidelines. Sedation, analgesia, and neuromuscular blockade are important considerations during the transport of patients with TBI to minimize changes in ICP and to maximize safety during transport. Hypoglycemia may mimic TBI and should be considered in all patients with altered mental status regardless of suspected etiology. HOSPITALTRANSPORT DECISIONS The management by EMS personnel of the headinjured patient prior to arrival at the hospital is influenced by a number of factors, including the mechanism of injury, the type and severity of injury, and the decision regarding choice of destination. When an integrated EMS and trauma system is in place and EMS agencies transport a patient directly fro the scene of the accident to an appropriate receiving facility (trauma center), the patient is entered into a system of care that has been shown to improve overall patient outcome. Interhospital transfers of these head injury patients are known to delay the time until neurosurgical consultation and intervention. This delay puts the patient at great risk for secondary insult to the brain. TRAUMASCORE FOR SURVIVALPROBABILITY RESPIRATORY EFFORT: Normal Shallow or Retractive SYSTOLIC BLOOD PRESSURE: Greater than 90 7090 5069 less than 50 no carotid pulse CAPILLARY REFILL: Normal (less than 2 seconds) Delayed (more than 2 seconds) No capillary refill 1415 1113 810 57 34 0 points 1 point 0 points 4 points 3 points 2 points 1 point 0 points
2 points 1 point 0 points 5 points 4 points 3 points 2 points 1 point
GLASGOW COMA SCALE SCORE:
WOUND CARE
All appropriate personal protective equipment should be used when treating patients. Flush wounds with a generous amount of sterile water or saline only when bleeding is at a minimum, (do not delay the control of bleeding to flush the wound). Hydrogen peroxide, betadine and scrubbing have been found to cause further injury and are therefore not recommended. Once dressings have been applied do not remove due to potential for further bleeding. Patient treatment/transport should not be delayed for wound care in lifethreatening situations. All other treatments should be performed following the appropriate guidelines. Bleeding control should be performed in the following order: Direct pressure Apply sterile dressing with pressure directly over the wound. Elevate Hold extremity above the patients heart while applying direct pressure to the wound. Pressure point Apply pressure to the artery proximal to the wound. Tourniquets Only to be used in a last resort effort to control bleeding, with the understanding that loss of the extremity distal to the tourniquet is likely.
Score
16 15 14 13 12 11 10 9 8 7 6 5 4 3 under 3 RESPIRATORYRATE: 1024 1535 greater than 35 less than 10
Interpretation
99% probability of survival 98% probability of survival 95% probability of survival 91% probability of survival 83% probability of survival 71% probability of survival 55% probability of survival 37% probability of survival 22% probability of survival 12% probability of survival 7% probability of survival 4% probability of survival 2% probability of survival 1% probability of survival 0% probability of survival 4 points 3 points 2 points 1 point
TYPES OF WOUNDS\TREATMENT:
E - 77 2/15/06

AbrasionsRemoval or destruction of the surface layers of the skin by friction. The depth of the penetration depends on the force and the duration of the contact with the damaging surface. Treatment: Irrigate with a sterile solution (NaCL or water), cover with a dry, sterile dressing. Note: Control bleeding, by proper technique, when appropriate. AmputationsAny injury that cuts off an appendage or projection of the body, (partially, or completely) Treatment: Control bleeding with proper technique, cover the stump with damp sterile dressing and an elastic wrap that will apply uniform, reasonable pressure across the entire stump. The amputated part should be placed in a dry plastic bag , (do not wrap in moistened dressing). Seal the bag , so the part will not lose moisture and place on cold packs, or in a container with ice and water (if available). Direct contact with freezing temperatures may cause tissue damage and should be avoided. Never use ice alone or dry ice. AvulsionsInvolves the tearing loose of a flap of skin, which may either remain hanging or be torn off altogether. Treatment: Control bleeding with proper technique, replace avulsed portion to its natural position (if still partially attached) and bandage with dry, sterile dressing. ContusionsA severe bruise in which the skin is intact but there is swelling and possibly a hematoma in the area of the injury. Contusions generally result from a blunt blow, with injuries to tissues present, deeper than the contusion itself. Fractures can commonly be found below contusions. Treatment: Apply ice packs to reduce the swelling, check for signs and symptoms of a fracture, such as deformities, reduced range of motion, pain etc.... Splint and treat per fracture guideline. EviscerationOpen wound to the abdominal area where any organ or viscera protrude from the wound. Treatment: Control bleeding with proper technique. Gently cover the area with sterile gauze moistened with saline or sterile water. Never attempt to reinsert the organs or viscera. Note: Make sure to keep organs moistened, otherwise irreversible damage will occur. Laceration Is an incision type wound, that can be clean or jagged, and can range from the skin surface to the underlying tissues. Lacerations may produce severe bleeding, or may bleed very little, therefore rapid assessment is necessary. Treatment: Control bleeding with proper technique, apply dry, sterile dressing, (clean with sterile water, or Saline, when appropriate). Maintain a high index of suspicion for damage/injury to underlying tissues/organs. E - 78 2/15/06 Open chest wound Usually a puncture type wound which is deep in nature, and is sometimes a sucking chest wound. Treatment: Control bleeding with proper technique, apply appropriate dressing (secure impaled objects, use occlusive dressings for sucking chest wounds) and maintain airway. This type of injury often requires advanced airway techniques, requiring that these patients be monitored closely for deterioration in respiratory status. PunctureA stab type wound from a knife or blunt object, this can include gun shot wounds and impaled objects. Treatment: Control bleeding with proper technique, secure impaled objects with exception to airway obstruction. Consider area of wound, underlying organs, point of entry/exit (if applicable) and prepare to treat for shock. Note: Chest injuries may require additional treatments including pleural decompression, pericardiocentesis, and cardiac/respiratory disturbances. Maintain a high index of suspicion when dealing with gun shot wounds due to the potential for extensive internal injury.
E - 79 2/15/06
PROCEDURAL GUIDELINES
Procedural Guidelines
03/01/05
P-1
Airway Management
Airway management should conform to accepted ACLS guidelines. Oxygen delivery systems and flow rates should conform to accepted ACLS guidelines. Accordingly, the Paramedic should choose the appropriate form and rate.
CAREVENT
Unit can be used as either a manual or automatic ventilator. Provides Demand Breathing with automatic cycling shut off and restart.
Application/Use
Manual Ventilations Select the tidal volume/frequency of ventilation for the size of patient being resuscitated. (Tidal volume= 1015 mls/kg, see chart below) Depress the manual button and observe the rise of the patients chest. Release the button when chest rise is adequate. Automatic Ventilation If you have been manually ventilating the patient, simply release the manual button and after a short pause (47 seconds) the ventilator will commence automatic cycling at the rate and volume selected on the indicator. If commencing automatic ventilations immediately, rotate the setting selector to t the setting appropriate for the size of the patient being ventilated and the ventilator will commence automatic cycling. Control Position Tidal Volume Vt (ml) Frequency (BPM) Automatic flowrate (LPM) Body Weight (kg) 73.3110 1 O F F 2 200 20 12 3 4 5 6 300 400 600 15 15 12 13.5 18 21.6 2030 7 800 12 28.8
1100 12 39.6
13.320
26.740 4060 53.380
CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP)

General:
CPAP stands for Continuous Positive Airway Pressure and is very useful in keeping the smaller airways open. The CPAP unit will supply approximately 130 liters of flow at an oxygen concentration (FiO2) of 30% (this can be increased to approx 50% with supplied supplemental oxygen tubing). It is important to remember that CPAP does not replace current treatment guidelines. Rather, it is an adjunct or in addition to them
Indications:
Pulmonary Edema
Contraindications:
Apnea Pneumothorax Gastric distention P-2 03/01/05
Severe facial injuries Hypotension secondary to trauma Asthma Altered LOC
Precautions:
Continuous monitoring of the patient is MANDATORY Watch for occlusion of the generator intake port Insure the supply tubing is not pinched, kinked, or occluded Observe the patient to insure they can exhale. If severe difficulty in exhaling, discontinue treatment and assist ventilations with BVM
Setup:
Connect flow generator to oxygen tank or oxygen outlet in Rescue Place filter on generator intake port Attach supply tubing to generator and to mask Explain procedure to patient Turn on oxygen supply and attach mask to patient using supplied straps After patient is accustomed to oxygen flow, attach 10.0 PEEP valve to mask
Guidelines:
Assess the patient (Vital signs and pre-oxygen SaO2) Administer Oxygen per protocol If wheezing present, administer one (1) Nebulizer treatment. If no improvement, administer CPAP treatment. If rales present, administer CPAP Monitor and record SaO2 Continue to follow Treatment Guidelines for underlying cause (i.e. Lasix, NTG, etc)
ESOPHAGEAL TRACHEAL DOUBLE LUMEN AIRWAY (COMBITUBE)

Indications
Cardiac arrest from any cause Respiratory arrest Unconscious patient with inadequate respirations and no gag reflex
Contraindications
Patient is under five (5) feet in height Patient is under sixteen (16) years of age Active gag reflex Patient has known or suspected esophageal disease Patient has ingested a caustic substance
Procedure
NOTE: The COMBITUBE Is Single Patient Use, This Device Is Not To Be Cleaned. Insure all necessary components and equipment are at hand Position the patients head in a neutral position Hyperventilate for at leased 30 seconds Lubricate tube for easier insertion Jawlift maneuver Insert COMBITUBE with curvature in same direction as natural curvature of pharynx 03/01/05
P-3

Insert gently DO NOT FORCE tube Stop when BLACK rings on the tube are positioned between the patients teeth If tube does not advance easily, redirect it or withdraw, reoxygenate, and reinsert (See Illustration A) To confirm tube placement Inflate pharyngeal cuff through line #1 (BLUE) with 100 ml of air and distal cuff through line #2 (WHITE) with 15 ml of air (See Illustration B) Ventilate through primary (BLUE TUBE) Tube placement is confirmed by auscultating breath sounds (high axillary & bilaterally) and auscultating over stomach Esophageal placement Breath sounds are present bilaterally with epigastric sounds absent continue to ventilate through primary (BLUE TUBE) (See Illustration C). Under this usage, the clear tube may be used for the removal of gastric fluids or gas with the catheter provided in the airway kit. Be careful as vomitus will frequently comeout of the clear tube with esophageal placement. Tracheal placement Breath sounds absent and epigastric sounds present, ventilate through secondary (CLEAR TUBE) continue to ventilate through secondary tube (See Illustration D) To Replace COMBITUBE with an endotracheal tube Deflate the #1 cuff labeled 100 ml If the tube is not already in the trachea, move the COMBITUBE to the left side of the mouth Intubate with an E.T. Tube using currently accepted medical techniques Deflate the distal cuff #2 labeled 15 ml and remove carefully
CRICOTHYROTOMY
Indications
Needle and surgical (scalpel) cricothyrotomy may be performed if more conventional techniques of controlling the airway are either unsuccessful or unobtainable as a result of edema, severe oropharyngeal hemorrhage, severe facial trauma, anaphylaxis, inhalation injury, or other severe airway complication. Both procedures are temporary stabilizing techniques and are relatively easy to perform.
Caution
The following are common complications: hemorrhage at the insertion site subcutaneous emphysema aspiration of blood into the lungs perforation/laceration of the thyroid cartilage, thyroid gland or esophagus laceration of carotid arteries or jugular veins
MINITRACH II CRICOTHYROTOMY KIT Contraindications

Children under 12 years of age
Figure 1
Application/Use
Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Stabilize the larynx with one hand, locate cricothyroid membrane with the other Find the landmark by palpating the patients neck from the top P-4 03/01/05
the first prominence felt is the thyroid cartilage; the second prominence is the cricoid cartilage (See Figure 1) the space between the two is the cricothyroid membrane Cleanse the site using antiseptic swab Using the guarded scalpel, position the cutting edge caudally, make a 1 cm midline vertical stab incision through the cricothyroid membrane into the airway Withdraw the scalpel ensuring the skin is pressed firmly against the larynx to prevent loss of alignment between the hole in the skin and the membrane Pass the introducer through the stab incision into the trachea Pass the 4.0 ET tube over the introducer and guide into the trachea until the flange of the tube rests against the skin some resistance may be noted when sliding the tube down the introducer if this occurs, gently rotate the tube between your thumb and forefinger while advancing the tube Withdraw the introducer Attach the 15 mm adapter to the flange of the catheter Secure the flange to the neck using the neck tie that is supplied with the kit if needed, suction the tube using the supplied catheter to remove excess blood or secretions suction should only be applied while withdrawing the catheter Ventilate with the highest available oxygen concentration Assess placement
PER TRACH Application/Use

Patient should be supine (ensure cervical spine immobilization if trauma is suspected) Hyperextend the patients head (unless trauma is suspected) Locate the cricothyroid membrane (See Figure 1) Prepare the site with a Betadine swab Perform a 1 horizontal incision on the skin over the cricothyroid membrane Insert a butterfly needle (with a syringe attached) into the cricothyroid membrane (angled slightly towards the feet). Once air is aspirated through the syringe, remove the syringe and advance the dialator (through the hub of the needle) as far as possible. Squeeze the butterflies on the needle to split the needle. Remove the needle pieces and advance the per trach until the tie down rests on the skin. Remove the dilator, inflate the cuff, check for breath sounds, and secure the trach. Ventilate with high flow oxygen.
NEEDLE CRICOTHYROTOMY Caution

This procedure does not provide airway protection or elimination of carbon dioxide
Procedure
Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Find the landmark by palpating the patients neck from the top (See Figure 1) the first prominence felt is the thyroid cartilage; the second prominence is the cricoid cartilage the space between the two, characterized by a small depression, is the cricothyroid membrane 03/01/05 P-5
Figure 2

Stabilize larynx with one hand, locate cricothyroid membrane with the other Cleanse the site using antiseptic swab Attach a 10 cc syringe to the needle of a 14 g catheter over needle set Insert needle through the cricothyroid membrane at a 4560 degree angle caudally (See Figure 2) Apply negative pressure to syringe during insertion Entrance of air into syringe indicates placement in trachea Advance catheter over needle, removing needle and syringe Secure hub Attach oxygen tubing kit to the catheter Obstruct thumb port to insufflate the chest; remove thumb from port allowing exhalation (See Figure 3)
Figure 3
Pediatric
For pediatric patients use the same procedure only use a 1418 g catheter over needle
SURGICAL (SCALPEL) CRICOTHYROTOMY Contraindications

Children 12 and under
Procedure
Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Stabilize larynx with one hand, locate cricothyroid membrane with the other Find the landmark by palpating the patients neck from the top (See Figure 1) the first prominence felt is the thyroid cartilage; the second prominence is the cricoid cartilage the space between the two, characterized by a small depression, is the cricothyroid membrane Cleanse the site using antiseptic swab Make a 2 cm horizontal incision with a scalpel through the membrane (See Figure 4) Insert handle of scalpel into incision and rotate 90 degrees to allow placement of a 5.0 to 6.0 mm ET Insert ET tube into the incision caudally and inflate cuff accordingly Ventilate with the highest available oxygen concentration Assess placement
Figure 4 St. Lucie County uses hemostats to dilate the surgical opening instead of the scalpel handle.
ENDOTRACHEAL INTUBATION
EXTUBATION Indications
Improper placement Occluded or damaged tube
Procedure
Ready suction unit Turn the patients head to one side if not contraindicated Deflate the cuff Remove the tube during exhalation (if applicable) Assess the airway
P-6
03/01/05
PROCEDURAL GUIDELINES NASOTRACHEAL INTUBATION Indications

Any patient in need of intubation who cannot protect and maintain their own airway and who has spontaneous respirations
Contraindications
Apnea Airway obstruction caused by foreign body obstruction Severe head injury or possible basilar skull fracture Bleeding disorders
Caution
Nasal intubation prevents a patient from receiving thrombolytic therapy. This consideration should be weighed when selecting the method of intubation Complications may include: bleeding from the nose nasal septal tear cranial perforation in basilar skull fractures injury to the pyriform sinus, epiglottis, and vocal cords No stylet is used during this procedure Never force the tube at any time as soft tissue trauma may cause excessive bleeding and damage to the vocal cords may occur
Application/Use
Select appropriate sized endotracheal tube, this will usually be 0.5 mm smaller than that used for orotracheal intubation. Once selected insert the distal end of the tube into the 15 mm adapter, forming a circle. This ensures anterior curvature of the tube making it easier to enter the trachea. Anesthetize the nostrils and pharynx with topical anesthetic if time permits Pick up the tube and release the previously formed circle, lubricate the tube generously with Xylocaine jelly or a waterbased jelly Keeping the bevel next to the nostril, gently insert the tube into the biggest nostril. With gentle and even pressure, advance the tube through the nostril into the pharynx. Listen down the tube for breath sounds and look for vapor condensation in the tube. Advancing the tube as the patient inhales will greatly enhance the chance of success When the 15 mm adapter is 12 cm from the nostril, confirm tube placement by auscultation of the epigastrium and lung fields. If the tube is in the esophagus, withdraw it back until the tip is in the pharynx and advance it again on the patients inspiratory breath. Once tube placement is confirmed, inflate cuff, secure the tube and ventilate patient using an appropriately sized BVM
OROTRACHEAL INTUBATION Indications

Any patient in need of intubation who cannot protect and maintain their own airway
Caution
Do not use the teeth as a fulcrum Remove loose dentures
Procedure
Use universal precautions Select the appropriate size ET tube Insert appropriate size stylet Inflate and test cuff 03/01/05 P-7

Deflate the cuff (leave syringe attached) Check laryngoscope light Preoxygenate the patient Place the patient in the sniffing position if not contraindicated Hold laryngoscope with the left hand Insert the laryngoscope blade in the mouth, sweeping the tongue to the left Visualize the vocal cords Insert the ET tube Maintain visualization as tube is passed Remove the laryngoscope blade Inflate the cuff with air and remove the syringe Ventilate the patient observing chest rise, auscultate epigastric and lung sounds Note the depth of the tube Secure the tube with a restraint device
Thomas ET Restraint Device
END TIDAL CO2 DETECTOR

Caution
This device is unable to indicate right mainstem intubation and has been known to produce a false positive or false negative reading. It is imperative that endotracheal tube placement be verified by alternate means. Documentation of verification is important especially in the incidence of a false reading.
Application/Use
Expiration date should be checked prior to being placed in service. Plug should not be unsealed longer then 24 hrs. (accuracy compromised) Verify initial colorshould be dark purple. Attach regulator to bag valve device and attempt to verify plug seal by squeezing bag without plug removal. Remove plug and squeeze bag again to verify valve will function properly. Attach unit, as close as possible, to the expired air output and ventilate pt. Compare color change on full expiration after the 6th ventilation. Variations in color range from light pink to bright yellow in the presence of CO2. (Depending on the percentage of CO2 detected.) Fluctuation of color strip during ventilation is normal. Attempts to read prior to the 6th ventilation can lead to a false positive or negative reading. If using device in conjunction with an endotracheal tube, verify placement by alternate means. The device can accurately monitor for up to 2 hours. Use of CO2 regulator should be continued while utilizing a ventilator. Regulator should be placed between the endotracheal tube and ventilator tubing to maintain the most accurate reading.
Pediatric
The CapnoFlo regulator may be used on pediatric as well as adult sized endotracheal tubes. However, caution is necessary due to the weight of the unit, which may dislodge the tube.
P-8
03/01/05
ESOPHAGEAL INTUBATION DETECTOR (EID)

Caution
Ventilating the patient with an automatic ventilator or BVM prior to using this device may cause the esophagus to fill with air and therefore give unreliable results.
Warning
Endotracheal tube obstruction, morbid obesity, pulmonary edema, mainstem bronchus intubation, severe bronchospastic or obstructive lung disease may lead to equivocal results due to decreased air available for aspiration. Direct larnyoscopy is always recommended in these situations.
Indication
To assist verification of placement of the endotracheal or Combitube into the trachea. The device is to be used in conjunction with all other means of establishing confirmation of placement. The O-ring design assures leak proof connection with tubes.
Contraindications
Children less than 5 years of age or less than 20kg (44) pounds. The EID is not to be used on pregnant patients.
Procedure
Perform leak test. Place a gloved finger over the end of the device and attempt to move air through. Discard if an air leak is detected. Immediately after intubation, and before ventilating the patient with an automatic ventilator or BVM, Compress EID, attach to the endotracheal or combitube and release. Allow the bulb to self-inflate If air returns and fills the bulb rapidly (less than 5 seconds); The endotracheal or combitube is likely in the trachea. As the trachea is rigid. If air slowly fills the bulb (5 to 30 seconds); Carefully assess tube location clinically, use direct laryngoscopic visualization if a question still exists. If location is in doubt re-intubate or support ventilation until you are prepared to attempt intubation again. Esophageal tissue will collapse around the EID. This is indicative of esophageal intubation.
ESOPHAGEAL OBTURATOR AIRWAY

Indications
The Esophageal Obturator Airway (EOA) is indicated for BLS airway control or in the event endotracheal intubation is not successful. The advantages of an EOA are its relative ease of placement, does not require visualization of the chords, helps prevent gastric distention and regurgitation, and ventilates at the level of the pharynx/ epiglottis.
Contraindications
Younger than 16 years old Less than 5 ft. tall or 100 lbs More than 6 ft. 7 in. tall Ingestion of caustic substances History of esophageal disease Alcoholism Conscious patient or patient with an intact gag reflex 03/01/05 P-9

Severe facial trauma preventing mask seal
Caution
Complications accompanying the use of an EOA may include unintended endotracheal intubation, traumatization of the pharynx and esophagus, assured vomiting on removal, and its dependence on a secure facemask seal for adequate ventilation. Endotracheal intubation may still be accomplished after placement of an EOA.
Procedure
Assemble EOA gather all parts inflate mask (if necessary) test cuff snap mask to tube lubricate tube Position yourself at patient's head Preoxygenate patient for 1 minute Have suction prepared Flex patient's head slightly inferior Grasp jaw and pull anterior and inferior (See Figure 5) Insert tube until mask is fully seated on face Check location of tube listen for lung sounds look for chest rise listen for exhalation Inflate cuff 2030 cc Detach syringe Recheck lung sounds
Figure 5
LARYNGEAL MASK AIRWAY

Indications
The Laryngeal Mask Airway (LMA) is a device used to assist in securing an airway in a deeply unconscious patient when other methods of airway control have been unsuccessful.
Procedure
Deflate the cuff completely. Mask should appear spoon shaped without any wrinkles. Lubricate the posterior surface. Hold the LMA like a pen, with the index finger at the junction of the cuff and tube. Press the tip of the cuff upward against the hard palate and flatten the cuff against it. Using one smooth movement, press first against the palate, then against the posterior pharyngeal wall, and advance the LMA into the hypopharynx until resistance is felt. Without holding the tube, inflate the cuff with just enough air to obtain a seal. Never overinflate.
Figure 6
P - 10
03/01/05
NASOGASTRIC TUBE
Indications
Nasogastric tube insertion is indicated for decompression of gastric distention and in poisoning or overdose cases when transport will be lengthy or delayed Nasogastric tube insertion in poisoning or overdose is a Physician Consult modality
Procedure
Select proper size nasogastric tube Warm nasogastric tube in hand to increase pliability Explain the procedure to the patient if indicated Measure the nasogastric tube from the patient's epigastrium to their nose and mark it with tape (See Figure 6) Lubricate the nasogastric tube with a generous amount of lubricant Insert the nasogastric tube into the largest nare until the tube is inserted to the tape mark Confirm placement by auscultating over the epigastrium while injecting air Secure the nasogastric tube to the patient's nose with tape using the chevron style
Figure 7
PLEURAL DECOMPRESSION
Indications
Figure 8 Tracheal shift towards the unaffected side of the chest Unequal breath sounds Jugular vein distention Increasing dyspnea Decreased lung sounds on the affected side Decreasing level of consciousness Decreasing oxygen saturation readings
Procedure
Primary midclavicular approach (See Figure 7) select site at the 2nd or 3rd intercostal space, midclavicular line cleanse the site with antiseptic swab insert a large bore over the needle catheter (14 gauge) just above the lower rib at a ninety degree angle advance the needle until the sound of escaping air is emitted advance the catheter and remove the needle apply appropriate one-way valve device secure catheter in place Alternate midaxillary approach (See Figure 8) select site at or around the 5th intercostal space at the midaxillary line cleanse the site with antiseptic swab insert a large bore over the needle catheter (14 gauge) just above the lower rib at a ninety degree angle advance the needle until the sound of escaping air is emitted advance the catheter and remove the needle apply appropriate one-way valve device secure catheter in place
CHEST DRAIN KIT

After performing a pleural decompression in the effort to relieve a tension pneumothorax, it is essential that an airtight one-way valve be utilized to prevent the condition from recurring. The pleural chest drain kit accomplishes this via the Heimlich chest drain P - 11 03/01/05

valve. The Heimlich valve is designed in a manner that allows air to pass out of it, thus preventing a tension pneumothorax, while also preventing air from reentering the thoracic cavity and thereby effecting a simple pneumothorax. The pleural chest drain kit consists of: 14 g over the needle catheter Luer Lock tubing Heimlich valve Three foot suction tubing
Indications
Whenever pleural decompression is employed to relieve the signs and symptoms of a tension pneumothorax Figure 9
Application/Use
Have the pleural chest drain kit assembled and ready for application prior to attempting pleural decompression Attach the Luer Lock tubing to the blue tip of the Heimlich valve, and tape in place to prevent accidental dislodging (correct valve operation is achieved when the arrow on the valve points away from the patient's chest) Attach the three foot suction tubing to the clear, distal tip of the Heimlich valve and drain into appropriate container; keep tubing lower than insertion site for draining (See Figure 9) Upon successful pleural decompression and removal of the needle, screw the Leur lock tubing onto the catheter. Observe the Heimlich valve to determine if it is operating correctly (the internal flutter valve will pulsate and collapse along with the patients respiratory efforts). Secure the catheter in place with tape and gauze as needed Continuously monitor the patient during treatment and transport for the signs and symptoms of a recurring tension pneumothorax, or other respiratory distress
PULSE OXIMETRY
Indications
All transported patients
Procedure
Select site Place SpO2 sensor on patients finger, earlobe, or toe as indicated Observe pulse indicator for synchronization with pulse Record oxygen saturation prior to oxygen administration if possible Record oxygen saturation after oxygen administration a reading below 90% may call for aggressive oxygenation and /or ventilatory assistance Monitor for changes
CAPNOGRAPHY(CO2):
Indications
All intubated patients
Procedure
Remove airway adapter from its package and inspect it Align the sensor over the adapter and between tabs P - 12 03/01/05
Slide the sensor onto the airway adapter Gently push and twist the larger end of the adapter onto the ET tube Push the smaller end of the adapter onto the sensor circuitry Position the adapter so the sensor is on the top
Printing Information:
Manually prints real time strips as it is monitored Snap Shot prints the last 8 seconds Print Trends prints all trends that are enabled
RETROGRADE INTUBATION
COOK RETROGRADE INTUBATION SET Indications
The Cook Retrograde Intubation Set has been designed to assist in the placement of an endotracheal tube during difficult or emergency airway access procedures. It is intended for use in situations where visualization of the vocal cords is not possible secondary to secretions, blood and/or anatomic abnormalities.
Contraindications
Ongoing coagulopathy Obsecure cricothyroid anatomy Infection of the cricothyroid membrane Mass (i.e.goiter)
Procedure
After standard prepping of the access site, advance the 18 gauge sheath needle (attached to a 6cc disposable syringe) in a cephalad direction through the cricothyroid membrane and into the trachea. Free flow of air aspirated into syringe will confirm positioning. Remove the needle and syringe leaving the sheath in place. Advance the J end of the wire guide through the sheath and up the trachea in a cephalad direction, until the tip of the wire guide can be retrieved through the mouth or nose. Note: The black proximal positioning mark of the wire guide should be visible at the access site. This will insure enough wire guide is exposed orally or nasally for control of subsequent 11.0 French TFE catheter introduction. Remove the sheath leaving the wire guide in place. Advance the 11.0 French black TFE catheter, antegrade over the wire guide via the mouth or nose and into the trachea until tenting is noted at the cricothyroid access site. With the TFE catheter in position, advance the endotracheal tube over the catheter and into position below the level of the vocal cords. Note: Always maintain control and position of wire guide during advancement of the endotracheal tube. Markings on the endotracheal tube should be in the range of 19cm to 23cm. Remove the wire guide and catheter from the endotracheal tube and check the tube with the EID bulb auscultate lung sounds x 5. Secure with a securing device and continuously monitor the end tidal CO2 indicator.
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RUSCH QUICKTRACH
CRICHOTHYROTOMY DEVICE Istructions for Use
Pre-Assembly: Open the package, remove the device, and familiarize yourself with its contents.
Step One
Place the patient in a supine position. Assure stable positioning of the neck region (place a pillow or piece of clothing under the patients shoulders) and hyperextend the neck (when applicable). Secure the larynx laterally between the thumb and forefinger. Find the cricothyroid ligament (in the midline between the thyroid cartilage and the cricoid cartilage). This is the puncture site.
Step Two
Firmly hold the device and puncture the cricothyroid ligament at a 90 angle. (Note: Because of the sharp tip and conical shape of the needle, an incision of the skin with a scalpel is not necessary. The opening of the trachea is achieved by dilating through the skin. This reduces the risk of bleeding as only the smallest necessary opening is made).
Step Three
After puncturing the cricothyroid ligament, check the entry of the needle into the trachea by aspirating air through the syringe. If air is present, the needle is within the trachea*. Now, change the angle of insertion to 60 and advance the device forward into the trachea to the level of the stopper. The stopper reduces the risk of inserting the needle too deeply and causing damage to the rear wall of the trachea.
Step Four
Remove the stopper. After the stopper is removed, be careful not to advance the device further with the needle still attached.
Step Five
Hold the needle and syringe firmly and slide only the plastic cannula along the needle into the trachea until the flange rests on the neck. Carefully remove the needle and syringe. Next, secure the cannula with the neck tape, apply the connecting tube to the 15mm connection, and connect the other end to the resuscitation bag or ventilation circuit.
*Warning
Should no aspiration of air be possible in Step Three because of an extremely thick neck, it is possible to remove the stopper and carefully insert the needle further until entrance into the trachea is made. Once this is verified, continue as in Step Five.
SUCTION
LAERDAL SUCTION UNIT (LSU) Indications:
It is intended for intermittent operation to remove secretions, blood or vomit from a patients airway to allow ventilation. Higher vacuum levels are generally selected for oropharyngeal suctioning, and lower vacuum levels are usually selected
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03/01/05
for tracheal suctioning and the suctioning of children and infants.
Contraindications:
None known.
Operating knob:
It is a combined ON/OFF switch and vacuum selector. Turn knob to desired vacuum amount. Unit is turned off by turning knob to the far left setting (0).
Indicator lights:
Power on indicator (circle with a colored in circle in it) This green LED has 3 functions: 1. Is lit continuously when the LSU is switched ON. 2. Flashes rapidly during Device Test. 3. Flashes slowly while the Automatic Power-save Function is activated, if the Device Test is interrupted and when the battery is discharged. External Power Indicator (circle with power cord in it) This green LED is continuously lit while external AC or DC power is connected. Failure Mode Indicator (circle with triangle and in it) The red LED is lit when a possible malfunction of the LSU has been detected. If lit turn the LSU OFF, and then ON again to check if the indication disappears. If it stays off, the LSU can be operated. If the indicator continues to be lit after three OFF/ON cycles and after replacing the battery with a fully charged battery, discontinue use. Vacuum Indicator: Green LED bargraph indicates the actual vacuum level. Battery Status Indicator: During operation from internal battery and during charging the displayed values must only be used as indications. The green LED bargraph has 3 functions: 1. During operation from internal battery- indicates approx. remaining battery capacity. 2. During charging- indicates approx achieved battery capacity. 3. During the Device Test- indicates which step of the test is currently in progress or which corresponding test result is being displayed. Test Button: This button allows you to run a user initiated Device Test program to identify whether the LSU operates satisfactory, is assembled correctly or if it needs service. Before you press the TEST-button, make sure the Patient Suction Tubing is not occluded or bent. Press and hold the TEST-button while setting the Operating Knob to 500+ mmHg. Note: Do not release the TEST-button until min. 2 seconds after the Operating Knob has been set to 500+. The test will start immediately. As soon as LED 2 of the Battery Status Indicator comes on fully occlude the Suction Tubing. Keep the tubing occluded until LED 1 comes on. Replacing the Canister:
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To remove the Canister, disconnect the angled connector from the vacuum inlet on the lid. To release the Canister Holder, press down the Canister Holder Release Arm while sliding the Holder toward you. Remove the canister from the holder. Replace the canister in the holder, slide the holder into position and connect the tubing to the canister. Replacing the Battery: Open the door. To remove the battery, push and move it slightly to the left and then release. Withdraw the battery from the LSU. To insert battery, push it fully in and then to the right to lock it. Close the battery door. After inserting the battery, place the LSU on charge unless a fully charged battery is inserted
MECONIUM SUCTIONING Caution

When the infant's condition is unstable, it may not be possible to clear the trachea of all meconium before positive pressure ventilation must be initiated This intervention should not be delayed while the infant is dried Mechanical suction should be set no higher than 100 mm/Hg
Figure 10
Procedure
Visualize hypopharynx with a laryngoscope and remove any residual meconium with suctioning Intubate the trachea and suction the lower airway utilizing a meconium trap connected to the ET tube (See Figure 10) Repeat as necessary After initial stabilization is achieved, an orogastric tube should be placed to empty the newborns stomach since it may contain meconium that could later be regurgitated and aspirated
PHARYNGEAL SUCTIONING Procedure

Use universal precautions Inspect unit for proper function and parts Switch on suction and clamp the tubing to note if the pressure dial registers at least 300 mm/Hg Attach the suction tip to the tubing Open the patients mouth Insert the suction tip in to the mouth and apply suction on the way out Do not suction for more that 15 seconds Reoxygenation should occur prior to repeated suctioning
TRACHEAL SUCTIONING Procedure

Prepare equipment Use universal precautions (should use sterile gloves) Hyperventilate the patient Grasp the suction catheter with the gloved hand Insert the suction catheter into the ET Tube without application of suction Apply suction during the withdrawal of the catheter P - 16 03/01/05
Remove the catheter Hyperventilate the patient Repeat as necessary
VENTILATOR
AUTOVENT 2000 Caution
Serial number of patient valve and serial number of module must match, otherwise settings may not be accurate
Application/Use
Determine the volume setting for the patient, use 810 ml per kg of ideal body weight or 5 ml per pound (70 kg = 700 ml). If unsure of proper weight, it is preferable to go with lower volume. Not recommended for use with patients less than 40 kg Normal BPM Adult 10 12 Should a mechanical problem develop or the patient appears to be experiencing difficulty while connected to the ventilator, disconnect and ventilate by other means Refer to manual for cleaning instructions and operating information
MINIVENT
The volume indicator on the device is set for LOW, MEDIUM, and HIGH. Tidal volumes range from 0500 ml for pediatric and 01,250 ml for adults. These are only approximates and are not exact volumes. It must not be assumed that the settings of LOW, MEDIUM, and HIGH are equally divided according to tidal volumes from 0500 or 1,250 ml. During tidal volume tests it was found that almost maximum volumes were obtained in the LOW to MEDIUM range (See Figure 16). Over ventilating a patient may have serious untoward effects.
Contraindications
This device should not be used for a patient less than 50 pounds body weight
Application/Use
Turn TIDALVOLUME control to 0 Turn MODE SELECTOR control to desired setting (ADULT, CHILD, HYPERVENTILATE, CPR) Connect the patient valve to the patient Slowly turn the TIDAL VOLUME control until the desired tidal volume is obtained Determine the volume setting for the patient, use 810 ml per kg of ideal body weight or 5 ml per pound (70 kg = 700 ml). If unsure of proper weight, it is preferable to go with lower volume.
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Cardiac
ALERTS CARDIAC AND STROKE
STROKE ALERT CRITERIA:
Time of onset <5 hours Any abnormal finding on examination? Deficit not likely due to head trauma? Blood Glucose >50
Caution
Prevent aspiration, keep NPO, elevate the head 30 degrees Avoid treatment of HTN, unless ordered per treatment guidelinesor on-duty ER Physician Avoid IV glucose (give glucose only if BGL is lower than 50 mg/dl and with Physician Consult)
Procedure
If patient meets inclusion criteria, they are considered priority 2, and a stroke alert is called to dispatch and the hospital transporting to Treatment as specified by treatment guidelines Perform thrombolytic exclusion check sheet Transport should not be delayed
CARDIAC ALERT CRITERIA:

Patient exhibiting signs and symptoms consistent with an AMI ST segment elevation present on 12lead EKG in 2 or more contiguous leads Patient is 18 years old or older
Caution
If QRS width is .12 sec or greater do not read ST segment changes Be aware of multiple conditions which may result in nonAMI ST segment changes. Be prepared to correlate clinically
Procedure
If patient meets inclusion criteria, even if they excluded from thrombolytics, they are considered priority 2 and a cardiac alert is called to dispatch Treatment as specified by guidelines Perform thrombolytic exclusion check sheet Emphasis is placed on expediting patient transport and performing treatments enroute to the hospital, not remaining on scene to fulfill protocol requirements
12 LEAD EKG
Indications
All chest pain including blunt trauma to the chest Any cardiac dysrhythmias or irregularities Heart rate less than 50 BPM or greater than 150 BPM Epigastric pain unless evidence of GI bleeding Thoracic back pain without trauma Diaphoresis not explained by fever or environment Difficulty breathing P - 18 03/01/05
Syncope without seizure or obvious blood loss (near syncopes included) CHF/Pulmonary edema Tricyclic antidepressant overdose
Caution
Treatment of life threatening problems such as dysrhythmias, acute pulmonary edema, shock, etc. should be initiated prior to obtaining a 12 lead ECG Obtaining a 12 lead ECG should not delay transport of critically ill patients
Procedure
Clean area for electrode placement with antiseptic swabs Shave area if needed being careful not to cause lacerations The midclavicular line may be found by dropping an imaginary line from the middle of the clavicle down The midaxillary line can be found by dropping an imaginary line from the armpit down Leads V4 through V6 must be in a straight line and this may not alys be in the intercostal space Run a V4R if ST changes seen in leads II, III or aVF. Move the V4 lead to the V4R position; manually print V4R. Running a second 12 lead with the V4 lead in the V4R position could result in a false impression or diagnosis advisory from the 12 lead monitor analysis. Place electrodes as per diagram (See Figure 11) RAright arm, upper arm or upper chest near the shoulder LAleft arm, upper arm or upper chest near the shoulder RLright leg, upper leg or lower abdomen near the hip LLleft leg, upper leg or lower abdomen near the hip V14th intercostal space, immediately to the right of the sternum V24th intercostal space, immediately to the left of the sternum V3placed between V2 and V4 V45th intercostal space, midclavicular line V55th intercostal space between V4 and V6 V65th intercostal space midaxillary line V4R5th intercostal space, right midclavicular line Figure 11
MARQUETTE RESPONDER 1500

CAPABILITIES
3 Lead ECG monitoring Defibrillation Cardioversion Transcutaneous pacing Diagnostic / interpretive 12-lead ECG
MONITORING
Patients can be monitored using either the Multifunction pads or by using the three lead patient cables.
Caution
If both the multifunction pads and the patient cables are connected to the patient and either a lead or a defibrillation cable becomes disconnected, the unit switches monitoring to the source that remains connected 03/01/05 P - 19
EMERGENCY MEDICAL GUIDELINES Application/Use

Multifunction pads turn the power on with the select energy switch; place switch in the ON/DISARM position the Marquette will enter a self test mode then indicate TEST OK turn the LEAD SELECTOR switch to the PADS position monitor will display ECG in Lead II only check expiration date on package pad position is anterior / anterior attach one pad to cable marked apex and the other pad to the cable marked sternum dry patient's chest peel off protective backing press the pads firmly onto the patient's chest in sternal / apex position monitor will display and print only in Lead II Using three lead patient cables turn power on and wait for the self test to be completed attach electrodes to patient cables using standard AHA code select the lead you wish to monitor ( I, II, or III ) the Marquette will display and / or print in the lead selected
RECORDING SELECTED LEAD

Paper pressing the button labeled PRINT starts the printer pressing the PRINT button a second time stops the printer Patient data card some Departments may use the optional patient data card to capture patient ECG information, please refer to the Operation Manual for more information
DEFIBRILLATION
Insure defibrillation pads are in place Select desired energy level on ENERGY SELECT 1 switch Press the white CHARGE 2 button The Marquette will indicate charging with an audible beep and the screen will state charging to XXX JOULES. When the unit has reached the selected charge the beeping will become rapid and continue to beep until the energy is delivered. The screen will show READY XXX JOULES After assuring the patient is clear, press the green SHOCK 3 button Controls and Indicators
1. EVENT MARK 2. PRINT 3. CHARGE 4. SHOCK 5. ENERGYSELECTAND POWER 6. ECG SIZE 7. LEAD SELECT 8. SYNC 9. POWER LIGHT 10. MENU SELECT 11. ENTER 12. VOLUME 13. LCD DISPLAY CONTRAST
SYNCHRONIZED CARDIOVERSION Caution

In order to activate the synchronized cardioversion function, the LEAD SELECT switch must be set to SYNC and you must press the SYNC button Once you press the SYNC button, you may use the LEAD SELECT switch to select PADS, LEAD I, II, or III while in synchronized mode
Application/Use
Connect both the three lead patient cables and the defibrillation cables to the patient as described in the monitoring section Select SYNC on the lead selector switch Press the SYNC button. The SYNC button will flash with each R wave detected and a marker will appear on each R wave on the display screen (if sync marker fails to appear, adjust ECG SIZE and / or select a different lead) Select the proper energy level with the ENERGY SELECT 1 switch P - 20 03/01/05
Press the white CHARGE 2 button When the unit is charged press and hold the green SHOCK 3 button until the energy is delivered Repeat as required
PACING
for The Marquette is capable of either fixed or demand pacing. The default setting is demand pacing. Place both multifunction pads and patient monitoring electrodes on patient as previously described Press SETUP on the pacemaker control panel. A marker will appear on the display screen on each R wave sensed. If the marker does not appear, adjust the ECG SIZE and / or use the LEAD SELECT switch to select a different lead. Set MODE, RATE, and OUTPUT parameters, refer to TRANSCUTANEOUS PACING PROCEDURAL GUIDELINE Press START / STOP button to begin pacing
Application/Use
RUNNING A DIAGNOSTIC 12 LEAD ECG

Connect the acquisition module to the A.M. INPUT on the left side of the Marquette Turn the LEAD SELECT to 12 LEAD (12 with QRS image) Prepare the patient, refer to 12 LEAD ECG PROCEDURAL GUIDELINE (SEE PAGE P-17) Then the message ACQUIRING DATA appears on the display screen, select START ANALYSIS and press ENTER The Marquette will automatically acquire, analyze, and print the 12 lead ECG without any further action on the operators part. Do not move the LEAD SELECT from 12 lead position until you are completely finished with the 12 lead operation.
PHYSIO CONTROL LIFEPAK 10

MONITORING
ECG monitoring may be done through the external paddles, disposable defibrillation electrodes, or through a 3lead patient cable.
Caution
Avoid contact with the conductive material
Application/Use
Paddles apply 1/4 1/2 of conductive gel over the entire surface of the paddles or use prejelled defibrillation pads and apply to the patient turn the monitor on by rotating POWER knob to any battery postion spare batteries are to be carried at all times; the LP 10 holds 3 batteries which are used individually until the power is depleted push LEAD SELECT to paddles postion assure that the gel is distributed evenly over the entire surface of the paddles place paddles on the patient's chest with approximately 25 pounds of pressure place APEX paddle on patient's lower left chest and STERNUM paddle on the sternum slightly to the right observe cardioscope for patient's rhythm Patient cable monitoring prepare the patient's skin surface, prior to the application of the electrodes assure the electrodes have sufficient gel to conduct secure and support the patient cable whenever possible, avoid monitoring in environments with significant electrical interference as noise may corrupt the ECG signal. 03/01/05 P - 21

if the ECG is unreadable due to the size of the QRS complex the ECG SIZE may be adjusted attach the 6 pin cable plug to the right side panel attach lead wires to the electrodes apply the electrodes to the prepared sites turn on the POWER select the proper lead with the LEAD SELECT adjust the ECG Size push the QRS VOL until audible Push the ECG SIZE up or down until systole beeper coincides with every QRS complex Adjust the QRS VOL as desired
CABLE PLACEMENT Application/Use

White (right arm or right upper chest) Black (left arm or left upper chest) Red (left leg or left lower chest)
RECORDING Application/Use
Push RECORD Adjust ECG SIZE if necessary If FREEZE is selected while recording, recording continues until FREEZE is released
CODE SUMMARY Application/Use

Push CODE SUMMARY; the recorder will print a full report of the information stored in memory Printing of the CODE SUMMARY report can be interrupted by pushing the CODE SUMMARY button pushing the CHARGE button pushing the CHARGE button pushing the RECORD button running out of chart paper turning off the POWER The code summary report may be resumed by pushing CODE SUMMARY whenever the Lifepak 10 is on Critical events will be retained in memory whenever the Lifepak 10 is turned on. If the power is turned off the code summary information will be retained for 5 minutes. After the 5 minutes the information will be erased
DEFIBRILLATION Application/Use
Apply conductive gel to paddles Turn the monitor on, O will be displayed under AVAILABLE ENERGY on status display Select energy to be delivered with ENERGY SELECT Push and release CHARGE button on APEX paddle; charge indicator will flash, a ramping tone will be heard, and numbers will scroll up under AVAILABLE ENERGY display until energy reaches preselected level at which time a charge tone will sound
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03/01/05
if the energy is changed after the charge has been initiated the energy will be discharged and the operator will have to reinitiate the charge by pushing the charge button Place the paddles firmly on the patient's chest in the same postion used for the QUICK LOOK procedure When the charge tones sound the defibrillator is ready for defibrillation Assure all personnel are clear from the patient as well as anything touching the patient, by looking and calling for Clear! Discharge the defibrillator by pushing both paddle DISCHARGE buttons simultaneously Observe patient and cardioscope to determine results To internally discharge an unwanted charge rotate ENERGY SELECT to another energy level Turn off monitor Thoroughly clean the paddles and store them in the storage area
SYNCHRONIZED CARDIOVERSION Application/Use

Rotate POWER to a power source Attach patient cable and ECG electrodes; electrodes should be placed away from paddle sites and such that resultant will give a tall QRS complex Select LEAD with optimum QRS complex amplitude Push SYNC button; SYNC message on status display will blink off with each detected QRS complex Observe cardioscope; adjust ECG SIZE so that sync markers occur only on the QRS complex. If markers do not occur on the QRS complexes adjust ECG SIZE, change the lead or move the electrodes on the patient. Prepare and postion the paddles on the patient's chest as described in the defibrillation procedure Select energy to be delivered with ENERGY SELECT Push the CHARGE button and wait for tone to sound indicating charge has completed. Push and hold paddle DISCHARGE buttons until discharge occurs with next QRS complex If rhythm does not convert and cardioversion is to be reattempted, it is necessary to push SYNC again since it switches back to defibrillate mode after each synchronous discharge Thoroughly clean and store paddles in storage area after procedure
PACING PROCEDURE Application/Use

Rotate POWER control to a power source Connect ECG electrodes to patient cable and attach to patient For better adhesion, clean and dry areas over which pacing electrodes will be placed Connect pacing cable to PACE connector at the right side of the LP 10 Connect the QUIKPACE electrodes to pacing cable matching electrode color to connector color Peel off protective covering from electrode to expose conductive surface; position electrodes on patient's chest Push PACER button; adjacent indicator will illuminate Select desired pacing RATE (pacemaker powers up at a rate of 40 bpm) CURRENT level will begin at 0 mA 03/01/05 P - 23

Observe cardioscope; SENSE marker should appear on each QRS complex. If SENSE marker is not present on QRS or appears elsewhere, adjust ECG SIZE control for optimal sensing. If this fails, select another lead and readjust ECG SIZE. If intrinsic beats are not present skip this step. When unit is sensing properly, activate pacing by pushing START/STOP button. Adjacent indicator will light and a positive going spike will be seen on the ECG display with each delivered pacing stimulus Increase current slowly while observing cardioscope for evidence of electrical pacing capture; palpate patient's pulse or check blood pressure to assess perfusion Recorder will document pacing parameters; each pacing stimulus will be marked with an arrow on the lower edge of ECG paper To terminate pacing, push START/STOP button again; adjacent indicator light will go out If a pacing cable lead or QUIKPACE electrode becomes detached during pacing, the LEADS message will be displayed on the status display along with an audible alarm. The pacing rate will maintain its prealarm setting, however, the current will reset to 0 mA.
LIFEPAK 12
GENERAL
The LIFEPAK 12 defibrillator/monitor series has five main operating modes: Advisory Mode (SAS): Provides all features available except manual defibrillation, synchronous cardioversion and pacing. Manual Mode: Provides normal operating capability for ALS users. Setup Mode: Allows operator to customize the device. Service Mode: Allows operator to execute device diagnostic tests and calibrations. Inservice Mode: Provides simulated waveforms for demonstration purposes
Low Battery Indication and Message:

Low battery icon at top of display and low battery message in status area foreach battery. When low battery is indicated, device autoswitches to second battery. When both batteries reach a low battery condition, there is a voice prompt toreplace battery.
DISPLAY
Size (active viewing area): LCD: 140.8mm (5.5 in) wide x 105.6mm (4.2 in) high EL: 165.1mm (6.5 in) wide x 123.8mm (4.9 in) high Resolution: 640 x 480 black and white LCD 640 x 480 amber and black EL display User selectable LCD contrast Displays a minimum of 4 seconds of ECG and alphanumerics for values, device instructions or prompts. Option to display one or two additional waveforms Waveform display sweep speed: 25mm/sec for ECG and 12.5mm/sec of CO2 P - 24 03/01/05
PROCEDURAL GUIDELINES DATA MANAGEMENT

The device captures and stores patient data, events (including waveforms and annotations), user test results and continuous ECG waveform records in internal memory. The user can select and print reports and transfer the stored information via an internal modem through landline or mobile phones.
Report Types:
Three format types of CODE SUMMARY critical event record (short, medium and long) Initial ECG (except short format) Automatic capture of vital signs measurements every 5 minutes 3-channel or 4-channel 12-lead ECG report Continuous waveform records (transfer only) Trend Summary . includes patient information, vital signs log and vital signs graphs Vital Signs . includes patient information, event and vital signs log. Snapshot . includes patient information and 8 seconds of ECG captured at the time of transmission
COMMUNICATIONS
The device is capable of transferring data records by internal modem, external EIA/TIA modem, cellular modem or serial connection. Supports EIA/TIA-602 compatible modems using Xon/ Xoff or RTS/CTS flow control at 9600 to 38400 bps. EIA/TIA-RS232E compatible at 9600, 19200, 38400 and 57600 bps. Group III, Class 2 or 2.0 fax
MONITOR
Voice Prompts: Used for selected warnings and alarms (configurable on/off).
ECG
ECG is monitored via several cable arrangements. A 3-wire cable is used for 3-lead ECG monitoring. A 5-wire cable is used for 7-lead monitoring. A 10-wire cable is used for 12-lead acquisition. When the chest electrodes are removed, the 10-wire cable functions as a 4-wire cable. Standard paddles or QUIK-COMBO pacing/defibrillation ECG electrodes or FAST-PATCH disposable defibrillation/ECG electrodes are used for paddles lead monitoring. Lead Selection: Leads I, II, III, (3-wire ECG cable) Leads I, II, III, AVR, AVL and AVF acquired simultaneously (4-wire ECG cable) Leads I, II, III, AVR, AVL, AVF, V1 (Labeled C on 5-wire ECG cable) Leads I, II, III, AVR, AVL, AVF, V1, V2, V3, V4, V5 and V6 acquired simultaneously, (10-wire ECG cable) ECG Size: 4, 3, 2.5, 2, 1.5, 1, 0.5, 0.25 cm/mV (fixed at 1 cm/mV for 12-lead) Heart Rate Display: 20 to 300 bpm digital display Out of range indication: Display symbol .- Heart symbol flashes for each QRS detection Continuous Patient Surveillance System (CPSS): In advisory mode while Shock Advisory System is not active, CPSS monitors the patient, via paddles or Lead II ECG, for potentially shockable rhythms. 03/01/05 P - 25

SpO2 Measurement Range: 50 to 100%
Trend
Display: Choice of HR, SpO2(%), EtCO2, RR, NIBP, P1, P2, ST shown in channels 2 or 3. Time scale: Auto, 30 minutes, 1, 2, 4 or 8 hours Duration: Up to 8 hours with -06 Memory PCB or later. Reduced storage capacity with earlier versions. ST segment: After initial 12-lead ECG analysis, automatically selects and trends lead with the greatest ST displacement. ALARMS Quick Set: Activates alarms for all parameters. VF/VT Alarm: Activates continuous CPSS monitoring in Manual Mode. Apnea alarm: Occurs when 30 seconds have elapsed since last detected respiration. INTERPRETIVE ALGORITHMS 12-lead Interpretive algorithm: GE Medical 12SL, includes AMI statements.
PRINTER
Prints continuous strip of the displayed patient information Paper Size: 50mm (2.0 in) or optional 100mm (3.9 in) Print Speed: 25mm/Sec +/- 5% (measured in accordance with AAMI EC-11, 4.2.5.2) Delay: 8 seconds Autoprint: Waveform events print automatically (user configurable) Optional 50mm/sec timebase for 12-lead ECG reports
MANUAL MODE
Energy Select (Monophasic): 2, 3, 4, 5, 6, 7, 8, 9, 10, 20, 30, 50, 70, 100, 150, 200, 300 and 360 joules or user configurable sequence 200/200/360 or 200/300/ 360 joules Energy Select (Biphasic): 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 30, 50, 70, 100, 125, 150, 175, 200, 225, 250, 275, 300, 325, and 360 joules or user configurable sequence 100 to 200, 100 to 300, 100 to 360. Charge Time: Charge time to 360J in less than 10seconds, typical Synchronous Cardioversion: Energy transfer begins within 60mS of the QRS peak
ADVISORY
Shock Advisory System (SAS) is an ECG analysis system that advises the operator if the algorithm detects a shockable or non-shockable ECG rhythm. SAS acquires ECG via therapy electrodes only. Shock Ready Time: Using a fully charged battery at normal room temperature, the device is ready to shock within 20 seconds if the initial rhythm finding is Shock Advised. Output Energy (Edmark): User configurable, sequence of 200/200/360 or 200/ 300/360 joules. Output Energy (Biphasic): User configurable, sequence of three sequential shock levels ranging from 200, 200 to 300, and 200 to 360 joules. Note: 5% accuracy applies when disposable therapy electrodes are attached. Energy output is limited to the available energy which results in delivery of 360 joules into 50 ohms.
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ZOLL M SERIES
MONITOR SELECTION AND GENERAL INFORMATION
Lead Placement- LA(black), RA(white), LL(red), RL(green) 12L- plugs into 4 lead. V1-V6 placement same as used now. Recap 4 lead when finished. 12 Leads are saved for a set time after unit is powered down. To do 12L- push 12 lead button, then aquire. 12L is then automatically ready for transmission. Strips print out with leads II, I, III. Print button marked Recorder. Paper: use the straight edge of the monitor to rip paper off. Use the perforation on the paper when cutting for pasting. Contrast and volume buttons are on the lower left corner. When placing a battery in the charger, do not take out until the ready light comes on. An alarm will sound reminding you to place the battery back in if you do. Pulse Ox- this monitor has a pulse ox built into it. Picks up minimal artifact from movement, etc Disposable probes can also be used (look like bandaids). Codemarker button- Lists the commonly used procedures and drugs. If these are pushed during a call, they will be listed on the summary printout.
Defibrillator
Biphasic waveform: Shocks at lower energy setting. Benefits by less skin effects and greater conversion rate. Keep the adult pads connected while in the case. The pads will still be sealed due to a double seal on the packaging. Use the anterior-posterior pad positioning for defib and pacing. If youre unsure if rhythm is shockable, press analyze button (if equipped). If it is shockable, shockable rhythm will be displayed. Charge unit to desired energy level. Cardioversion: Synch pad placement is the front pad goes on the 3rd intercostal space midclavicular and the posterior pad goes in the standard place. Energy settings: 03/01/05 P - 27
Adult defib for V-fib & Pulseless VT: 120j, 150j, 200j (progressive) Ped defib for V-fib & Pulseless VT: 1 j/kg, 2 j/kg, 2 j/kg (progressive) Adult Synch Cardioversion for Atrial & Ventricular Tachys w/pulses: 50j, 75j, 120j, 150j, 200j (progressive) Ped Synch Cardioversion for Atrial & Ventricular Tachys w/pulses: 1 j/kg, may repeat at 2 j/kg (progressive).
Pacer
Unit is automatically set to 70 beats per minute. User needs to adjust the milliamps. The settings that are being used will be remembered if switch is changed to defib or monitor. 4:1 button: when pressed and held, temporarily withholds pacing. Pacing will be delivered at the set ppm setting. (approx 1 every 4th beat).
ZOLL PD 1400 PACEMAKER/DEFIBRILLATOR

MONITORING Application/Use
Attach the patient electrodes to the patient and plug in the cable connector to the ECG INPUT Turn selector switch to the MONITOR ON position Press the LEAD button until the desired lead is displayed on the monitor Press the ECG SIZE button until the desired waveform size is displayed Adjust the systole beeper tone volume to the desired level Set HEART RATE ALARM by depressing the ALARM SET button and press the ALARM ON/OFF button Refer to the operator's manual to change the alarm limits To record the ECG tracing, press the RECORDER ONOFF button beside the monitor; the recorder will continue to run until the button is pressed again Figure 11
DEFIBRILLATION Caution
The pediatric paddles are built into the adult paddles (See Figure 12). To access the pedi paddles push the PEDI button on the side of each paddle and slide the adult paddle forward. When replacing the adult paddles be sure the paddles lock into place.
Application/Use
Select DEFIB ON, this automatically sets the energy level to 200 joules Select the lead to use; remember the patient must have the electrodes already attached in order to use lead I, II, III Apply conductive material to the patient or the paddles (multifunction electrodes are pregelled) Apply the paddles to the chest or attach the multifunction electrodes to the chest select the ENERGY LEVEL, if 200 is not the desired level, by either depressing the UP/DOWN buttons located on the front of the panel or the sternum paddle charge the paddles by depressing the CHARGE button on the front panel or on the apex paddle discharge the defibrillator by holding both DISCHARGE buttons on the paddles or both buttons on the multifunction cable at the connection site P - 28 03/01/05
Figure 12
repeat steps for each subsequent shock (the device is marked 123 for each step to be taken and the order of which it should be taken)
PACING Application/Use
Select MONITOR ON Set OUTPUT to 0 mA Apply pacer pads Connect pacer electrodes to the output cable Select PACER ON Set pacer RATE, observe the pacing artifact and confirm it is well positioned in diastole Increase output until capture
STANDBY PACING Indications

Indicated for patients in a bradycardic rhythm expected to drop below levels sufficient to maintain adequate cardiac output
Application/Use
Establish effective pacing Set the mA OUTPUT to 10% higher than the minimum mA output necessary to effect consistent capture Turn the pacing RATE below the patient's heart rate. This suppresses pacing unless the patient's rate drops below the set pacing rate. The pacing rate should be set at a level needed for adequate cardiac output. Check the threshold periodically MCFR and SFR perform pericardiocentesis
MULTIFUNCTION ELECTRODES
The multifunction electrodes allow for hands free defibrillation, cardioversion, pacing, and monitoring with a single pair of electrodes. The placement for the pregelled electrodes are anterior/posterior. The multifunction electrodes can only be used with a multi function cable.
PERICARDIOCENTESIS
Indications
Emergency relief of cardiac tamponade on critically injured patients accompanied by severe hemodynamic impairment
Contraindications
Hemodynamically stable patients
Caution
Figure 13 This is a sterile procedure; use appropriate sterile technique Hazards cardiac arrhythmias including VFib and Asystole puncture or laceration of cardiac chambers or coronary arteries hemothorax, pneumothorax, or both. injection of air into cardiac chambers if catheter is left open to air
Procedure
Place patient on 3lead EKG monitoring if not already done Locate the entry site (between the xiphoid process and left costal margin) Prep the entrance site with antiseptic swabs and provide an aseptic area Place the 16 g intracardiac needle (34 inches in length) on a 3050 cc syringe Consider sedation if patient is conscious Insert needle at 3045 degree angle to the skin and advance toward left shoulder while aspirating continuously (See Figure 13, 14) P - 29 03/01/05
Figure 14

As the needle is advanced beneath the skin the tight pericardium may be felt. Entry in to the pericardial space may produce a giving sensation. Contact of the needle against the epicardium my give a scratching sensation and the needle should be withdrawn slightly.
TRANSCUTANEOUS PACING
Indications
Symptomatic Bradycardia Pulseless Electrical Activity with bradycardia unresponsive to drug therapy Asystole
Contraindications
Traumatic asystole prior to fluid replacement and PASG application Overdrive pacing Figure 15
Caution
Muscle twitch will make carotid pulse assessment difficult at best with output settings in excess of 100 mA; assess femoral, brachial, or radial pulses in these instances
Procedure
Leads applied, monitor set to Lead II Pad placement anteriorposterior is preferred (See Figure 15) anterioranterior should be used in spinal immobilization and when defibrillation is also being performed (See Figure 16) Perform pacer set up set RATE to 70 beats per minute set OUTPUT for symptomatic bradycardia set OUTPUT to minimum for asystole and bradycardic PEA set OUTPUT to maximum Initiate pacing Increase or decrease OUTPUT as needed to establish and maintain capture and pulses
Figure 16
AUTOMATED EXTERNAL DEFIBRILLATOR

The AED is for use by emergency care personnel specifically trained in the operation of the AED, and qualified by Training in Advanced Cardiac Life Support, Basic Life Support, or in other physicianauthorized emergency medical response.
Indications
The AED is semiautomatic, and is for the use on victims of sudden cardiac arrest, on whom lack of circulation is indicated by: Unconsciousness Absence of breathing Absence of pulse
Contraindications
Consciousness Presence of breathing Presence of pulse Any condition incompatible with life P - 30 03/01/05
Conditions deemed environmentally unsafe Valid and verified DNRO present Patients less than 8 years old ( AHA) Patients weighing less than 2530 kg. (5566 lbs.) (AHA)
Caution
Assure scene safety! Assess for hazards! Do not place pads directly over artificial pacemaker sites, use alternative site. Any medication including a NITROPATCH OR NITROPASTE should be removed from the patient prior to AED application.
Special Considerations
Hypothermia Associated with Cardiac Arrest Defibrillation should not be withheld from the cold patient in ventricular fibrillation (core < 85 F). If the hypothermic patient does not respond to three shocks, stop defibrillation attempts, resume CPR and rewarming efforts, and transport. Cardiac Arrest Associated with Trauma Seldom responds to defibrillation Begin CPR if indicated Assess rhythm Initiate BLS interventions including: airway, oxygenation, control of hemorrhage, and cervical spine immobilization. Defibrillate as indicated by AED Automatic Internal Cardiac Defibrillators (AICD) For patients with known ICDS, attach the AED and follow standard operating procedures. If the ICD is in the process of shocking a patient, allow the ICD to complete its cycle for approximately 3060 seconds before applying AED pads.
On Scene Trained Personnel and the arrival of ACLS Providers

ACLS providers have authority of patient care over AED personnel. On arrival ask for a quick report from the AED providers concerning patient condition and performance of the AED. ACLS providers should consider shocks delivered by the AED providers and incorporate that into the treatment of the patient. For example, if the AED has delivered the first three shocks of a Vfib sequence, the ACLS providers should then move towards intubation, IV access, and drug therapy.
Procedure
Scene Survey. Primary Survey: Verify unresponsiveness and then ABCS. Airway Open the airway; nontraumatic, use head tilt / chin lift. Traumatic, use jaw thrust method. Breathing Look, listen, and feel for air movement from the mouth or nose. If no breathing present, give 2 artificial ventilations. If no spontaneous respirations follow, proceed to pulse check. Circulation Check for carotid pulse. If no pulse is felt in 510 seconds then: 2 Rescuers initiate CPR until AED is attached. 1 Rescuer attach AED then follow algorithm. After 1 minute of CPR you will be instructed to stop and let the AED analyze rhythm for 515 seconds. 03/01/05 P - 31
EMERGENCY MEDICAL GUIDELINES Application/Use

If the patient has met the AED criteria: Make sure the patient is not wet and in contact with water. Assess entire scene for life safety. Apply pads per training instructions. Activate AED. Follow algorithm prompts
ARREST NOTIFICATION:
Notify Dispatch if cardiac arrest in progress. Radio transmission must be at least 6 feet away when AED is operating.
PATIENT STABILIZATION:
If at any time the patient develops a pulse, but no respirations, continue to provide rescue ventilations and monitor the pulse. If the patient has a return of pulse and adequate respirations, place in the recovery position and continue to monitor all vital signs until ACLS personnel arrive. Different brands and models of AEDs have a variety of features and controls that may differ in characteristics such as paper strip recorders, rhythm display methods, energy levels, and messages to the operator. Operators can orient themselves best by understanding how each brand and model approaches the operational phase by referring to the training they received and the manufacturers recommendations. Please refer to departmental procedure for retrieving the patient data after the AED has been used.
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Medication and Fluid Administration

AVAILABLE ROUTES OF ADMINISTRATION
Endotracheal Inhalation Intramuscular Intranasally Intraosseous Intravenous Optic Oral Rectal Subcutaneous Sublingual Topical
BONE INJECTION GUN (B.I.G.)

Adult- blue 15g Pediatric- red 18g
Indications:
Rapid infusion of fluids and drugs.
Contraindications:
Skin infection. Tumor and fracture at insertion site.
Site Location:
Adults- 1-2cm medially and 1cm proximally to the tibial tuberosity. Pediatrics below age 6 and in the elderly- 1-2cm medially and 1-2cm distally to the tibial tuberosity.
Recommended Depth:
Adults: 2.5cm (Adult B.I.G. is NOT adjustable) Infants 0-3 yrs: 0.5 0.7cm Pediatrics 3-6 yrs: 1cm 1.5cm Pediatrics 6-12 yrs: 1.5cm
Procedure:
1. Choose either Adult or Pediatric B.I.G. If pediatric, choose the desired depth by unscrewing the sleeve from the cylinder housing. 2. Use a povidone iodine tincture to clean the selected site for injection. 3. Position the front of the B.I.G. at the selected site, holding and pushing firmly on the rear part. 4. Pull out the safety latch from the instrument by squeezing its two sides together. 5. Triggering the B.I.G. can be done by pressing the rear part against the two handles of the housing or by pushing the rear part firmly against the injection site. P - 33 03/01/05

6. Remove the B.I.G. and separate the trocar needle from its housing. 7. Pull out the stylet trocar to separate it from the needle. Only the needle cannula must remain in the bone. 8. Connect the safety latch to the cannula. 9. Connect a syringe or infusion set to the needle. 10. To reduce the pain in conscious patients, it is recommended to start a slow flushing of the inserted needle with 1-5cc of Lidocaine over 1-2 minutes, then inject the fluid drug (bolus) or infusion. To maintain optimal flow, high pressure up to 300 mmHg to the infusion bag is recommended.
Miscellaneous Information:
The B.I.G. can be left in for up to 6 days. The needle should be cleaned with an antiseptic solution everyday. Flow Rates: Gravity fed: 10 20cc/min 300mmHg with pressure bag: 30 40cc/min Syringe: 60 100cc/min Shelf life is 3 years. Needle cannot be inserted next to a previous injection site; the fluid will drain out through the other site.
BURETTE ADMINISTRATION SET

The burette administration set is used when a medication needs to be mixed in 100 cc or less of fluid or any pediatric patient requiring IV therapy where fluid volume administered requires precise measurement. It should not be used when large fluid volumes are needed. The burette is distinguished from other administration sets by the 150 cc chamber located within the tubing. It is especially useful when dealing with pediatric patients when fluid or medication administration is crucial. The chamber can be filled with the exact required amount of fluid or medication to prevent overdosing or bolusing with too much fluid.
Application/Use
Choose appropriate fluid Close the upper roller clamp on the tubing and spike the IV bag Open the upper roller clamp and fill the burette to the desired level; close the upper roller clamp If applicable add medication to the chamber and gently invert to mix the drug with the fluid Squeeze the drip chamber and fill Open the lower roller clamp and allow the solution to fill the entire set Connect the solution set to the IV catheter and set desired rate Open lower roller clamp and verify proper flow rate
Caution
Prior to removing the cassette from the pump, ensure that the lower roller clamp is closed to prevent bolusing the patient with fluid or medication
Application/Use
Choose appropriate fluid Close the upper roller clamp on the tubing and spike the IV bag Open the upper roller clamp and fill the burette to the desired level; close the upper roller clamp
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03/01/05
If applicable add medication to the chamber and gently invert to mix the drug with the fluid Squeeze the drip chamber and fill to 1/3 full Invert the cassette with the flat side facing you Open lower roller clamp and allow solution to fill entire set Close the lower roller clamp and insert the cassette into the pump Connect the solution set to the IV catheter and set desired RATE on the Pump Open lower roller clamp and press OPR on pump
DOUBLE LUMEN IV CATHETER

This device is intended for use in the patient who requires multiple IV access. The two lumen design prevents mixing of medications within the catheter. Use of the double lumen catheter eliminates the need to establish a second IV site for medication administration.
Indications
Administration of IV nitroglycerin Preparation of the cardiac patient for thrombolytic therapy
Caution
Device is not intended for fluid resuscitation; lumens are 20 g and 22 g (See Figure 17) Figure 17
Application/Use
Flush the secondary access port with saline Cannulate the vein with the double lumen catheter the double lumen catheter is inserted as a standard IV catheter, refer to INTRAVENOUS CATHETER INSERTION PROCEDURAL GUIDELINE (SEE PAGE P-47) After removing the introducer needle, attach the IV line to the main port and flush, assuring infiltration has not occurred, and secure appropriately To attach the second IV line, remove the male adapter plug from the second port by twisting. The second IV line may be attached either directly or by Luerlock (this will avoid the need for needle insertion into the male adapter plug). The infusion pump IV line should be connected to the secondary port; the small 22g lumen of the secondary port will not restrict the positive pressure flow of the infusion pump as it might a gravity fed IV line
DRAWING UP MEDICATIONS
AMPULE Procedure
Prepare a syringe of the appropriate volume with a needle Verify the name and concentration of the medication printed on the ampule; inspect the solution for discoloration, cloudiness, or particles; check expiration date Tap ampule with finger to move the solution down into the well Using a 4x4 gauze pad (See Figure 18), face ampule away and break off the top of the ampule neck along scored area. Some ampules have colored rings that mark the scored area of the ampule. Break along the colored mark. Insert the needle into the ampule making sure the needle does not touch the rim of the ampule. Pull back on the plunger of the syringe to withdraw the needed amount (dosage) of medication. 03/01/05 P - 35
Figure 18

Expel any air present in the syringe and carefully recap the needle with appropriate technique (if it will not be used immediately)
VIAL Procedure
Prepare a syringe of the proper volume with a needle Verify the name and concentration of the medication printed on the vial; inspect the solution for discoloration, cloudiness, or particles; check expiration date Disinfect the rubber stopper of the vial using an antiseptic swab Draw air into the syringe of equal volume to solution to be withdrawn Insert the needle at an angle through the rubber stopper, and inject the air inside the vial (See Figure 19) Invert the vial and draw out the needed solution (volume); carefully withdraw the needle from the vial Expel any air present in the syringe and carefully recap the needle with appropriate technique (if it will not be used immediately)
Figure 19
ENDOTRACHEAL MEDICATION ADMINISTRATION

Procedure
Verify the name and concentration of the medication; inspect the solution for discoloration, cloudiness, or particles; check expiration date Hyperventilate the patient prior to drug administration Inject medication through the endotracheal tube medication port (See Figure 20) for endotracheal tubes without a medication port, drugs should be administered through an appropriate size suction catheter inserted through the endotracheal tube into the bronchial tree Resume ventilation Monitor the patient No more than 10 cc of fluid should be given endotracheally Endotracheal drug dosages should be 22.5 times the normal IV dose The drug should be diluted to 10 cc of fluid in an adult patient, 5 cc of fluid in a child, 2 cc of fluid in an infant
Figure 20
EPI-PEN AUTO INJECTOR

The EMT (or Paramedic) may administer prescribed Epinephrine via an auto-injector for patients who are exhibiting signs of respiratory distress associated with allergic reaction. These signs include: dyspnea, hives, flushing of the skin, wheezing, edema, and possible unstable vital signs.
Procedure
Primary Assessment Assure auto-injector is prescribed for the patient (EPI-Pen for adult patient and EPI-Pen Jr. for pediatric patient), check expiration date and cloudiness or discoloration if possible. If patient is exhibiting signs of moderate to severe allergic reaction as described above, assist patient in administering Epinephrine via auto-injector. Remove auto-injector safety cap. P - 36 03/01/05
Select appropriate injection site. Thigh lateral portion of thigh, midway between waist and knee. Shoulder fleshy portion of upper arm. Push auto-injector firmly against site until injector activates. Hold in place until medication is fully injected (minimum of 10 seconds). Record time. Dispose of injector in biohazard container. Reassess patient.
F.A.S.T. 1 INTRAOSSEOUS INFUSION SYSTEM

WARNING
Safety of the F.A.S.T. 1 Intraosseous Infusion System in patients with very severe osteoporosis has not been proven. Insertion of the F.A.S.T. 1 Intraosseous Infusion System in sites other than the adult manubrium may result in ineffective infusion and may result in ineffective infusion and may result in overpenetration of the infusion tube with consequent serious injury to the patient.
PRECAUTIONS
For use with adult patients. The F.A.S.T. 1 Intraosseous Infusion system is designed to penetrate 6.0 mm into the manubrium. Adult patients are expected to have a manubrium thickness greater than 6.0 mm. Qualified professionals should determine any appropriate or necessary exceptions, either inclusions or exclusions, to the criterion For use with adult patients. Severe skin compromise such as trauma, infection or burns over the infusion site may interfere with use of the device. Check for fracture of the sternum or vascular injury which may compromise the integrity of the manubrium or its vascularization. Check for midline sternotomy scars the device may be less effective in patients with a previous midline sternotomy.
Indications
The F.A.S.T.1 Intraosseous Infusion System is intended for intraosseous infusion as an alternative to intravenous access to facilitate emergency resusitation through the use of drugs and fluids. It is not intended to be used for more than 24 hours.
CONTRAINDICATIONS
None Known
DESIGNATED INSERTION SITE

The single designated site of insertion is the adult manubrium, on the midline and 1.5 cm (5/8 inch) below (inferior to) to supra-sternal notch (sternal notch). Proper placement of the patch helps ensure insertion at the site.
Caution
Do not use this product until you have been trained and evaluated for F.A.S.T. 1 use.
Instructions for placement

Administer local anaesthetic if the patient is conscious and alert. Expose sternum. Prepare insertion site with iodine and alcohol swabsprovided. Maintain aseptic technique throughout the procedure.
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P - 37

Remove top half of patch baking (labeled Remove1). Locate sternal notch with index finger held perpendicular to manubrium. Using index finger, align notch in patch with patients sternal notch. Verify target zone (circular hole in patch) is over patients midline. Secure top half of the patch to patient. Remove bottom half of patch backing. Press firmly to secure patch to patient. Verify location; the notch in the patch should match the sternal notch, and the target zone should be over the patients midline. Take corrective action if error is greater than about 1 cm (3/8). Twist and pull back to remove sharps cap from introducer. Place bone probe cluster in larget zone. Ensure that the introducer axis is perpendicular (90 degrees) to the skin at the insertion site. Ensure the entire bone probe cluster is within the target zone. Pressing straight along the introducer axis, with hand and elbow in line, push with firm and constant force until a distinct release is heard and felt. The introducer must remain perpendicular to the skin during insertion. After release, pull straight back to remove the introducer, exposing the infusion tube. NOTE: As the insertion force required in Step #5 can be considerable, some users may find that a two-handed grip on the introducer allows better control during insertion of the infusion tube. Push the used bone probe cluster into the foam-filled sharps plug. If desired, place the original sharps cap over the sharps plug. Attach right-angle female connector on patch to infusion tube. Optional Steps: Verify placement by attaching syringe to straight female connector and withdrawing marrow into infusion tube. Increase fluid flow rate by flushing system with 10 ccs of saline. Attach straight female connector on patch to purged source of fluid or drugs. Fluid can now flow to the site. NOTE: If fluid does not flow at all or if extravasation (leakage of fluid) occurs, infusion should be discontinued and an alternative vascular access method should be used. Place dome over patch and press down firmly to engage Velcro fastening. Attach unopened sterile remover package to the patient (arm, leg, attach to IV bag, etc.) THIS PACKAGE MUST BE TRANSPORTED WITH THE PATIENT. The remover is needed to eventually remove the infusion tube from the patients bone when intraosseous access is no longer required.
REMOVAL OF THE DEVICE

Remove the dome from the patch. Disconnect the infusion tube from the male connector. Maintaining aseptic technique, open the remover package, take out the remover, remove the tubing protecting the threaded tip, and insert the remover into the infusion tube. Hold the infusion tube straight out from the patient (90 degrees to the patch) as the remover is being placed. Advance the remover and turn it clockwise until it stops turning, to engage the threads in the proximal tip of the infusion tube. Pull straight out on the remover to remove the infusion tube. Dispose of the remover in a manner appropriate for contaminated sharps. Remove the patch. Apply pressure after removing the patch and then dress the wound using aseptic technique.
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NOTE: The F.A.S.T. 1 may be used to administer drugs or fluids as boluses from a syringe, or from fluid sources such as IV bags using gravity drip, pressure cuffs, or the syringe/stopcock pumping method. Fluid flow rates during intraosseous infusion are typically determined by the pressure source and limited by the emissary veins of the bone, rather than by the intraosseous infusion system. Fluids have been infused into adult sternums through F.A.S.T. 1 Intraosseous Infusion System at 30 ml/min using a one meter gravity drip (75 mmHg), and at over 120 ml/min using a pressureized fluid source.
DRUG HANDLING
INVENTORY
Central Supply All receiving/issuing of controlled substances from the controlled substance locker in the central supply shall be performed by the inventory control officer, inventory clerk or other designated personnel. The receipt/issue of controlled substance shall be logged on the controlled substance log and shall note the following: date and time of the transaction name/initials of employee/supplier receiving/issuing substance name/initials of designated person conducting transaction name of substance received/issued amount of substance received/issued expiration date of substance received/issued (in case of multiple units, the earliest expiring unit shall be listed) Receiving/issuing of medications shall be performed by the inventory control officer, inventory clerk or other designated personnel Shipping documents (packing slips) shall be handled in accordance with department policies. The shipment shall be inspected and checked for the following by the inventory control officer, inventory clerk or other designated personnel : breakage or damage accurate quantities (shipped vs. backordered) accurate items (correct product shipped) expiration dates (drugs with less than one year left on expiration should be returned to supplier as Expiration Unacceptable) Inventory shall be placed in stock utilizing First In, First Out (FIFO) stock method (stock is rotated so earliest expiring units are in front, latest expiring units are in back) Rescue Vehicle The department paramedic and EMT on shift should conduct a physical inventory of the rescue vehicle every morning utilizing the par levels established by the department. Any item found below par level should be requisitioned in accordance with department policy. The appropriate stock should be pulled and issued to the crew by the inventory control officer, inventory clerk or other designated personnel in accordance with department policy.
SECURITY
Access department personnel shall have access to IV fluids as necessary department paramedics, inventory control officer, inventory clerk or other designated personnel shall have access to medications as necessary Controlled Substances access to the controlled substance locker shall be limited to the inventory control officer, inventory clerk or other designated personnel P - 39
03/01/05

the department paramedic on shift shall have access to the controlled substances maintained within the drug box on the apparatus Central Supply all IV fluids shall remain locked within the central stock area all medications shall remain locked within the locked central stock area all controlled substances (Morphine, Valium) shall remain double locked within the locked central stock area Rescue Vehicle all IV fluids shall remain within the locked apparatus when not in use all medications shall remain within the locked apparatus when not in use all controlled substances (Morphine, Valium) shall remain locked within the controlled substance lockbox which shall remain within the locked apparatus when not in use
USE
Central Supply no IV fluids, drugs or controlled substances should be used directly out of central supply for direct patient care Rescue Vehicle use of IV fluids, drugs and controlled substances shall be at the paramedic's discretion within the guidelines promulgated by the department medical director, Emergency Medical Guidelines and/or online medical control
INFUSAPORTS
Indications
IV access for necessary fluid or drug administration
Figure 21
Contraindications
Precautionary IV access
Caution
Do not use a saline lock with an InfusaPort Do not force fluid into a port to flush it This is a sterile procedure; use aseptic technique and extra caution to avoid infection at the port site
Procedure
Attach Huber needle to IV setup and flush Identify InfusaPort location Put on sterile gloves. Cleanse the area with antiseptic swabs in a circular outward motion each time; repeat twice (2). This step is absolutely necessary. Advance the needle into the port until it hits the solid template; open the IV line to flush the port (See Figure 33, 34). If the IV will not run, have the patient turn their head and/or shrug their shoulders. If it still will not run and the needle is properly placed, the port may be clotted and is not usable. Apply an antibacterial ointment, dress the area with 2x2 IV sponges using enough so the needle is resting on them. Loop the tubing and secure the needle and the tubing to the patient. Figure 22
INFUSION PUMP
AVI MODEL 400, 400A
The AVI Model 400A Volumetric Infusion Pump is indicated for use in venous pharmacological IV therapy to assure accurate, continuous, nonpulsatile delivery. The P - Model 40 03/01/05 AVI 400A is equipped with a full range of comprehensive alarms to alert the
operator when a problem occurs.
Indications
The AVI Infusion Pump is indicated for use whenever a medication IV drip is established or precise delivery of fluids is required
Caution
If piggybacking AVI administration set into a standard IV set, be certain the roller clamp on the standard IV set is also closed
Application/Use
Select appropriate IV set AVI Model 4220 Check valve IV Administration Set used for standard IV medication administration AVI Model 290 Low Absorption IV Administration Set used for Nitroglycerin IV administration only AVI Model 1230 Burette Administration Set used for IV medication administration where the medication requires specific volume dilution in less than 250 mL of fluid Select appropriate fluid and follow instructions for specific IV set chosen AVI Model 4220 Check valve IV Administration Set AVI Model 290 Low Absorption IV Administration Set AVI Model 1230 Burette Administration Set Turn on the POWER SWITCH, the LOAD KNOB to its OUT position; press STBY to silence the audio alarm Loosen the DOOR LOCK by turning the knob counterclockwise; release the DOOR LATCH and open the door Install the AVI cassette in the pump with the flat side facing outward. Match the four small holes in the cassette with the four locating pins on the cassette housing. Close the door, making sure the DOOR LATCH engages. Turn the DOOR LOCK clockwise until finger tight. With the set's lower roller clamp closed and the upper clamp open, turn the LOAD KNOB to its fully IN position. When loading an administration set in an AVI pump be sure the set's upper clamp is open; the pump may be damaged if the upper clamp is closed when the LOAD KNOB is turned to its IN position Never push on the door when turning the LOAD KNOB to its IN position; pump and/or cassette damage could result Attach the AVI administration set (with roller clamp closed) to the IV catheter Open the administration set's lower roller clamp Press RATE and enter the desired rate in mL/h using the NUMBER KEYS Press LIMIT and enter the desired VOLUME LIMIT in mL using the NUMBER KEYS Press CLEAR to return the VOLUME INFUSED display to zero Verify displayed settings and press OPR to begin the infusion To stop the infusion, either press STBY or move the pump's POWER SWITCH to the OFF/CHARGE position Always close the administration set's lower roller clamp before turning the LOAD KNOB either in or out; unrestricted gravity flow will occur if the DOOR LATCH is released and the clamp is not closed Always verify infusion settings are correctly displayed prior to pressing OPR to avoid incorrect infusion Air Removal 03/01/05 P - 41

The insistent audio alarm and the AIR and EMPTY BAG visual alarms are activated if air is detected in the upper cassette chamber. Air is removed from the AVI administration set in an upstream direction, away from the patient, without violating the integrity of the sterile fluid pathway. press STBY close the administration set's lower roller clamp If removing air from a piggyback set and an AVI check valve administration set, close the primary set's upper clamp before proceeding. Failure to close the proper clamp may cause piggyback solution to be flushed into the primary solution container. turn the LOAD KNOB to its OUT position, loosen the DOOR LOCK, release the DOOR LATCH, and open the door Remove the cassette from the pump and hold it with the flat side facing you. Tilt the cassette so the upper chamber is slightly away from you. Gently squeeze each chamber in sequence from bottom to top, keeping each previous chamber depressed as you move upward along the cassette. This method forces the air through the upper tubing to the drip chamber and solution container. release the chambers and allow gravity to refill the cassette; repeat procedure if all air is not expelled reinstall the cassette in the pump, close and latch the door, tighten the DOOR LOCK, and turn the LOAD KNOB to its IN position open the set's lower roller clamp (and the check valve set's upper clamp, if applicable) and press OPR to restart the infusion Titration the AVI pump has the ability to titrate, or change flow rates instantly without interrupting the administration of fluid press CLEAR while the pump is operating (do not press STBY first) enter the new rate using the NUMBER KEYS (it is not necessary to press RATE first); verify displayed rate within 10 seconds of pressing CLEAR, press OPR to instantly begin infusing at the new rate When a new rate is entered as above, it is immediately displayed in the RATE display while the pump continues to infuse at the original rate. If OPR is not pressed within 10 seconds of pressing CLEAR, the noninsistent audio alarm sounds and the RATE display changes back to the original rate. If this occurs, press OPR to silence the alarm and repeat the correct titration procedure.
BAXTER COLLEAGUE INFUSION PUMP Powering On

Turn power on by pressing the ON/OFF button When all self tests are complete, the CHANGE PERSONALITY and NEW PATIENT soft keys will be showing If NEW PATIENT soft key is present, information from the previous program is still retained in memory. To clear memory, press the NEW PATIENT soft key From the power on screen after self test, press the MAIN DISPLAY key (top right of front panel) to view the main display screen
Powering Off
While the pump automatically closes the dark blue slide clamp, always close the roller clamp before removing the tubing from the pump Press the ON/OFF key
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03/01/05
PROCEDURAL GUIDELINES Loading the Tubing

After turning the power on, press the OPEN key. The automatic tube loading mechanism open. If tubing is not loaded within 60 seconds, the loading mechanism closes Ensure that the dark blue slide clamp occludes the tubing. When the loading mechanism is open and STOPPED is displayed on the pump, insert the dark blue slide clamp into the slot. Pull tubing taut and slide it all the way into and along the tubing channel When the pump detects the tubing, the loading mechanism automatically pulls in the dark blue slide clamp, then closes and loads the tubing into the pumping mechanism After the tubing is loaded, confirm that the tubing entering the pump on the left side is going to the solution container Open the roller clamp. Verify that no solution is flowing (no drops falling in drip chamber and/or no flow from the end of the tubing) Attach the tubing to the patient access site
Unloading the Tubing

If the pump is running, press the STOP key on the pump Close the roller clamp on the tubing Press the OPEN key The loading mechanism automatically closes the dark blue slide clamp and opens the tubing channel so you can remove the tubing Ensure that the tubing channel is completely open (arrow displayed on the pump display) When the mechanism is opened completely, grasp the tubing on both sides of the pump and remove the tubing from the pump. The mechanism closes automatically 60 seconds after the tubing is removed
Manual Tube Release

Use the Manual Tube Release ONLY when the automatic tube release is not functioning Close the roller clamp on the tubing Locate the manual tube release on the right side of the pump, as you face the panel Push and grasp the release tab, turning it out Rotate the tab counterclockwise to its stop. This closes the dark blue slide clamp and opens the pump mechanism Remove the tubing from the pump
Resetting the Manual Release

Ensure there is no tubing or foreign objects in the tubing channel Turn the release tab clockwise to its stop and push the tab into its socket The DONE soft key is displayed when the manual tube release is reset. Press the DONE soft key to clear the alarm The pump cannot be powered off until the manual tube release is reset
Programming the Primary Rate

When the main display screen is shown, press the RATE key. The display then changes to the programming screen and the rate field is highlighted Program the desired flow rate (in ml/hr) using the keypad Press the VOL key or use the arrow keys to highlight the volume field Program the desired volume to be infused After programming is complete, verify the information before starting the pump Press START to being infusing 03/01/05 P - 43
EMERGENCY MEDICAL GUIDELINES Completing or Stopping the Infusion

When the volume remaining reaches zero (0), the pump automatically goes to KVO mode To exit this mode, press the STOP key or turn off the pump
Changing the Flow Rate during Infusion

Press the RATE key and enter the new value Press the START key to save the change and being infusing at the new rate
Programming a Dose Based on Patient Weight

On the primary screen, press the CHANGE MODE soft key. The programming modes screen is then displayed Use the arrow keys and/or PAGE UP/PAGE DOWN soft keys to highlight the mg/ kg/min selection Press the SELECT soft key to display the programming screen Program each field listed When finished, verify all values and press the CONFIRM SETTINGS soft key Press the START key to begin the infusion
Using the Volume-Time Function

Press the appropriate programming key (Primary or Piggyback) From the programming screen, press the CHANGE MODE soft key Highlight either PRIMARY VOLUME-TIME or PIGGYBACK VOLUME-TIME then press the SELECT key Enter the volume to be infused Highlight TIME DURATION using the arrow keys. Enter the time period for the infusion in hours and/or minutes. The pump automatically calculates the flow rate Verify that the information is correct, then press the CONFIRM SETTINGS soft key, then press the START key to being the infusion
Air Alarm
If the air detected alarm sounds, the advance air pop-up window is displayed. Press the UP arrow key next to the YES label for pump-assisted viewing of detected air. If pump-assistance is not desired, press the DOWN arrow key to manually purge the air. Remove the tubing from the pump and flush the air from the tubing, then replace the tubing in the pump Press and hold the ADVANCE AIR key. The pump continuously pumps until the key is released. When the pump detects fluid, a FLUID DETECTED icon is displayed When the FLUID DETECTED icon is displayed, the alarm is reset. Visually inspect the air bubble, disconnect the tubing from the patient, and flush the air from the tubing When the air has been removed, the infusion may be restarted. Press the Primary or Piggyback key then START
IVAC 530
Notes
Delivers at 45 psi and useful for intraosseous infusions Use vented tubing with glass NTG infusion bottles The pump does not detect infiltrations (monitor the site) Four hours of operation time on a fully charged battery The white drop indicator illuminates with each drop Close the drip clamp prior to opening the pump door. P - 44 03/01/05
PROCEDURAL GUIDELINES Application/Use

Prepare IV set with all air remove from the tubing and the drip chamber half full Place the drip sensor on the chamber above the fluid level Open the pump door, place tubing between the guide posts. Close the door, secure the latch, and ensure the tubing is not kinked. Attach the tubing to an IV site (preferably a seperate site or twincath). If piggybacking into a standard IV set, be sure the roller clamp on the standard IV set is closed. Turn the machine on (green power button)and select the gtts/min setting. Start the infusion by pressing the red start button.
IVAC MED SYSTEM 3

MultiChannel Infusion Pump Application/Use
Priming the Administration Set use only IVAC 25 or 28 series Administration sets. close regulating clamp. Spike container, fill drip chamber to the fill line. check vent position. slowly prime set, tapping and inverting cassette and any Y sites to expel all air. Cassette Insertion turn instrument ON before inserting cassette. ensure slide clamp is pulled out completely. insert cassette at an upward angle, then snap in place. slide clamp must be flush with cassette. ensure tubing collar correctly seated. three beeps indicate proper placement. Instrument Quick Setup verify instrument is turned on. select Channel by pressing desired channel key (A, B, C). press Select to move highlighted bar to choose setting to change, i.e. Rate, Volume Remaining or to clear Volume Infused. use (up) arrow,(down) arrow, Fast (up) arrow, or Fast (down) arrow to program new settings. to change direction of the Fast keys, press the corresponding (up) or (down) arrow. to recall a setting before Enter is pressed, press More Options, press Recall. press Enter when programming complete. press START/STOP key to begin or stop infusion. verify settings on Standard Display page. verify infusion status INFUSING, STOPPED, ALARM, KVO, STANDBY, FAULT, SERVICE. verify flow of solution from the drip chamber. Titration of Rate access desired channel by pressing channel key (A, B, C). change the rate by using the up arrow, down arrow, Fast (up) arrow, or Fast (down) arrow. press Enter. Clearing the Volume Infused access desired channel by pressing channel key (A, B, or C). press Select until Volume Infused (VI) is highlighted. press Clear to reset to zero. 03/01/05 P - 45

press Enter. Clearing the Total Volume Infused for all channels, primary and secondary press MORE OPTIONS until the Tot Vol softkey appears. press Tot Vol. Total volume page appears. press Clr Tot. All values for each channel will clear and flash. press Enter. Stopping a channel temporarily access channel by pressing channel key (A, B, C). press START/STOP key. Infusion status STOPPED on Channel page. indefinitely access desired channel by pressing channel key (A, B, C). press START/STOP key. Infusion status STOPPED on Channel page. return to the Standard Display page. press Stndby softkey standby option is only available on Standard Display page, when cassette is in a STOPPED channel. Clearing information from the standard display page when not in use the channel must be stopped and the cassette removed. the channel must not be selected, i.e. Status line for that channel must not be highlighted. to clear the Status line highlighting, press any infusing channel key. the information for the channel not in use will disappear from the Standard Display page after 2 minutes. Figure 23
INTRAMUSCULAR MEDICATION ADMINISTRATION

Procedure
Explain the procedure to the patient Verify the patient has no allergies to the medication Prepare a syringe of proper volume and attach a 21 gauge 1 inch needle Verify the name and concentration of the medication; inspect the solution for discoloration, cloudiness, or particles; check expiration date Disinfect the deltoid muscle using an antiseptic swab medication can also be given in the upperouter quadrant of the buttocks Recheck the medication Using one hand, stretch skin layer apart and flatten between fingers. Holding the syringe in the other hand, quickly insert the needle at a 90 degree angle in to the muscle (See Figure 23, 24). Pull back on the plunger to insure the needle has not entered an artery or vein by accident; there should be no blood return into the syringe Inject the medication Quickly remove the syringe and apply firm pressure over the injection site Properly dispose of the needle and monitor the patient for adverse reactions
Figure 24
Pediatric
Needle size should be 2325 gauge and length 1 inch Recommended site is anterior thigh or upperouter quadrant of the buttocks
Figure 25 P - 46 03/01/05
INTRAOSSEOUS INFUSIONS
Indications
Multi system trauma with associated shock and/or severe hypovolemia Unresponsive and in need of immediate drug or fluid resuscitation due to: burns cardiac arrest anaphylaxis neardrowning status asthmaticus severe dehydration associated with vascular collapse and/or loss of consciousness
Figure 25a
Contraindications
Fracture or crush injury to the same extremity Gross infection at the intended site of puncture Responsive patient (unless cardiac arrest is imminent)
Caution
No more than one insertion attempt per bone If the needle becomes obstructed, attempt to clear by flushing with saline. If this is unsuccessful, insert a clean needle of a smaller diameter through the center of the original needle Use of sterile procedure should be documented on the run report due to rare but serious side affect of osteomyelitis (inflammation of the bone, especially the marrow, caused by a pathogenic organism)
Figure 26
Procedure
There are two sites available for intraosseous infusion in the tibia. Children under seven years old, use the proximal tibia, which is located two finger widths below the tibia tuberosity on the anterior medial aspect of the leg (See Figure 25, 25a). Children over seven years of age, use the flat portion of the lower tibia approximately 2 cm above the medial malleolus (See Figure 26) due to the thickness of the proximal tibia compared to that of the distal tibia in that age group. Choose appropriate site and cleanse with antiseptic swab Insert the intraosseous needle, directed slightly inferior to avoid the epiphyses (See Figure 27), into the tibia using firm pressure and a boring motion until entering the medullary cavity which is noted by a lack of resistance. The needle will feel firmly fixed in place. Remove the stylet and attach a 3way stopcock with 10 cc syringe to the needle and flush. Look for infiltration around the site or no flow of the intravenous fluid. If either of these two are present discontinue the procedure, remove the needle and apply firm pressure for a minimum of 10 minutes. Once placement is confirmed, open fluid administration set. All fluids and medications may be administered via the intraosseous route. Secure the needle as you would an impaled object
Figure 27
INTRAVENOUS CATHETER INSERTION

Procedure
Explain the procedure to the patient Assemble the equipment needed appropriate infusion set intravenous fluid select the catheter to be inserted antiseptic swab 03/01/05 P - 47
Figure 28

tourniquet Apply tourniquet if appropriate Select a suitable vein Prepare the venipuncture site Scrub the area with antiseptic swab starting above the vein and wiping vigorously in widening circles Align the catheter. With the bevel up, enter the skin at a 3045 degree angle (See Figure 28). After entering the skin, lower the catheter to approximately a 15 degree angle to enter the vein. Enter the vein from the side or from the top. A pop should be felt upon entering the vein. Note blood return in the catheter. a bevel down technique may be used in pediatric patients or patients with fragile veins Slightly advance the catheter beyond this point to insure placement inside the lumen of the vein. Advance the catheter inside vein and withdraw the needle while holding the catheter steady. (A Venoject with adapter may also be used) If blood is required, it can be drawn from the IV catheter using a 10cc syringe, prior to attaching IV fluid tubing Release the tourniquet Attach the IV tubing, and allow unimpeded flow of the IV solution. The flow should be steady. If the fluid is unsteady in nature, the catheter tip may be against the vein wall; pull back slightly
Figure 29
INTRAVENOUS MEDICATION ADMINISTRATION

BOLUS Caution
Beware of run away IV flow rate Figure 30
Procedure
Verify the name and concentration of the medication; inspect the solution for discoloration, cloudiness, or particles; check expiration date Disinfect the drug administration port of the IV line using an antiseptic swab Uncap the needle Recheck the medication Insert the needle in to the administration port; take care not to jam the needle straight through and out the opposite side Pinch the tubing above the port to prevent back flow of medication into the IV bag (See Figure 29); inject the medication (See Figure 30) check the IV site for patency to prevent any medication infiltration Open the IV line clamp to flush any remaining medication from the IV line, reset the clamp to the proper flow rate
MUCOSAL ATOMIZATION DEVICE (MAD)

INTRANASAL DRUG DELIVERY
The nasal route is an attractive method of drug delivery due to the rich vascular plexus that is present within the nasal cavity and the easy accessibility of this vascular bed. Because of this easily accessed vascular bed, nasal administration of medications is emerging as a promising method of delivering medications directly to the blood stream. This method of delivery can eliminate the need for intravenous catheters while still achieving rapid, effective blood levels of the medication administered. P - 48 03/01/05
PROCEDURAL GUIDELINES Advantages

The rich vascular plexus of the nasal cavity provides a direct route into the blood stream for medications that easily cross mucous membranes. Due to direct absorption into the blood stream, gastrointestinal destruction and hepatic first pass metabolism (destruction of drugs by the liver enzymes) are avoided, allowing more drug to be bioavailable than if it were administered orally. For many medications the rates of absorption and plasma concentrations are relatively comparable to that obtained by intravenous administration. Ease and convenience: This method of drug administration is essentially painless, does not require sterile technique, intravenous catheters or other invasive devices and it is immediately and readily available in all patients. Due to the close proximity of the olfactory nasal mucosa to the central nervous system, CSF drug concentrations may exceed plasma concentrations, making this an attractive method of rapidly achieving adequate CSF drug concentrations for centrally acting medications.
Caution
Do not give more than 2ml of medication, more than that will just run out of the nose
Indications
Fast medication delivery for: Seizures Sedation Opiate overdose Hypoglycemia Intravenous access unobtainable or with a combative patient
Contraindications
Bloody nose Large volumes of mucous production
Medications able to be given intranasally

Ativan (Lorazepam) Glucagon Narcan (Naloxone) Versed (Midazolam)
Procedure
Draw desired amount of medication into a syringe with luer-lock tip Attach MAD nasal atomizer to syringe Place atomizer within nostril Briskly compress syringe to administer 1/2 of the volume as atomized spray Remove and repeat in other nostril, so all the medication is administered Reassess the patient and continue with treatment protocol
NEEDLESS IV SYSTEMS
Should be used when available. Reduces the risk of accidental needle sticks.
Components
Syringe Cannula For drawing and administering medications from an ampule. Blunt tipped. Vial Access Cannula 03/01/05 P - 49

For drawing and administering medications from a vial; pointed tip will remain in vial. Saline lock device (i.e. Multiaccess Port or MAP, Heplock) Used for precautionary IV access Threaded Lock Cannula or Lever Lock Cannula Used to secure IV tubing to saline lock device or medication access port on compatible tubing. Drug Vial Adapter Used on multidose vials for syringe cannula usage.
NERVE AGENT AUTO INJECTORS

The Paramedic may administer the prescribed nerve agent antidotes via an auto-injector for rescuers or patients who are exhibiting signs of organophospate poisoning. These signs include: pinpoint pupils, salivation, lacrimation, urination, defication, gastrointestinal discomfort, emesis, respiratory difficuty, seizures, coma, or death. The Nerve Agent Auto Injectors include the Mark I, Atropen, and the CANA Kit. These kits should be used as indicated in the Hazmat Section. Only the Atropen is available in pediatric dosages. EMTs may self administer.
Procedure
Primary Assessment Verify the appropriate dosage auto-injector based on age and weight, check expiration date. Ensure patient is exhibiting signs of organophosphate poisoning as described above. Remove auto-injector safety cap. Select appropriate injection site. Thigh lateral portion of thigh, midway between waist and knee. Buttock upper outer quadrant. Push auto-injector firmly against site until injector activates. Hold in place until medication is fully injected (minimum of 10 seconds). Record time. Dispose of injector in biohazard container. Reassess patient. Re-adminster per dosing schedule in Hazmat Section
NITROGLYCERIN IV
Indications
ST elevation in two or more contiguous leads of the 12 Lead EKG Continued chest pain partially relieved after 3 SL nitroglycerin when ST elevation is not present Congestive heart failure with moderate to severe dyspnea Hypertension with Physician Consult
Contraindications
Systolic blood pressure less than 100 mm/Hg Known allergy to nitrates Head trauma Hypovolemia
P - 50
03/01/05
PROCEDURAL GUIDELINES Caution

Low absorption tubing does not have to be used in order to deliver accurate amounts of the medication. The use of PVC tubing does not alter the dose being received by the patient. Utilize a double lumen catheter IV catheter or establish a second IV line. At the medic's discretion, IV Nitro may be piggybacked as a last resort if no other IV site is available. If this becomes necessary, piggyback the line at the lower hub of the regular tubing and use an 18 g needle advanced as much as possible through the lower hub. When transferring patient to ER staff be sure to close the lower roller clamp on the IV tubing. If this is not done a large bolus of Nitro will be administered to the patient with potentially disastrous results. Nitro is absorbed through the skin; use caution not to expose any unprotected skin to this medication
NITROUS OXIDE
NITRONOX
Nitronox is a mixture of 50% Nitrous Oxide and 50% Oxygen
Nitronox Equipment
Nitronox units are comprised of a Nitrous Oxide cylinder, a blending regulator and an Oxygen cylinder. The Oxygen cylinder may or may mot be part of the Nitronox unit. Some Nitronox units require a separate oxygen unit to connect the Nitronox unit. When turning the Nitronox unit on, turn on the Nitrous Oxide cylinder and the Oxygen cylinder. The blending regulator gauge should indicate green. This green zone indicates that the proper blending of Nitrous Oxide 50% with Oxygen is being maintained. Nitronox units that require a separate oxygen unit use a small Nitrous Oxide cylinder that is intended for single use. This will require that the Nitrous Oxide cylinder be changed after each use.
Indications
Nitronox is indicated for pre-hospital relief of pain.
Contraindications
Any altered level of consciousness (i.e. alcohol intoxication or drug overdose). Head injury Hypotension or shock COPD Acute PE Chest Trauma, especially pneumothorax Nausea and vomiting Decompression sickness Air embolism Abdominal pain with distension or suspicion of obstruction Pregnancy (except during delivery, if mother is stable). Patient is unstable to self-administer Nitronox.
Procedure
After the above contraindications have been excluded, Nitronox may be selfadministered by the patient. 03/01/05 P - 51

All vitals signs are to be monitored frequently and documented. The pulse oximeter should also be used. If the patients vital signs become unstable or the patient becomes symptomatic from the side effects, discontinue Nitronox. Whenever Nitronox is administered to a patient, the patient will be transported ALS. Patients will not be released to a BLS unit for transport. Nitronox should be considered a drug and as with any drug, complications may develop. Proper precautions should always be taken. The patient may also be given Oxygen via nasal cannula @ 4-6 LPM to maintain oxygen therapy when the Nitronox is not being administered by the patient.
PIGGYBACK
Indication
IV drug Therapy
Contraindications
Allergies to medication Infiltration at IV Site
Procedure
Prepare the necessary equipment Confirm that the patient is not allergic to medication Select the proper medication Verify the name and concentration of the medication; inspect the solution for discoloration, cloudiness, or particles; check expiration date Draw up medication / assemble prefilled syringe Clean the medication administration port on IV bottle/bag, with antiseptic swab Carefully add medication to bottle Mix the fluid by inverting the bottle several times Place label on bottle/bag, identifying the medication and concentration Connect the administration set using aseptic technique Flush IV line and expel air Attach needle to IV line; use luerlock application when available Clean medication port with antiseptic swab and insert needle Secure needle Stop flow of primary line Set pump infusion rate Monitor patient for desired affect
RECTAL MEDICATION ADMINISTRATION

Indications
For emergent medication administration when IV access is unobtainable in adults and children
Procedure
Place medication in a needleless syringe Attach the plastic catheter of a 14 gauge IV catheter on the end of the syringe Lubricate the catheter Insert catheter past anal sphincter Inject medication; withdraw syringe
P - 52
03/01/05
SALINE LOCK
Indications
Patients who need or require IV access, but will probably not require fluids Hemodynamically stable patients complaining of: COPD dialysis problems hypertension post seizure other precautionary IV access
Procedure
Cannulate vein, refer to INTRAVENOUS CATHETER INSERTION PROCEDURAL GUIDELINE (SEE PAGE P-47) Screw the saline lock onto the hub of the catheter Flush the saline lock with 23 cc of bacteriostatic 0.9% NaCl to confirm placement in the vein and to flush the saline lock and catheter of blood Fluids may be piggybacked to the saline lock if needed If medications are administered via the saline lock, flush the saline lock with 12 cc of NaCl after the medication is given
Figure 31
SUBCUTANEOUS MEDICATION ADMINISTRATION

Procedure
Figure 32 Explain the procedure to the patient Verify that the patient has no allergies to the medication Prepare a 1 cc syringe and attach a subcutaneous needle (short 2530 g) Verify the name and concentration of the medication; inspect the solution for discoloration, cloudiness, or particles; check expiration date Disinfect the site using an antiseptic swab With one hand, gently grasp the skin over the injection site and pull it away from the underlying muscle (See Figure 47) Insert the needle into the subcutaneous tissue at a 45 degree angle to the skin (See Figure 48) Gently pull back on the plunger to verify an artery or vein has not been entered; there should be no blood return Inject the medication Quickly withdraw the needle at the same angle it was inserted; apply firm pressure to the injection site Properly dispose of the syringe Monitor the patient for adverse reactions
UMBILICAL VENOUS CATHETERIZATION

Indications
Asphyxiated newborn Hypovolemia Last resort for venous catheterization 03/01/05 P - 53
EMERGENCY MEDICAL GUIDELINES Contraindications

NonSymptomatic newborn Other venous access available
Caution
Hypertension Thrombosis To far of a placement of the catheter, may irritate the liver Reassessment of vascular site for patent access IV overload
Procedure
Obtain the proper equipment needed for procedure Umbilical tape or equivalent Scissors Select appropriate size catheter (14g IV catheter, 5fr nasogastric tube) Appropriate infusion set Appropriate infusion fluid 3 Way stop cock (optional) Antiseptic swab
Application/Use (see figure below)

Prepare Equipment place newborn on a warm flat surface encircle the umbilical tape as close to the clamp and distal to the newborn, loose enough to control bleeding use aseptic technique to prepare site cut cord advance catheter into vein attach appropriate IV catheter set to catheter adjust umbilical tape to control bleeding, but not to constrict vascular access suture (if jurisdiction allow) into position and tape onto the abdomen to secure line monitor IV flow rate to avoid overload
P - 54
03/01/05
General
BLOOD ALCOHOL SAMPLING
Legal Interpretation
FS Chapter 316.1932(2)(f)(2) Only a physician, certified paramedic, acting at the request of a law enforcement officer, may withdraw blood for the purpose of determining the alcohol content thereof or the presence of chemical substances or controlled substances thererin
Caution
Drawing a blood alcohol sample SHOULD NOT DELAY TRANSPORT of the critical patient!
Procedure
The EMS run report shall contain the following information (if applicable) A blood alcohol kit was used Betadine (providone-iodine) solution (or hydrogen peroxide/acetone if allergic to iodine) was used for the skin preparation Name of the law enforcement officer requesting blood sample Time of draw If paramedic drawing samples is different from the one signing the report, that paramedic will sign under the above information All blood samples taken shall be surrendered to the requesting law enforcement officer The paramedic May be required to obtain multiple samples Shall obtain a minimum of two samples per person/per draw Shall render emergency medical service or treatment as necessary prior to the drawing of blood and alcohol samples Shall obtain alcohol samples only at the request of a law enforcement officer either in the field, upon arrival in the Emergency Department, or in the law enforcement facility
03/01/05
P - 55
BLOOD GLUCOSE LEVEL

This procedure is used as a gauge for treatment. Consider administration of D50 for any reading of 60 mg/dl or less. D50 use not considered in CVA unless reading less than 50mg/dl
Indications
Any change from the patients normal mental status Unconscious/unresponsive patients Stroke victims Alcoholic patients Seizure patients Patients with known diabetes, if the complaint warrants a glucose check
GLUCOMETER ELITE Application/Use

Insert the lancet into the glucolet pen Insert the test strip into the glucometer until an audible beep is heard Cleanse the finger with a antiseptic swab and allow to dry Perform a finger stick using a lancing device; dispose of the device once used If necessary, gently squeeze the finger to obtain a sufficient blood sample Touch the tip of the strip to the blood; the blood will be automatically be drawn into the test strip. Once the meter beeps remove the strip from the blood source. The blood glucose level will be shown after 60 seconds Once the blood is obtained remove and dispose of the strip and record the reading a reading of LO indicates a blood glucose level less than 40 mg/dl a reading of HI indicates a level above 500 mg/dl
ONE TOUCH Application/Use

Press the ON/OFF button to turn the meter on When the meter reads INSERT STRIP carefully remove a test strip from the package being careful not to touch the white test area, and insert into the meter Apply the blood sample to the white test area The meter will begin a count down and will show the results within 45 seconds the meter will show readings between 0600 mg/dL if the results are above 600 mg/dl the meter will read HIGH Clean unit after each use
BROSELOW PEDIATRIC EMERGENCY TAPE

Application/Use
Place the Broselow tape, with the multicolored side facing up, next to the supine child with the red tip at the head. Measure from the top of the head to the soles of the feet. Whichever color zone the bottoms of the child's feet align with will provide the appropriate size and type of airway equipment to be utilized. If patient's length falls at the extremes (upper or lower) of a respective color, consider the next closest color category and follow clinical guidelines. Immediately next to the color zones are the weight zones which provide the proper drug dosages for seizures, increased intracranial pressure, overdose, and cardiac resuscitation within a respective weight class. As with the color / airway zones, P - 56 03/01/05
consult the weight / dosage zone that aligns with the bottom of the patients feet. If the actual weight of the patient is available, however, use the tape as a calculator by going directly to the respective weight / dosage zone. On the opposite side of the tape are weight zones which, when measured against the supine child in the above described manner, provide the appropriate calculations for infusions, fluid volume expansion, paralytics, defasciculating agents and induction agents
COLIN BLOOD PRESSURE MONITOR

Indications
Continuous blood pressure monitoring
Caution
Unusual readings need to be confirmed with traditional procedures The machine will reinflate if the systolic pressure is high
Application/Use
Select the proper sized cuff Be sure the air line is without any kinks Turn the unit on and allow it perform its selftest Press the start button Adjust the interval times (5 to 10 min for stable patients) The alarm may be silenced by pressing the white alarm button The alarm limits may be adjusted
CRITICARE 506DX2 VITALCARE VITAL SIGNS MONITOR

Indications
Automatic monitoring of Noninvasive Blood Pressure (NIBP) and Pulse Oximetry (SpO2) Temperature monitoring (oral and rectal)
Caution
Use only Criticare blood pressure cuffs for accurate readings Prolonged use of blood pressure cuffs and pulse oximetry probes can cause tissue damage. Periodically check patient.
Procedure
1. 2. 3. 4. 5. 6. Turn power on and allow unit to selftest Blood Pressure Select proper size cuff and secure onto patients arm Make sure that there are no kinks or other obstructions in the hose Press the NIBP Start /Stop button to take the reading. Adjust the interval time
03/01/05
P - 57
EMERGENCY MEDICAL GUIDELINES Pulse Oximetry

1. Place the finger sensor on the patients finger with the LEDs positioned on the nail side. 2. Attempt to place sensor on the opposite extremity that the blood pressure cuff is on. 3. Reading will automatically appear
Temperature (if installed on machine)

1. Install the desired probe (blue for oral, red for rectal) 2. Place IVAC brand probe cover onto probe 3. Temperature will start to be taken when probe makes contact with tissue. 4. Temperature is done when you hear an audible tone and either F or C will be displayed with the reading. 5. Eject probe cover by pushing on the colored end of the probe.
DO NOT RESUSCITATE ORDER (DNRO)

WHAT TO DO
Get the original Florida Prehospital Do Not Resuscitate Order (DNRO), DOH Form 1896, Oct 93, or substantially equivalent. Copies of the form are acceptable. Validate the form for completeness patient or surrogates signature properly executed physicians signature properly executed Identify the patient photo identification (i.e. drivers license), or witness Provide any care and comfort measures indicated Document information effective date of DNRO witness used for identification (if applicable) attending physician name of patient or surrogate who signed DNRO attach original (or validated copy) DNRO to run report
DOPPLER MEDISONIC
Indications
Used for detecting very faint sounds (PEA, bruits, distal pulses, etc) Used in Obstetrics (fetal heart tones and stress detection during birth)
Application/Use
Sparingly apply ultrasound gel over the area to be assessed Place the doppler over the test site Press and hold the buttom until the audio is heard at a comfortable level Move the doppler in a circular motion until the desired sound is located
FOLEY CATHETERIZATION
Indications
To relieve bladder distention and maintain urinary tract patency, usually associated P - 58 03/01/05
with long patient transfers
Caution
This procedure requires the use of sterile technique, the provider must be familiar with the aspects of this techniques prior to attempting this procedure
Procedure
Obtain catheter insertion kit Explain procedure to patient Open catheter insertion kit and place in an accessible location Put on sterile gloves using sterile technique Place drapes over perineal area Examine catheter and check to see if it is securely attached to drainage bag and attach syringe with sterile water to injection port Apply lubricant to catheter tip Cleanse urinary meatus using cotton soaked with antiseptic solution femalesstart above the meatus and wipe downward to the perineum, repeat several times using a new cotton ball each time malescleanse in a circular motion from the meatus downward to the base of the glans, repeat several times using a new cotton ball each time Insert lubricated catheter tip into urethra and ask patient to take a deep breath and exhale slowly Advance catheter until urine is noted and advance approx. 23cm further to ensure balloon is in the bladder Inject the sterile water into the port and pull gently on the catheter until resistance is met Place drainage bag below level of the bladder Tape catheter to inner thigh and make sure the system drains freely Measure and document amount of urine output
MORGAN MEDIFLOW LENS

Indication
Anytime an eye injury needs to be irrigated.
Procedure
Insertion Apply topical anesthetic to eye, if available. Attach IV set or Morgan delivery set. Begin flow. Have patient look down, insert lens under upper eyelid. Have the patient look up, retract lower lid, and drop lens in place. Absorb outflow with towels or other cloth device. Removal Have patient look up, retract lower lid. Slide lens out.
03/01/05
P - 59
PHLEBOTOMY
Procedure
Assemble all equipment necessary for the procedure Explain the procedure to the patient Apply the tourniquet and visualize/palpate for a suitable vein Cleanse the venipuncture site using an antiseptic swab, moving in a circular motion from the center of the site to the outer portion of the site. Remember to cleanse the fingertip of the glove that is to used for palpating the site. Inspect the needle, syringe, or evacuated tube before performing the procedure Perform the venipunture using one of the following methods: evacuated tube method grasp the patient's arm firmly, using the thumb to draw the skin taut; the vein is entered with the bevel of the needle upward; one hand should hold the tube while the other pushes the tube onto the holder the tube should fill until the vacuum is exhausted and blood flow has ceased; if blood does not readily flow into the tube change the tube. If blood flow stops before an adequate amount of blood has been collected then pull back on the needle slightly once the tube has filled, pull the tube off the holder prior to exiting the vein to avoid developing a hematoma at the site syringe method this method should be used on patients with more difficult veins once venipuncture has been performed, if the blood flow stops, determine if the plunger is being pulled back too hard and adjust accordingly once the venipuncture is complete, the blood must be transferred to a tube (the top of the red top tube may be removed for filling) transfer the blood into a tube being certain not to force the blood into the tube (this could cause the tube to explode); hold the tube at a slight angle so that the blood flows down the side of the tube to avoid breakage of the blood cells other methods a winged infusion set with a vacutainer is generally used on pediatric patients and patients with very small/ fragile veins Once the procedure has been completed be sure to remove the tourniquet, place a dressing on the site and label the tube with the patient's name, date, time, and collector's initials All supplies should be disposed of properly ions chest trauma with dyspnea where inflation of the abdominal compartment will interfere with oxygenation distended abdomen (aortic aneurysm is possible exception)
P - 60
03/01/05
PROPAQ
CAPABILITIES:
ECG monitoring Respirations Noninvasive Blood Pressure(NIBP) Pulse Oximetry (Nellcor) Mainstream CO2
OPERATION:
Initial Power Up: Turn unit on by using on/off switch located on the right side panel Select patient mode (adult, child, infant) adult 9 years old child = 45 weeks to 9 years infant = neonate to 44 weeks To change mode, select: setup > more > change Unit is already set up for adult
MONITOR ECG:
Apply leads as in normal ECG Respirations: Respirations will automatically be recorded through the ECG
NIBP:
Place the proper sized cuff on the patients arm or thigh Auto or manual intervals may be set by: Pressing Auto/Man button Pressing Interval button to desired interval Pressing Start to initiate a measurement
RADIO COMMUNICATIONS
Standard rules for open air communications will be used, and the team is encouraged to keep radio air time to less than 30 seconds for routine encodes. Describe the problem in enough detail to explain treatment initiated and rationale for request, and to advise the hospital of the nature and seriousness of the patients problem so that they can be appropriately prepared for your arrival. Significant objective findings may need to take precedence over a detailed history.
SUGGESTED ENCODE FORMAT

Identify unit ID and paramedic/EMT name, priority/level of care, objective of communication (i.e. request for orders, notification, consultation, etc.) History to include patient description (number, age, sex), chief complaint, pertinent additinal symptoms, pertinent past history, pertinent medications Objective findings of patients current condition, level of consciousness, vital signs, EKG rhythm, pertinent findings Treatment in progress and response to treatment, requests Estimated time of arrival at ER
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RESPONDER INFLATABLE PEDIATRIC SEAT

Indications
Properly secure pediatric patients that weight between 20 and 40 pounds with a maximum height of 40 inches during transport to the Emergency Department. Note: The Responder Inflatable Pediatric Seat is certified for use in motor vehicles and aircraft. The kit contains one (1) pediatric seat, (1) 12volt DC pump, (1) I-clip, (1) corrugated hose.
Caution
Make sure the pump is switched off before plugging it into the cigarette lighter.
To Inflate
Connect one end of the corrugated hose to inflate on pump and the other end to the valve on the seat. You will hear a click when properly attached. Open the Pedi-Seat. Do not put anything on the seat during inflation. Turn the pump switch on and inflate for approximately 60 seconds (the sides will be firm and the bottom will be softer. Turn the pump switch off, unplug hose from seat and cap the seat valve. Secure Pedi-Seat to rescue. Use the I-clip if securing with a lap-shoulder belt.
To Deflate
Connect one end of hose to deflate on pump and the other end to the valve on seat. Some air will be released at this time. Make sure the pump is off before plugging into cigarette lighter. Turn the pump switch on and deflate for approximately 60 seconds. Turn the pump switch off, unplug the hose and cap the seat valve. Ensure seat is properly cleaned with mild soap / disinfectant such as Cidex Fold the seat and store all components in carrying case.
SUSPECTED CHILD/OTHER ABUSE

The State of Florida has strict concise laws regarding the reporting of suspected abuse and/or neglect of children, the elderly and the disabled. Should the team encounter a patient within one of these three groups whom they know or have reason to suspect has been abused or neglected, they have both a legal and moral obligation to report same. Suspected instances of abuse or neglect are to be reported. Even though local authorities have been advised, notification of DOH is mandatory (per state law). The following action shall be taken: Recognition of possible abuse or neglect Notify attending EDP and local law enforcement official Notify DOH Abuse Hotline 180096ABUSE Notify supervisor Complete written incident report (to be forwarded to DOH) Document notification steps on the completed run report Forward written incident report to administration as soon as possible
Figure 33
Figure 34 P - 62 03/01/05
THERMOSCAN THERMOMETER
Caution
The Pro2 should not be used on any patient's ear which exhibits symptoms of an acute or chronic inflammatory condition of the external ear canal Do not take a temperature on an ear that contains blood or purulent discharge
Application/Use
Make sure the thermometer is in the proper mode for the patient's age Install a cover on the probe by pressing the probe barrel straight down into the opened cover until you feel and see the cover seat securely, this will automatially turn the unit on All display segments will momentarily be displayed. When this is complete the display will show the temperature mode selected (i.e. ORAL F) and the word READY If the patient is under one year of age, pull the ear pinna straight back, insert the probe, carefully but firmly to seal the ear canal and press the top button (See Figure 33); the button should be held down for one second If the patient is over one year of age or an adult the ear pinna should be pulled both up and back (See Figure 34); the button should be held down for one second Eject the disposable probe cover by pressing the eject button
TRAUMADEX
INDICATIONS
Temporary treatment of severe bleeding
Contraindications
Not for intravenous application and should never be injected into blood vessels. Should not be used on sucking chest wounds, open brain injuries with exposed brain tissue, and open fractures with exposed bone.
Procedure
Tear open package and remove the cover, using a twisting and bending motion. Clean and remove excess blood from the wound site, using a sterile bandage or gauze. Identify the source of the bleeding, again removing any excess blood, then thoroughly cover the source and the wound bed with the TraumaDEX powder. Immediately reapply and maintain pressure at the source of the bleeding with a bandage or gauze
Other information
This is a singlepatient, single use product. TraumaDEX will not interfere with would treatment at the ED. Can be easily washed away without disturbing the clot. P - 63 03/01/05
Immobilization
AMBU PERFIT ACE
Collar Assembly
Hold collar near tracheal opening with one hand and place the index finger on the foam side of the chin piece and the thumb on the plastic side of the chin piece Simply flip the chin piece from the back of the collar to the front of the collar This automatically forms the chin piece and places it in position of function
Procedure for use

Have one rescuer gently hold the head and neck in neutral alignment Second rescuer applies the collar to the patient Collar comes packaged to a Neckless Size 3. If a larger size is needed, disengage safety locks by pulling up on the safety buttons. Simply pull the collar apart until the appropriate size is reached Reengage the safety locks by pushing down on the safety buttons If a smaller size is needed, disengage the safety locks and pull out the arrows. Adjust the collar to appropriate size then push in the arrows and reengage the safety locks.
CERVICAL IMMOBILIZATION DEVICE (C.I.D.)

Approved devices: Ferno CID, Headbed II, Sta-Blocks
Indications
Used in conjunction with a rigid cervical collar to secure a patients head to a long spine board or similar device, when a neck injury is suspected
Application/Use
Apply a rigid cervical collar per guidelines Transfer the patient to a backboard using accepted technique Position approved device under the patients head and affix to the board (Ferno CID is attached to the board prior to patient transfer and is reusable) Position support blocks or side panels against the head on each side Ferno CID only- the angled side of the support blocks may be placed next to the patients head in cases where inline position cannot be maintained and the patient must be immobilized in position found Maintain neutral alignment of the head and neck and use straps provided to secure patient to the device Clean or dispose of the devices per department guidelines
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HALF BACK EXTRICATION/LIFT HARNESS

Indications
The LSP Half Back (See Figure 35) is a versatile, short body immobilization board designed for suspected cervical/ spinal injuries during confined space extrication, i.e. auto accident, storage tank, sewer, construction area, etc. This device will be employed when a patient has a suspected cervical/spinal injury and must be extricated from any position other than lying (where the patient could be log rolled directly onto a backboard) except as noted below
Caution
The device is applied quickly with very little time cost, but a patient with immediate life threatening injuries is extricated directly without employing the Half Back (at the discretion of the onscene medical authority)
Application/Use
Manual Cspine immobilization Ccollar applied Remove any eyeglasses and articles from shirt pocket(s) Open Half Back, remove head harness, do not remove straps from pockets Insert Half Back behind patient Position sides under patient's arms Release padded leg straps to expose torso strap pockets Connect torso straps (color coded); leave loose Connect shoulder straps (color coded); adjust to bring sides of Half Back against patient's underarm Tighten torso straps Remove a leg strap from pocket; place webbing portion (not padding) under patient's leg at knee; work webbing back and forth under leg to the groin area; pull padded section under leg; connect (color coded) and tighten strap; repeat with other leg Disengage velcro from chin and forehead strap on head harness; grasp head harness by velcro flaps that attach harness to Half Back; position top of head harness to patients head; secure velcro flaps to Half Back; secure forehead strap (near eyebrows); secure chin strap Release manual Cspine immobilization Extricate patient Place patient on backboard/Miller Board Loosen leg straps Secure patient on backboard/Miller Board
Figure 35
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KENDRICK EXTRICATION DEVICE (KED)

Indications
The KED (See Figure 36) device is employed when a patient has a suspected cervical/spinal injury and must be extricated from any position were the patient cannot be directly placed (log roll or standing) onto a backboard.
Caution
The device is applied quickly with very little time cost, but a patient with immediate life threatening injuries is extricated directly without employing the KED (at the discretion of the onscene medical authority).
Application/Use
Establish manual cervical support Apply cervical collar Maintain inline cervical support Move patient's torso forward as a unit Place the KED behind the patient, ensuring it is all the way down to the seat Position side flaps under patient's armpits and around torso Fasten the mid torso strap Fasten the lower torso strap Position and fasten the groin straps Pad any space between the occiput and the upper portion of the KED Attach the forehead strap Attach the lower strap around the collar roller bandage (Kling) may be used in place of head straps as long as it secures the head in the same manner as the straps Fasten the upper torso strap Check all straps to ensure they are snug Loosen groin straps when placing patient supine for immobilization
Figure 36
LONG SPINE IMMOBILIZATION

Indications
Any patient of an MVA, fall, or where mechanism of injury suggests possible spinal injury Any trauma patient who complains of pain in the head, neck, or back Any trauma patient who may have injury to the spine but in whom evaluation is difficult due to altered mental status (i.e. drugs, alcohol, unconsciousness)
Application/Use
Manual Cspine immobilization Ccollar applied Halfback/KED applied (if applicable) Position rescuer 1 at the head of patient (maintaining Cspine), rescuer 2 at the shoulders, rescuer 3 at the hips; backboard is place alongside the patient Rescuer 1 commands all movements Log roll placement rescuer 1 makes a preparatory count to three and the patient is gently log rolled up on the three count; Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral Cspine alignment
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the backboard is slid into place by Rescuer 3 (with one hand) or by additional personnel rescuer 1 makes a preparatory count to three and the patient is gently log rolled down on the three count; Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral Cspine alignment Alternative placement techniques standing sliding placement with scooptype device Double X Strapping there are four preconnected female straps attached to the long board. Two are placed over the shoulders and onto the chest, with the other two attached at mid chest (just under arm pit). there are four male straps with speed clips. Two are to be speed clipped to the pins by the patients's upper thighs and crisscrossed to the shoulders. The other two males will be speed clipped to the pins by the patient's ankles and crisscrossed to the females at mid chest (just under arm pit). Single X Strapping same as Double X Strapping except uses a single X strap method on the top and a single horizontal strap across the lower extremities Apply Cervical Immobilization Device Release manual Cspine immobilization; patient is ready for transport Remember that the head is only immobilized after the body has been immobilized.
Helmet Removal
Important Points About Helmet removal Athletes wearing both helmets and shoulder pads (Football, Hockey and Rugby) are another special set of patients. Helmets used in different sports present different management problems for rescuers. The above-mentioned helmets are custom fitted to the individual and are therefore more difficult to remove. Unless special circumstances exist, such as respiratory distress coupled with an inability to access the airway, THESE TYPE HELMETS SHOULD NOT BE REMOVED IN THE PREHOSPITAL SETTING. The athlete wearing shoulder pads has his neck in a neutral position when lying supine with a helmet in place. Athletic helmet design will generally allow easy access once the face guard is removed. The face guard can easily be removed with a screwdriver or a pair of trauma scissors. On occasion, face guard screws may be rusted and you will be unable to remove it in the normal fashion. This occurs predominately with adolescents and nonprofessional athletes. In this case, the helmet must be removed and padding must be inserted under the head to keep the neck from hyperextending, or the shoulder pads must be cut away and removed. After arrival at the emergency department the C-spine can be x-rayed with the helmet in place. Once the spine is evaluated, the helmet can be removed by stabilizing the head and neck, removing the cheek pads, releasing the air inflation system, and then sliding the helmet off in the usual manner. In contrast, motorcycle helmets often must be removed in the prehospital setting. The removal technique is modified to accommodate the different designs. Motorcycle helmets are often designed with a continuous solid face guard that limits airway access. These helmets are not custom designed and frequently are poorly fitted to the patient. Their large size will usually produce significant neck flexion if left in place when the patient is placed on a backboard. Motorcycle accidents are usually associated with much more violent forces than are athletic injuries, The motorcycle helmet will make it 03/01/05 difficult to
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stabilize the neck in a neutral position, may obstruct access to the airway, and may hide injuries to the head or neck; MOTORCYCLE HELMETS SHOULD BE REMOVED IN THE PREHOSPITAL SETTING.
Removing A Motorcycle Helmet From A Patient With A Possible Cervical Spine Injury
Position yourself above or behind the patient, place your hands on each side of the helmet, and immobilize the head and neck by holding the helmet and the patients neck Your partner positions himself to the side of the patient and removes the chin strap Chin straps can usually be removed easily without cutting them. Your partner then assumes the stabilization by placing one hand under the neck and the occiput and the other hand on the anterior neck with the thumb pressing on one angle of the mandible and the index and middle fingers pressing on the other angle of the mandible You now remove the hekmet by pulling out laterally on each side to clear the ears, and then up to remove. Tilt full-face helmets back to clear the nose (tilt the helmet, not the head) If the patient is wearing glasses, remove them through the visual opening before removing the full-face helmet. Your partner maintains steady immobilization of the neck during this procedure After removal of the helmet, you again assume immobilization of the neck by grasping the head on either side with your fingers holding one angle of the jaw and the occiput Your partner now applies a suitable rigid extrication collar.
MILLER BOARD
Indications
Any victim of trauma with obvious neurological deficit such as paralysis, weakness, or paresthesia (numbness or tingling) Any victim of trauma with severe facial or head injuries Any victim of trauma to multiple systems Any victim of trauma in critical condition (priority one or two) or is unconscious
Contraindications
Patient weight greater than 250 pounds Children less than 65 pounds
Caution
Overtightening straps may obstruct chest expansion or inhibit respiratory effort
Application/Use
Manual Cspine immobilization Ccollar applied Halfback / KED applied (if applicable) Open harness system and place board alongside the patient Position rescuer 1 at the head of patient (maintaining Cspine), rescuer 2 at shoulders, rescuer 3 at the hips Rescuer 1 commands all movements Rescuer 1 makes a preparatory count to 3 and the patient is gently log rolled up on the three count. Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral Cspine alignment. The Miller Board is slid into place by Rescuer 3 (with one hand) or by additional personnel. The shoulder pins of the board are aligned with the top of the patient's shoulders; this03/01/05 alignment is essential to providing proper Tspine immobilization.
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Rescuer 1 makes a preparatory count to three and the patient is gently log rolled down on the three count. Rescuers 2 and 3 perform the roll while Rescuer 1 maintains neutral Cspine alignment. Place the chest strap loosely over the patient's chest, excluding the arms, and thread through the pin. Thread both shoulder straps through their corresponding pins and leave loose. Position shoulder straps based on anatomical considerations and the condition of the victims chest. Tighten the chest strap; tighten the shoulder straps Thread and tighten the lower torso strap; patient's hands may be placed inside or outside of strap based on patient consideration Thread and tighten the leg and ankle straps Disengage velcro from chin and forehead strap on head harness; grasp head harness by velcro flaps that attach harness to Miller Board; position top of head harness to patient's head; secure velcro flaps to Miller Board; secure forehead strap (near eyebrows); secure chin strap Release manual Cspine Extricate patient; patient is ready for transport
NAJO PEDIAIRALIGN BACKBOARD

Indications
Infants and children needing cspine immobilization Weight rating up to 100 pounds
Strapping Technique
Chest straps crisscross across patients chest Remainder of straps go across the body Wrist restraints can be used if needed.
Broselow Color Coding

If the board is equipped with the Broselow Color Coding and the top of the patients head starts in the brown area, follow the colorcoding down the patients left side of the board. If the top of the patients head starts in the green area, follow the color-coding down the patients right side of the board.
RIGID CERVICAL COLLAR

Approved devices: Stiffneck, Stiffneck Select, SureLoc, WIZLoc and Philadelphia
Indications
Suspected cervical injury. All approved rigid cervical collars are designed to limit movement of the cervical spine in all patients in whom a cervical injury is suspected.
Caution
These devices must always be used in conjunction with other immobilization adjuncts. Proper sizing is critical for good patient care, improper sizing can cause hyperextension or lack of support.
Procedure Sizing
All approved devices rely on the same key dimension in sizing (figure 37,38,39) 03/01/05
Figure 37 P - 69

The key dimension is the distance between the top of the patients shoulders where the collar will rest and the bottom plane of the patients chin (angle of the jaw)
Stiffneck, Stiffneck Select and Philadelphia

While the patients head is being held in neutral alignment use finger width to visually measure the distance from the shoulder to the chin (key dimension) Use the finger measurement to select the collar size or adjustment that matches the key dimension Maintain neutral alignment of the head throughout application Position the chin piece by sliding the collar up the chest wall. Be sure the chin extends far enough onto the chin piece to cover the central fastener. Difficulty in positioning the chin piece may indicate the need for a shorter collar Slide the back portion of the collar behind the patients neck and affix the hook and loop fastener strap to the collar, the strap should be snug enough to maintain the chin piece in position Ensure that the chin piece stays in position during the application
Figure 38
SureLoc and WIZLoc

Maintain neutral alignment of the head throughout application The key dimension on the collar is the distance between sizing indicator and the lower rigid plastic band, not the foam padding WIZLoc OnlyPre adjust the occipital support based on visual inspection of the neck (Thick, Regular or Tall) Position the chin piece under the patients chin Slide the back portion of the collar behind the patients neck and loosely affix the hook and loop fastener strap to the collar Hold the bottom of the collar downward in contact with the patients chest Raise the mandibular support until contact is made with the chin (do not exert upward pressure on the chin, the may cause further injury to the patient), lock the support in position Adjust the hook and loop fastener snug enough to maintain the chin piece in position SureLoc OnlyAdjust the occipital support until contact is made with the patients occiput (do not exert upward pressure after contact with the occiput is made, this may cause further injury to the patient), lock the support in position Ensure that the chin piece stays in position during the application Clean or dispose of collars according to department guidelines
Figure 39
PATIENT RESTRAINTS
Restraints have the potential to produce serious consequences such as physical and psychological harm, loss of dignity, violation of an individuals rights, and even death. Accordingly, the use of restraints will be limited to situations where other treatment interventions have clearly failed to address the patients presenting clinical needs and safety. Examples of alternative interventions may include but are not limited to utilization of adjustable stretcher restraint straps, soft roller bandage to cover and protect IV sites. Restraint is any method of physically restricting a persons freedom of movement, physical activity or normal access to his or her body.
Indications
Patients with Endotracheal tubes/trachs Patients with Invasive Catheters, lines and tubes Patients with Brain pathologies or injury P - 70 03/01/05
Patients who are violent or could inflict potential harm to self or others due to an impaired psychological state and/or substance abuse
Contraindications
The potential risks of restraints are believed to be offset by the potential benefits of a better patient outcome (such as the patient being safer from activities and behaviors that could cause physical harm and lead to a chance of increased morbidity) as well as being safer for crew members.
Caution
Loss of pulses, capillary refill and sensation can occur if restraints are overtightened Neurovascular exams shall be performed at 5 minute intervals during restraint
Procedure
Explain reason for restraint to the patient, family, or significant other, prior to being initiated. Reassure the patient that this is not a punishment, but a safety precaution. Select the appropriate restraint, this should be adjusted to provide for patient comfort, but secure enough to assure effectiveness of device Apply according to the manufacturers instructions. When wrist restraints are used cocurrently with ankle restraints, the restraint should be applied to one arm and the opposite leg (two point restraint) or to all four extremities (four point restraint) you should be able to slip one finger between the restraint and the patients skin. Tie with easily released hitches (Quickrelease knots) out of patients reach. Position patient to prevent aspiration and to allow visual contact, maintain proper body alignment. Check pulses below the point of restraint to ensure circulation Check restraint integrity
PEDIATRIC PATIENT IMMOBILIZATION

Indications
Spinal immobilization, of pediatric patients who fit within the height and weight guidelines specific to the brand of pediatric immobilizer used A.A. Kinder (See Figure 40) infants and children up to 60 pounds Ferno PediPac (See Figure 41) patients 2854 inches, and between 2090 pounds LSP PediImmobilizer (See Figure 42) infants and children up to 75 pounds Figure 40
Application/Use
While applying gentile inline manual Cspine , immobilize the patient's head and neck (cervical spine) with a cervical collar or similar device. Do not release until immobilization is complete. Place the immobilizer behind the patient for extrication (if applicable), or beside them if application is only for a backboard type use. For this type of application, a proper log rolling technique should be used. While continuing manual cspine, apply the straps to the body and extremities Secure the head with the CID, supplied by the manufacturer, and release manual c spine Device should be secured to either stretcher or bench seat, prior to transportation Figure 41
Figure 42
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SPIDERTYPE PATIENT STRAP

Procedure
Lay strap over patient with V toward the head and feet and centered on body Open Velcro straps Secure top V strap over patient's shoulders and through backboard Secure center body straps through backboard openings: top strap over mid chest mid strap over pelvis lower strap over thighs above the knees Secure lower V strap around ankles and through the backboard Ensure all straps are snug before moving patient
SPLINTING
The decision to splint should be based upon patient condition. When patient condition warrants load and go, transport should not be delayed to splint extremity fractures. In the stable trauma patient, extremity fractures should be splinted prior to moving the patient.
Caution
Loss of pulses, capillary refill, movement and/or sensation can occur if the splint is overtightened or overinflated Care should be taken to carefully assess circulation, sensation and movement prior to and after splinting. If there is a loss of circulation after splinting make one attempt to realign the injury and reassess. Gross angulation of limbs that require alignment in order to stabilize, should be realigned along the long axis of the limb. Close straps and evacuate air from splint; discontinue air evacuation when splint is rigid Further immobilize as needed Reassess circulation, sensation and motor function
Procedure
Remove or cut away clothing to expose area of injury Control active bleeding Check distal pulses, capillary refill, sensation/movement prior to splinting if distal pulses are absent in fractures or dislocations, one attempt to place the injury into anatomical position, may be attempted (consider pain control) Open wounds should be dressed and bandaged Use the most appropriate splint to immobilize the joint above and below the fracture site Dislocations should be immobilized to prevent any further movement of the joint Check distal pulses, capillary refill, sensation, and motor function after splinting
VACUUM SPLINT Indications

Any extremity fracture or injury
Procedure
Take CSpine precaution as indicated by mechanism of injury Manually stabilize the extremity Expose the injury P - 72 03/01/05
Assess circulation, sensation and motor response Choose appropriate size vacuum splint and form to injury; consider application of ice or cold pack to injury Close straps and evacuate air from splint; discontinue air evacuation when splint is rigid Further immobilize as needed Reassess circulation, sensation, and motor function
STA-BLOCK HEAD IMMOBILZER

WARNING
In cases of suspected spinal cord injury, proper immobilization is only one part of the total immobilization. It is imperative that the patient be properly immobilized to prevent any movement of the spinal column.
POSITIONING THE STA-BLOK OCCIPITAL PAD

Remove the occipital pad from the package and place pad under patients head while maintaining neutral alignment of the patients head and neck. Center the pad at the patients temporal area. While holding the Sta-Blok occipital pad in place, pull the release liner to expose the adhesive backing material. After removing the release liner, press down firmly on the occipital pad.POSITIONING SIDE SUPPORT BLOCKS Place side support blocks against the head just above the patients ears and press the hook down on the occipital pad.
SECURING PATIENTS HEAD

Take the soft white strap material and attach to the Sta-Blok support blocks with the hook. Make sure the strap goes over the forehead.
FOR EXTRA SUPPORT AS CHIN STRAP or FOR PATIENT WEARING HELMET

Severe weather strap will also be used, in addition to the hook and loop strap, around patients neck for extra stability. Because of its length, the severe weather strap is ideal for use with a patient wearing a motorcycle or football helmet. The patients face and airway must be accessible at all times.
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Multiple Casualty Incidents

The Multiple Casualty Incident can be effectively managed if the appropriate command is established and necessary resources committed. The difficulty lies in recognizing the size of command structure and quantity of resources needed for small to medium size inidents. This guideline quantifies command structure size and function based on the number of medical units responding to a given incident and/or the number of persons involved. This method will eliminate the possibility of too small a command structure for incoming units and will help avoid confusion. The triage system used with the MCI guideline is the START Method. This method will allow rapid triage to be performed in an efficient manner. The unit responses defined in the following MCI Level declarations are additional to the initially assigned ambulance.
LEVEL 1 RESPONSE
Defined as a single additional ambulance response, OR Incident involving 59 persons
COMMAND
Incident Command established per Department SOG
COMMUNICATIONS
Request designation of staging area from Command Assign tactical channel Notification only to local hospital Notification of EMS and shift supervisor
TRIAGE
Performed by senior medical officer or designee Triage tagging not performed Patient log not used
TREATMENT
Initiated at patient location Package per guidelines
SUPPORT PERSONNEL
One engine
LEVEL 2 RESPONSE
Defined as a two or three additional ambulance response, OR Incident involving 1020 persons
COMMAND
COMMUNICATIONS
Request designation of staging area from Command Assign tactical channel Notify closest 2 hospitals, request number of patients they can receive Notification of EMS and shift supervisor
MEDICAL COMMAND
Medical Command established by senior medical officer and reports directly to Incident Commander or Operations (if established) Management of patient area; refrain from patient involvement until all patients triaged Medical command assumes triage, treatment and transport officer roles Coordinates triage Establishes patient log P - 74 03/01/05
Additional resources should be requested through Incident Command and given access and assignment instructions Assign resources to triaged patients based on priority
TRIAGE
Triage performed by designee of medical command Perform appropriate triage Note location of patient on tag (i.e. driver red vehicle) Triage results are reported to medical command
SUPPORT PERSONNEL
Two or three engines
LEVEL 3 RESPONSE
Defined as a four or greater ambulance response, OR Incident involving more than 20 persons
COMMAND
COMMUNICATIONS
Request designation of staging area from Command Assign tactical channel Notify closest 3 hospitals, request number of patients they can receive Notify additional hospitals as needed Notification of shift supervisor
MEDICAL COMMAND
Medical Command established by senior medical officer and reports directly to Incident Commander or Operations (if established) Assign Triage Officer to establish Triage group Identify areas to be used for treatment Identify ambulance transport staging area (coordinated with Incident Command) Assign Treatment Officer to establish Treatment area in preselected location (8 or more patients) Assign Transport Officer to establish Transport area in preselected location (8 or more patients) Assign Medical Communications Officer (as needed; Transport Officer may double as Medical Communications in smaller incidents)
TRIAGE
Triage performed by Triage Officer and/or designee(s) when possible, patients are triaged where found and moved to appropriate treatment area; it may be appropriate to establish a triage area where patients are first moved from the incident site, triaged, then moved to appropriate treatment area All patients should be tagged with priority only for tracking Keep tally of total number of patients triaged and number assigned to each category Report patient numbers to Triage Officer at regular intervals Repeat triage sequence to monitor changes in condition If time and circumstances allow; perform more detailed assessment and write information on the tag while the Treatment group continues to move patients out of the triage area Depending on the incident size and available number of tags, colored tape may be substituted 03/01/05 P - 75
TREATMENT
Establish patient treatment area after conferring with Medical Command regarding location Assemble Treatment group personnel into two subgroups, one to perform basic packaging in triage area and then move patients to Green, Yellow or Red treatment areas and one to provide treatment within the treatment area so packaging groups may Treatment personnel should continue evacuating patients from the triage area fill out triage tag information as completely as possible noting patient, assessment and treatment information Uninjured victims should be kept in the Green treatment area until evaluated and released at the appropriate time by the Transport Officer (who must log all patients) or taken in a controlled manner away from the incident by the Transport Group A patient whose condition changes inside the treatment area should be moved to the appropriate Green, Yellow or Red area Name of person providing treatment should be noted on triage tag
TRANSPORT
Establish loading zone after conferring with Medical Command regarding location; consider proximity to treatment area and ambulance approach and exit routes Make sure transport personnel stay with their vehicles Assign patients from treatment areas to ambulances for transport Determine patient destination through coordination with Medical Communications Officer Only two stretcher patients and one ambulatory patient (in front seat) per ambulance Attempt to assign one Red, one Yellow and one Green patient per ambulance Do not assign more than one Red (priority 1) patient per ambulance As patients are queued for transport, separate transport control portion of triage tag Triage tag remains with patient for transport Supervise the actual loading of patients; if necessary, delegate the loading of ambulatory patients on buses As patients are loaded, give the transport control portion of the triage tags to the Medical Communications Officer and advise ambulance unit and destination Keep a unit ready for loading in the loading zone Do not allow patients to stack up in the loading zone
MEDICAL COMMUNICATIONS OFFICER

Record all patients and disposition in patient log Ensure all patients accounted for when loaded ambulance departs; request another ambulance move into loading zone from ambulance staging area unit, total number of patients, priority and brief description (chief complaint) of each patient's condition Transporting units should not communicate directly with the receiving hospital unless the condition of the patient deteriorates and Medical Control contact is necessary for the management of the patient
SUPPORT PERSONNEL
Must be scaled to the size and nature of the response Consider the following needs: number of personnel (command, medical, fire, law enforcement) number of engines special needs (buses, heavy equipment, etc.) P - 76 03/01/05
INTERFACILITY TRANSPORTS
Purpose
A patient may be transferred to another hospital if: The patient, family, or personal physician desires The sending physician must be in compliance with EMTALA guidelines on patient transfers, if the trip is a transfer as defined by EMTALA. Completion of the Physicians Certificate of Transfer form accomplishes this purpose. This transfer is arranged as a physician to physician transfer. Either the attending physician, or the Emergency Department Physician are authorized to arrange such transfers. Communications will verify acceptance of the patient by the receiving facility before the patient is moved.
Procedure
Transport caregivers must receive a thorough and complete summary of the patients condition, current treatment, possible complications, and other pertinent medical information. Patient ID must be verified. Transfer papers (summary, lab work, H&Ps, consults, x-rays, cath films or CDs, etc.) should be given to the paramedic. If the patient has DNR orders, the original should always accompany the patient, once he or she is discharged. Treatment orders should be given to the paramedic. These orders should be in writing, or direct verbal order from the doctor who is initiating the transfer. All Code Three transports must have at least one IV access before going enroute. The only exception would be for a pediatric patient where the physician has determined that an IV would be detrimental to the patient. A specialty team member should accompany any patient whose needs exceed the scope and training of the transport personnel, e.g. obstetrics, neonates, or criticalcare. If the hospital denies the request for additional personnel, the Medical Director, or supervisor should be contacted immediately. All medicated IV drips should be controlled by a battery-powered IV pump, with the only possible exceptions being vitamin or electrolyte drips.
EMTALA Transfer Criteria

EMTALA: EMERGENCY MEDICAL TREATMENT AND ACTIVE LABOR ACT All previous references to COBRA have been replaced by EMTALA. At the time of this writing, new definitions and interpretations of this act are in the process of determination, and are essentially in a state of flux that is not likely to be resolved completely in the near or distant future, as change is a part of the nature of social legislation. Although it has been designed to cover emergency transports, whenever you have any doubt in your mind about the nature of a transport, a supervisor, or the Medical Director should be consulted. Transferring physician certifies the need/risk/benefits of transport. The patient must be accepted at the receiving facility, and has a designated accepting physician. The patient (or surrogate) agrees to the transfer. The level of care to be provided is specified and appropriate to the patients condition to treat any reasonably foreseeable complication during transport. All orders from the transferring (sending) physician are clearly specified in writing and are appropriate for the level of training of the attending personnel and equipment provided.
Ob Triage Guidelines
The final decision with acceptance of an OB transport rests with the supervisor of MD. 03/01/05 P - 77
EMERGENCY MEDICAL GUIDELINES Routine Interfacility Tranports

Routine Interfacility transports by private providers characteristically do not destinate in the ER. For this reason, normal communications via Medcom for physicians orders are not appropriate. If specific orders are not secured from the sending physician prior to transport, arrangements should be made to contact the appropriate physician via cell phone, or through dispatch as needed. The other alternative is to provide direct communications with the providers Medical Director for physicians orders as needed. Because the documentation of medical necessity for authorization (especially by Medicare) of interfacility transports is done post facto, it is essential that copies of the History and Physicals, Consultations, laboratory results, Nursing Notes, Discharge Planners instructions and Interfacility Transfer Summary be included with the patient care report. ICD-9 Codes are generally more geared toward prehospital, rather than interfacility transports. BLS transports, in most cases can only be justified by documentation of underlying conditions still present at the time of transport that support evidence that transport by other means is medically contraindicated.
Arterial Lines Procedure

Make sure that the line remains open at all times by insuring that the pressure infuser has approximately 300mm Hg pressure on the bag at all times. Flush the line by squeezing the flush valve. Periodically check the integrity of the tubing and all connections to the catheter, as well as catheter placement to avoid a bleed-out from a disruption of the system. Monitor the patients hemodynamic and perfusion status. If the catheter should dislodge, hold direct pressure and treat as an arterial bleed.
Specialty Team Transports

During specialty transports, patient care is to be provided by the Specialty Transport Team. The EMS Team should assist within their level of training. Although the Specialty Transport Team is directly responsible for the care of the patient, the EMS Paramedic is nonetheless responsible for a full and complete Patient Care Report, including vital signs and an assessment consistent with state standards Balloon Pump for documentation.
Procedure
All balloon pump transfers require additional manpower. An RN, Perfusionist, Critical-Care Paramedic or Respiratory Therapist trained in balloon-pump operation should accompany the crew. Modern balloon pumps no longer mount to the bottom of the stretcher and are self-standing units with their own set of wheels. Every effort must be taken to ensure that the members of the team transfer the stretcher, patient, and pump as a unit. Special care must be given to insure that the balloon pump is moved with the patient in a manner so as to prevent any compromise of the electronic and pressure lines connecting the balloon pump to the patient.
P - 78
03/01/05
JUMP START PEDIATRIC TRIAGE

Step 1 All children who are able to walk are directed to the area designated for minor injuries, where they will undergo secondary (more involved) triage. At a minimum, secondary triage should consist of the RPM components of the JumpSTART algorithm. Infants who are developmentally unable to walk should be screened at the initial site (or at the secondary triage site for green patients if carried there by others), using the JumpSTART algorithm. If they satisfy all of the physiologic delayed criteria (i.e., fulfill no immediate criteria) and appear to have no significant external injury, infants may be triaged to the minor category. NOTE: Children with special health care needs are often chronically unable to ambulate. These children can be triaged similar to infants who are developmentally unable to walk. Respiratory and circulatory parameters remain unchanged, although those with chronic respiratory problems may routinely have elevated respiratory rates. Neurological status may be difficult to judge due to lack of knowledge of a given patients baseline function. A caregiver with knowledge of the children involved would be of invaluable assistance in this case, usually in the secondary triage stage. Be on the lookout for information about special needs children. There is a trend favoring brief medical data cards to be stored in the drivers area of buses and other vehicles routinely transporting children with special health care needs. Step 2A Nonambulatory pediatric patients are initially assessed for presence/absence of spontaneous breathing. Any patient with spontaneous respirations is then assessed for respiratory rate (see Step 3). Any patient with absolute apnea or intermittent apnea (periods of more than 10 sec.) must have their airway opened by conventional positional techniques, including (limited) BLS airway foreign body (FB) clearance only if there is an obvious FB. If the patient resumes spontaneous respirations, a red ribbon (immediate) is applied and the triage officer moves on. Step 2B If upper airway opening does not trigger spontaneous respirations, the rescuer palpates for a peripheral pulse (radial, brachial, pedal). If there is no peripheral pulse, the patient is tagged as deceased (black ribbon) and the triage officer moves on. Step 2C If there is a palpable peripheral pulse, the rescuer gives 5 breaths (about 15 sec.) using mouth-to-mask/barrier technique. This is the pediatric jumpstart. One mask (with one-way valve) should be available on every potential first-in EMS unit. (An adult mask may be used for a child if inverted.) Ventilatory face shields such as those marketed for CPR classes and public use may also be used. Crosscontamination is a minimal issue, as this is already occurring because triage personnel do not change gloves between patients. Also, children are somewhat less likely to have dangerous transmissible diseases and the number of children satisfying the criteria for a ventilatory trial will be relatively small. If the ventilatory trial fails to trigger spontaneous respirations, the child is classified as deceased. If spontaneous respirations resume, the patient is tagged as immediate and the triage officer moves on without providing further ventilations. The child may or may not still be breathing on arrival of other non-triage personnel. Appropriate intervention can then be determined based upon the resources available at the designated treatment site.
03/01/05
P - 79

Step 3 All patients at this point have spontaneous respirations. If the respiratory rate is roughly 15-45 breaths/min proceed to Step 4 (assess perfusion). If the respiratory rate is less than 15 (slower than one breath every 4 seconds) or faster than 45 or very irregular, the patient is classified as immediate (red ribbon) and the triage officer moves on. Step 4 All patients at this point have been judged to have adequate respirations. Assess perfusion by palpating peripheral pulses on an (apparently) uninjured limb. This has been substituted for capillary refill (CR) because of the variation in CR with body and environmental temperature and because it is a tactile technique more adaptable to poor environmental conditions. If there are palpable peripheral pulses, the rescuer assesses mental status (Step 5). If there are no peripheral pulses, the patient is categorized as an immediate patient (red ribbon) and the triage officer moves on. Step 5 All patients at this point have adequate ABCs. The rescuer now performs a rapid AVPU assessment, keeping in mind the apparent developmental stage of the child. If the patient is alert, responds to voice, or responds appropriately to pain (localizes stimulus and withdraws or pushes it away), the patient is triaged in the delayed category (yellow ribbon). If the child does not respond to voice and responds inappropriately to pain (only makes a noise or moves in a nonlocalizing fashion), has decorticate or decerebrate posturing, or is truly unresponsive, a red ribbon (immediate) is applied and the triage officer moves on.
P - 80
03/01/05
SIMPLE TRIAGE AND RAPID TREATMENT (START)

The system is a method of triage that is proved to be very effective and is based on three observations(i.e. RMP):
Respiration Perfusion Mental status

The four levels of triage are identified by color codes: Priority One (Red Tag)immediate care; life threatening Priority Two (Yellow Tag)urgent care; can delay treatment and transport up to one hour Priority Three (Green Tag)delayed care; can delay treatment and transport up to three hours Priority Four (Black Tg)no care required; dead patient Use the blue tags for contaminated patients in need of decontamination Move all walking wounded to the Green treatment area Begin by moving from patient to patient to assess the remaining victims Stop at each person for a quick assessment and tagging Each stop should not take more than 1 minute (Purpose at this point is to define and tag patients) Refer to the flow chart for methodology and corrective actions to be taken during triage
NO INJURY OR COMPLAINTS
DELAYED TRANSPORT UP TO THREE (3) HOURS
No
BREATHING?
DEAD
Yes
CONTAMINATED?
DECONTAMINATION
RESPIRATION EFFORT?
Inadequate <10 or >30
Adequate and <30
PERFUSION?
Cap refill >2 sec or radial pulse absent
CRITICAL/ IMMEDIATE TRANSPORT
LOC?
Unconscious or altered L.O.C.
DELAYED TRANSPORT UP TO ONE (1) HOUR
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TRAUMATIC BRAIN INJURY

TRAUMA Traumatic Brain Injury
Complete trauma assessment per Trauma Guidelines Stabilize C-Spine and assure adequate airway Perform baseline Glascow Coma Scale (GCS) Treat per pre-hospital triage for TBI guideline Maintain an SAO2 > 90% Maintain a systolic BP of >100 mmHg Transport to most appropriate receiving facility by most appropriate means per Trauma Transport Protocol (TTP) Recover any avulsed tissue if possible (ear, nose) and wrap in moist gauze
Ocular Injury
Treat specific ocular injury - blunt or penetratingAdminister Tetracaine 1-2 gtts. in affected eye prn for pain. Can be used with contact lens Control bleeding with gentle pressure over wound site Stabilize protruding foreign bodies with moist sterile dressings, protect and cover both eyes if applicable Remove contact lenses if management of injury is complicated by their presence (ie. chemical burns)
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03/01/05
TRIAGE FOR THE TRAUMATIC BRAIN INJURY PATIENT
Mild, Moderate TBI
Severe TBI (Comatose)
Score GCS Eyes
Eyes open, open to voice, or open to pain
Eyes do not open to pain
Score GCS Verbal
Says at least words
Incomprehensible sounds or none
Score GCS Motor
Any motor response
Localization or withdrawal
Extensor or flaccid response
Assess Pupils
Any pupil response
Pupils equal and reactive
Pupils asymmetric or fixed and dilated
Treatment
Oxygenate
Intubate (ventilate and oxygenate if intubation not available) Normoventilate
Intubate (ventilate and oxygenate if intubation not available) Hyperventilate
Transport
Transport to: Emergency Room (GCS 14, 15) Trauma Center (GCS 9-13)
Transport to: Trauma Center with TBI Resources* if available (GCS<9)
First Priority: Asses, Treat, Stabilize
Airway Breathing Circulation
Ensure: Systolic blood pressure > 100mmHg and SaO2 > 90%
*Trauma center with 24 hour scanning capabilities, 24 hour available operating room, prompt neurosurgical care and the ability to monitor intracranial pressure and treat intracranial hypertension as delineated in the Guidelines for the Management of Severe Head Injury (www.braintrauma.org)
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P - 83
Treatment: Ventilation Rates (approximate) Normal Ventilation Breaths Per Minute Adults Children Infants 10 bpm 20 bpm 25 bpm
Transport Decisions
Hyperventilation Breaths Per Minute Adults Children Infants 20 bpm 30 bpm 35 bpm
The recommended hospital destination may not always be possible given the variality of local resources and transport times. The decision for EMS personnel to follow these recommendations should be based upon discussion and approval by the EMS Division Chief and/or local Medical Control.
P - 84
03/01/05
ENDOTRACHEAL TUBE INTRODUCER

PURPOSE: TO FACILITATE DIFFICULT INTUBATIONS Indications for use:
1. 2. 3. 4. 5. 6. 7. Difficult intubations If the laryngeal opening is not fully visible To control the direction of the endotracheal tube during insertion Short-bull neck Laryngeal edema ( i.e. burns, anaphylaxis ) Anatomical abnormalities ( congenital / tumors ) Inability to position the pt due to entrapment or confined space etc.
Contraindications for use:

1. Pediatric pts under 14 y/o
Precautions:
1. Soft tissue damage or bronchial rupture may occur: a. During blind intubation b. Positioning past the carina c. When undue pressure is applied d. Endotracheal tube is threaded over introducer without using a laryngoscope
Equipment:
1. 2. 3. 4. 5. 6. 7. 8. Appropriate level of universal precautions Laryngoscope with appropriate blade E.t. tube 6.0 or greater Gum elastic bougie Have suction available Lubrication ( sterile h2o, ky jelly ) Means of ventilation ( bvm, auto vent ) Thomas lock
Technique / procedure:
1. Hyperoxygenate the pt 2. Perform an optimal direct laryngoscopy 3. At a minimum, the tip of the epiglottis must be visible in order to direct the introducer into the glotic opening. 4. Tactile confirmation of tracheal clicking will be felt as the distal tip of the introducer bumps against the tracheal rings. If the tracheal clicking cannot be felt, continue to gently advance the introducer until hold up is felt. Tracheal clicking and hold up are positive signs that the introducer has entered the trachea. No tracheal clicking or hold up is indicative of esophageal placement. 5. Advance the introducer to a depth of approximately 25cm so that the distal tip lies at least 2-3cm beyond the glottic opening. 6. While holding the introducer securely and without removing the laryngoscope, advance the endotracheal tube over the proximal tip of the introducer. Once the endotracheal tube passes beyond the teeth, rotate the endotracheal tube 90* counter clockwise (1/4 turn to the left) so that the endotracheal tube lies in the mid trachea.
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P - 85

7. Advance the endotracheal tube to the proper depth so that the tip of the endotracheal tube lies in the mid-trachea. 8. Holding the endotracheal tube securely, remove the introducer. 9. Confirm endotracheal intubation: Esophageal detector device (self inflating bulb) Chest auscultation along the mid-axillary lines and the epigastrium End tidal c02 detection 10. Secure the pts head ( lsb, cid) *** do not clean or sterilize the introducer *** dispose of after each use .
P - 86
03/01/05
03/01/05
P - 87
TREATMENT GUIDELINES
Treatment Guidelines
10/7/2009
M-1
GENERAL TREATMENT PRECAUTIONS
Medical
The following statements apply throughout the treatment guidelines If your agency does not utilize a specific treatment you are not responsible for its application.
Monitor blood pressures when...

100mm/Hg systolic shall be the lower limit for medications that may cause hypotension The target blood pressure for maintaining hypotensive patients shall be 100mm/Hg systolic 180mm/Hg systolic or 110mm/Hg diastolic (with associated symptoms) shall be the hypertensive limits for consideration of treatment
When administering nitrates...

Other forms of nitroglycerine shall be discontinued when IV nitroglycerine is initiated Remove all forms of patients own nitroglycerine prior to treatment with nitroglycerine Concurrent use of PDE-5 inhibitors with nitrates, either episodic or continuous, is contraindicated. Nitroglycerine will not be given to patients within 24 hours of PDE-5 inhibitors: sildenafil citrate (Viagra) vardenafil (Levitra) tadalafil (Cialis)- 48 hours Administration of nitrates should be done with extreme caution, if at all, in patients with right ventricular infarct. These patients may be sensitive to nitrates. Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine sulfate
For other drugs...

Epinephrine should be administered with caution to patients over 60 years of age, pulse above 120 BPM, systolic blood pressure above 160mm/Hg or with a hypertensive or cardiac history Labetalol should be administered with caution to patients with heart rates less than 100 BPM Labetalol should be administered with caution to patients on Lasix When administering magnesium sulfate closely monitor the respiratory rate, blood pressure and reflexes Calcium channel blockers are contraindicated with history of Wolf Parkinson White syndrome, use caution when administering to patients with wide QRS, short pr interval or presence of a delta wave Albuterol (Proventil, Ventolin) 2.5 mg may be given diluted in 3 cc saline nebulized in line via ETT with BVM
SLCFD paramedics must accompany all transported patients to hospital.
Pediatrics...
A Paramedic should attend all pediatric patients five (5) years or younger during transport. A child restraint seat should be used when appropriate
Fluids...
All fluid boluses should be in 250cc increments allowing intervals for vital sign and lung sounds assessment Fluid hydration rates shall be 250cc/hr IV 0.9% NaCl 250 cc/hr 62 gtts/min with 15 gtt set IV 0.9% NaCl 250 cc/hr 41 gtts/min with 10 gtt set Fluid resuscitation (patients with signs of severe hypotension) rates shall be wide open rate
M-2
10/7/2009
Medical
ABDOMINAL PAIN
CAUTION!
Limit the use of phenergan in pediatrics with prolonged vomiting of unknown etiology.
BLS
Vitalize/Prioritize Oxygen/Airway
ALS
EKG monitor IV 0.9% NaCl or LR KVO Nausea/Vomiting Promethazine (Phenergan) 6.25 - 12.5 mg IV (Max 25 mg.) or Dolasetron Mesylate (Anzemet) 12.5mg IV
PHYSICIAN CONSULT
Nasogastric tube if indicated (prolonged transport time, GI bleed, distention, and hemoptysis)
Dilute Phenergan in 10cc NaCl before IV administration.
Medical
Pediatric
Nausea/Vomiting Promethazine (Phenergan) 0.25mg/kg IV not to exceed 12.5mg or Dolasetron Mesylate (Anzemet) 0.35mg/kg not to exceed 12.5mg for children 2-16 years
MCFR uses Ondansetron (Zofran) 4mg IV /IM over 30 seconds. Ped 0.1mg/ kg over 30 seconds in place ofor Anzemet
ALLERGIC REACTIONS
CAUTION
Epinephrine should be administered with caution to patients > 60 years of age, pulse rate above 120, systolic blood pressure above 160 mm Hg, or hypertensive or cardiac history. Epinephrine and albuterol should be administered 2 to 3 minutes apart. Rapid infusion of cimetidine (Tagamet) may cause hypotension and cardiac dysrhythmias. Atrovent is CONTRAINDICATED in allergic reactions to peanut and soy products.
BLS
Vitalize/Prioritize Oxygen/Airway Identify the cause of the reaction. Remove source if possible (i.e. stinger from bee) Assist patient with personal EpiPen and/or personal albuterol inhaler PRN
ALS
EKG monitor IV 0.9% NaCl KVO Large bore IVs wide open for severe reactions until systolic BP of 100 mm Hg is maintained. Mild Reaction (itching and hives) Diphenhydramine (Benadryl) 25 mg IVP Cimetidine (Tagamet) 300 mg / 50 cc IV 0.9% NaCl infused over 15 minutes (50 gtts/ min 15gtt set) Methylprednisolone (SoluMedrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP
MCFR mixes Tagamet 300 mg in 100cc 0.9% NaCl run over 15 minutes. (100 gtts/min with a 15 gtt set)
M-3
10/7/2009
IM injection of Benadryl, Moderate Reaction (dyspnea, wheezing, chest tightness, or edema) Albuterol (Proventil, Ventolin) 2.5 mg and Atrovent 0.5mg via mininebulizer or via Tagamet, and SoluMedrol ETT with a BVM - repeat as needed are appropriate when IV Diphenhydramine (Benadryl) 50 mg IVP access is unobtainable. Methylprednisolone (SoluMedrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP SLCFD does not administer Tagament IM. MCFR mixes Tagamet 300 mg in 100cc 0.9% NaCl run over 15 minutes. (100 gtts/min with a 15 gtt set)
Cimetidine (Tagamet) 300 mg / 50 cc IV 0.9% NaCl infused over 15 minutes (50 gtts/ min 15 gtt set) Epinephrine 1:1,000 0.3 mg SQ repeated q 20 minutes to total of (3) doses. Alternate extremities. Severe Reaction (Hypotension, i.e. anaphylatic shock) IV 0.9% NaCl fluid bolus as needed Epinephrine 1:1,000 0.3 mg SQ repeated q 20 minutes to total of (3) doses. Alternate extremities Diphenhydramine (Benadryl) 50mg IVP CARDIAC ARREST IMMINENT epinephrine 1:10,000 0.3 mg IVP (instead of SQ 1:1,000) May be given ETT if no IV access Albuterol (Proventil, Ventolin) 2.5 mg and Atrovent 0.5mg via mininebulizer or via diluted in 3 cc saline nebulized inline via ETT with BVM - repeat as needed Methylprednisolone (SoluMedrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP Cimetidine (Tagamet) 300 mg / 50 cc IV 0.9% NaCl infused over 15 minutes (refer to Drip Chart) Epinephrine 210g/min or dopamine drip 510 g/kg/min titrated to systolic BP of 100 mm/Hg
Medical
PEDIATRIC
MCFR mixes Tagamet 300 mg in 100cc 0.9% NaCl run over 15 minutes. (100 gtts/min with a 15 gtt set)
Albuterol (Proventil, Ventolin) 1.25 mg/3 cc Diphenhydramine (Benadryl) 1 mg/kg Cimetidine (Tagamet) contraindicated under 16 years of age Methylprednisolone (SoluMedrol) 2 mg/kg maximum dose 125 mg or dexamethasone (Decadron) 0.2mg/kg to maximum dose 4mg Epinephrine 1:1,000 0.01 mg/kg SQ (0.01 cc/kg) maximum single dose 0.3 mg
ALTERED LEVEL OF CONSCIOUSNESS

BLS
Vitalize/Prioritize Oxygen/Airway Protect from injury / Restrain PRN Attempt to identify cause (i.e. stroke, diabetic, head injury, overdose, and seizures)
ALS
Only administer Narcan in increments of 0.4mg to maintain airway.
EKG monitor IV 0.9% NaCl KVO Blood glucose level >300 or <60 (<50 in newborn) refer to DIABETIC TREATMENT GUIDELINE (see page M6) Thiamine 100 mg IVP if alcohol abuse is suspected Naloxone (Narcan) 0.42 mg slow IVP or nasally, titrate to resp. rate of 12 (Max 10 mg) Chemical sedation of the violent patient, refer to SEDATION GUIDELINE (SEE PAGE M-13) Physical restraint of the violent patient, refer to PROCEDURAL GUIDELINE (SEE PAGE P-70)
PEDIATRIC
Apply appropriate pediatric immobilization device Naloxone (Narcan) 0.01 mg/kg initial dose then 0.1 mg/kg second dose (if needed) maximum cumulative dose of 2.0 mg Chemical sedation of the violent patient, refer to SEDATION GUIDELINE (SEE PAGE M-13) M-4
10/7/2009
ASTHMA
CAUTION
Epinephrine and albuterol should be administered with caution to patients over 60 years of age, pulse above 120 BPM, systolic blood pressure above 160mm/Hg, or hypertension or cardiac history. Abort continuous nebulized treatment if any of these signs are observed.
BLS
Vitalize/Prioritize Oxygen/Airway Assist patient with personal autoinhaler
ALS
EKG Monitor IV 0.9% NaCl 250 cc/hr (62 gtts/min with 15 gtt set) infusion Mix ipratropium (Atrovent) 0.5 mg with albuterol (Proventil) 2.5 mg and administer via mininebulizer May repeat Proventil after 10 minutes (Do not repeat Atrovent) Continuous nebulized albuterol treatment may be appropriate in severe distress. Methylprednisolone (SoluMedrol) 125 mg IVP over 23 minutes or dexamethsone (Decadron) 4mg IVP Epinephrine 1:1000 0.3 mg SQ Repeat epinephrine 1:1000 0.3 mg SQ 20 minutes after first dose in opposite extremity Magnesium Sulfate 2gm/10cc 0.9% NaCl over 3 minutes, up to 4-6 gm if severe distress Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or in line nebulizer via ETT)
Medical
MCFR administers Magnesium Sulfate as 2 grams in 100cc over 10 min.
PEDIATRIC
12 years of age and younger IV 0.9% NaCl or LR 2 cc/kg bolus Epinephrine 1:1,000 0.01 mg/kg (0.01 cc/kg) SQ Albuterol (Proventil) 1.25 mg via mininebulizer Methylprednisolone (SoluMedrol) 2 mg/kg maximum dose of 125 mg IVP or dexamethasone (Decadron) 0.2mg/kg maximum dose of 4mg
CHRONIC OBSTRUCTIVE PULMONARY DISEASE

CAUTION
Continuous nebulized albuterol should be aborted in patients who are: > 60 years of age, pulse rates above 120 BPM, systolic blood pressure above 160mm/Hg, or with hypertension or cardiac history.
BLS
Vitalize/Prioritize Oxygen/Airway Low flow (24 LPM) to maintain SaO2 of 95% or higher concentrations until improved
ALS
EKG Monitor IV 0.9% NaCl KVO or saline lock (if stable) Mix ipratropium (Atrovent) 0.5 mg with albuterol (Proventil) 2.5 mg, administer via mininebulizer May repeat Proventil after 10 minutes (Do not repeat Atrovent) Continuous nebulized albuterol treatment may be appropriate in severe distress Assess for secondary signs of cardiac failure: edema, jugular vein distention, rales, and frothy sputum, refer to CHF/PE GUIDELINE (see page C-5) Intubate if no improvement or marked respiratory distress, refer to RSI TREATMENT GUIDELINE (see page M-11)
10/7/2009
M-5

Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or inline nebulizer via ETT) Methylprednisolone (SoluMedrol) 125 mg IVP over 23 minutes or dexamethasone (Decadron) 4mg IVP
PEDIATRIC
Albuterol (Proventil) 1.25 mg via mininebulizer Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or inline nebulizer via ETT) Methylprednisolone (SoluMedrol) 2 mg/kg over 23 minutes maximum dose of 125 mg IVP or dexamethasone (Decadron) 0.2mg/kg maximum dose of 4mg
DIABETIC EMERGENCIES
CAUTION
A physician consult should be obtained regarding treatment of low blood glucose levels Rescue Lieutenants and Flig associated with pregnancy and stroke. If BGL is less than 60 in pregnancy and/or stroke, a physician consult should be obtained.
BLS
Medical
Vitalize/Prioritize Oxygen/Airway Obtain blood glucose reading Assist with the administration of oral glucose when consciousness permits
ALS
EKG Monitor IV 0.9% NaCl KVO 250 cc/hr (62 gtts/min with 15 gtt set) infusion if blood glucose level > 300 mg/dl 250cc bolus, repeat if necessary, if blood pressure is less than 100mm systolic Thiamine 100 mg IVP or IM if alcohol abuse is suspected Dextrose 50% 25 gm IVP if blood glucose level is less than 60 mg/dl Repeat blood glucose within 15 minutes Repeat Dextrose 50% 25 gm IVP PRN Glucagon 1 mg IM or intranasally if no IV access
Pediatric
Age: birth to 1 month Dextrose 12.5% 0.5 gm/kg IVP slow Expel 37.5 cc of D50% and draw 37.5 cc of 0.9% NaCl Age: 1 month to 8 years Dextrose 25% 0.5 gm/kg IVP slow Expel 25 cc of D50% and draw 25 cc of 0.9% NaCl Age: 8 years and older Dextrose 50% 0.5gm/kg Glucagon 0.5 mg IM for children less than 20kg 1.0 mg IM for children more than 20kg
M-6
10/7/2009
DIALYSIS PROBLEMS
BLS
ALS
EKG Monitor IV 0.9% NaCl KVO or saline lock (if stable) If IV access is unobtainable, access dialysis port if applicable (critical pts only) Cautious incremental boluses of NaCl up to 250 cc, repeat as necessary if patient is in frank shock immediately post dialysis, reassess vital signs and lung sounds Blood glucose level, refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) ACLS guideline Sodium Bicarbonate should be considered early in cardiac arrest Calcium Chloride 10% 10 cc IVP if ventricular tachycardia, ectopy or fibrillation are nonresponsive to appropriate ACLS treatment (after lidocaine and/or sodium Flight Medics may administer bicarbonate)
MCFR uses Amiodarone as the prefered antiarrhymic
HYPERTENSION
CAUTION
Labetalol (Trandate) is contraindicated in acute coronary syndrome, cardiogenic shock, heart block (2nd and 3rd degree), sinus bradycardia, CHF, bronchial asthma, and COPD when these conditions are acute. Patients should be in supine position during and after the administration of Labetalol. Patients who maintain a chronic hypertensive status may require a higher than normal systolic blood pressure to maintain cerebral perfusion. This should be considered when administering treatment to lower blood pressure. Other forms of nitroglycerin should be discontinued when IV Nitro is initiated. Labetalol (Trandate) will decrease heart rate and should be used with extreme caution in patients with heart rates less than 100 BPM.
Medical
BLS
Vitalize/Prioritize Oxygen/Airway Confirm with two(2) sets of vital signs (right & left) Place the patient supine during drug administration Obtain additional blood pressures immediately prior to and at 5 and 10 minutes after drug administration
ALS
EKG monitor IV 0.9% NaCl KVO or saline lock (if stable) Symptomatic (headache, visual disturbances, epistaxis, nausea/vomiting) and blood pressure: Greater than 180mm/Hg systolic, or Greater than 110mm/Hg diastolic Nitroglycerin IV Initiate at 5-10g/min IV infusion pump or dial-a-flow Increase 5-10g/min q 5 minutes until desired response Labetalol (Trandate) 0.25 mg/kg IVP over 2 minutes (300 mg max dose) Target blood pressure (160/90) Repeat Labetalol after 10 minutes if BP remains > 180/110
IRSDPS uses Labetalol 20mg q10min, doubling each sequential dose until a BP of 140/90 or max of 300mg Discontinue all Nitrates prior to administering Labetalol. MCFR requires IV Nitro to be place on an IV pump only.
M-7
10/7/2009

Hypertensive patients listed under Caution should receive nitroglycerin Nitroglycerin contraindicated if within 24 hours of sexual enhancing medication use, (48 hours for Cialis) Nitroglycerin 1 (one) 1/150gr SL Tab or 0.4mg Spray SL 1 inch of paste (may be administered concurrently with SL nitro)
PEDIATRIC
The safety of labetalol has not been established in children. Nitroglycerin is not indicated for use in children
MEDICAL SHOCK SYNDROMES

CARDIOGENIC SHOCK HYPOVOLEMIC SHOCK (MEDICALLY INDUCED) SEPTIC SHOCK
BLS
Vitalize/Prioritize Oxygen/Airway Trendelenberg positioning as tolerated by patient Body Temperature
Medical
ALS
EKG Monitor IV 0.9% NaCl Hypotensive (BP less than 100mm/Hg systolic) 250 cc bolus repeated as necessary to maintain systolic BP 100mmHg Dopamine 520 g/kg/min titrated to effect Congestive Heart Failure / Pulmonary Edema, refer to CHF/PE TREATMENT GUIDELINE (see page C-5) Chest Pain / Suspected Myocardial Infarction, refer to CHEST PAIN TREATMENT GUIDELINE (see page C-4) If fever is present and altered LOC, administer Acetaminophen Suppository 325mg rectally
MCFR does not carry Acetaminophen suppository
PEDIATRIC
Fluid bolus of 20 cc/kg repeated as necessary to maintain blood pressure Dopamine 220 g/kg/min titrated to effect If fever is present, administer Childrens Acetaminophen Liquid 10mg/kg PO If altered LOC, administer Acetaminophen Suppository 125mg
MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds Ped 0.1mg/kg over 30 seconds in place of Phenergan or Anzemet
NAUSEA / VOMITING
Caution
The use of Promethazine (Phenergan) should be used with caution in patients that are hypotensive
BLS
ALS

M-8
EKG Monitor IV 0.9% NaCl KVO Promethazine (Phenergan) 6.25 - 12.5 mg IV or Dolasetron Mesylate (Anzemet)12.5mg IVP
10/7/2009
repeat Promethazine (Phenergan) to max 25mg IV if vomiting continues. Physician Consult for repeat Dolasetron Mesylate (Anzemet) Nasogastric tube (prolonged transport time, GI bleed, distention, and hematemesis)
IRCEMS gives Phenergan without consult.
PEDIATRIC PHYSICIAN CONSULT
MCFR uses Ondansetron Promethazine (Phenergan) 0.25 mg/kg IV not to exceed 12.5 mg or Dolasetron Mesylate (Zofran) 4mg IV/IM over 30 (Anzemet) 0.35mg/kg IVP to max of 12.5mg seconds Ped 0.1mg/kg IV Nasogastric tube (prolonged transport time, GI bleed, distention, and hematemesis) over 30 seconds in place of Phenergan or Anzemet
OBSTETRICS/GYNECOLOGY
BLS
Vitalize/Prioritize Oxygen/Airway (100% high flow for mother, blow by for neonate) Obtain BGL from mother Positioning If delivery is not in progress, transport the patient in the left lateral recumbant position If perineal inspection reveals abnormal presentation (i.e. foot, buttocks, hand or face), place the patient in the knee-chest or left lateral recumbant position with immediate transport Delivery Slow, controlled delivery of the head; apply gentle perineal pressure Observe for meconium staining; if present, vigorously suction oral pharynx during delivery and immediately after (intubation may be required) Double clamp cord 1012 inches from abdomen Dry, stimulate and maintain body temperature PostPartum Check APGAR at 1 and 5 minutes (Appendix D) Assess for postpartum hemorrhage
Medical
ALS
EKG Monitor IV 0.9% NaCl KVO large bore
SEIZURES OR COMA (ECLAMPTIC)

Magnesium Sulfate loading dose of 4 gm/100cc (piggyback) wide open Magnesium Sulfate drip 2gm/100cc at 100cc/hr (25 gtts/min with 15 gtt set) Utilize a Burette, Volutrol administration set, or IV pump
SLCFD administers Mag. Sulfate in Eclampsia 4gm diluted IVP over 3 minutes.
FIRST/SECOND TRIMESTER BLEEDING

Apply maternity or 5x9 pad to vaginal area If hypovolemic establish two large bore IVs wide open using trauma tubing and pressure infusers to maintain systolic blood pressure of 100mm/Hg PostPartum bleeding, apply trauma dressing to vaginal area
PHYSICIAN CONSULT
PostPartum hemorrhage (post placenta delivery) Oxytocin (Pitocin) 20units/1000 cc 0.9% NaCl infused at 120150 cc/hr (30 gtts/ min with 15gtt set) if extended transport time and/or distance Hypertensive disorder of pregnancy (Preeclamptic) using a burette or Volutrol drip set: Magnesium Sulfate loading dose 4 gm/100cc IV 0.9% NaCl over 15 minutes Magnesium Sulfate maintenance dose 2 gm/100cc at 100 cc/hr Seizures unresolved by magnesium sulfate (Eclamptic) Diazepam (Valium) 3-5 mg IV over 2 minutes May repeat to a total of 10 mg or Lorazepam (Ativan) 0.5 - 1 mg IVP or nasally may repeat twice q5 minutes
10/7/2009
M-9
PAIN MANAGEMENT
Caution
Pain medications may produce respiratory depression Pain medications are not to be used in the presence of abdominal pain, head injury, kidney stones, or altered LOC
Indications:
Relief of moderate to severe pain associated with trauma, fractures, dislocations, myocardial infarction, and burns
BLS
Vitalize/Prioritize Oxygen/Airway Monitor patients level of consciousness and respiratory status
ALS
EKG monitor IV 0.9% NaCl KVO or saline lock if stable Nitrous oxide for minor musculoskeletal pain May use either of the following medications: Dilaudid (hydromorphone hypochloride) 1-2mg slow IV or IM titrated to effect may repeat to a total of 4mg In elderly (65 years or older) 0.25 - 0.5mg slow IV or IM titrated to effect may repeat as tolerated Morphine or Nubain 1-5mg IV or IM titrated to effect may repeat in small increments until desired effect is achieved Promethazine (Phenergan) (to be given with the selected pain medication) 6.25 - 12.5mg IV or Dolasetron Mesylate (Anzemet) 12.5mg IVP
Medical
MCFR first line drug for pain management is Dilaudid unless contraindicated. SLCFD, IRSDPS & IRCEMS can use Nubain for pain management with the same dosage as Morphine. Dilute Phenergan in 10cc NaCl before IV administration. MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. Ped 0.1mg/kg in place of Phenergan or Anzemet MCFR Rescue Lieutenants and Flight Medics may administer Fentanyl 25-50 mcg IVP every 5 min.in patients 16 years old and older. Patients under the age of 16 years old use Morphine 0.1-0.2mg/kg IVP.
M - 10
Pediatrics
Morphine 0.1 - 0.2mg/kg IV or IM slowly Dilaudids safety and effectiveness in children has not been established
10/7/2009
RAPID SEQUENCE INTUBATION

This procedure is for patients requiring total airway control who may be fully or partially conscious. Two (2) paramedics must be in attendance with the patient before RSI can be performed and must accompany the patient to the hospital
SLCFD requires a paramedic Lt. or a Flight Medic to be present. They need not IMPORTANT accompany patient to the A secondary airway device must be ready to use if endotracheal intubation cannot be ER. successfully performed (i.e. Combitube, LMA, surgical airway, etc...) MCFR requires a Rescue Lt. Indications or Flight Medic presence Seizure/ convulsion disorder and accompaniment with Multi-system trauma patient to ER Head injury
When other methods of airway control or treatments have failed or are either not possible or practical
Contraindications
It must be kept in mind that all contraindications are relative and risk must be weighed against possible benefits Digitalis toxicity Increased intracranial pressure Increased intraoccular pressure Known electrolyte imbalance Skeletal muscle myopathy Acute malignant hyperthermia
MCFR uses a different Guideline for RSI. Refer to pages M 16 & 17
Medical
Caution
It is important to remember that neuromuscular blockade does not alter the patients level of consciousness, therefore it does not reduce pain
Pre-medication Procedure
O2 100% via mask or BVM. Pre-oxygenation is REQUIRED for a minimum of 2 minutes before proceeding with paralysis. The purpose is to cause a nitrogen washout in the lungs and create an oxygen reservoir. This oxygen reservoir will allow approximately 3 to 4 minutes of apnea without hypoxemia in a normal patient. Atropine Pediatrics 16 years of age or less 0.02mg/kg (0.1mg minimum dose) Adults 1mg IVP If bradycardia present or potential MUST be given before any repeat doses of Anectine Lidocaine 1.5mg/kg Do not use if administering Etomidate Hydromorphone (Dilaudid) for pain control, if needed 1-2mg IV titrated to effect may repeat to a total of 4mg In elderly (65 yrs and older), 0.25mg - 0.5mg IV titrated to effect may repeat as tolerated Promethazine (Phenergan) or Dolasetron Mesylate (Anzemet) to be given with Dilaudid Adults: 6.25-12.5mg IV, Dolasetron Mesylate (Anzemet) 12.5mg IV Pediatrics: 0.5mg/kg not to exceed 6.25mg IM or Dolasetron Mesylate (Anzemet) 0.35mg/kg
10/7/2009
M - 11

Etomidate (Amidate) 0.3mg/kg may repeat x1 If allowed may administer 20mg non-weight based Lidocaine is not used with Etomidate If Etomidate is contraindicated or unavailable Midazolam (Versed) Adults over the age of 60yrs: 2.5mg IV or IM titrated to effect. may repeat to a total of 5mg Adults under the age of 60yrs: 5mg IV or IM titrated to effect may repeat to a total of 10mg Pediatric dose: 0.3mg/kg Allow adequate time to assess the effectiveness of sedation
SLCFD does not administer Etomidate under the age of 10yrs.
PARALYTICS
Procedure Succinycholine Chloride (Anectine) may be repeated in 2 minutes for desired effect Adult: 1.5mg/kg IV Pediatric and Infants: 2mg/kg IV Onset <1 minute Duration of approximately 4-6 minutes Caution Hyperthermia: presents as jaw spasm or general rigidity Monitor body temperature Cool as needed Hyperkalemia: presents as tall, peaked T waves Constant monitoring of EKG Administer calcium chloride 500mg slow IV Increased intracranial pressure Increased intraoccular pressure Sudden cardiac arrest in children with Duchennes muscular dystrophy (children usually undiagnosed) Observe for peaked T waves Administer calcium chloride 500mg IV Administer sodium bicarbonate 1mEq/kg Administer glucose per DIABETIC EMERGENCIES GUIDELINE (see page M-6) Vercuronium Bromide (Norcuron): indicated if transport time is > 15 minutes, patient becomes combative after the effects of the Anectine have worn off, or the patient is still combative after sedation Adult and pediatric: 0.1mg/kg IV Onset in 2-4 minutes Duration of 20-40 minutes Side effects: hyperthermia
Medical
M - 12
10/7/2009
SEDATION
Indications
Airway management (when RSI is not indicated or available) Cardioversion External pacing Altered level of consciousness, violent patient
Caution
Diazepam (Valium) may cause respiratory depression or compromise.
ALS
Anesthetic spray to posterior pharynx (for intubation) For combative patient and external pacing Diazepam (Valium) 5mg IV/IM may repeat once after 5 minutes MCFR refer to Post Intubation Guideline page M-18 OR Lorazepam (Ativan) 1 mg IVP or nasally may repeat as needed up to a max. of 4 mg For intubation (also see RSI TREATMENT GUIDELINE, page M-11) MCFR Rescue Lieutenants Midazolam (Versed) and Flight Medics may 2.5mg IV, IM (if over 60yrs), or nasally administer propofol 5mg IV, IM (under 60 yrs), or nasally (Diprivan) for sedation, OR refer to Guideline page MEtomidate (Amidate) 0.3mg/kg IV For Cardioversion 17 for dosing. Midazolam (Versed) 2.5mg IV, IM (if over 60yrs), or nasally 5mg IV, IM (under 60 yrs), or nasally OR Lorazepam (Ativan) 1mg IVP or nasally may repeat as needed up to a max. of 4 mg MCFR refer to Post Post Intubation Intubation Guideline page Re-evaluate the tube placement after movement or transfer of patient. Reassess every 5 minutes M-18 if a Rescue Consider further sedation or paralytic agent (see page M-12 for dosages) Lieutenant or Flight Medic Evaluate the need for effective neurological exam versus paralytic agent. is present. Consider PAIN MANAGMENT GUIDELINE (see page M-10) Look for increased BP, tearing, evaluate physiological response to pain Etomidate (Amidate) 0.3mg/kg IV MCFR Rescue Lieutenants OR and Flight Medics may Lorazepam (Ativan) 1 mg IVP or nasally administerEtomidate 0.03 May repeat as needed up to a max. of 4 mg
Medical
0.05mg/kg IVP (may repeat x1) during extended extrication to aid in ease and safety of extricating combative or uncooperative patients. Due to the short half life of Etomidate (6 min or less) administration must be carefully coordinated with the actual patient removal.
Pediatric
Diazepam (Valium) 0.2-0.5 mg/kg IV / IM / PR no faster than 3mg/min Midazolam (Versed) 0.3-0.6mg/kg IV / IM or nasally Lorazepam (Ativan) 0.05-0.1mg/kg IV / IM or nasally
10/7/2009
M - 13
SEIZURES
Caution
Refer to OBSTETRICS/GYNECOLOGY TREATMENT GUIDELINE (See Page M-9) for seizures associated with pregnancy Consider etiology of seizure for possible infectious disease isolation. The Team should utilize appropriate personal protective equipment. Use caution not to over cool a febrile patient to the point of shivering. Use of PO medications should be avoided in patients with decreased level of consciousness. Vitalize/Prioritize Oxygen/Airway Protect from injury Consider C-Spine precautions if suspected injury
BLS
ALS
EKG monitor IV 0.9% NaCl KVO Glucose level possible or suspected hypoglycemia, refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) prior to administration of diazepam (Valium) or lorazepam (Ativan) Diazepam (Valium) 35 mg IV/IM may repeat to a total of 10 mg may be administered rectally if no IV access OR Lorazepam (Ativan) 1mg IV, nasally, or rectally may be repeated to a max of 4mg OR Versed 0.1mg/kg IM, IV, or nasally Febrile seizures If altered LOC, administer acetaminophen suppository 325mg
Medical
MCFR uses Lorazepam (Ativan) 1mg IVP, nasally, or rectally as first line drug
Physician Consult
diazepam (Valium) 35mg IV for doses greater than 10 mg lorazepam (Ativan) 0.5mg - 1mg IV for doses greater than 4mg
Pediatric
Idiopathic (nonfebrile) seizures Diazepam (Valium) 0.2-0.5 mg/kg IV or rectal (no faster than 3 mg/min if IV) OR Lorazepam (Ativan) 0.1mg/kg IV or nasally Febrile seizures treat febrile seizures by cooling. (Use caution to avoid rapid temperature change.) consider Diazepam (Valium) 0.2-0.5 mg/kg IV or rectal (no faster than 3 mg/min if IV) or Ativan 0.1mg/kg if seizures are continuous childrens Acetaminophen liquid 10 mg/kg PO when level of consciousness permits If altered LOC, administer Acetaminophen suppository 125mg
MCFR does not carry Acetaminophen suppository
M - 14
10/7/2009
SICKLE CELL ANEMIA

BLS
Vitalize/Prioritize Oxygen/Airway (High flow) Emotional support
ALS
EKG monitor IV 0.9% NaCl infusion 250 cc/hr Pain control, refer to PAIN MANAGEMENT TREATMENT GUIDELINE (See page M-10)
MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. Ped 0.1mg/kg over 30 seconds in place of Phenergan or Anzemet
Pediatric
Promethazine (Phenergan) 0.25 mg/kg IV not to exceed 12.5 mg or Dolasetron Mesylate (Anzemet) 0.35mg/kg IVP to max of 12.5mg Pain control, refer to PAIN MANAGEMENT TREATMENT GUIDELINE (See page M-10)
STROKE
Caution
All medications given in the presence of a Stroke must be Physician consult.
Medical
BLS
Vitalize/Prioritize Oxygen/Airway (Oxygen as per patients need) Evaluate for stroke alert Elevate patients head 30 degrees Do not delay transport
ALS
EKG Monitor IV 0.9% NaCl KVO or saline lock (if stable) Blood glucose level, refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) Hypertension above 180 systolic or 110mm diastolic, refer to HYPERTENSION TREATMENT GUIDELINE (SEE PAGE M-7) Treat arrhythmias per appropriate Guideline Complete Stroke Alert check sheet If possible airway instability, refer to RSI TREATMENT GUIDELINE (see page M-11)
MCFR refer to RSI Treatment Guideline page M-16 and M-17
10/7/2009
M - 15
RAPID SEQUENCE INTUBATION (MCFR ONLY)

MCFR requires a Rescue Lt. or Flight Medic presence and accompaniment with patient to ER
This procedure is for patients requiring total airway control who may be fully or partially conscious. Two (2) paramedics must be in attendance with the patient before RSI can be performed and must accompany the patient to the hospital
IMPORTANT
A secondary airway device must be ready to use if endotracheal intubation cannot be successfully performed (i.e. Combitube, LMA, surgical airway, etc...)
Indications
Seizure/ convulsion disorder Multi-system trauma Head injury When other methods of airway control or treatments have failed or are either not possible or practical
Contraindications
Medical
It must be kept in mind that all contraindications are relative and risk must be weighed against possible benefits Digitalis toxicity Increased intracranial pressure Increased intraoccular pressure Known electrolyte imbalance Skeletal muscle myopathy Acute malignant hyperthermia
Caution Use extreme caution in pregnancy as Caution: opiates and Norcuron will cross the placental barrier. Pre-medication Procedure
O2 100% via mask or BVM. Pre-oxygenation is REQUIRED for a minimum of 2 minutes before proceeding with paralysis. The purpose is to cause a nitrogen washout in the lungs and create an oxygen reservoir. This oxygen reservoir will allow approximately 3 to 4 minutes of apnea without hypoxemia in a normal patient. The acronym LOADS is used to dictate proper administration L-Lidocaine O-Opioid A-Atropine D-Defasciculation S-Sedation Lidocaine 1.5mg/kg IVP Fentanyl - MUST be given slowly (Over 60 seconds) Adults < 60 years old 3 mcg/kg IVP Adults > 60 years old 1.5 mcg/kg IVP Pediatrics 1-2 mcg/kg IVP Atropine All pediatrics < 10 years of age 0.02mg/kg IVP (0.1mg minimum dose) Adults 1.0mg IVP MUST Administer prior to second dose of Anectine If bradycardia present or potential Norcuron 0.01mg/kg IVP for defasiculation (withhold in children <10 years old) Etomidate (Amidate) 0.3mg/kg IVP (may be used with pediatrics) M - 16
10/7/2009
If Etomidate is contraindicated or unavailable Midazolam (Versed) Adults < the age of 60: 5mg/kg IVP or IM titrated to effect May repeat to a total of 10mg Adults > the age of 60: 2.5mg IVP or IM titrated to effect May repeat to a total of 5mg Pediatric dose: 0.1mg/kg Allow adequate time to assess the effectiveness
PARALYTICS
Succinycholine Chloride (Anectine) may repeat in 2 minutes Adult 1.5mg/kg Pediatric 2.0mg/kg
Caution
Hyperthermia: presents as jaw spasm or general rigidity
Monitor body tempature Cool as needed

Hyperkalemia: presents as tall, peaked T waves
Medical
Constant monitoring of EKG Administer Calcium Chloride 500mg slow IVP Increase ICP Increase IOP Sudden cardiac arrest in children with Duchennes muscular
dystrophy.
Observe for peaked T waves Administer Calcium Chloride 500mg IVP Administer sodium bicarbonate 1mEq/kg IVP Administer glucose per Diabetic Emergency Guideline
(page M-6) Diprivan (if available) may be used for sedation or intubation. Use with extreme caution in the potentially hypotensive patient. The absolute contraindication is systolic BP of less than 100mm/hg. Loading dose (adults < 55) 2-2.5mg/kg given as 40mgIVP every 10 secondsuntil desired level of sedation is reached with maximum single not to exceed 120mg (eldery 1-2 mg/kg given as 20mg every 10 seconds), followed by a drip 25-120mcg/kg/min. Start at 25mcg/kg/min and increase 5-10mcg/kg/min until desired level of sedation is maintained. Reassess blood pressure frequently and adjust Diprivan as needed.
10/7/2009
M - 17
POST INTUBATION MANAGEMENT
Administer longer acting sedation for transport prior to Norcuron consideration Versed
Adults 0.1 mg/kg IVP (adults over 60 years old 0.05 mg/kg IVP) Pediatrics 0.1 mg/kg IVP
Assess for signs of pain and ensure systolic BP greater than 100mm/hg Fentanyl - MUST give slowly (over 60 seconds). May repeat after 10 minutes
Medical
Adults 2mcg/kg IVP (over 60 years old 1mcg/kg IVP) Pediatrics 1-2mcg/kg IVP
Vercuronium Bromide (Nurcuron) 0.1mg/kg IVP if the patient is unmamageable i.e. fighting the ET Tube and ventilator or becomes combative only after intubation, sedation and pain management.
Pain management is not to be withheld in the intubated head injured or stroke patient where signs of pain exist. Patients with traumatic injuries especially warrant re-evaluation for signs of pain. This also includes medical patients with pain complaints prior to intubation i.e. severe headache with a stroke. Baseline neurological assessments must be determined prior to administering sedation and pain medications with the initiation of RSI and reported to the receiving physician accordingly.
M - 18
10/7/2009
CARDIAC GUIDELINES
Cardiac
ASYSTOLE
Caution
Ask and verify DNR Orders (Must see original) or other acceptable form refer to page E-18 for information on DNRO
Sodium bicarbonate 1 mEq/kg
definitely helpful known preexisting hyperkalemia acceptable, probably helpful known preexisting bicarbonateresponsive acidosis overdose with tricyclic antidepressants to alkanize urine in overdoses acceptable, possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated, may be harmful hypoxic lactic acidosis
BLS
Consider TERMINATION GUIDELINE ( See page E-43) Vitalize/Prioritize Secure airway with appropriate adjunct Application of AED, refer to AED GUIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions)
ALS
Intubate EKG monitor IV 0.9% NaCl Confirm asystole in more than one lead Vasopressin 40u IVP to replace first or second dose of Epi or Epinephrine 1.0mg 1:10,000 IVP/IO q 35 minutes Atropine 1.0mg IVP/IO, repeated every 35 minutes up to a total of 3mg (0.03 0.04mg/kg) Consider possible causes: 6H 6T Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia, refer to HYPOTHERMIA TREATMENT GUIDELINE (SEE page T-5) Hydrogen Ion (acidosis) (sodium bicarbonate) Hyper/Hypokalemia (consider calcium chloride or sodium bicarbonate) Hypoglycemia Tamponade (pericardiocentesis) Tension pneumothorax (needle decompression) ThrombosisCoronary (ACS) ThrombosisPulmonary (embolism) Toxins Trauma Calcium Chloride 10mg/kg IVP if patient on calcium channel blocker or history of renal failure
Atropine 1.0mg IVP

the shorter atropine dosing interval (3 min) is possibly helpful in cardiac arrest
Cardiac
Patient remains in asystole

if patient remains in asystole or other agonal rhythm after successful intubation and initial medications and no reversible causes are indentified, consider termination of resuscitative efforts by a physician. Consider interval since arrest.
Vasopressin 40u IV push is first line for MCFR
Physician Consult
Consider termination of efforts after 10 minutes of treatment with no change
Pediatric
Refer to Broselow/Pediatric Resuscitation Tape Epinephrine Epinephrine repeated every 35 minutes 0.01mg/kg (0.1cc/kg) Epinephrine 1:10,000 IV/IO, or 0.1mg/kg (0.1cc/kg) Epinephrine 1:1,000 ET
IRCEMS does not use termination guidelines SLCFD considers termination of efforts after 20 minutes of treatment with no change
C-1
10/7/2009

Atropine 0.02mg/kg minimum dose 0.1mg maximum single dose 0.5mg for a child (1-8 yrs), 1.0mg for adolescent (8-16 yrs) may repeat after 35 minutes maximum cumulative dose 0.030.04mg/kg Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4.2% solution expel 25cc of sodium bicarbonate 8.4% and draw 25cc of 0.9% NaCl
BRADYCARDIA
Caution
Patients with 2nd degree type II or 3rd degree block should recieve TCP as first treatment
BLS
Serious symptoms
chest pain shortness of breath decreased level of consciousness
Cardiac Cardiac
Serious signs
hypotension shock pulmonary congestion congestive heart failure acute myocardial infarction
Vitalize/Prioritize Oxygen/Airway Observe closely
ALS
EKG monitor IV 0.9% NaCl Consider transcutaneous pacing Serious signs or symptoms: Atropine 0.5mg, repeated as necessary every 35 minutes up to a total of 3mg (0.030.04mg/ kg) Transcutaneous pacing pt severely symptomatic or delay in drug administration consider pacing before atropine use discretion for transthoracic versus A/P placement sedation, refer to SEDATION TREATMENT GUIDELINE (SEE PAGE M-13) Dopamine (Intropin) 520 g/kg per minute Epinephrine 210 g/min
Atropine
atropine should be given in repeat dose every 3-5 minutes up to total of 0.03-0.04mg/kg. Use the shorter dosing interval (3 minutes) in severe clinical conditions. It has been suggested that atropine should be used with caution in atrioventricular (AV) block at the His-Pukinje level (type II AV block and new thirddegree block with wide QRS complexes) (acceptable, possibly helpful); trans-cutaneous pacing is recommended.
Third-degree heart block

never treat third-degree heart block plus ventricular escape beats with lidocaine
Pediatric
* Give atropine first for bradycardia due to suspected elevated vagal tone or primary AV block, if heart rate <60 with poor perfusion start CPR if Atropine ineffective Atropine 0.02mg/kg minimum dose 0.1mg maximum single dose 0.5mg for child (1 - 8 yrs) may repeat after 35 minutes maximum cumulative dose 0.030.04mg/kg Epinephrine repeated every 35 minutes 0.01mg/kg (0.1cc/kg) epinephrine 1:10,000 IV or IO 0.1mg/kg (0.1cc/kg) epinephrine 1:1,000 ET Dopamine (Intropin) 5 - 20 ug/kg/min Transcutaneous pacing profound symptomatic bradycardia refractory to BLS and ALS anteriorposterior position is preferred, but anterioranterior is acceptable provided the negative () pad is placed near the apex of the heart
Epinephrine drip is appropriate with Atropine and TCP if the patient appears to be in a prearrest state
C-2
10/7/2009
CARDIAC GUIDELINES
CARDIOGENIC SHOCK
BLS
Vitalize/Prioritize Oxygen/Airway Trendelenburg position
ALS
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF IV 0.9% NaCl KVO Hypotensive (blood pressure less than 100 mm/Hg systolic) 250cc fluid bolus, repeat as necessary, to maintain systolic of 100 mm/Hg contraindicated if lung sounds indicate pulmonary edema Dopamine (Intropin) 520 g/kg per minute titrated to BP of 100mm/Hg systolic Evidence of right ventricular infarct (ST elevation in lead V4R) treat hypotension with cautious fluid bolus up to 2,000cc frequently check blood pressure and lung sounds Congestive heart failure / pulmonary edema, refer to CONGESTIVE HEART FAILURE/ PULMONARY EDEMA (See Page C-5) Chest pain / suspected myocardial infarction, refer to CHEST PAIN / MYOCARDIAL INFARCTION (SUSPECTED) (See Page C-4)
Cardiac
Pediatric
Dopamine (Intropin) 520 g/kg per minute
CARDIOVERSION / DEFIBRILLATION
BLS
Vitalize/Prioritize Oxygen/Airway Check oxygen saturation Ready suction device
Delays in synchronization
if delays in synchronization occur or clinical conditions are critical, go immediately to unsynchronized shocks
ALS
IV access established per primary Treatment Guideline Premedicate whenever possible, see SEDATION TREATMENT GUIDELINE (See Page M-13) Synchronized cardioversion/Defibrillation See Appendix A for specific Joule Settings.
10/7/2009
C-3
CHEST PAIN / MYOCARDIAL INFARCTION(SUSPECTED)

Contraindications
Aspirin or aspirin based products are contraindicated in children 16 years of age or younger due to Reyes syndrome allergy Heparin is contraindicated if recent bleeding, surgical procedure, gastrointestinal bleeding, bleeding ulcers, head trauma, stroke, transient ischemic attack (TIA) or history of bleeding tendencies
Caution
Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine. These patients may be sensitive to nitrates. Other forms of nitroglycerine should be discontinued when IV Nitro is initiated
BLS
ALS
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF Evaluate for Cardiac Alert IV 0.9% NaCl KVO double lumen IV catheter is preferred for the MI patient Hypotensive (blood pressure less than 100 mm systolic), refer to CARDIOGENIC SHOCK TREATMENT GUIDELINE (See Page C-3) Perform cardiac enzymes using Field Test Kit, draw green top tube Nitroglycerine (contraindicated if sexual enhancing medications were taken within past 24 hours [i.e. Levitra, Viagra] and within 48 hours for Cialis) contraindicated if blood pressure less than 100 mmHg systolic 1/150gr or 0.4mg spray SL (may administer 1 SL prior to 12 lead or IV access) may repeat at five minute intervals to a total of three (3) 1 inch paste (may be administered concurrently with SL nitroglycerine) 510 g/min IV infusion pump, increased 510 g/min every 35 minutes until pain is relieved or 100 mmHg systolic blood pressure is maintained if either of the following two conditions exist: ST elevation in any two contiguous leads of 12 lead ECG (it is not necessary to administer 3 SL nitro prior to initiating IV nitro), or pain partially but not completely relieved by 3 nitroglycerine SL Aspirin 324325mg chewable (4 pediatric chewable aspirin) Pain relief (one of the following) Morphine Sulfate in 2 mg increments IVP until desired effect max. dose 10 mg and Promethazine (Phenergan) 12.5 mg IVP or Dolasetron Mesylate (Anzemet) 12.5mg IVP Dilaudid (hydromorphone hypochloride) 1-2mg slow IVP titrated to effect may repeat to a total of 4mg. In elderly (65 years and older) 0.25 - 0.5mg slow IVP titrated to effect, may repeat as tolerated Promethazine (Phenergan) 12.5mg IVP or Dolasetron Mesylate (Anzemet) 12.5mg IVP Ventricular ectopy, refer to VENTRICULAR ECTOPY TREATMENT GUIDELINE (See Page C-8) ACLS guideline
Cardiac Cardiac
Cardiac
MCFR does not use double IV catheters. Two (2) separate IV lines must be established
Cardiac Enzyme Field Test Kit used by SFR Dilute Phenergan in 10cc before IV administration. MCFR drug of choice for pain relief is Dilaudid unless contraindicated
MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. Ped 0.1mg/kg over 30 seconds in place of Phenergan or Anzemet
C-4
10/7/2009
CARDIAC GUIDELINES
Physician Consult
Nitroglycerine IV if pain unaffected by 3 nitroglycerine SL contraindicated if blood pressure less than 100 mmHg systolic initiate at 510 g/min IV Infusion Pump increase 510 g/min every 35 minutes until pain is relieved or 100 mmHg systolic blood pressure is maintained Heparin 60 units/kg (max.4,000 units) IV in suspected acute MI draw blue top blood tube for prothrombin time and partial thromboplastin time (PT, PTT) prior to administration of Heparin
IRCEMS does not need orders for Ntg Drip MCFR does not carry Heparin
CONGESTIVE HEART FAILURE/PULMONARY EDEMA

Caution
If patient is febrile, consult EDP before administering furosemide or nitroglycerine, consider respiratory distress etiology of infection (pneumonia) rather than CHF Administration of nitrates should be done with caution in patients with right ventricular infarct. These patients may be sensitive to nitrates. Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine.
Cardiac
BLS
Vitalize/Prioritize Oxygen/Airway (high flow) Body temperature
ALS
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF Consider using CPAP early Intubate if marked (extraordinarily severe) respiratory distress sedation for conscious patients, refer to RSI TREATMENT GUIDELINE (See Page M-11) IV 0.9% NaCl KVO Nitroglycerine (Contraindicated if sexual enhancing medications were taken within past 24 hours [i.e. Levitra, Viagra] and within 48 hours for Cialis) contraindicated if blood pressure less than 100 mm systolic moderate to severe distress, administer IV nitroglycerine as soon as possible 1/150 gr SL may administer 1 SL prior to 12 lead or IV access may repeat after five minutes to a total of three (3) 1 inch paste (may be administered concurrently with SL nitroglycerine) Nitroglycerine 5-10 g/min IV Infusion Pump increase 5-10 g/min every 35 minutes maintain at least 100 mmHg systolic blood pressure Furosemide (Lasix) 0.51.0mg/kg IVP not to exceed 80mg Dopamine (Intropin) 520 g/kg per minute titrated as needed for hypotension Morphine Sulfate in 2 mg increments IVP until desired effect max. dose 10 mg and Promethazine (Phenergan) 12.5 mg IVP or Dolasetron Mesylate (Anzemet) 12.5mg IVP contraindicated if blood pressure less than 100 mmHg systolic
IRCEMS uses up to 100mg of Lasix Dilute Phenergan in 10cc before IV administration. MCFR uses Ondansetron (Zofran) 4mg IVP/IM over 30 seconds. Ped 0.1mg/kg over 30 seconds in plave of Phenergan or Anzemet
C-5
Pediatric
Furosemide (Lasix) 1.0mg/kg IVP slowly over 12 minutes Morphine Sulfate 0.10.2mg/kg IVP slowly, maximum single dose 4mg
10/7/2009
NARROW COMPLEX TACHYCARDIA

BLS
ALS
Serious signs or symptoms
chest pain, shortness of breath, decreased level of consciousness, low blood pressure, shock, pulmonary congestion, congestive heart failure, acute myocardial infarction unstable condition must be related to the tachycardia
Vagal maneuvers
carotid sinus pressure is contraindicated in patients with carotid bruits avoid ice water immersion in patients with ischemic heart disease
IRCEMS uses Adenocard 12mg for each dose.
MCFR administers Cardizem by IV infusion only, over 5 minutes. The max first dose is 25 mg with a max second dose of 35 mg.
Lifeline uses Verapamil 2nd line.
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF IV 0.9% NaCl KVO Unstable, with serious signs or symptoms ventricular rate greater than 150 beats per minute may give brief trial of medications (see STABLE OR BORDERLINE below) refer to CARDIOVERSION TREATMENT GUIDELINE (See Page C-3) immediate cardioversion seldom needed for rates less than 150 beats per minute (see SERIOUS SIGNS OR SYMPTOMS at left) Regular Rhythm further treatment not recommended if patient stable vagal maneuvers Adenosine Phosphate (Adenocard) 6mg IVP over 13 seconds (As rapid as possible in the most proximal IV port, followed by a rapid fluid bolus.) after 12 minutes, 12mg IVP over 13 seconds; may repeat once Diltiazem (Cardizem) 0.25mg/kg IV over 2 minutes may repeat, if necessary, 15 minutes after first dose, 0.35mg/kg IVP over 2 minutes, consider synchronized cardioversion if rhythm does not convert and / or patient becomes unstable Irregular Rhythm (A-Fib, A-Flutter, MAT {multifocal atrial tachycardia}) > 130 symptomatic Diltiazem (Cardizem) 0.25mg/kg IV over 2 minutes may repeat, if necessary, 15 minutes after first dose, 0.35mg/kg IVP over 2 minutes, synchronized cardioversion if rhythm does not convert Wide QRS complex refer to WIDECOMPLEX TACHYCARDIA TREATMENT GUIDELINE (See Page C-10)
Cardiac
Pediatric
Adenosine (Adenocard) 0.1 mg/kg IVP rapid push maximum single dose 6 mg second dose 0.2 mg/kg IVP rapid push maximum single dose 12 mg third dose 0.2 mg/kg IVP rapid push maximum single dose 12 mg
C-6
10/7/2009
CARDIAC GUIDELINES
PULSELESS ELECTRICAL ACTIVITY

BLS
Vitalize/Prioritize Oxygen/Airway Application of AED, refer to AED G UIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions)
ALS
EKG monitor Intubate IV 0.9% NaCl Consider possible causes: 6H 6T Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia, refer to HYPOTHERMIA TREATMENT GUIDELINE (See Page T-5) Hydrogen Ion (acidosis) (sodium bicarbonate) Hyper/Hypokalemia (consider calcium chloride or sodium bicarbonate) Hypoglycemia Tamponade (pericardiocentesis) Tension pneumothorax (needle decompression) ThrombosisCoronary (ACS) ThrombosisPulmonary (embolism) Toxins blockers Trauma Vasopressin 40u IVP to replace 1st or 2nd dose of Epi or Epinephrine 1.0mg 1:10,000 IVP/IO q 35 minutes Absolute or relative bradycardia give Atropine 1.0mg IVP, repeated every 35 minutes up to a total of 3mg (0.04mg/kg) Sodium Bicarbonate 1 mEq/kg IVP Calcium Chloride 10mg/kg IVP if patient on calcium channel blocker or history of renal failure Glucagon 1-5mg IVP for blocker overdose
Sodium Bicarbonate 1mEq/kg

definitely helpful in known preexisting hyperkalemia acceptable, probably helpful in known preexisting bicarbonateresponsive acidosis overdose with tricyclic antidepressants to alkanize urine in overdoses acceptable, possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated, may be harmful hypoxic lactic acidosis
Atropine 1.0mg IVP

the shorter atropine dosing interval (3 min) is possibly helpful in cardiac arrest
Cardiac
Vasopressin 40u IV push is first line for MCFR
SFR uses Vasopressin in place of Epi in PEA
Pediatric
Epinephrine Epinephrine repeated every 35 minutes 0.01mg/kg epinephrine (0.1cc/kg) 1:10,000 IVP or IO, or 0.1mg/kg epinephrine (0.1cc/kg) 1:1,000 ET Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4.2% solution expel 25cc of sodium bicarbonate 8.4% and draw 25cc of 0.9% NaCl
10/7/2009
C-7
VENTRICULAR ECTOPY
Caution
Although the loading dose of lidocaine does not need to be reduced, the maintenance dose should be decreased by 50% in the presence of jaundice, acute MI, congestive heart failure, circulatory shock, JVD, unconsciousness, or in patients older than 70 years of age. AHA recognizes that mixing two or more antiarrythmics can cause ectopy.
BLS
ALS
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF IV 0.9% NaCl KVO Determine need for acute suppressive therapy (use only 1 antiarrhythmic) suspected MI or acute chest pain with one or more of the following: multiformed PVCs couplets runs of VT Amiodarone 150mg IV over 10 minutes, may repeat once Maintenance drip- 1mg/min Lidocaine 0.50.75 mg/kg IVP repeated every 510 minutes to cumulative total of 3 mg/kg maintenance infusion 24 mg/min Procainamide (Pronestyl) 20mg/min IV drip until: 1) ectopy suppressed or, 2) hypotension ensues or, 3) QRS is widened by 50% of its original width or. 4) 17 mg/kg is reached (12 mg/kg for patients with cardiac or renal dysfunction) maintenance infusion 14 mg/min
Cardiac Cardiac
MCFR uses Amiodarone as the preferred antiarrhymic
MCFR does not carry Procainamide (Pronestyl)
C-8
10/7/2009
CARDIAC GUIDELINES
VENTRICULAR FIBRILLATION / PULSELESS VTACH

Caution
Although the loading dose of Lidocaine does not need to be reduced in the pulseless patient, the maintenance dose should be decreased by 50% in the presence of jaundice, acute MI, congestive heart failure, circulatory shock, JVD, unconsciousness or in patients older than 70 years old.
Sodium Bicarbonate 1 mEq/kg

definitely helpful known preexisting hyperkalemia acceptable, probably helpful known preexisting bicarbonate-responsive acidosis, overdose with tricyclic antidepressants, to alkanize urine in overdoses acceptable, possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated, may be harmful hypoxic lactic acidosis
BLS
Vitalize/Prioritize Oxygen/Airway Perform CPR until defibrillator attached; continue through arrest Application of AED, refer to AED GUIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions)
Fluid bolus after drug administration

be prepared to administer a 20-30cc bolus of IV fluid and elevate the arm after each IV medication
ALS
Defibrillate with single shock For specific Joule settings refer to APPENDIX A Resume CPR immediately (give 5 cycles or aproximately 2 minutes of CPR) Return of spontaneous circulation assess vital signs, support airway, breathing provide medications appropriate for blood pressure, heart rate and rhythm Rhythm change without spontaneous circulation PEA, refer to PULSELESS ELECTRICAL ACTIVITY TREATMENT GUIDELINE (See Page C-7) asystole, refer to ASYSTOLE TREATMENT GUIDELINE (See Page C-1) Hypothermic, refer to HYPOTHERMIA TREATMENT GUIDELINE (See Page T-5) Persistent or recurrent VF/VT intubate IV 0.9% NaCl KVO Vasopressin 40u IVP to replace 1st or 2nd dose of Epi Epinephrine 1.0mg IVP every 3-5 minutes defibrillate (refer to Appendix A for Joule settings) administer medications of probable benefit in persistent or recurrent VF/VT Amiodarone 300mg IVP repeated at 150mg IVP in 5 minutes Maintenance drip of 1mg/min after conversion Lidocaine 1.5mg/kg IVP repeated at 0.5 - 0.75 mg/kg every 35 minutes to a cumulative total of 3mg/kg Magnesium Sulfate 12 g IVP in torsades de pointes or suspected hypomagnesemic state or severe refractory VF defibrillate (refer to Appendix A for Joule settings) Sodium Bicarbonate 1 mEq/kg
Cardiac
or
Vasopressin 40u IV push is first choice for MCFR AHA recommends: Avoid mixing antiarrhymics if possible. MCFR uses Amiodarone as the preferred antiarrhymic
Pediatric
Defibrillate with a single shock (refer to Appendix A for Joule settings) Epinephrine Epinephrine repeated every 35 minutes 0.01mg/kg Epinephrine (0.1cc/kg) 1:10,000 IVP or IO, or 0.1mg/kg Epinephrine (0.1cc/kg) 1:1,000 ET Amiodarone 5mg/kg IVP my be repeated up to max 300mg Maintenance drip refer to Broselow for dose Lidocaine 1mg/kg IVP or IO, repeated every 35 minutes to a total of 3mg/kg Magnesium Sulfate 25 to 50 mg/kg max 2 gm IVP in torsades de pointes or suspected hypomagnesemic state or severe refractory VF Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4.2% solution expel 25cc of sodium bicarbonate 8.4% and draw 25cc of 0.9% NaCl
MCFR uses Amiodarone as the preferred antiarrhymic
10/7/2009
C-9
WIDECOMPLEX TACHYCARDIA
If there is any doubt whether monomorphic or polymorphic VT is existant in the unstable patient, cardiovert refer to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3)
BLS
ALS
EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF IV 0.9% NaCl KVO Unstable, with serious signs or symptoms ventricular rate greater than 150 beats per minute (monomorphic VT) may give brief trial of medications (see STABLE OR BORDERLINE below) refer to CARDIOVERSION TREATMENT GUIDELINE (See Page C-3) immediate cardioversion seldom needed for rates less than 150 beats per minute (see SERIOUS SIGNS OR SYMPTOMS at left) ventricular rate greater than 150 beats per minute (polymorphic VT) consider sedation refer to APPENDIX A for cardioversion settings Regular Rhythm (V-Tach or Uncertain) Amiodarone 150mg IV over 10 minutes repeated as needed to max of 2.2g in 24 hrs Maintenance drip of 1mg/min Lidocaine 0.50.75mg/kg IVP repeated every 510 minutes to cumulative total of 3mg/kg SVT with Aberrancy Adenosine Phosphate (Adenocard) 6 mg IVP over 13 seconds after 12 minutes, 12 mg IVP over 13 seconds; may repeat once consider synchronized cardioversion or defibrillation if patient becomes unstable, go to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) Irregular Rhythm (Polymorphic V-Tach) Unstable - Defibrillate refer to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) Amiodarone 150mg IV over 10 minutes repeated as needed to max of 2.2g in 24 hrs Lidocaine 0.50.75mg/kg IVP repeated every 510 minutes to cumulative total of 3mg/kg Magnesium Sulfate 1-2g IV diluted in 10cc over 2 minutes for Torsades de Pointe
Serious signs or symptoms

chest pain, shortness of breath, decreased level of consciousness, low blood pressure, shock, pulmonary congestion, congestive heart failure, acute myocardial infarction unstable condition must be related to the tachycardia
Cardiac
Lidocaine
use lower doses and longer intervals for: patients older than 70 years liver failure heart failure smaller body size bradycardias conduction disturbances (particularly blocks)
Maintenance drip
initiate maintenance drip of drug that converts rhythm
MCFR uses Amiodarone as the preferred antiarrhymic IRCEMS uses 12mg doses of Adenosine only Adenosine is used for diagnostic reasons after Lidocaine
Pediatric
Adenosine (Adenocard) 0.1 mg/kg IVP rapid push maximum single dose 6 mg second dose 0.2 mg/kg IVP rapid push maximum single dose 12 mg third dose 0.2 mg/kg IVP rapid push maximum single dose 12 mg Amiodarone 5mg/kg IV over 20 - 60 minutes Synchronized cardioversion go to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) if conversion to sinus rhythm does not occur after two attempts, the diagnosis of SVT should be reconsidered; sinus tachycardia may actually be present
C - 10
10/7/2009
TRAUMA AND ENVIRONMENTAL GUIDELINES
Trauma / Environmental
Evaluate all trauma patients for Trauma Alert Criteria
BITES AND STINGS
Trauma/Environmental
BLACK WIDOW BLS Prioritize/Vitalize Oxygen/Airway ALS EKG monitor IV 0.9% NaCl KVO in large vein Diazepam (Valium) 5 mg IVP to max of 10mg or Lorazepam (Ativan) 1mg IVP or nasally may be repeated to a max of 4mg Pain control (see Pain Management Treatment Guideline, page M10) Physician Consult Calcium chloride 10% (request dosage) Pediatric Calcium chloride 10% (request dosage) Diazepam (Valium) 0.3 mg/kg IV no faster than 3 mg/min or lorazepam (Ativan) 0.1mg/kg IV Rationalization: Benzodiazepines (Valium/Ativan) potentiate the effects of GABA (gamma-amino butyrate) which will facilitate inhibitory GABA neurotransmission and other inhibitory transmitters, blocking the pain. BROWN RECLUSE BLS Prioritize/Vitalize Oxygen/Airway ALS EKG monitor IV 0.9% NaCl KVO Pain control (see Pain Management Treatment Guideline, page M10) MARINE INJURIES BLS Prioritize/Vitalize Irrigate area with 0.9% NaCl, sea water, vinegar or ammonia Jellyfish or Man-of-war stings Apply meat tenderizer paste Remove barbs or tentacles if visible (scrape off, do not try to grab it or more poison will be released) Apply hot packs to relieve pain
10/7/2009 T-1
Observe for shock or allergic reaction; if allergic reaction, please refer to Allergic Reaction Treatment Guideline (see page M-3) ALS EKG monitor IV 0.9% NaCl KVO Pain control (see Pain Management Treatment Guideline, page M10)
SNAKE BITE
CONTRAINDICATIONS
The use of ice, tourniquet or constricting bands is contraindicated.
Caution
If a tourniquet is applied prior to arrival, physician consult is indicated prior to removing the tourniquet. Let the physician decide whether or not it should be removed.
BLS
Prioritize/Vitalize Oxygen/Airway Mark initial edematous area Keep patient calm Rapid, undelayed transport If snake is DEAD, bring to ED for identification
ALS
EKG Monitor IV 0.9% NaCl KVO Allergic reaction or anaphylaxis, refer to Allergic Reaction Treatment Guideline (see page M-3) Refer to apropriate guideline for arrhythmias
Physician Consult
Pain control, refer to Pain Management Treatment Guideline, ( see page M-10) Rationale: may potentiate the toxin
SLCFD uses Kool-A-Burn for 1st, 2nd and 3rd degree burns less than 15% BSA.
BURNS
Caution
Burn patients are at high risk of developing hypothermia. Observe closely for any signs of shivering
BLS
Prioritize/Vitalize Oxygen/Airway High flow for inhalation burn (strongly consider advanced airway control) Remove or cool heat source if present (i.e. tar, clothing) Cool compress dressing on minor burns with sterile saline (1st degree only) (do not apply ice directly to burns) Dry, sterile burn sheet for 2nd and 3rd degree burns Use Rule of Nines to determine percentage of body surface area involved in burn, (see Appendix D, page AD-1) Consider a Trauma Alert for 2nd and 3rd degree burns greater than 15% BSA Electrical and chemical burns Spinal immobilization on electrical burns, if patient has had loss of consciousness, fall, or pain from trauma T-2 10/7/2009
TRAUMA AND ENVIRONMENTAL GUIDELINES ALS

EKG monitor IV 0.9% NaCl, two (2) lines if major burns If hypotensive (blood pressure less than 100 mm systolic), 250 cc bolus, repeat as necessary, then 250 cc/hr infusion Pain control (see Pain Management Treatment Guideline, page M-10)
Pediatric
Bolus 20 cc/kg, then 20 cc/kg hr Pain control (see Pain Management Treatment Guideline, page M-10) SLCFD requires two or more of the following to perform Pleural Decompression: *Altered LOC or unconscious *Respiratory distress and/or cyanosis * Loss of radial pulse or hypotension
CHEST INJURY
BLS
Vitalize/Prioritize Oxygen/Airway (high flow) reevaluate oxygenation Spinal immobilization if indicated Repeat chest exams Consider the following treatments leave any penetrating object, stabilize and seal around it
ALS
EKG monitor 12 Lead EKG if time allows IV 0.9% NaCl set as needed Consider the following treatments tension pneumothorax refer to PLEURAL DECOMPRESSION GUIDELINE (See Page P-11) dress open chest wounds, seal on three (3) sides (observe for signs of tension pneumothorax) pericardiocentesis refer to PERICARDIOCENTESIS GUIDELINE (See Page P-29) Refer to apropriate guideline for arrhythmias
CRUSH INJURY
Caution
Compressive force to the head, neck, chest, or abdomen should be removed immediately
Indications
Compression in excess of 60 minutes Involvement of large muscle mass Absent pulse / capillary return in distal limb Weak, rapid pulse Usually absence of pain in affected region Onset of shock The activation of specialized teams (i.e. Technical Rescue and HAZMAT) should be considered early.
BLS
Vitalize / Prioritize Oxygen / Airway
ALS
EKG monitor IV large bore 0.9% NaCl 1000cc bolus then 250-500cc/hr infusion Sodium Bicarbonate 50mEq IVP Pain control, refer to Pain Management Treatment Guideline (see page M-10) 10/7/2009 T-3
EMERGENCY MEDICAL GUIDELINES Pediatric

IV 0.9% NaCl 40cc/kg bolus (max 1000cc) Sodium Bicarbonate 1mEq/kg IVP Above treatments should be done concurently with extrication.
DROWNING/NEAR DROWNING
Caution
Consider the possibility the drowning may be secondary to some other trauma MCFR consider CPAP if lungs sound wet and no history of barotrauma.
BLS
Vitalize/Prioritize Oxygen/Airway Spinal immobilization if indicated
ALS
EKG monitor IV 0.9% NaCl KVO if hypotensive (blood pressure less than 100 mm systolic) run wide open until blood pressure is 100 mm systolic, then 250 cc/hr ACLS guideline
Physician Consult
sodium bicarbonate 1 mEq/kg IVP for near drowning MCFR and SFR carry the Morgan Lens
Pediatric
Do not delay transport for multiple IV attempts; drugs may be given endotracheally or intraosseous
EYE INJURIES
BLS
Vitalize/Prioritize Oxygen/Airway Toxic chemical/burns remove any contacts flush eyes with 0.9% NaCl; minimum of 20 minutes for acids and alkalines use Morgan Eye Lens, if available Trauma stabilize any penetrating objects apply sterile dressing to both eyes
ALS
Toxic chemical/burns tetracaine 12 gtts in the affected eye(s) prior to flushing
FRACTURES
BLS
Vitalize/Prioritize Oxygen/Airway Spinal immobilization if indicated Immobilize, refer to SPLINTING PROCEDURAL GUIDELINE (See Page P-72) Dress open wounds with sterile dressings T-4 10/7/2009

ALS transport is indicated for any multiple, long bone, pelvic or open fractures EKG monitor IV 0.9% NaCl 250 cc/hr infusion (if lungs clear) when patients condition permits, establish IV access prior to moving patient if multiple, long bone or pelvic fracture administer 250 cc bolus, repeat as necessary Pain control (see Pain Management Treatment Guideline, page M-10) line, page M-10)
HEAD INJURIES
BLS
Vitalize/Prioritize Oxygen/Airway Spinal immobilization Transport with backboard elevated 30 degree headup position
ALS
EKG monitor IV 0.9% NaCl KVO 250 cc bolus if blood pressure less than 100 mm systolic
HEAT TRAUMA
Caution
Do not over cool to the point of shivering
BLS
Vitalize/Prioritize Oxygen/Airway Cool patient
ALS
EKG monitor IV 0.9% NaCl 250 cc bolus, repeat as necessary, then 250 cc/hr
Passive Rewarming
Methods include removing wet clothes, covering with blankets or sheets and turning the heat on in the vehicle.
HYPOTHERMIA
Caution
Certain brands of thermometers may not read as low as the temperatures listed in this section.
Active external warming

Methods include electric or charcoal warming devices, hot water bottles, heating pads, radiant heat sources, and warming beds, hot packs
BLS
Determine patient priority Remove wet garments Protect against heat loss and wind chill (blankets) Maintain horizontal position Avoid rough movement and excess activity Core temperature: mild hypothermia, 3436 C (93.296.8 F) passive rewarming active external rewarming moderate hypothermia, 3034 C (86.093.2 F) 10/7/2009 T-5

passive rewarming active external rewarming of core areas Severe hypothermia, less than 30 C (86.0 F) Vitalize/Prioritize Oxygen/Airway
ALS
EKG monitor IV 0.9% NaCL KVO Cardiac arrest VF/VT initial treatment, refer to Ventricular Fibrillation Treatment Guideline, (see page C-9) CPR Intubate Core temperature less than 30 C (86.0 F) Continue CPR Withhold IV medications Limit shocks for VF/VT to 3 maximum Transport Core temperature greater than 30 C (86 F) Continue CPR Give IV medications as indicated, but at longer intervals Repeat defibrillation for VF/VT as core temperature rises Notification of receiving facility early to place rewarming equipment on standby
MCFR does not use this procedure.
LOCAL ANESTHESIA
Indications
Anesthetize insertion area for sternal IO
BLS
Vitalize/Prioritize Oxygen/Airway Circulatory support as necessary
ALS
EKG monitor Lidocaine 1% with Epinephrine 1:100,000 10cc Create wheel with approximately 5cc SQ in area to be injected Allow for the initial effect of SQ Lido/Epi, then administer remainder of solution onto the periosteum / bone cortex and surrounding tissues After 90 seconds, the site is anesthetized
Hyperbaric Facilities: St. Marys Medical Center
SCUBA DIVING INJURIES

Do not use Nitrous Oxide in SCUBA injuries CAUTION The following are CONTRAINDICATED CPAP, Trendelenburg positioning, and massage of the affected joints. Helicopter transport necessitates the pilot maintaining altitude at less than 1000 feet.
BLS
Vitalize/Prioritize Oxygen/Airway (High flow) via non-rebreather mask or BVM T-6
10/7/2009

Contact the nearest hospital with HBOC ASAP. This will initiate recall of the hyperbaric diving medicine specialists to the receiving facility. Contact St. Marys ER Nurses Desk (561) 8812900 Spinal immobilization if suspected trauma Immobilize prior to removal from water if possible Transport supine Monitor for complications Consider bringing in dive tables, dive computer, and water sample from scene Treat for associated hypothermia with passive re-warming PRN Obtain a thorough clinical history of the event For Professional consultation contact: DAN 24 hours/day 1919684 4 DAN
ALS
SaO2 readings that do not improve with supplimental O2 may require RSI EKG monitor Perform 12 lead in patients with Arterial Gas Embolism (AGE) symptoms IV 0.9% NaCl 250 bolus until normotensive, then 250cc/hr Aspirin 324-325mg chewable (4 pediatric chewable aspirin) Pneumothorax / Tension Pneumothorax consider the following treatments: MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. Ped 0.1mg/kg in place of Phenergan or Anzemet
10/7/2009
T-7

observe for signs of tension pneumothorax decompression of tension pneumothorax, refer to PLEURAL DECOMPRESSION PROCEDURAL GUIDELINE (See Page P-11) Pain control, referrunoff to Pain Management *Contain irrigation if possible Guideline (see page M-10) Phenergan 6.25 - 12.5mg IM or Anzemet 12.5mg IVP for nausea/vomiting
Physician Consult
Pericardial emphysema with signs of pericardial tamponade, refer to PERICARDIOCENTESIS PROCEDURAL GUIDELINE (See Page P-29) Consider transport to facility with hyperbaric chamber early
Toxicology
Toxicology
OVERDOSE
BLS
Vitalize/Prioritize Oxygen/Airway consider notification of poison control Poison Control Center 18002823171
ALS
EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Altered LOC, refer to Altered Level of Consciousness Treatment Guideline (see page M4) Seizures, refer to Seizure Treatment Guideline (see page M-14)
Physician Consult
Nasogastric tube
SPECIFIC TOXICOLOGICAL EMERGENCIES

BENZODIAZEPINE OVERDOSE
Common Benzodiazepines: Alprazolam (Xanax) Clonazepam (Klonopin) Chlorazepate (Tranxene) Diazepam (Valium) Esfazolam (Prosom) Flurazepam (Dalmane) Halazepam (Paxipam) Lorazepam Midazolam Oxazepam Prazepam Quazepam Temazepam Triazolam (Ativan) (Versed) (Serax) (Centrax) (Doral) (Restoril) (Halcion)
T-8
10/7/2009
TRAUMA AND ENVIRONMENTAL GUIDELINES BLS

ALS
EKG monitor IV 0.9% NACL KVO Altered LOC, refer to Altered Level of Consciousness Treatment Guideline (see page M4) Seizures, refer to Seizure Treatment Guideline (see page M-14)
NARCOTIC OVERDOSE Caution

Administer Narcan with caution in patients that are chronic users of narcotics. Only administer Narcan to maintain airway.
Common Narcotics
Codeine Darvocet Demerol Dilaudid Fentanyl Heroin Lortab Methadone Morphine MS Contin Oxycontin Percocet Percodan Ultram Vicodin
Toxicology
BLS
ALS
EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Alerted LOC, refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures, refer to Seizure Treatment Guideline (see page M-14)
TRICYCLIC ANTIDEPRESSANT OVERDOSE (TCA) Contraindications

Administration of Procainamide, Magnesium Sulfate, Ipecac, Romazicon, or Calcium Chloride is contraindicated.
Common Tricyclics
Amitriptyline Clomipramine Doxepin Maprotiline Protryptyline (Elavil) (Anafranil) (Sinequan) (Ludiomil) (Triptil, Vicatil) Amoxapine Desipramine Imipramine Nortriptyline Trimipramine (Asendin) (Norpramin) (Tofranil) (Pamelor) (Surmontil)
BLS
ALS
EKG monitor 12 Lead EKG IV 0.9% NACL KVO or Saline Lock (if stable) Alerted LOC, refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures, refer to Seizure Treatment Guideline (see page M-14) Sodium Bicarbonate 8.4% 50cc IVP Sodium Bicarbonate 8.4% 50cc/500cc NACL infused @ 50cc/hr 10/7/2009 T-9

Refer to appropriate guideline for arrhythmias
Physician Consult
Nasogastric tube
Pediatric
Sodium bicarbonate 1 mEq/kg Under 1 year of age use 4.2% solution (expel 25 cc out of 8.4% solution and draw up 25 cc of 0.9% NaCl)
CARBON MONOXIDE
Caution
If intubation is necessary, DO NOT HYPERVENTILATE (hypervetilation hinders the elimination of carbon monoxide) SaO2 readings may be inaccurate. Pulse oximetry does not read carbon monoxide
BLS
Toxicology
Remove patient from contamination source while maintaining rescuer safety Use personal protective equipment w/respiratory protection (i.e. air packs) if indicated If multiple patients, refer to MCI Procedural Guideline, page P-74) Vitalize/Prioritize Oxygen/Airway Consider aeromedical transport with long transport distance to a facility with a hyperbaric chamber Transport in semifowlers position
ALS
EKG monitor IV 0.9% NACL KVO
Physician Consult
Request orders for transport to a hyperbaric chamber facility
MCFR drug of choice is Ativan 1mg IV push or nasally
COCAINE OVERDOSE
BLS
ALS
EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Seizures, refer to Seizure Treatment Guideline (see page M-14) 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II, III, or aVF Valium 5mg IVP, Ativan 1mg IVP, or Versed 1-2mg IVP for relief of chest pain may be administered rectally if no IV access (also nasally for Ativan or Versed) may repeat once after 10 minutes if chest pain persists Chest pain unrelieved by Valium, Ativan, or Versed or chest pain greater than 12 hours after use, refer to Chest Pain Treatment Guideline (see page C-4)
Physician Consult
Repeat Valium, Ativan, or Versed Notify emergency department if patient ingests cocaine powder, crack, or packed condom
Pediatric
Valium 0.2-0.5mg/kg no faster than 3mg/min, Ativan 0.1mg/kg, or Versed 1-2mg T - 10 10/7/2009
ECSTASY (MDMA) OVERDOSE

CAUTION
Hyperthermia associated with MDMA overdoses can reach as high as 109 degrees Fahrenheit (42.7 degrees Celsius)
BLS
Vitalize/Prioritize Oxygen/Airway Ice packs in the axilla and groin areas and / or cover patients with wet sheets and fan them.
ALS
EKG Monitor IV 0.9% NaCl or LR KVO Altered level of consciousness, refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Hypotension, refer to Medical Shock Syndromes Treatment Guideline (see page M8) Seizures, refer to Seizure Treatment Guideline (see page M-14)
Toxicology
PHYSICIAN CONSULT
Nasogastric tube
GHB (GAMMA HYDROXYBUTYRATE) OVERDOSE

CAUTION
The patient, despite a comatose condition, will occasionally respond to stimuli violently. This includes fighting attempts at ventilation. Assistance will normally prove necessary to adequately restrain the patient in the ambulance during transport.
BLS
Vitalize / Prioritize Oxygen / Airway Restrain patient if necessary
ALS
EKG Monitor IV 0.9% NaCl or LR KVO Altered level of consciousness, refer to the ALTERED LEVEL OF CONSCIOUSNESS TREATMENT GUIDELINE (SEE PAGE M-4) Seizures, refer to the SEIZURE TREATMENT GUIDELINE (SEE PAGE M-14)
PHYSICIAN CONSULT
Nasogastric tube
TOXIC CHEMICAL EXPOSURE

Caution
Consider early notification of your Hazardous Materials Team. Do not handle any toxic chemical exposure without the correct level of personal protective equipment (PPE) Consult DOT Handbook.
BLS
Remove the patient from the contamination source while maintaining rescuer safety Remove contaminated clothing Brush off dry chemicals T - 11
10/7/2009

Make sure chemical is not water reactive Flush with copious amounts of water for at least 20 minutes Contain runoff of toxic chemicals If multiple patients, refer to MCI PROCEDURAL GUIDELINE (see page P-74) Vitalize/Prioritize Oxygen/Airway
ALS
EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Altered LOC, refer to ALTERED LEVEL OF CONSCIOUSNESS TREATMENT GUIDELINE (see page M-4) Seizures, refer to SEIZURE TREATMENT GUIDELINE (see page M-14) Inhaled toxins, refer to INHALED TOXINS TREATMENT GUIDELINE (see page T-12)
Physician Consult
Use of any chemical antidote kit available on scene
Toxicology
INHALED TOXINS BLS

If multiple patients, refer to MCI Procedural Guidelines (see page P-74) Vitalize/Prioritize Oxygen/Airway
ALS
EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Albuterol (Proventil) 2.5mg via mininebulizer for wheezing may repeat once methylprednisolone (Solu-Medrol) 125mg IVP or dexamethasone (Decadron) 4mg IVP furosemide (Lasix) 40mg IVP with PE signs and/or symptoms Atropine 0.5-1mg IVP, repeat as needed up to 3mg
Pediatric
Albuterol 1.25mg via mininebulizer for wheezing Atropine 0.02mg/kg minimum dose 0.1mg maximum single dose 0.5mg for child, 1mg for adolescent methylprednisolone (Solu-Medrol) 2mg/kg or dexamethasone (Decadron) 0.2mg/kg maximum dose 125mg of Solu-Medrol maximum dose 4mg of Decadron furosemide (Lasix) 1.0mg/kg IVP slowly over 12 minutes
ORGANOPHOSPHATE POISONING
BLS SLUDGE
Remove the patient from the contamination source while maintaining rescuer safety Remove contaminated clothing Brush off dry chemicals Make sure chemical is not water reactive Flush with copious amounts of water for at least 20 minutes Contain run-off of toxic chemicals If multiple patients, refer to MCI Procedural Guideline (see page P-74) Vitalize/Prioritize Oxygen/Airway 10/7/2009
SSalivation LLacrimation UUrination DDiarrhea GGastrointestinal EEmesis

T - 12

EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Altered LOC, refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures, refer to Seizure Treatment Guideline (see page M-14) Inhaled toxins, refer to Inhaled Toxins Treatment Guideline (see page T-12) Atropine 2.0mg IVP every 5 minutes until SLUDGE symptoms are controlled No maximum dose of Atropine
Pediatric
Atropine 0.02mg/kg minimum dose 0.1mg maximum single dose 0.5mg for child and 1mg for adolescent
Toxicology
T - 13
10/7/2009
DRUG REFERENCE
Drug Reference
D-1 03/01/05
ACETAMINOPHEN (TYLENOL*, APAP)

CLASS Non-narcotic analgesic/Antipyretic ACTIONS Reduces fever May block pain impulses peripherally INDICATIONS Pediatric fever over 101 degrees F. when level of consciousness permits. CONTRAINDICATIONS History of hypersensitivity Intolerance to tartrazine, alcohol, table sugar, and saccharin. WARNINGS Verify fever SIDE EFFECTS Anemia, rash, hives DOSAGE Pediatric: 10 mg/kg PO
ACETAMINOPHEN SUPPOSITORIES (RECTAL TYLENOL)

CLASS Non-narcotic analgesic/Antipyretic ACTIONS Reduces fever May block pain impulses peripherally INDICATIONS Use in febrile seizures post Valium administration Establish time of last dose of Tylenol if possible. Tylenol is given every 4-6 hours PRN. CONTRAINDICATIONS History of hypersensitivity Intolerance to tartrazine, alcohol, table sugar, and saccharin. WARNINGS Verify fever SIDE EFFECTS Anemia, rash, hives DOSAGE Adult: 325mg Pediatric: 125mg
D-2 03/01/05
DRUG REFERENCE
ACETYLSALICYLIC ACID (ASPIRIN, ASA)

CLASS Salicylate, anti-platelet ACTIONS Impedes clotting by anti-prostaglandin properties INDICATIONS Chest pain of suspected cardiac origin CONTRAINDICATIONS Active gastro-intestinal bleeding Patient taking coumadin Allergy Children under 16 due to Reyes Syndrome SPECIAL CONSIDERATIONS Some asthmatics, especially those with environmental allergies, consider themselves allergic to acetylsalicylic acid. Often this allergy is actually a predisposition toward acetylsalicylic acid induced bronchospasm. DOSAGE 324mg PO (4 Tablets)
ADENOSINE (ADENOCARD)
CLASS Nucleoside, antiarrhythmic ACTIONS Adenocard is a naturally occurring nucleoside (a glycoside formed by the union of a purine base with sugar) which is normally present in all cells of the body. It directly slows electrical conduction through the AV node of the heart. It interrupts the reentry circuit the etiology of most SVTs (WPW included). Adenocard is rapidly eliminated by vascular components (halflife <10 seconds so side effects are minimal and short-limiting). INDICATIONS To convert hemodynamically stable supraventricular tachycardia (rate above 160) after vagal maneuvers were unsuccessful for conversion. CONTRAINDICATIONS Second- or third- Degree A-V blocks Sick sinus syndrome History of hypersensitivity SIDE EFFECTS Hypotension < 1% of time used May produce short lasting 1st, 2nd, or 3rd degree heartblocks 55% of patients develop a few seconds of conversion arrhythmias (asystole, PVCs, or PACs) at the time of conversion Facial flushing, headache and shortness of breath, lightheadedness and nausea WARNINGS No studies have been performed on the effects of Adenocard in pediatrics. DOSAGES Initial dose 6 mg rapid IV push (60% conversion). If rhythm has not converted in 1 to 2 minutes, 12 mg rapid IVP (92% conversion), may be repeated. HOW SUPPLIED 6 mg and 12mg prefilled syringes
D-3 03/01/05
ALBUTEROL (PROVENTIL, VENTOLIN)

CLASS Adrenergic bronchodilator ACTIONS Albuterol is primarily a beta-2 sympathomimetic and as such produces bronchodilation. Because of its greater specificity for beta-2 adrenergic receptors, it produces fewer cardiovascular side effects and more prolonged bronchodilation than Isuprel. Onset is within 15 minutes; peaks in 60-90 minutes. Therapeutic effects may be active up to 5 hours. INDICATIONS Albuterol inhaler is indicated for relief of bronchospasm in patients with reversible obstructive airway disease including asthma. CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS AND ADVERSE REACTIONS CNS: Nervousness, tremor, headache, dizziness, insomnia CV: Tachycardia, hypertension, angina GI: Drying of oropharynx, nausea, vomiting, unusual taste WARNINGS Use cautiously in patients with coronary artery disease, hypertension, hyperthyroidism, diabetes. Epinephrine should not be used at the same time as Albuterol, however, either may be used subsequent to a failure of the other. Administer cautiously to patients on MAO inhibitors (Nardil, Marplan, Eutonyl) or tricyclic antidepressants. Beta- blockers and Albuterol will inhibit each other. DOSAGE 2.5 mg in 3 ml in a nebulizer at 6 lpm.
AMIODARONE (CORDARONE, PACERONE)

CLASS Antiarrythmic ACTIONS Slows nerve impulses on the heart and acts directly on heart tissues. INDICATIONS Used to correct ventricular arrythmias to a regular rhythm. CONTRAINDICATIONS Known allergy Pregnancy Liver disease Thyroid problems Patients taking Dilantin. SIDE EFFECTS Cough, painful breathing, shortness of breath, dizziness, lightheadedness, syncope, numbness or tingling in fingers or toes, unusual and uncontrolled movements of the body. DOSAGE
V-Fib / Pulseless V-Tach

300 mg IVP may repeat with 150mg IVP
Perfusing patients (V-Tach, Rapid atrial dysrhythmias with poor LV function.)

150mg IV given over 10 min
Maintenance Drip
Infuse 1mg/min (40gtts/min) with mini drip Mix 150mg in 100cc of D5W (1.5mg/cc) IV Infusion pump: 40cc/hr with 100cc volume to be infused. IV drip set (60gtts/cc) 40gtts/min (1.5gtts/sec)
D-4 03/01/05
DRUG REFERENCE
AMYL NITRATE
CLASS Vasodilator ACTIONS Amyl nitrate is chemically related to nitroglycerin. Effective in the treatment of cyanide poisoning by causing the oxidation of hemoglobin to the compound methemoglobin. Methemoglobin reacts with the cyanide ion to form cyanomethemoglobin, which has less affinity for oxygen, thus freeing the hemoglobin to react with oxygen. INDICATIONS Cyanide poisoning Angina CONTRAINDICATIONS None when used for cyanide poisoning SIDE EFFECTS Hypotension, Tachycardia, palpitations, syncope, headache, nausea / vomiting, dizziness, blurred vision WARNINGS Use with caution when treating poisoning with a combination of cyanide and carbon monoxide DOSAGE Administer vapors from crushed inhalant for 30 60 seconds. Repeat continuously as needed.
ATROPINE SULFATE (AS A CARDIAC AGENT)

CLASS Anticholinergic ACTIONS Atropine is a potent parasympatholytic anticholinergic that reduces vagal tone and thus increases automatically the SA node and increases A-V conduction. INDICATIONS Asystole Bradycardia, either absolute (<60 BPM) or relative
A. Serious signs and symptoms must be related to the slow rate. Clinical manifestations include: 1. Signs: Low BP, shock, pulmonary congestion, CHF, Acute MI 2. Symptoms: Chest pain, shortness of breath, decreased level of consciousness
Do not delay TCP while awaiting IV access or for Atropine to take effect if patient is symptomatic. Denervated transplanted hearts will not respond to atropine. Go at once to pacing, catecholamine infusion, or both. CONTRAINDICATIONS None in emergency situations for adults Not to be used in infants below 1 month in age SIDE EFFECTS CNS: Restlessness, agitation, confusion, psychotic reaction, pupil dilation, blurred vision, headache CV: Increase heart rate, may worsen ischemia or increase area of infarction, ventricular fibrillation, ventricular tachycardia, angina, flushing of skin GI: Dry mouth, difficulty swallowing GU: Urinary retention Other: Worsened pre-existing glaucoma WARNINGS Too small of a dose (<0.5 mg in the adult or 0.1 mg in the pediatric patient) or if pushed too slowly may initially cause the heart rate to decrease. Atropine is potentiated by antihistamines and antidepressants. A maximum dose of 0.04 mg/kg should not be exceeded. DOSAGES Adult: Bradycardia: 0.5 to 1 mg IV or ET may repeat every 3 5 minutes until improved or total dose of 0.04 mg/kg has been reached. Asystole: 1 mg IV or ET; then repeat in 3 5 minutes. Pediatric: 0.02 mg/kg IV or ET minimum dose is 0.1 mg and maximum dose is 1 mg. HOW SUPPLIED Prefilled syringes containing 1 mg in 10 cc of solution Multi-dose vials containing 4 mg in 10 cc of solution D-5
03/01/05
ATROPINE SULFATE (AS AN ANTIDOTE FOR POISONINGS)

CLASS Anticholinergic ACTIONS Atropine is a potent parasympatholytic that binds to acetylcholine receptors thus diminishing the actions of acetylcholine. INDICATIONS Organophosphate (e.g. parathion, malathion, rid-a-bug) and carbamate (baygon, sevin and many common roach and ant sprays). POISONING SIGNS ARE SLUDGE: Salivation Lacrimation Urination Defecation GI Cramping Emesis Also: pinpoint pupils, bradycardia and excessive sweating. CONTRAINDICATIONS None when used in the management of severe organophosphate poisoning. SIDE EFFECTS Victims of organophosphate poisoning can tolerate large doses (1000 mg) of atropine. Signs of atropinization is the end point of treatment: flushing, pupil dilation, dry mouth, tachycardia. WARNINGS It is important that the patient be adequately oxygenated and ventilated prior to using atropine as atropine may precipitate ventricular fibrillation in a poorly oxygenated patient. DOSAGE Adult: 2 mg IV. May repeat with 2-5 mg q 5 minutes until atropinization occurs. Pediatrics: 0.05 mg/kg repeat q 25 minutes if necessary
CALCIUM CHLORIDE
CLASS Elemental Calcium for electrolyte balance ACTIONS Calcium chloride is a calcium salt that maintains cell membrane and capillary permeability. Also acts as an activator in the transmission of nerve impulses and contraction of cardiac, skeletal and smooth muscles. INDICATIONS Magnesium sulfate toxicity As an antidote to calcium channel blocker overdose Hyperkalemia (renal dialysis, cardiac arrest) To relieve muscle spasm and pain caused by a black widow spider bite or portuguese man-o-war sting CONTRAINDICATIONS Hypercalcemia Renal calculi SIDE EFFECTS Arrhythmias, cardiac arrest, bradycardia, syncope, phlebitis at IV site, nausea and vomiting SPECIAL CONSIDERATIONS Should be given with extreme caution and in reduce dosage to persons taking digitalis. IV line should be flushed between calcium chloride and sodium bicarbonate administration. DOSAGE ADULT: 10 mg/kg of a 10% solution slow IVP, may be repeated every 10 minutes PEDIATRIC: 5 to 7 mg/kg of a 10% solution slow IVP
D-6 03/01/05
DRUG REFERENCE
CALCIUM GLUCONATE
CLASS Calcium electrolyte ACTIONS Supplemental Calcium therapy INDICATIONS Hypocalcemia Hyperkalemia Hypermagnesemia Calcium channel blocker overdose CONTRAINDICATIONS Hypercalcemia V-fib Digitalis toxicity SIDE EFFECTS Venous irritation, bradycardia, hypotension, cardiac dysrhythmias WARNINGS Patients EKG must be monitored Necrotic to exposed tissue if infiltration occurs DOSAGE 500mg 1000mg IV over 5 10 minutes Peds: 20-25mg/kg IV or IO slowly
CIMETIDINE (TAGAMET)
CLASS H2 blocker ACTIONS Inhibits the action of histamine on the stomach cells, thus reducing acid production. INDICATIONS Allergic reaction Anaphylaxis CONTRAINDICATIONS None in the emergency setting SIDE EFFECTS Fatigue, headache, dizziness, nausea and vomiting WARNINGS May alter blood levels in patients taking Coumadin, Dilantin and Theophylline. DOSAGE 300mg in 50cc infused over 15 minutes
D-7 03/01/05
DEXAMETHASONE (DECADRON)
CLASS Steroid ACTIONS Anti-inflammatory Suppresses immune response (especially in allergic reactions)
INDICATIONS
DIAZEPAM (VALIUM)
CLASS Anticonvulsant/sedative ACTIONS Diazepam suppresses the spread of seizure activity through the motor cortex of the brain. INDICATIONS Major motor seizures Status epileptieus Premedication before cardioversion Skeletal muscle relaxant Acute anxiety states Airway management (when RSI not indicated or available) External pacing Altered L.O.C., violent patient (physician consult) Eclampsia (physician consult) CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS Hypotension, drowsiness, headache, amnesia, respiratory depression, blurred vision, nausea and vomiting. WARNINGS Diazepam is incompatible with many medications. It should not be mixed with any other drugs. IV line should be adequately flushed. May cause respiratory depression or compromise. Flumazenil should be readily available to reverse sedation effects. DOSAGES Adult: 2 10 mg IV, IM or rectal Pediatric: 0.25 0.5 mg/kg IV or rectal HOW SUPPLIED Ampule containing 10 mg in 2 cc
Anaphylaxis (after epinephrine and diphenhydramine) Asthma COPD

CONTRAINDICATIONS
None in the emergency setting

PRECAUTIONS
Should be protected from heat Onset of action may be 2-6 hours and thus should not be considered to be of use in the critical first hour following an anaphylatic reaction
SIDE EFFECTS
Gastrointestinal bleeding Prolonged wound healing

DOSAGE
4-24 mg IV or IM 0.2-0.5mg/kg in Pediatrics
D-8 03/01/05
DRUG REFERENCE
DILTIAZEM (CARDIZEM)
CLASS Calcium Channel Blocker ACTIONS Inhibits calcium influx through slow channels into the cells of the myocardium and smooth muscle. Also dilates coronary arteries and inhibits coronary artery spasm. INDICATIONS PSVT Rapid atrial fibrillation Atrial flutter CONTRAINDICATIONS 2 or 3 degree block Hypotension Sick sinus syndrome VT WPW Do not give with oral beta blockers Do not give with Furosemide in the same IV line (flush the line first) SIDE EFFECTS Hypotension, bradycardia, headache, N/V, CHF, dizziness, weakness, WARNINGS Use with caution for patients with a heart rate of less than 100 bpm. May cause hypotension. DOSAGE 0.25mg/kg slow IVP over 2 minutes. If no effect in 15 minutes:0.35mg/kg slow IVP
DIPHENHYDRAMINE (BENADRYL)
CLASS Ethanolamine derivative antihistamine ACTIONS Diphenhydramine is an antihistamine with anticholinergic (drying) and sedative side effects. Antihistamines appear to compete with histamine for cell receptor site on effector cells. Diphenhydramine prevents, but does not reverse histamine medicated response, particularly histamines effects on the smooth muscle of the bronchial airways, gastrointestinal tract, uterus, and blood vessels. INDICATIONS Allergic reactions Anaphylaxis CONTRAINDICATIONS Newborns Premature infants Nursing mothers Lower respiratory tract symptoms Asthma SIDE EFFECTS AND ADVERSE REACTIONS Hypotension, headache, palpitations, drowsiness, tachycardia, sedation and disturbed coordination. WARNINGS In infants and children especially, antihistamines in overdosage may cause hallucinations, convulsions, or death. As in adults, antihistamines may diminish mental alertness in children. In young children, they may produce excitation. Diphenhydramine has additive effects with alcohol and other CNS depressants (hypnotics, sedatives, tranquilizers, etc.) DOSAGE Adult: 25 50 mg IVP Pediatric: 1 mg 1.25 mg/kg HOW SUPPLIED 50 mg diphenhydramine HCL in 1 ml ampules/prefilled syringes
D-9 03/01/05
DOBUTAMINE (DOBUTREX)
CLASS Inotrope ACTIONS Stimulates beta-1 receptors in the heart, therefore increasing cardiac function, cardiac output, and stroke volume with only minor effects on the heart rate. INDICATIONS Congestive Heart Failure CONTRAINDICATIONS Shock Hypovolemia Tachydysrhythmias SIDE EFFECTS Tachydysrhythmias, Acute Coronary Syndrome, ventricular ectopy, V-fib, V-Tach, nausea / vomiting, hypertension, headache DOSAGE 2-20ug/kg/min IV infusion. Mix 250mg in 250cc (1mg/cc)
DOLASETRON MESYLATE (ANZEMET)

CLASS Antiemetic INDICATIONS Nausea and Vomiting CONTRAINDICATIONS Hypersensitivity to Anzemet SIDE EFFECTS Headache, diarrhea, dizziness, arrhythmias DOSAGE Adult: 12.5 mg
Pediatric: 0.35mg/kg (not to exceed 12.5mg) 2 yrs 16 yrs
D - 10 03/01/05
DRUG REFERENCE
DOPAMINE (INTROPIN)
CLASS Sympathetic Agonist ACTIONS Intropin stimulates dopaminergic beta-adrenergic and alpha-adrenergic receptors of the sympathetic nervous system. It exerts an inotropic effect on the myocardium resulting in an increased cardiac output. Intropin produces less increase in myocardial oxygen consumption than does isoproterenol and its use if usually not associated with tachydysrhythmias. Intropin dilates renal and mesenteric blood vessels at low doses that may not increase heart rate or blood pressure. Therapeutic doses have predominant beta adrenergic receptor stimulating actions that result in increases in cardiac output without marked increases in pulmonary occlusive pressure. At high doses, Intropin has alpha receptor stimulating actions that result in peripheral vasoconstriction and marked increases in pulmonary occlusive pressure. INDICATIONS To treat shock and correct hemodynamic imbalances Improve perfusion to vital organs and to increase cardiac output. CONTRAINDICATIONS Intropin should not be used in patients with tumor of the adrenal gland. SIDE EFFECTS AND ADVERSE REATIONS CNS: Headache CV: Ectopic beats, tachycardia, anginal pain, palpitations, hypotension. GI: Nausea, vomiting Local: Necrosis and tissue sloughing with extravasation. Other: Piloerection, dyspnea WARNINGS Do not administer Intropin in the presence of uncorrected tachyarrythmias or ventricular fibrillation. Do not add Intropin to any alkaline diluent solution since the drug is inactivated in alkaline solution. Patients who have been treated with monoamine oxidase (MAO) inhibitors will require substantially reduced dosage. DOSAGE Mix 400 mg into 250 cc NaCl or 800 mg into 500 cc NaCl to yield a concentration of 1,600 mcg/ml. Begin infusion at 2 to 5 mcg/kg/min and titrate to effect. Dosages of over 20 mcg/kg/ min have been required occasionally to obtain desired effect. HOW SUPPLIED Intropin is supplied in 5 ml ampules containing 400 mg.
EPINEPHRINE (1:1000)
CLASS Sympathetic Agonist ACTIONS Epinephrine is a sympathomimetic which stimulates both alpha and beta adrenergic receptors causing immediate bronchodilation increase in heart rate and an increase in the force of cardiac contraction. Subcutaneous dose lasts 5-15 minutes. INDICATIONS Asthma Anaphylaxis Allergic reaction CONTRAINDICATIONS Hyperthyroidism Hypertension Cerebral arteriosclerosis in asthma In anaphylaxis, however, there are no contraindications SIDE EFFECTS Same as epinephrine 1:10,000 WARNINGS Same as epinephrine 1:10,000. Also causes hyperglycemia. 1:1000 epinephrine cannot be given intravenously, unless diluted first to 10 cc 0.9 % NaCl. Epinephrine should be used with caution to patients >60 years of age, pulse above 120 bpm, systolic blood pressure above 160 mm Hg, hypertensive or cardiac history. DOSAGE Adult: 0.3-0.5 mg (0.3-0.5 cc) subcutaneously. Can also be given sublingually. May be repeated every 15 minutes x 3 if patient in anaphylaxis is hypotensive, start an IV and administer 3-5 cc of a 1:10,000 solution IV push. Pediatric: 0.01 mg/kg up to 0.3 mg subcutaneously. HOW SUPPLIED Ampule containing 1mg/cc Multi-dose vial containing 30 mg in 30 cc
D - 11 03/01/05
EPINEPHRINE (1:10,000)
CLASS Sympathetic Agonist ACTIONS Epinephrine is a sympathomimetic which stimulates both A & B receptors. As a result of its effect, myocardical and cerebral blood flow are increased during ventilation and chest compression. Epinephrine increases systemic vascular resistance and thus may enhance defibrillation. INDICATIONS Asystole, Ventricular fibrillation unresponsive to defibrillation PEA and severe anaphylaxis Other pediatric indications: Hypotension in patients with circulatory instability Bradycardia unresponsive to atropine CONTRAINDICATIONS None in the cardiac arrest situation. SIDE EFFECTS CNS: Anxiety, headache, cerebral hemorrhage CV: Tachycardia, ventricular dysrythmias, hypertension, angina, palpitations GI:Nausea and vomiting WARNINGS Epinephrine is inactivated by alkaline solutions never mix with Sodium Bicarbonate. Do not mix Isuprel and Epinephrine will get exaggerated response. Action of catecholamines is depressed by acidosis attention to ventilation and circulation is essential. Antidepressants potentiate the effect of Epinephrine. DOSAGES Adult: 0.5 to 1.0 mg (5-10 cc) IV every 5 minutes Can also be given double-dose down the ET tube repeat every 5 minutes. As a vaso-pressor infusion 1 mg/ 250 cc NaClstart 1 mcg/min And titrate to desired effect. For Cardiac Arrest: 1 mg IVP every 3 to 5 minutes Pediatric: 0.01 mg/kg (0.1 ml/kg) IV or Double-Dose down ET tube, repeat every 5 minutes as necessary as in infusion start at 0.1 mcg/kg/min up to 1.0 mcg/kg/min. HOW SUPPLIED Prefilled syringes containing 1 mg/10 cc
ETOMIDATE (AMIDATE, HYPNOMIDATE)

CLASS Short acting non-barbiturate hypnotic ACTIONS Etomidate is a short acting non-barbiturate hypnotic that acts at the level of the reticular activating system thereby causing sedation and amnesia. It also works well as an anti-convulsant since it does not require locked access. Lowers ICP and cerebral metabolic rate of oxygen consumption Duration of action 3-5 minutes INDICATIONS Pre-medication for RSI Cardioversion Convulsions. CONTRAINDICATIONS Under 10 years old Hypoventilation Laryngospasm Bradycardia Vomiting SIDE EFFECTS Respiratory depression, apnea WARNINGS Be aware of increased myoclonic activity. Nausea is common post recovery. DOSAGE 0.2mg/kg-0.6mg/kg (usually 0.3mg/kg) IVP over 30-60 seconds Some agencies administer 20mg non-weight based
D - 12 03/01/05
DRUG REFERENCE
FLUMAZENIL (ROMAZICON)
CLASS Benzodiazepine antagonist ACTIONS Antagonizes the actions of benzodiazepines on the central nervous system. Flumazenil competitively inhibits the activity at the benzodiazepine receptor site to reverse the sedative effects of the benzodiazepines INDICATIONS Benzodiazepine overdose CONTRAINDICATIONS Tricyclic antidepressant overdose Status epilepticus Increased ICP SIDE EFFECTS Nausea / vomiting, seizures, agitation, withdrawal symptoms, dizziness, blurred vision WARNINGS Not recommended for use in the elderly Can possibly cause seizures in the overdose patient DOSAGE 0.2mg IVP over 30 seconds, after 30 seconds, 0.3mg IVP over 30 seconds, after 1 minute 0.5mg IVP over 30 seconds, repeat in 20 minute intervals to a total of 3mg. Peds: 0.01mg/kg IV, IO up to 0.2mg single dose. Max dose of 1mg.
FUROSEMIDE (LASIX)
CLASS Diuretic ACTIONS Furosemide is a loop diuretic which inhibits the reabsorption of sodium and chloride in the kidneys. Following administration, venous dilation occurs within 5 minutes which causes reduction in pre-load, thus decreasing cardiac work. Onset of diuresis is 5-15 minutes and effects can last up to 2 hours. INDICATIONS Pulmonary edema Hypertension Congestive heart failure Cerebral edema CONTRAINDICATIONS Furosemide is contraindicated in patients who are allergic to sulfa. Should be used in pregnancy only when benefits clearly outweigh risks. Not to be used on renal dialysis patients. SIDE EFFECTS CNS: Dizziness, tinnitus, hearing loss, headache, blurred vision, weakness GI: Anorexia, vomiting, nausea CV: Hypotension Others: Pruritus, urticaria, muscle cramping WARNINGS Furosemide should be protected from light. Dehydration and electrolyte imbalance can result from excessive dosages. Rapid diuresis can lead to hypotension and thromboembolic episodes. DOSAGE Adult: 0.5 1.0 mg/kg IV slowly over 1-2 minutes (40-80 mg) Can be given IM or double patients daily dose. HOW SUPPLIED Ampules of 10 cc containing 10 mg/cc Prefilled syringes containing 40 mg/4 cc or 100 mg/10cc
D - 13 03/01/05
GLUCAGON (GLUCAGON)
CLASS Polypeptide Hormone ACTIONS Assists with the breakdown of glycogen into glucose. INDICATIONS Hypoglycemia when IV access is unobtainable b-blocker overdose CONTRAINDICATIONS Hyperglycemia SIDE EFFECTS Hyperglycemia DOSAGE Reconstitute glucagen powder with 1cc of diluting solution, then 1mg IM
GLUCOSE 50% (DEXTROSE 50%)

CLASS Carbohydrate ACTIONS A monosaccharide which provides calories for metabolic needs, spares body proteins and loss of electrolytes. Readily excreted by kidney producing diuresis. Hypertonic solution. INDICATIONS Hypoglycemia Coma of unknown origin. CONTRAINDICATIONS CVA with suspected intracranial or intraspinal hemorrhage DTs with dehydration SIDE EFFECTS CV: Thrombosis, sclerosing if given in peripheral vein INTEG: Tissue irritation if infiltration occurs OTHERS: Acidosis, alkalosis, hyperglycemia, hypokale - mia WARNINGS May cause Wernicke-Korsakoff syndrome in acute alcohol intoxication usually this is prevented by administering Thiamine 100 mg. IM or IV. Perform an Accucheck (if possible) and draw a blood sample (red top tube) prior to administering Dextrose. Physician consult should be obtained regarding treatment of low blood glucose levels associated with pregnancy and stroke. DOSAGE Adult: 50 cc of a 50% solution (25 grams) IV Pediatric: Age: birth 1 year Dextrose 12.5% 0.5 1 gm/kg slow IVP Expel 37.5 cc of D-50 and draw 37.5 cc 0.9% NaCl Age: 1 - 8 years Dextrose 25% 0.5 1.0 gm/kg slow IVP Expel 25 cc of D-50 and draw 25 cc of 0.9% NaCl
D - 14 03/01/05
DRUG REFERENCE
GLUCOSE ORAL (GLUTOSE)

CLASS Carbohydrate ACTIONS Glutose 15 is oral Glucose gel containing 40% Dextrose (dglucose), the kind of sugar the body most readily absorbs. INDICATIONS Hypoglycemia in the emergent setting when IV access cannot be obtained. CONTRAINDICATIONS Airway obstruction When suction is not available to maintain the airway of a patient with altered level of consciousness. SIDE EFFECTS Other: Acidosis, alkalosis, hyperglycemia, hypokalemia WARNINGS For oral use only. Use extreme precautions and aggressive management to protect the airway of patients with altered level of consciousness (LOC) providing suction PRN. Use care in application to avoid being bitten by patient. Use reasonable doses in amounts small enough not to occlude the airway. DOSAGE Adult: utilize 15 gm dosage tube PRN Pediatric: utilize 15 gm dosage tube PRN HOW SUPPLIED Prefilled tube containing 15 grams of Glucose (d-glucose), purified water, glycerin, lemon flavoring, and preservatives in an oral gel base.
HEPARIN
CLASS Anticoagulant ACTIONS Inhibits the action of antithrombin III on various coagulation factors including factors IIa, IXa, Xa, XIa and XIIa. Inhibition of factor Xa results in interference with thrombin generations; therefore the action of thrombin in coagulation is inhibited. Heparin also increases the rate of formation of antithrombin III-thrombin complex causing inactivation of thrombin and preventing the conversion of fibrinogen to fibrin. By inhibiting the activation of fibrin-stabilizing factor by thrombin, heparin also prevents the formation of a fibrin clot. INDICATIONS Acute Coronary Syndrome Pulmonary embolism Stroke CONTRAINDICATIONS Active bleeding Hemophilia Thrombocytopenia Suspected intracranial hemorrhage SIDE EFFECTS Hemorrhagic reaction WARNINGS Use with caution in women who are menstruating and pregnancy. Use with caution in geriatric patients. Draw a blue top tube for PT and PTT levels. DOSAGE 5000 units IVP
D - 15 03/01/05
HYDROMORPHONE HCL (DILAUDID)

CLASS Narcotic analgesic ACTIONS Binds with opiod receptor sites in the CNS, altering perception of and emotional response to pain. INDICATIONS Relief of moderate to severe pain from trauma, fractures, dislocations, myocardial infarction, and burns CONTRAINDICATIONS History of hypersensitivity Presence or possibility of intracranial pressure (ICP) Pre-existing respiratory depression (i.e. COPD, emphysema, status asthmaticus CAUTIONS May produce respiratory depression Not to be used in abdominal pain or head injury patients SIDE EFFECTS Respiratory depression Nausea and vomiting Circulatory depression and cardiac arrest have occurred after rapid intravenous injection DOSAGE 1-2mg slow IV, IM. May repeat to a total of 4mg In elderly (65 yrs and older), 0.25 - 0.5mg slow IV, IM. May repeat as tolerated Pediatric: not approved for pediatric use
IPRATROPIUM (ATROVENT)
CLASS Parasympatholytic Bronchodilator ACTIONS Anticholinergic agent acts directly on the smooth muscles of the bronchial tree, by inhibiting acetylcholine at receptor sites. Also reduces vagally mediated reflexes bronchospasms. INDICATIONS COPD Bronchospasm Asthma CONTRAINDICATIONS History of hypersensitivity Glaucoma Allergy to soy or peanut products Use caution in pregnancy, nursing mothers. SIDE EFFECTS Dry mouth, headache, cough, blurred vision, rash, hives DOSAGE One time use. 0.5mg nebulized with 2.5mg of albuterol
D - 16 03/01/05
DRUG REFERENCE
KETOROLAC (TORADOL)
CLASS Analgesic/Non-steroidal anti-inflammatory ACTIONS Ketorolac is a non-steroidal anti-inflammatory drug (NSAID). It has analgesic, anti-inflammatory, and antipyretic effect. Unlike narcotics which act on the central nervous system, Ketorolac is considered a peripherally acting analgesic. It does not have the sedative properties of the narcotics. Ketorolac has been used with morphine and meperidine without adverse effects. INDICATIONS Mild to moderate pain. CONTRAINDICATIONS History of hypersensitivity Not administered to patients with allergies to aspirin or the non-steroidal anti-inflammatory drugs. WARNINGS May cause gastrointestinal irritation and bleeding. SIDE EFFECTS Can cause edema, hypertension, rash, itching, nausea, heartburn, drowsiness, and dizziness. DOSAGE 30 60 mg IM 30 mg IVP HOW SUPPLIED Prefilled syringes containing 15, 30, and 60 mg of the drug
LABETALOL (NORMYDYNE, TRANDATE)

CLASS Beta blocker ACTIONS Adrenergic receptor blocker (both alpha and beta), causing a fall in blood pressure and a slight decrease in heart rate. INDICATIONS Hypertension CONTRAINDICATIONS Bronchial asthma Congestive heart failure Heart blocks greater than first degree Cardiogenic shock Severe bradycardia Chronic bronchitis Emphysema COPD Preexisting vascular disease SIDE EFFECTS Dizziness, nausea, vomiting, diarrhea, increased airway resistance. WARNINGS Use with caution in patients with heart disease. Orthostatic hypotension will occur so patients must remain supine. Nitroglycerine and Labetalol have additive effects and should not be used together except with great caution. This drug masks common signs of shock and hypoglycemia. Dizziness is the most common side effect and tends to occur in earlier stages of the treatment, in patients also receiving diuretics. When administered IV for hypertensive emergencies, Labetalol produces a rapid, predictable fall in blood pressure within 5 to 10 minutes. Will decrease heart rate and should be used with extreme caution in patients with heart rates less than 100. DOSAGE 0.25 mg/kg IV slowly over 2 minutes (20 mg dose for average adult) 5 mg IV over 2 minutes (max 300 mg) NOT FOR USE IN PEDIATRICS
D - 17 03/01/05
LIDOCAINE HCL (XYLOCAINE)

CLASS Antiarrhythmic ACTIONS Decreases ventricular automaticity and raises the ventricular fibrillation threshold. INDICATIONS PVCs: >6 minute. R-on-T phenomenon, multifocal, or in bursts of >2 or more in a row. Ventricular tachycardia Ventricular fibrillation Prophylactic treatment in patients highly suspected of having myocardial infarction. CONTRAINDICATIONS Lidocaine is contraindicated in second-degree heart block Mobitz II: complete A-V block; and Stokes-Adams syndrome If PVCs occur in conjunction with sinus bradycardia, the bradycardia should be treated first SIDE EFFECTS CNS: Drowsiness, numbness, dizziness, blurred vision, tinnitus, euphoria, muscle twitching, Convulsions, tremors. CV: Rare, but with toxic levels hypotension, widening of QRS complex, bradycardia, cardiac arrest. RESP: At toxic levels respiratory depression and/or arrest. WARNINGS Lidocaine is metabolized in liver. Maintenance infusion should be decreased by half in patients with liver disease and low cardiac output states, (i.e. shock, congestive heart failure and/or patient older than 70 years of age.) DOSAGE Adults: 1.0 1.5 mg/kg* IV bolus, repeat with 0.5 1.5 mg/ kg q 5-10 minutes if necessary to a total of 3 mg/kg. Can also be administered IM or Double-Dose down ET tube followed by an infusion at 2-4 mg/min. Pediatrics: 1 mg/kg IV bolus. IV infusion should contain 120 mg LIDOCAINE/100 cc D5W, infuse at a rate of 20-50 mcg/ kg/min. NOTE: The larger dosage approach is recommended in cardiac arrest HOW SUPPLIED Prefilled syringes: 1% = 100 mg/10 cc 2% = 100 mg/5 cc Prefilled bag: 2 gm/500 cc D5W NOTE: Lidocaine jelly is a viscous preparation of 2% Lidocaine that facilitates nasotracheal intubation by providing lubrication and acting as a local anesthetic. D - 18
LIDOCAINE HCL 2% WITH EPINEPHRINE 1:100,000

CLASS Amide derivative ACTIONS Provides profound local anesthesia of intermediate duration. Average anesthesia of at least 60 minutes. INDICATIONS Utilized prior to sternal interosseous infusions (FAST 1 or BIG). CONTRAINDICATIONS None SPECIAL CONSIDERATIONS None
03/01/05
DRUG REFERENCE
LIDOCAINE HCL TOPICAL (XYLOCAINE 2% JELLY)

CLASS Amide derivative ACTIONS Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action. The onset is 3-5 minutes. It is effective when applied to intact skin. Lidocaine may be absorbed following topical administration to mucus membranes, its rate and extent of absorption depending upon concentration and total dose administered, the specific site of application, and duration of exposure. In general, the rate of absorption of local anesthetic agents following topical application occurs most rapidly after itratracheal administration. Lidocaine is metabolized rapidly by the liver. INDICATIONS As an anesthetic lubricant for endotracheal intubation (Oral or Nasal). CONTRAINDICATIONS History of hypersensitivity to local anesthetics. SPECIAL CONSIDERATIONS Use caution in patients with severe shock or heart block. Debilitated elderly patients, acutely ill patients, and children should be given reduced doses commensurate with their age and physical status. Excessive dosage, or short intervals between doses, can result in high plasma levels and serious adverse effects. xylocaine 2% Jelly should be used with extreme caution in the presence of sepses or severely traumatized mucosa in the area of application, since under such conditions there is the potential for rapid systemic absorption. When used for endotracheal tube lubrication, care should be taken to avoid introducing the product into the lumen of the tube. Do not use the jelly to lubricate the endotrachial stylette. If allowed into the inner lumen, the jelly may dry on the inner surface leaving a residue which tends to clump with flexion, narrowing the lumen. There have been rare reports in which this residue has caused the lumen to occlude. DOSAGE Adults: No more than 600 mg in a 12 hour period.
LORAZEPAM (ATIVAN)
CLASS Anticonvulsant/Sedative, Benzodiazepine ACTIONS Lorazepam is a benzodiazepine with a shorter half-life than diazepam. It suppresses the spread of seizure activity through the motor cortex of the brain. INDICATIONS Major motor seizures Status epilepticus Premedication before cardioversion Acute anxiety states CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS Hypotension, drowsiness, headache, amnesia, respiratory depression, blurred vision, nausea and vomiting. WARNINGS Because of its short half-life, seizure activity may recur. In such cases, additional doses may be required. May cause respiratory depression. Monitor respiratory status closely. Romazicon can be used as an antidote. DOSAGE Anxiety: 0.5 2 mg IVP Seizures: 0.5 mg 1.0 mg, may repeat after 15 minutes Neonate (<1 month): 0.05 mg/kg not to exceed 2 mg. May be repeated after 10 minutes. Infants & Children: 0.1 mg/kg over 2 5 minutes. Maximum single dose 4 mg. May be Repeated after 15 20 minutes. HOW SUPPLIED Lorazepam is supplied in ampules and tubex syringes containing 1, 2, and 4 mg in 2 ml of solvent.
Pediatrics: Not to exceed 4.5 mg/kg (2.0mg/lb) of body weight.

HOW SUPPLIED
30 ml Aluminum tube
D - 19 03/01/05
MAGNESIUM SULFATE
CLASS Anticonvulsant/Antiarrhythmic ACTIONS Magnesium Sulfate is a central nervous system depressant and vasodilator. INDICATIONS Eclampsia including pre-eclampsia Torsades De Pointes Refractory V-fib/pulseless v-tach Status asthmaticus CONTRAINDICATIONS Renal diseases Heart blocks CHF Bradycardia Cardiogenic shock SIDE EFFECTS Respiratory depression, bradycardia, heart block, CHF, bronchospasm, postural hypotension. DOSAGE Eclampsia: Loading dose 4 gm/100 cc IV 0.9% NaCl wide open Maintenance dose 2 gm/100 cc at 100 cc/hr Pre-Eclampsia: Loading dose 4 gm/100 cc IV 0.9% NaCl over 15 minutes Maintenance dose 2 gm/100 cc at 100 cc/hr Refractory V-fib: 1 2 gm slow IVP over 1-2 minutes Torsades De Pointes: 1 2 gm diluted in 10 cc NaCl administered IV over 3 minutes, up to 4 6 gms. Status Asthmaticus: 2 gm diluted in 10 cc NaCl administered IV over 3 minutes, up to 4 6 gms. Dose may be repeated if patient is still symptomatic. The time interval to repeat the dose will be based on the patients condition. HOW SUPPLIED 50% Magnesium Sulfate injection, 5 grams {500 mg/ml (4mEq/ml)} prefilled syringe. Vials containing 5 grams in 10 cc solution (0.5 g/cc)
MEHTYLPREDNISOLONE (SOLU-MEDROL)
CLASS Corticosteroid/Anti-inflammatory ACTIONS Steroid which is used to stabilize cell membranes to decrease edema in head trauma and used as an anti-inflammatory drug. Decreases inflammation, mainly by stabilizing leukocyte lysosomal membranes. Also suppresses the immune response, stimulates bone marrow and influences protein, fat and carbohydrate metabolism. Onset of action may be 2-6 hours and thus should not be of use in the critical first hour following an anaphylactic reaction. INDICATIONS Head trauma Severe asthma Allergic reactions COPD CONTRAINDICATIONS Patients with reduced immune system. SIDE EFFECTS May cause fluid retention, CHF, hypertension, abdominal distension, vertigo, headache, malaise, and hiccups. WARNINGS Must be reconstituted and used promptly. DOSAGE Usual dose is 125 mg IV but can be up to 30 mg/kg IV over 30 minutes. HOW SUPPLIED Vial containing 125 mg
D - 20 03/01/05
DRUG REFERENCE
MIDAZOLAM (VERSED)
CLASS Benzodiazepine ACTIONS Short acting CNS depressant that impairs the memory. INDICATIONS Conscious sedation, Premedication for tracheal intubation CONTRAINDICATIONS History of hypersensitivity Glaucoma Shock Alcohol intoxication Overdose Hypotension SIDE EFFECTS Over sedation, hypotension, blurred vision, headache, respiratory depression / arrest, nausea and vomiting WARNINGS Sedative effects may be accentuated by concomitant use of barbiturates, alcohol, or narcotics. Should not be used in patients who have taken CNS depressants. Avoid high doses! May cause hypotension. DOSAGE 2.5mg 5.0mg IVP over 60 years old 5.0mg 10.0mg IVP below 60 years old Peds: 0.1mg/kg IV, max of 2.5mg/kg dose 0.2mg/kg IM, max 5mg
MORPHINE SULFATE (MS)

CLASS Narcotic Analgesic ACTIONS Morphine is a narcotic analgesic which depresses the central nervous system and sensitivity to pain. It increases venous capacitance, decreases venous return and produces mild peripheral vasodilation. Morphine also decreases myocardial oxygen demand. INDICATIONS Pain from acute MI Pulmonary edema Pain from burn Pain from Fx or dislocation to facilitate moving patient CONTRAINDICATIONS Pain due to trauma or acute abdomen Volume depletion or hypotension Head trauma Acute alcoholism Acute asthma History of hypersensitivity SIDE EFFECTS CNS: Euphoria, drowsiness, pupillary constriction, respiratory arrest CV: Bradycardia, hypotension GI: Decreases gastric motility, nausea and vomiting GU: Urinary retention RESP: Bronchial constriction, decrease cough reflex WARNINGS Morphine is detoxified by the liver. It is potentiated by alcohol, antihistamines, barbiturates, sedatives and beta-blockers. DOSAGE Adults: 1 5 mg IV slowly. Repeat with small increments every 5 minutes until desired response is achieved. Can also be given IM or SC. Pediatrics: 0.1 0.2 mg/kg IV slowly. HOW SUPPLIED Ampule containing 10 mg/l cc
D - 21 03/01/05
NALBUPHINE (NUBAIN)
CLASS Synthetic narcotic agonist / analgesic ACTIONS Nubain is a potent analgesic. Analgesic potency is essentially equivalent to that of morphine on a milligram basis. INDICATIONS Pain Management (burns, marine injuries, chest pain, fractures, sickle cell crisis) CONTRAINDICATIONS History of hypersensitivity Respiratory depression Hypotension SIDE EFFECTS Respiratory depression, nausea/vomiting, headache, dry mouth, sedation, hypotension WARNINGS Not indicated for use in children Use may impair the mental or physical abilities Use care with susceptible individuals, might result in physical dependence DOSAGE 2mg 4mg IVP or IM
NALOZONE (NARCAN)
CLASS Narcotic Antagonist ACTIONS Naloxone is chemically similar to narcotics. However, it has only antagonistic properties. It competes for opiate receptors in the brain. It also displaces narcotic molecules from opiate receptors. It can reverse respiratory depression associated with narcotic overdose. INDICATIONS Complete or partial reversal of narcotic depression Respiratory depression secondary to narcotics or related drugs: heroin, methadone, lomotil, pentazocine (talwin) , meperidine (Demerol), propoxyphene, codeine, hydromorphone (darvon), morphine (dilaudid), percodan Suspected acute opiate overdose Unconscious/unresponsive patient of unknown origin. CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS AND ADVERSE REACTIONS CNS: Tremor, agitation, belligerence, pupillary dilation seizures, increased tear production, sweating. CV: Hypertension, hypotension, ventricular tachycardia, pulmonary edema, ventricular fibrillation. GI: Nausea, vomiting WARNINGS
Naloxone should be administered cautiously to persons including newborns of mothers who are known or suspected to be physically dependent on opiates may precipitate an acute abstinence syndrome. May need to repeat Naloxone since duration of action of some narcotics may exceed that of Naloxone. Naloxone is not effective against a respiratory depression due to non-opiate drugs. Use caution in patients with pre-existing cardiac disease or who have received potentially cardiotoxic drugs. Use caution during administration as patients may become violent as level of consciousness increases.
DOSAGE Adult: An initial dose of 0.4 mg 2 mg may be administered IV, IM, or SC. May be titrated to effect and repeated in 2-3 minutes if necessary. If no response after 10 mg, then condition is probably not due to narcotic. Pediatric: 0.01 mg/kg initial dose. 0.1 mg/kg second dose if needed. Maximum cummlative dose of 2.0 mg. HOW SUPPLIED NALOXONE is available in 1 ml (0.4 mg/ml), 10 ml (.04 mg/ ml), and also 1 mg/2 ml prefilled syringes. For childern: 2 ml (0.2 mg/ml) ampule
D - 22 03/01/05
DRUG REFERENCE
NITROGLYCERINE IV (TRIDIL)
CLASS Nitrate, antianginal agent (coronary vasodilator) ACTIONS Increases coronary blood flow by dilating coronary arteries and improving collateral flow to ischemic regions. Produces vasodilation (venous greater than arterial), decreases preload and afterload, reduces myocardial oxygen demand. INDICATIONS Chest pain of suspected cardiac origin Acute pulmonary edema Hypertension CONTRAINDICATIONS Hypotension Patients <12 years old SIDE EFFECTS Headache Nausea and vomiting Hypotension Dizziness, flushing Tachycardia SPECIAL CONSIDERATIONS Avoid Nitroglycerin in the setting of right ventricular infarction; monitor vital signs often. Use IV pump or Dial-A-Flow to deliver specific ml/hr. DOSAGE 5 10 mcg/min IV drip, may increase by 5 to 10 mcg/min until desired effect is achieved or systolic blood pressure <100 mmHg. Pediatric dosage is contraindicated.
NITROGLYCERINE SL (NITROLINGUAL) (NITROBID) (NITROSTAT)

CLASS Nitrate, antianginal agent (coronary vasodilator) ACTIONS Nitroglycerin is a direct vasodilator which acts principally on the venous system although it also produces direct coronary artery vasodilation as a result. There is a decrease in venous return which decreases the workload on the heart and thus decreases myocardial oxygen demand. Sublingual Nitroglycerin is readily absorbed. Pain relief occurs within one minute and therapeutic effects can last up to 30 minutes. INDICATIONS Angina Pectoris Hypertensive crisis Pulmonary edema with hypertension CONTRAINDICATIONS Patients with increased intracranial pressure Systolic blood pressure <100 mmHg Children under age 12 SIDE EFFECTS CNS: Headache, dizziness, flushing, nausea and vomiting CV: Hypotension, reflex tachycardia PRECAUTIONS Tolerance to nitrates easily develops which necessitates increasing the dosage. DOSAGE 1 spray or 1 SL tab contains 0.4 mg Nitroglycerin Adult: 1 spray or 1 tab SL. May repeat in q3-5 minutes for total of 3 doses. Pediatrics: Not indicated
D - 23 03/01/05
NITROGLYCERINE TOPICAL (NITRO-BID)

CLASS Nitrate, antianginal agent (coronary vasodilator) ACTIONS Transdermal absorption, causes coronary vasodilation INDICATIONS Prophylaxis Treatment of angina pectoris CONTRAINDICATIONS History of hypersensitivity Hypotension (systolic < 100mmhg) SIDE EFFECTS Hypotension, headache, nausea and vomiting, blurred vision, dizziness WARNINGS Use with caution for right side injury / infarct. Dosage has not been established in children. DOSAGE 1 inch applied topically to the chest wall. 1 inch = 15mg nitroglycerin
NITROPRUSSIDE (NIPRIDE)
CLASS Vasodilator ACTIONS Directly acts on vascular smooth muscle, therefore results in peripheral vasodilation of arteries and veins. Decreases systemic resistance, preload and afterload and increases cardiac output. INDICATIONS Hypertensive Crisis Congestive heart failure CONTRAINDICATIONS Recent use of Viagra within 24 hours Hypotension Aortic stenosis SIDE EFFECTS Tachycardia, hypotension, dizziness, hypoxemia, CO2 retention, headache, nausea / vomiting WARNINGS Wrap IV set in an opaque cover because the drug is light sensitive. Caution must be used, can result in toxic levels of cyanide. DOSAGE 0.1 10ug/kg/min. Start at 0.1ug/kg/min and titrated to effect. Increase dose every 3-5 minutes until desired effects are achieved. Mix 50mg in 250cc of D5W (200ug/cc)
D - 24 03/01/05
DRUG REFERENCE
NITROUS OXIDE (NITRONOX)

CLASS Analgesic/Anestetic Gas ACTIONS Nitrous Oxide is a central nervous system depressant that causes rapid but easily reversible pain relief. INDICATIONS Substernal chest pain of suspected cardiac origin that does not respond to nitroglycerin or morphine sulfate. Musculoskeletal pain Burns, (excluding respiratory tract burns) Normal and breech childbirth ?? CONTRAINDICATIONS Altered level of consciousness Patients intoxicated with drugs or alcohol COPD Acute pulmonary edema Pneumothorax Barotrauma Acute abdomen Head injury Respiratory tract burns SIDE EFFECTS Headache, dizziness, giddiness, nausea and vomiting. SPECIAL CONSIDERATIONS Vehicle should be well ventilated during Nitrous Oxide administration (turn on the exhaust fan and open windows). When administering Nitrous Oxide to a minor, obtain parental consent or contact the EDP for orders. DOSAGE 50% N2O/50% O2 self administered by patient through the mask or mouth piece. Upon discontinuation of Nitronox, administer supplemental O2 4 lpm/nasal cannula approx. 15 minutes.
OXYTOCIN (PITOCIN)
CLASS Hormone/Uterine stimulant ACTIONS Oxytocin is a naturally occurring hormone. It is used in the emergency setting to control post partum hemorrhage by contracting uterine smooth muscle and lactation. INDICATIONS Post partum hemorrhage CONTRAINDICATIONS Oxytocin should be administered only to patients suffering from severe post-partum bleeding. It is essential to verify that the baby and the placenta have been delivered, and that there is not an additional fetus in the uterus. WARNINGS Can cause overstimulation of the uterus and uterine rupture. SIDE EFFECTS Can cause hypotension, arrhythmias, tachycardia, seizures, coma, nausea and vomiting DOSAGE 20 units/1000 cc 0.9% NaCl infused at 120 150 cc/hr. HOW SUPPLIED Vials containing 10 units in 1 cc
D - 25 03/01/05
PROCAINAMIDE (PRONESTYL)
CLASS Antiarrhythmic ACTIONS Slows conduction through myocardium Elevates V-fib threshold Suppresses ventricular ectopic activity Decreases automaticity of ectopic pacemakers INDICATIONS Persistent cardiac arrest due to ventricular fibrillation and retractory to lidocaine. PVCs refractory to lidocaine V-tach refractory to lidocaine Patients allergic to lidocaine CONTRAINDICATIONS High degree heart blocks PVCs in conjunction with bradycardia (treat rate first) Torsades de Pointes WARNINGS Procainamide should be discontinued when any of the following four occurs: Rhythm resolved Hypotension QRS widens by 50% Maximum dose of 17mg/kg administered SIDE EFFECTS May cause drowsiness, seizures, hypotension, bradycardia, heart blocks, nausea, vomiting, respiratory and cardiac arrest. DOSAGE Bolus drip mix 2 grams in 50 cc 0.9% NaCl run at 20mg/min. Maintenance drip 2 grams in 500 cc run 1-4 mg/min. May give up to 50 mg/min. for shock resistant or recurrent pulseless VT/VF. HOW SUPPLIED Vials containing 1 grams in 10 ml
PROMETHAZINE (PHENERGAN)
ACTIONS A derivative of phenothiazine (thorazine) with antiemetic; anticholinergic and antihistamine effects. INDICATIONS Severe nausea and vomiting Antiemetic Sedation CONTRAINDICATIONS Abdominal pain SIDE EFFECTS Dry mouth, blurred vision, dizziness, confusion, extra pyramidal symptoms (muscle rigidity, tremor) may occur. It may also worsen glaucoma, bladder obstruction or stenosis peptic ulcer. Hemothiazines tend to lower blood pressure and also lower the seizure threshold (i.e. make seizures more likely in seizure prone patients such as alcoholic or epileptics). DOSAGE Adult: 6.25 25 mg IM, IV, oral or rectal Pediatric: 0.2 0.5 mg/kg not to exceed 12.5 mg NOTE: Should be used following Morphine Sulfate administration.
D - 26 03/01/05
DRUG REFERENCE
PROPOFOL (DIPRIVAN)
ACTIONS Diprivan injectable emulsion is an intravenous sedativehypnotic agent producing rapid sedation with minimal excitatory activity, however it has no analgesic properties. The actual mechanism of action is unknown. Onset of sedation usually occurs within 1-3 minutes. After bolus, titrating a maintenance infusion can control the level of sedation. After discontinuing the infusion the effects of the sedation clear within 5-7 minutes. INDICATIONS Induction and maintenance of general anesthesia in the intubated and mechanically ventilated patients. CONTRAINDICATIONS History of hypersensitivity to Propofol or its components (soybean oil, egg lecithin, glycerol) Patients in which sedation is not needed. SIDE EFFECTS Hypotension Bradycardia and decreased cardiac output Respiratory acidosis during weaning May produce copious secretions, larnygospasm and hypotension. Pain or burning at the injection site is common especially when the IV is in a small peripheral vein. SPECIAL CONSIDERATIONS Diprivan is extensively distributed throughout the body. It is eliminated from the body by the liver and the pulmonary system. No dosage adjustments are needed for patients with renal or hepatic failure.
SODIUM BICARBONATE
CLASS Alkalizing agent ACTIONS An alkalizing agent used to buffer acids present in the body during and after severe hypoxia. Bicarbonate combines with excess acids (usually lactic acid) present in the body to form a weak, volatile acid. This acid is broken down into CO2 and H2O. Sodium Bicarbonate is effective only when administered with adequate ventilation and oxygenation. INDICATIONS Metabolic acidosis due to: Cardiac arrest Shock Salicylate overdose Barbiturate overdose Keto acidosis Hyperkalemia Tricyclic antidepressant overdose CONTRAINDICATIONS Congestive heart failure Alkalotic states SIDE EFFECTS Metabolic alkalosis Hypernatremia Cerebral acidosis Sodium and H2O retention which can cause CHF WARNINGS Excessive Bicarbonate therapy inhibits the release of oxygen. Bicarbonate does note improve the ability to defibrillate. May inactivate simultaneously administered catecholamines. Will precipitate if mixed with Calcium Chloride. Administration should be guided by arterial blood gasses and ph. DOSAGE Adult: 1 meq/kg IV. Repeat with 0.5 meq/kg q 10 minutes Pediatric: 1 meq/kg IV. Repeat with 0.5 meq/kg q 10 minutes Infants: 0.5 meq/kg IV (diluted) slowly. May repeat in 10 minutes HOW SUPPLIED Prefilled syringes containing 50 meq/50 cc
D - 27 03/01/05
SUCCINYLCHOLINE CHLORIDE (ANECTINE, QUELICIN)

CLASS Depolarizing neuromuscular blocker ACTIONS Succinylcholine Chloride is a depolarizing muscle relaxant that prevents acetylcholine from binding to receptors on the post-synaptic neuron, thereby inhibiting the generation of an action potential and effectively paralyzing skeletal muscle. Complete paralysis is obtained within 1 minute and persists for approximately 2 minutes. It has no effects on consciousness whatsoever. INDICATIONS To facilitate intubation in patients where other efforts to obtain definitive airway control have failed. CONTRAINDICATIONS Any patients who can not be effectively ventilated with a BVM and oral airway. SIDE EFFECTS Prolonged apnea, bronchospasm, sinus arrest, tachycardia, bradycardia, PVCs, increased ICP, muscle fasciculations. SPECIAL CONSIDERATIONS Since Succinylcholine Chloride effects only skeletal movement and not sensation, the patient should be sedated prior to administration. The use of Succinylcholine will not reduce the patients level of consciousness. The paramedic should verbally reassure the patient before intubation. If unable to intubate the patient, ventilate with BVM and oral airway until spontaneous respirations return (this should occur in approximately 5 to 7 minutes). Less than one percent of the population, and a higher percentage of the pregnant population, lack sufficient pseudocholinesterase to rapidly metabolize Succinylocholine. Paralysis may be dramatically prolonged in these patients. DOSAGE Adult: 1 mg/kg IVP repeated in 1 to 2 minutes if desired effect is not achieved. Pediatric: Same as the adult dose. Can be given IM if needed 3 mg/kg HOW SUPPLIED Vials containing 10 ml of a 20 mg/ml Concentration (200 total milligrams)
TETRACAINE HCL (PRONTOCAINE)

ACTIONS Tetracaine is an ophthalmic solution that produces anesthesia by preventing initiation and transmission of impulses at the nerve-cell membrane. INDICATIONS As an adjunct to facilitate irrigation of foreign bodies in the eye. Toxic/chemical burns to the eye. CONTRAINDICATIONS None in the emergency setting SIDE EFFECTS Rash, irritation, sensitivity SPECIAL CONSIDERATIONS Do not use if the Tetracaine HCL solution contains crystals, or if it is cloudy or discolored. Do not let patient touch or rub the eye after it is anesthetized as this can cause corneal abrasions. May be administered with contact lenses left in eye(s). Patch eye after administering. DOSAGE 1 to 2 drops of a 0.5% solution instilled into the affected eye. Pediatric dose will be the same.
D - 28 03/01/05
DRUG REFERENCE
THIAMINE (VITAMIN B-1)

ACTIONS Thiamine is a sterile solution of Vitamin B1 (can not be produced by the human body). With total absence of Thiamine in the diet, body depletion occurs in approximately three weeks. INDICATIONS For the treatment of Thiamine deficiency Rapid restoration of Thiamine to prevent WernickeKorsakoff in the alcoholic and malnourished patient. Administered to individuals (prior to dextrose) with marginal thiamine status to avoid precipitation of heart failure. CONTRAINDICATIONS History of hypersensitivity WARNINGS Serious hypersensitivity/anaphylactic reactions can occur, especially with repeated dosages. SIDE EFFECTS A feeling of warmth pruritus, urticaria, weakness, sweating, nausea, restlessness, throat tightness, cyanosis, pulmonary edema, and GI bleeding. DOSAGE 100 mg IVP prior to administration of highly concentrated Dextrose solutions. HOW SUPPLIED 100 mg in 1 ml
VASOPRESSIN (PITRESSIN)
CLASS Antidiuretic Hormone ACTIONS Systemic vasoconstriction, increased contractility, increased cerebral and coronary perfusion without undesired effects of myocardial ischemia and irritability. INDICATIONS Ventricular fibrillation Pulseless ventricular tachycardia CONTRAINDICATIONS All other pulseless dysrhythmias SIDE EFFECTS None in the pulseless patients WARNINGS Currently only to be used for pulseless V-fib and V-tach patients DOSAGE 40 units IVP, one time administration. No Epinephrine for 10 min post administration.
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VECURONIUM BROMIDE (NORCURON)

CLASS Nondepolarizng neuromuscular blocker ACTIONS Norcuron is a nondepolarizing neuromuscular blocking agent of intermediate duration. It acts by competing for cholinergic receptors at the motor end-plate. Clinically required neuromuscular blockade will occur in 2.5 to 3 minutes and last approximately 25 to 30 minutes. INDICATIONS Long term paralysis for flight or ground transport to facilitate control of combative patients that have already been intubated. CONTRAINDICATIONS Any patient that an RSI has NOT been successful. SIDE EFFECTS Prolonged apnea, tachycardia, bradycardia, bronchospasm, muscle fasciculations. SPECIAL CONSIDERATIONS If Succinylcholine is used prior to Norcuron, the administration of Norcuron should be delayed until the patient starts recovering from the Succinylcholine-induced neuromuscular blockade. Prior administration of Succinylcholine may enhance the neuromuscular blocking effect of Norcuron and its duration of action. The effect of prior use of other nondepolarizing neuromuscular blocking agents on the activity ofNorcuron has not been studied. Norcuron should only be given to a pregnant woman if clearly needed. DOSAGE Adult: Initial dose: 0.1 mg/kg IVP Maintenance dose: 0.015 mg/kg IVP (25 40 min. after initial dose) Subsequent maintenance doses, if required, may be administered at 12 15 minute intervals. Pediatric: Same as the adult dose. HOW SUPPLIED Vial with 10 mg of a sterile nonpyrogenic freeze-dried buffered cake.
VERAPAMIL (ISOPTIN OR CALAN)

CLASS Calcium channel blocker ACTIONS Inhibits slow channel calcium activity in cardiac and smooth muscles. It blocks the slow inward current due to changes in both calcium and sodium flux. INDICATIONS Paroxysmal Supraventricular Tachycardia refractory to Adenocard in the stable patient Symptomatic Atrial Fibrillation and Atrial Flutter (above 130 BPM with chest pain and SOB) CONTRAINDICATIONS Hypotension (Blood pressure below 120 systolic) Bradycardia History of Wolf-Parkinson-White syndrome SIDE EFFECTS Causes reflex increase in adrenergic tone due to peripheral vasodilation if given for tachycardia due to Wolf-Parkinson-White syndrome. Decreased blood pressure and increased adrenergic response may extend an acute M.I.. May also cause symptomatic bradycardia. Dizziness, headache, fatigue, AV block, peripheral edema, nausea, and asystole. WARNINGS Verapamil may induce severe hypotension and pre-dispose to V-fib if given to V-Tach. If uncertain of origin (V-Tach or wide complex PSVT) treat the rhythm as V-Tach; Verapamil should be avoided. DOSAGE 5 mg slow IVP (0.075 0.15 mg/kg) 10 mg slow IVP in 15 minutes, if necessary
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AEROMEDICAL
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primarily funded through local taxing districts. The private service model represents primarily fixedwing aircraft vendors. These services generally do not respond directly to the scene. They use an on-call staff and perform long-rang missions. These models are primarily funded through insurance and direct cash-for-transport exchanges. The government/private partnership has just came into existence over the last several years. The LifeStar aeromedical program was the first in the nation to use this model. The government agency supplies the crew housing, equipment, supplies, and medical flight personnel. The private industry aviation vendor supplies the aircraft, maintenance, and pilots. This model has proven to be the most economical by far. No taxing districts are needed and the start up fees are minimal for the local government. This model is funded primarily through automobile and private insurance billing.
AEROMEDICAL GUIDELINES, EDUCATIONAL SECTION

THE HISTORY OF AEROMEDICAL TRANSPORT
Transport of injured patients by air can be traced to World War I, when a French fighter plane was used to evacuate a wounded Serb. Fixed-wing transport had limited use until World War II, when the Allies evacuated large numbers of casualties by air, primarily in C-47 transports. The modern era of air medical transport began during World War II, when helicopters transported wounded patients in Burma. During the Korean and Vietnam conflicts, helicopter air medical transport significantly reduced battlefield mortality and became an important and highly visible part of the military trauma system. The successful air medical experience in Vietnam proved the ability of helicopters to transport injured patients directly from trauma scenes to specialized trauma care centers. Awareness of the role military air medical transport made the extension of helicopter use to the civilian arena inevitable. The first air medical transport program was established in 1972 at St. Anthonys Hospital in Denver, Colorado. Since then, the number of air medical programs has grown steadily, reaching more than 160 programs today. Some services that began with a single rotor-wing aircraft have added additional helicopters, fixed-wing, or ground critical care transport capability. Air medical transport services now provide much more than trauma scene response. Transfers from rural emergency departments into tertiary care centers occur on a routine basis and in some cases account for 100% of the call volume of the program. Fixed-wing transports are particularly useful for long distance (i.e. >150-200 miles) interfacility transports and can operate in weather conditions that may restrict rotorwing aircraft.
AIRCRAFT TYPES OPERATING IN FLORIDA Aeromedical providers who utilize the BK117:
Orange County Fire-Rescue Aeromed Bayflite Trauma One Air Care Team Life Flight Eurocopter Kawasaki BK117 Power: 2x684 shp Allied Signal LTS B-1, B-2 Power: 2x738 shp Turbomeca Arriel 1E2 C-1 MTOW: 3,350kg (7,385lb) Maximum useful weight: 1,595kg (3,156lb) Maximum cruise speed: 133kt Maximum range: 294nm (B-2), 292nm (C-1)
Aeromedical providers who utilize the Dauphin:

ShandsCair Eurocopter AS365N2 Dauphin Power: 2x739 shp Turbomeca Arriel 1E2 N2 Power: 2x851 shp Turbomeca Arriel 2C N3 MTOW: 4,250kg (9,370lb) Maximum useful weight: 1,980kg (4,365lb) N2 Maximum useful weight: 1,950kg (4,299lb) N3 Maximum cruise speed: 150kt Maximum range: 464nm
ORGANIZATIONAL MODELS
The hospital based model represents the most common type of approach for providing air medical service to the community. A hospital usually a tertiary or academic center sponsors and/or owns the air medical program. Aircraft, pilots, and maintenance services are often provided by an aviation vendor. (i.e. Tampa General Hospital-Aeromed) The governmental agency model has been used successfully for years. These models are predominantly operated by a law enforcement agency with medical staffing being supplied by the local hospital or fire department. These models are A-2
Aeromedical providers who utilize the S-76C+:

Palm Beach County Health Care District Miami Childrens Hospital Sikorsky S-76C+ Power: 2x856 shp Turbomeca Arriel 2S1 MTOW: 5,307kg (11,700lb) Maximum useful weight: 1,618kg (3,562lb)
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Maximum cruise speed: 155kt Maximum range: 385nm Max Useful Wt: 7,360lbs Max Cruise Speed: .82 Mach, 465kts, 535mph Max Range: 1,436NM, 1,651SM
Aeromedical providers who utilize the EC-135:

Martin County Fire Rescue Holmes Regional First Flight Collier County EMS Baptist Life Flight Florida Flight 1 Eurocopter EC-135 P1/T1 Power: 2x732 shp Turbomeca Arriel 2B1 T1 Power: 2x621 shp Pratt & Whitney PW206B P1 MTOW: 2,720kg (5,996lb) Maximum useful weight: 1,240kg (2,734lb) P1 Maximum useful weight: 1,255kg (2,767lb) T1 Maximum cruise speed: 139kt Maximum range: 322nm
AEROMEDICAL PROGRAM OPERATION

HELICOPTER ORIENTATION AND SAFETY
Aeromedical providers who utilize the A119 Koala:

St. Lucie County Sheriffs Office & St. Lucie County FireDistrict Agusta A119 Koala Power: 1x1002 shp Pratt & Whitney MTOW: 2,720kg (5,996lb) Maximum useful weight: 1,290kg (2,845lb) Maximum cruise speed: 140kt Maximum range: 353nm
Because of their unique capabilities, helicopters are increasingly used for emergency medical services. The ability of the helicopter to get in an out of accident scenes, remote areas and hospital pads quickly is key in delivery of lifesaving care. Training, teamwork and coordination are essential for safe helicopter EMS operations. Aeromedical crew members (ACMs) can contribute significantly to the safety of the mission, the patient, ground personnel and themselves. It is imperative that ACMs receive mission-specific training to ensure a safe standard of operation and preclude any errors which could effect the safety of flight. Types of Helicopters There are many types of helicopters in service in the EMS industry. The helicopter most commonly used in EMS programs are as follows: Single Engine: Single-engine aircraft include but are not limited to, the bell 206 BIII Jet Ranger, Bell 206 LIII Long Ranger, Aerospatiale A Star AS 350 and the Agusta A119 Koala. Twin Engine: Twin-engine aircraft include but are not limited to, the MBB BK117, MBB BO105, Aerospatiale Twinstar AS 355F, Aerospatiale Dauphin SA 365N, Bell 222, Bell 412, Agusta 109A and Sikorsky S76. Helicopter Capabilities Each helicopter has different capabilities. In general, however, single-engine helicopters require less time to start, use less fuel and cost less to operate. Twin-engine helicopters offer a increased safety margin, usually provide increased payload and require more maintenance and more time to start than the single engine aircraft. The standard in the EMS industry is the twin-engine aircraft due to the increased safety margin to the aircraft personnel and patient. Operational Limitations Ceiling/Visibility - Limitations exist under both visual flight rules (VFR) and instrument flight rules (IFR). Ambient Temperature - Most aircraft have both an
Aeromedical providers who utilize the BO105:

Life Net Life Flight Lee County EMS Eurocopter BO105 Power 2x500 shp Rolls-Royce Allison 250 C28C MTOW: 2,600kg (5,732lb) Maximum useful weight: 1,170kg (2,550lb) Maximum cruise speed: 130kt Maximum range: 278nm
Aeromedical providers who utilize the A109:

Baptist Aeromed Agusta A109 KII Power: 2x640 shp Pratt & Whitney Canada MTOW: 2,850kg (6,203lb) Maximum useful weight: 1,280kg (2,822lb) Maximum cruise speed: 156kt Maximum range: 550nm
Aeromedical providers who utilize the Gates Learjet 25:

Power: GE CJ610 MTEW: 15,000lbs
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upper and lower ambient temperature limit. Icing - Flight is prohibited in known icing conditions Wind - The amount of wind in which a helicopter can operate varies, depending on factors such as aircraft type, pilot experience, gust spread, turbulence (mountains, tall buildings, etc.) and other factors. Head winds affect the range of the helicopter and may extend the ETAs. Thunderstorm and severe weather (TRW) - These situations should be avoided unless circumnavigation can be safely accomplished. Altitude Limitations Service ceiling - The limitations section of the helicopter flight manual contains service ceiling information. This figure represents the highest altitude at which flight characteristics and handling for the aircraft have been satisfactorily demonstrated. Oxygen requirements - The FAA requires the use of supplemental oxygen by the pilot and passengers above 10,000 feet under certain conditions. Medical oxygen does not comply with this regulation. Performance - Aircraft performance is adversely affected by increasing altitude. High-altitude landings may not be possible without decreasing the weight of the helicopter. Terrain Slopes - Slope landings require greater precision on the part of the pilot. The degree of the slope that may be negotiated varies, depending on factors such as aircraft type, pilot experience, surface condition, wind direction and velocity. Confined areas - Most programs require a minimum clear area (i.e. 60' x 60' day, 100' x 100' night) for use as a helicopter landing zone. Confined areas present special problems such as obstacles, vertical let-downs, hover OGE (out of ground effect - increased power requirements), safe approach and departure, etc. The use of canned landing zones are being discouraged due extended transport times from the scene to the canned area. It is recommended that the helicopter LZ be located as close to the actual scene as possible. This decreases the Golden Hour time that the patient needs to have the best chance of survival. Surface conditions - Extremely dusty landing zones can reduce visibility to zero due to rotorwash disturbance. Excessively rocky or otherwise uneven landing surfaces may not provide a solid enough base for the aircraft. Flotation devices may be required for the aircraft for over the water operations. Helicopter Safety Pilot-In-Command Responsibilities According to federal air regulations, responsibility for all aspects of the safe operations of the aircraft rests with the pilot-in-command. All passengers must function in and around the aircraft under the pilots direction. The safety of the EMS mission can be enhanced through ACM cooperation. ACM Duties - Normal Operations Seat belts and shoulder harnesses must be used by all personnel. ACMs must know the location and operation of all exits. Loose articles must be securely stowed when no in use. Sharp objects, such as needles and IV catheters, should be protected. ACMs must be trained to use all medical equipment and systems used for patient care.ACMs must be trained to use all the radio equipment located on board the aircraft. ACMs must always remain clear of the flight controls and switches not designated specifically for medical personnel use. Communications with the pilot must be maintained at all times. The pilot should be warned of converging traffic or of obstructions on landing or takeoff. The ACM should advise the pilot prior to use of distracting medical equipment, such as on board suction, lighting, etc. Patient needs, such as altitude or heating/air conditioning requirements, also should be discussed with the pilot. Non-essential conversation should be kept to a minimum during critical phases of the flight. The hot-mike should be used appropriately. ACMs should be highly disciplined in the use of proper terminology to avoid confusion or misinterpretation of instructions during any phase of the mission. ACMs should direct the activities of ground personnel around the helicopter. The number of assistants approaching the helicopter should be kept to a minimum. ACMs also will ensure the tail rotor is secured by either standing watch themselves or by designating a public safety official upon landing. Night protocols should be strictly adhered to. The use of red or amber lighting inside the cabin is preferred because bright
Federal Aviation Regulations (FARs)

FARs are written and enforced by the Federal Aviation Administration. All civil aviation operations, including aeromedical flights, are governed by appropriate FARs. FAR Part 91 - details general operating and flight rules for aircraft flying within U.S. airspace. FAR Part 135 - specifies rules for air taxi and commercial operators. Most aeromedical programs, other than local government (local sheriffs offices) or military, are regulated under Part135 of the FAR.
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white lights destroy the pilots night vision. Lights should be off or dimmed during night landing approaches. ACM Duties - Emergency Procedures Some of the malfunctions/emergencies that may occur during transport include engine failure, tail rotor failure, hydraulic failure, electrical failure, autorotation, fire, inadvertent meteorological conditions (IMC) and emergency aircraft shutdown. ACMs should be aware of these conditions so they can respond appropriately. Emergency procedures should be discussed and planned as part of the pre-flight briefing. Emergency training should include the topics listed in Title 14 Code of Federal Regulations Part 135.331, Crewmember Emergency Training, as appropriate. The following topics also should be covered: Pilot directives Stow all equipment, restrain the patient securely and lock and tighten seat belts/shoulder harness. After the emergency, transfer the patient to a safe location, remove all survival equipment and check to ensure the proper operation of the ELT. Remain at or near the aircraft, providing the aircraft can be seen from the air. If immediate egress is warranted, the ACM should proceed to a pre-designated point referenced from the aircraft. hit the rotor blades. Noise Helicopter engines, transmissions and rotor systems emit loud, high-frequency noise. Permanent high-frequency hearing loss can occur with extended exposure if hearing protection is not used. Wires Wires tend to be more hazardous than other obstructions because they are difficult to see. ACMs and ground personnel must ensure all wires are clear in the approach and departure path of the aircraft. Unsecured Landing Zone The ACM shall ensure adequate security of the helicopter while the pilot remains in the aircraft. Ground agencies who have been trained in helicopter/landing zone safety can be used to secure the area while the aircraft is on the ground. The ACMs assigned to the aircraft and the pilot have the final word when it comes to the safety and operation of the aircraft on the scene. Safety Attitudes Safety is everyones responsibility. Question anything that you do not fully understand regarding aircraft operation and safety. Success or failure in dealing with an emergency usually depends on how prepared you are. Dont be complacent. Safety is a dynamic concept and must be continually addressed. Stay up to date on the latest changes in aircraft safety. Make suggestions to improve current conditions. Safety is the highest priority. Never attempt to influence the decision of the pilot or that of another ACM. The degree of patient injury or illness has absolutely no bearing on whether or not a flight may be safely accomplished. Always conduct yourself as a role model for safety around the aircraft. Observers When operating in and around the aircraft, the observer is under the direction of the pilot and air crew members. The observer will adhere to strict aircraft discipline at all times. The observer shall not disturb or manipulate any equipment. When the observer is occupying the aft compartment, he or she shall always follow the flight teams instructions. The safety of the aircraft and its personnel are paramount.
Hazard Recognition
Main Rotor System On slopes or uneven ground, blade clearance may be deceptive. Blades may flex downward, especially when turning slowly in windy conditions. ACMs or ground crews should not carry tall objects, such as IV poles, or initiate CPR on stretchers under turning rotor blades. NEVER approach or leave an aircraft uphill. ALWAYS approach or leave an aircraft downhill. Tail Rotor System All personnel should be alert to the hazards of the tail rotor system. It is low enough to cause severe injury or death. High speed makes tail rotor blades difficult to see. NEVER approach a aircraft without the pilots or the ACMs permission to do so. Rotor Wash During the landing and departure of helicopters, extremely strong winds are produced. Lightweight articles, such as sheets, mattress pads and gravel, can cause injury, especially to the eyes. Standing downwind can dramatically increase the severity of rotor wash. Avoid tall objects which may
AIR TRANSPORT GENERAL INFORMATION

Training of flight has evolved into a process of acquiring specialized knowledge, skills, and experience. The A-5
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stresses of flight, affecting not only the patients condition but the flight crew as well, are a subject of great concern but one that has been given little consideration. There are nine stresses of flight that we will go over. These stresses are barometric pressure, hypoxia, fatigue, noise, vibration, thermal stress, dehydration, third spacing, and gravitational forces. Conditions that influence these stresses include altitude, duration of flight, pressurized versus unpressurized environment, weather, and the physical condition of both the patient and the flight team.
Hypoxic hypoxia is an inadequate Pa02 caused by reduced oxygen in the atmosphere or an inadequate gas exchange at the alveolar - capillary membrane. Anemic hypoxia is caused by a reduction in the oxygen - carrying capacity of hemoglobin, as demonstrated in sickle cell anemia, CO poisoning, etc. Stagnant hypoxia occurs when the cardiac output does not meet the demands of the tissues, resulting in shock, venous pooling and possibly cardiac arrest. Histotoxic hypoxia is prevalent when the tissues are unable to utilize the available oxygen, as with cyanide poisoning.
Other contributing factors also can increase the incidence of hypoxia. These include pneumonia, COPD, acute asthma, pneumothorax, heart attack, shock, blood loss, smoking, temperature, fitness, alcohol, and other factors. Hypoxia resulting from any abnormal condition experienced by the air crew member or patient is intensified by altitude change. There are four stages of hypoxia, they are:
BAROMETRIC PRESSURE
The effects of barometric pressure change and hypoxia are best represented through a combination of the gas law of Boyle and that of Dalton. Boyles law states that at a constant temperature, the volume of a given gas is inversely proportional to the pressure to which it is subjected. The significance of this law, when applied to flight, is that as altitude increases, barometric pressure decreases, allowing for increased expansion of a gas within a closed or semi closed space. This is especially critical in the transport of patients in an unpressurized aircraft, in which altitude and pressure changes are more extensive than in a pressurized cabin. When transporting patients with such conditions as pneumothorax, bowel obstruction, or gastrointestinal or genitourinary complications, it is advisable to leave nasogastric tubes, foley catheters, chest tubes, and similar equipment open to gravity or low suction. Internal gas expansion and possible deterioration of the patients status are thus minimized. The use of endotracheal tubes, air splints, and MAST (Military Anti-Shock Trousers) warrants frequent volume checks of the cuff and bladder, especially during ascent and decent. Glass bottles should be vented if they cannot be replaced with plastic bags. Crew members must be aware that flying with upper respiratory complications can lead to damage to the eardrum, particularly in an unpressurized cabin at higher altitudes. Daltons law of partial pressure states that the pressure of a gaseous mixture is equal to the sum of the partial pressures of the gases in the mixture. Oxygen accounts for 20.95% to 21% of the earths atmosphere. This percentage remains constant, but the gas expands at altitudes directly related to the change in barometric pressure and there is less oxygen available at higher altitudes. Hypoxia and hypoxemia results and can manifest itself in crew members, as well as in patients.
Indifferent stage - night vision decreases by approximately 28%, heart and respiratory rate increases, and the person is unaware of the symptoms.
Compensation stage - in addition to all indifferent stage signs, night vision is reduced 50%.
Disturbance stage - initial awareness of symptoms. Air hunger, headache, nausea, amnesia, decreased level of consciousness and belligerence are experienced. Nausea and vomiting occur, mainly in children. Critical stage - inability to remain upright is rapidly followed by unconsciousness, seizures, coma and death.
If signs and symptoms of hypoxia in patients or air crew members are ignored, they may result in death. Supplemental oxygen therapy is a prime intervention for both air crew members and patients alike. The type and amount of oxygen delivery depends upon the condition of the patient and/or air crew member.
FATIGUE HYPOXIA
Hypoxia is defined as a inadequate supply of oxygen for cell function. Hypoxemia is an abnormal deficiency of oxygen content in the blood. The four categories of hypoxia are: A-6 A multitude of factors contribute to fatigue in the transport team. Several general factors contribute to the stress of the flight: general health status, smoking, alcohol use, vibration, noise, temperature, rotational shifts, diet, hypoxia, Gforces, and barometric changes. When any crew member has an upper respiratory tract infection, smokes, consumed alco-
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AEROMEDICAL
SIGNS AND SYMPTOMS OF HYPOXIA
Objective Signs:
At 10,000 feet At 18,000 feet At 20,000 feet hyperventilation and impaired task performance. cyanosis, confusion, poor judgment and muscular incoordination. jerking of upper limbs, seizures and rapid unconsciousness.
Subjective Signs:
At 5,000 feet At 10,000 feet At 15,000 feet blurred vision and/or tunnel vision air hunger, apprehension, fatigue, headache, nausea, dizziness and hot and cold flashes. numbness, tingling, euphoria and belligerence.
hol 8 to 12 hours before the flight, did not eat properly before or during the shift, or has not had a restful sleep, the incidence of significant fatigue increases. The mechanical function of the aircraft contributes to fatigue. The noise level and vibration created by the propellers of the fixed-wing aircraft or the rotor blades of the helicopter are continual stressors to the crew and the patient, both mentally and physically, throughout the flight. In addition, weather conditions such as high or low temperatures, storms, winds, and thermal changes (turbulence caused by the meeting of two air masses of different temperatures) contribute to fatigue. Compounding these stresses are the crews emotional and physical stresses of treating a critically ill patient who is enduring the same physiologic effects. Whether the duration of the flight is a short 15 to 30 minutes or is extended for 4 to 6 hours, the effects of fatigue will be noticed by the crew and patient.
late vasoconstriction and decrease sweating. Consequently, in rotorcraft, particularly during hot-weather operations, the vasoconstriction caused by vibration can override or impair the function of the bodys cooling mechanism by decreasing the ability to sweat.
THIRD SPACING AND DEHYDRATION

The aforementioned vasoconstrictive and vasodilatory effects can contribute to the stressors that cause third spacing and dehydration. Since the majority of flights are at lower altitudes and of short duration, the effects are not often evident. However, flight crews must be cognizant of these physiologic stressors in long-distance, high-altitude, or multiple short-scene flights. Signs and symptoms may include edema, dehydration, increased heart rate and decreased blood pressure.
NOISE, VIBRATION, AND THERMAL STRESS

Noise creates a twofold problem for the flight crew. First, increased decibel levels in the aircraft interfere with the ability to properly auscultate lung, heart, and bowel sounds along with blood pressures. Adaptive monitoring procedures include palpation of blood pressures and observation and palpation of the chest (for abnormal excursion or increased dyspnea) and abdomen (for increased distension or guarding). Second, constant exposure to aircraft noise not only temporarily affects hearing ability but may promote hearing loss over a long period. Vibration and thermal changes, depending on whether the change is to greater heat or more cold, can have either an antagonistic or a synergistic effect. The bodys primary response to heart exposure is vasodilatation and activation of the cooling mechanisms. Cold exposure and vibration stimu-
GRAVITATIONAL FORCES
Gravitational (G) forces are most relevant in relation to the patients position in the aircraft, particularly in a fixedwing aircraft. Factors influencing (G) forces are weight and its distribution, gravitational pull, and centrifugal force. The latter two factors relate to blood pooling. Centrifugal force tends to alter the blood flow in the body in proportion to the amount of force imposed. When positive (+G) forces are applied to the body, blood tends to pool in the lower portions of the body; the opposite occurs during negative (-G) application. Patient positioning in some aircraft may minimize or enhance the effects of G-forces, as follows:
Cardiac - consider positioning the patient with head toward the back (aft) position of the aircraft. On ascent, this may enhance the -G forces by pooling the blood in the
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upper part of the body, which may assist in myocardial perfusion.
Obstacles: High-tension wires, cell-phone towers, trees or bushes in LZ, uneven terrain Communications: Should be kept to a minimum. Only transmit needed safety information when on approach. Weather: Advise dispatch to relay on-site information to inbound helicopter.
GPS: Advise ASAP landing zone coordinates. If no GPS available, give nearest cross street reference.
Fluid Overload - Consider positioning the patient with head toward the front of the aircraft. This may enhance the +G forces by pooling the blood in the lower extremities.
Head Injury - Consider positioning the patient head first, with feet toward the back (aft) portion of the aircraft. This may enhance the +G forces by pooling the blood in the lower extremities. This may help reduce the risk of a transient increase in ICP on lift-off.
AIR TRANSPORT PRE-HOSPITAL

Radio communication with scene contacts shall be limited to information that affects the flight crews preparation (i.e. number of patients, presence of hazardous materials, etc.). When the aircraft is on location, no information shall be given unless its related to the landing zone and safety of the aircraft until the aircraft is on the ground. Do not delay the response of the aircraft because of extended extrication. The reason being is two-fold, firstly, upon the aircrafts arrival you not only receive the benefit from its equipment but you also obtain more manpower to treat the patient. Secondly, the main purpose of rotor-wing aircraft in the EMS environment is for rapid transport to specialized tertiary care centers (i.e. trauma centers). This cannot be obtained if the aircraft is sitting at the base site 20 minutes from the scene with extrication in progress. Remember, we have only one (1) hour/60 minutes from the TIME OF INJURY to get the patient to the OPERATING ROOM. The general rule for flight programs is to be on scene no more than 10 minutes from the time of initial landing unless extrication or airway problems arise. All activity at the scene should be directed toward moving the patient to the helicopter. Starting IVs or splinting is not justification for a delay. Once the extrication (if needed) is completed, cervical spine immobilize the patient and prepare to move toward the aircraft. If multiple patients are involved, the flight team must communicate carefully with the incident commander, the pilot, and ensure appropriate loading of the most critical patients take place. If multiple patients are involved, it is highly recommended that shutting down of the aircraft be accomplished if reconfiguration of the aircraft is needed.
Patients: Advise ASAP if multiple patients. Notify aircrafts dispatch as soon as possible if more than one aeromedical provider is responding to the scene. This will allow the pilots to communicate and coordinate their approach. Scene Personnel: Never approach the aircraft unless directed to do so by the pilot or air crew members on scene. Security: Aircraft safety is a priority. No unauthorized vehicle traffic around the aircraft. Placement of a tail rotor guard is a priority once the aircraft has arrived and is secured on the ground. Hazardous Material: No patient will be transported via helicopter unless they are first decontaminated if pesticides, herbicides, or weapons of mass destruction (WMD) are involved.
References: Airborne Patient Care Management Mosbys Medical and Nursing Dictionary, 2003 Thermoregulatory Responses to heat and vibration in men, Aviation, Space and Environmental Medicine 57, No. 11 Basic Human Physiology, The Effects of Long Duration Acceleration Aviation Medicine. The nine stresses of Flight, Journal of Emergency Nursing 13, No. 4 NEMSPA, National EMS Pilots Association, Guidebook to Landing Zones FAMA, Florida Air Medical Association, www.fama.org Physiological Training, DOT Manual, FAA, 1980: 3 Air-Medical Crew National Standard Curriculum, 1st Ed
SELECTING AN ON-SCENE LZ
First, determine if the area is large enough to land a helicopter safely. The landing surface should be flat and firm, free of debris that would blow up into the rotor system. A paved roadway, parking lot or other concrete surface is preferred.
PRE-HOSPITAL CONSIDERATIONS

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Day Landing Zone Size: 60 feet x 60 feet Night Landing Zone Size: 100 feet x 100 feet
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Touchdown Area: the touchdown area should be a square with 60-foot sides, increased to100 x 100 feet at night. The landing site should be clear of people, vehicles, and obstructions such as trees, poles and wires. Keep in mind that wires are extremely difficult at best to see from the air during the day and nearly impossible at night. This is the one time utilization of a spotlight pointed up at the pole where wires make their connection is suggested. Utilization of a fire engines mounted spotlights are preferred while the engine is parked under the wires. Handheld lights may also be used. Furthermore, the landing site must be free of stumps, brush, posts and large rocks. LZ by utilizing the nose of the aircraft as your 12 oclock marker. He should stand with his back to the wind and with his arms raised over his head to indicate he is the ground guide. Once verbal and visual communication is established with the flight crew and a LZ brief is given, the ground guide should clear the LZ. The helicopter will orbit the LZ conducting recon prior to landing. This action is performed to further identify potential problems and execute the proper approach should the pilot need to abort the landing.
GROUND GUIDE CONTINUED

The Ground Guides sole purpose is to ensure scene security thru protection from the dangers of an idling helicopter. Deploy as many public safety officials as necessary to meet the security requirements of each LZ. Ensure that personnel understand their assignment. The tail rotor guards are especially important to the operation. Scene security does not end when the helicopter lands, it is just beginning. DO NOT under any circumstances abandon your responsibility. Scene security MUST be maintained and not abandoned at any time during flight operations. This responsibility includes (1) helicopter stand-by as medical flight crews package one patient, (2) shut down to reconfigure the aircraft for two patients, loading of the patient (s), (3) clearing scene personnel from the LZ during power up and the subsequent lift-off of the helicopter. The ground guide should be far enough from the touchdown area that he can maintain eye to eye contact with the pilot and remain outside the rotor arch. Your job is to STOP anyone (other than those escorted by flight crew members) from approaching the aircraft at anytime. The only hand signal that you need to be aware of is the WAVE-OFF. Anyone at anytime can wave-off the helicopter should you see anything of concern to you. (i.e. people in the LZ, a previously unseen safety hazard, or equipment hanging outside the aircraft). If you have a radio and are monitoring the LZ frequency announce WAVE OFF, WAVE OFF, WAVE OFF. If you do not have a radio, ensure that the pilot or flight crew member aboard the helicopter see your hand gestures in order to acknowledge your request.
WIND DIRECTION & TOUCHDOWN AREA

Consider the wind direction. Helicopters land and take off into the wind. Is the approach and departure path free of obstructions (wires, poles, antennas, trees, etc?)? If there are obstructions, please tell the helicopter crew on the initial radio call.
PERSONAL SAFETY & NIGHT LANDING

When an LZ is established other than on a roadway that has been shut down by public safety, and if time and personnel permit, mark the touchdown area with a light source other than road flares. Road flares are an intense source of ignition and are not appropriate. Nighttime operations may facilitate the need to illuminate the corners of the LZ to make it identifiable to the helicopter. At night . . . assure the spotlights, floodlights and hand lights used to define the touchdown area are not pointed toward the helicopter. Turn-off non-essential lights. White lights, such as spotlights flash bulbs and hi-beam headlights ruin the pilots night vision and temporarily blind him. Red lights, however, are very helpful in finding accident locations and do not affect the pilots night vision. Keep spectators at least 200 feet from the touchdown area. Keep emergency service personnel at least 100 feet away. Have fire equipment (if available) standing by. There is no need to deploy a charged hose line. Assure that everyone wears eye protection. If helmets are worn, chinstraps must be securely fastened (no loose ball caps or helmets blowing up through rotors). Do not land the helicopter in an extremely dusty area or areas with excessive loose debris. (i.e. hay, fresh cut grass) Choose a more appropriate location. This action may cause the helicopter to ingest debris thereby making it mechanically compromised and unsafe to fly.
AVOIDING PATIENT TRANSFER DELAYS

Remember, the reason you called for a helicopter is to expedite transport. Every minute that you delay the transfer of the patient to the flight crew takes away from their golden hour. The Golden Hour can be further broken down. The EMT-Paramedic has a Golden 10 Minutes to assess the critical trauma patient and provide ESSENTIAL needed on-scene management. There is no excuse for holding critical trauma patients at the scene for unmeaningful or unnecessary intervention (i.e. IV attempts) that can be accomplished in flight. Once the helicopter has landed, the only delay should result A-9
GROUND GUIDE
When you hear or see the helicopter, one person should help guide the helicopter into a safe landing. That person must wear eye protection. Guide the helicopter to the
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from an inability to secure a difficult airway and requiring the assistance of the flight crew to do so. Please bring the patient to the flight crew the aircraft were to fly through the hazardous gases, the crew could be poisoned and/or the engines could develop mechanical problems. Poisonous or irritating gases may cling to a victims clothing and go unnoticed until the patient is loaded And the doors of the helicopter are closed; the crew is then compromised.
ASSISTING THE FLIGHT CREW

Once the helicopter has landed, DO NOT approach the helicopter. The flight crew will approach you when it is safe to do so. It is the goal of the flight crew to be off the scene within minutes of their arrival. A patient not requiring additional interventions by the flight crew may be transferred to the helicopter stretcher as report is being taken from the onscene paramedic. Please have any pertinent information written down. Once the patient is cocooned, secured to the stretcher and ready to load, the flight crew may select two or three personnel to assist with movement to the helicopter. PLEASE BE PREPARED WITH PROPER PERSONAL SAFETY EQUIPMENT to assist. Failure to be prepared will cause delay in transport. Helmet with chinstrap fastened, eye protection and hearing protection is recommended. These additional items can be found in the LZ kits located on each fire engine. In order to facilitate lift-off, additional personnel are generally not required on paved roadways. When approaching or departing the helicopter, always be aware of the tail rotor and always follow the flight crews directions for your safety.
HAZARDOUS MATERIAL LIZS

Helicopter landing zones must be selected to avoid ALL possibility of compromising the safety of the helicopter and its crew. When explosives, poisonous gases/vapors, or chemicals in danger of exploding and burning are on site, helicopter landing zones must be prepared UPWIND at least ONE MILE from the hazardous material accident site and never in lowlying areas. For hazardous material accidents involving radioactive materials, the helicopter landing zone must be prepared UPWIND, at least ONE QUARTER MILE from the accident, unless there are radioactive gases (steam or smoke), and in this case, the landing zone must be at least one mile upwind of the accident site. A Final Note Your helicopter ambulance can serve you only if we arrive safely. Our safety and the safety of the people on the ground depends on you, the professionals on the scene.
GENERAL HELICOPTER SAFETY RULES

When working around helicopters, never approach from the rear. Always approach and depart the aircraft towards the front so you can see the pilot, and he can see you. When approaching the helicopter, remember to keep low to avoid the main rotor, because winds can cause the rotor to flex downward. If the helicopter is landed on a slope, approach and depart from the down-slope side only. When the helicopter is loaded and ready for take off, keep the departure path free of vehicles and spectators. If an emergency were to occur, we would need this area to execute our landing. SIDE BAR NOTE - **Martin County Fire-Rescue LifeStar1 will not be transporting any patients exposed to a hazardous or radioactive material.
HAZARDOUS CHEMICALS/GASES
Hazardous chemical and gases are extremely dangerous to the unprotected person and may be fatal if inhaled or absorbed through the skin. Upon initial radio contact, the helicopter crew must be made aware of any hazardous gases in the area of a scene or LZ. Never assume that the crew has already been informed. If A - 10 03/01/05
Haz-Mat Guidelines
Haz-Mat Guidelines
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respond in a defensive fashion without actually trying to stop the release from a safe distance, keep it from spreading, and preventing exposures. ~. 9329). Sixteen hours of training is required for this level by Federal OSHA mandates. Again, additional medical training to decontaminate and manage victims would probably be necessary. The 40hour Haz-Mat Medic or Tox-Medic class is recommended. 29 CFR 1910.120 regulations state that EMTs and Paramedics cannot wear special protective gear, SCBA or respirators unless they have been trained to use them and their responsibilities at the scene require it. In the vast majority of cases, they should be trained to recognize a hazardous materials incident and be able to initiate a response. Decontaminated victims should be brought to them for medical care so that untrained and unprotected EMTs and Paramedics are not put at risk.
HAZARDOUS MATERIALS MEDICAL MANAGEMENT PROTOCOLS

INTRODUCTION
The NIOSH EPA hazardous waste site operations document is helpful in defining the EMT / Paramedics role. It categorizes medical support as involving offsite personnel. Ambulance personnel provide emergency treatment procedures appropriate to the hazards on site. Given EMS personnels medical duties, and responsibilities at a haz-mat spill site (particularly if they are not part of the fire service) they should be trained at least at the First Responder Awareness Level. EMTs and paramedics should be trained at the First Responder Operations Level if they are expected to select and don protective equipment, conduct rescues, decontaminate victims or response personnel. In any case, these two EMS classifications should take a course on the medical management of haz-mat victims that is based on these protocols or their equivalent. Fire service personnel, will be trained at a higher level because of their fire service duties and functions. All of this must be consistent with the haz-mat role that the local EMS agency has defined for EMS personnel. Again, it is the employers responsibility to see that their personnel are properly trained to meet these requirements. First responders at the awareness level are individuals who are likely to witness or discover a hazardous substance release and who have been trained to initiate an emergency response by notifying the proper authorities of the release. They would take no further action beyond notifying the authorities of the release. Given their typical daily responsibilities and training, EMTs and Paramedics clearly are not responsible for making a rescue wearing protective gear, for controlling and containing the release, stopping its spread, or for decontamination of protective equipment. However, they can provide medical care to a fully decontaminated victim. The federal rule does not specify how many hours of training are necessary for this level. We have evaluated the rule and recommend no less than four hours of training as being sufficient to meet the OSHA requirements for this category of responder. Additional medical training to manage hazardous materials victims would probably be necessary. First responders at the operations level are individuals who respond to releases or potential releases of hazardous substances, as part of the initial response to the site for the purpose of protecting nearby persons, property or the environment from the effect of the release. They are trained to H-2
INTRODUCTION TO PROTOCOLS
Health care providers who care for injured persons exposed to hazardous materials must know how to evaluate and manage a contaminated victims medical problems while protecting themselves and others from potential hazardous exposure (secondary contamination). The following treatment protocols provide stepbystep information on how to manage medical problems arising from the most common kinds of hazardous materials (haz-mat) scenes. These protocols are designed for use by Haz-Mat entry team members, paramedics or other rescue health workers in the field, and hospital emergency department physicians and nurses. The protocols are intended as guidelines. They may require modification depending on the resources of a particular department or the needs of a particular patient. It is essential for the safety of health care personnel and patients that hospitals and emergency medical services agencies have a written plan for management of the contaminated victim, and that their personnel are trained to follow it. In all incidents, health care providers should immediately contact the receiving hospital, or Regional Poison Control Center for advice on managing victims of hazardous materials exposure. Controversies abound in the evolving field of environmental toxicology. For this reason, the protocols are sometimes vague or ambiguous. For example, no consensus exists on what specific protective gear, if any, is appropriate for emergency departments and prehospital medical care providers because most authorities agree that it is unacceptable to provide sophisticated protective gear to persons who have not been previously properly fitted and trained in its use.
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Haz-Mat Guidelines
It is imperative that proper decontamination has been initiated by the haz-mat team or other trained responders in the hot zone/decontamination area. Rescuers who are trained to use self contained breathing apparatus, to select the appropriate chemical protective suits, and know how to function in them, are the only ones who should assist with decontamination or enter the hot zone. covering the rest of the body and exposed skin should be carefully checked for contamination. If victims are already properly decontaminated before they are brought to health care providers at the perimeter of the hot zone/decon area, they will pose very little, if any, risk to the prehospital health provider or their vehicle. Thus, health care providers will not generally need to use any specialized protective gear, even for substances considered as potential secondary contaminants. In many cases (e.g., corrosive materials in the eye; oily pesticide skin exposure), prehospital health care personnel may need to repeat or continue decontamination procedures (e.g., eye irrigation; soap/water skin wash) after receiving the victim at the perimeter. Although specialized protective gear should not be necessary, it is prudent for providers to don the protective gear when appropriate. All leather items, wool or other highly absorbent materials that cannot be decontaminated should be removed prior to providing care.
PreHospital Care
Consult the specific protocols for recommended pre hospital care of exposed victims. Note that some of the management protocols may exceed the paramedic scope of practice in a local area. Refer to your local EMS agency medical director for guidance. Victims with few or minimal symptoms are not necessarily safe from progression of illness. Many toxic substances have delayed onset effects, which may appear several hours later, after the victim has returned home. If the toxic substance is known, obtain consultation from the Regional Poison Control Center to determine if delayed effects might be seen and for guidance on triage of asymptomatic or mildly symptomatic exposure victims. Any persons suspected of being exposed should be seen and evaluated by emergency department staff.
No provider should put on a respirator or other specialized gear unless that worker has been previously fitted and trained in its use.
If the transport vehicle is inadvertently contaminated, advice from the local environmental health department, hazardous materials team, or local hazardous materials spill clean up companies should be sought on how to determine the level and location of the contamination and on how to clean it up. Advice should also be sought on how to preserve evidence for law enforcement, and dispose of or clean contaminated clothing and personal items.
Decontamination of Prehospital Personnel

Prehospital workers will not normally need personal decontamination. In those rare circumstances where they have been in the hot zone or have attended to a victim who was not properly decontaminated, they should consider themselves to be potentially contaminated. Consult the lists above or knowledgeable sources to determine the risk of secondary contamination, since in many, if not most cases; no personal decontamination will be necessary. Information can be obtained from the Incident Command Safety Officer at the scene, the receiving hospital, or the Regional Poison Control Center. If in doubt, decontaminate.
Prehospital Triage
Victims with obvious significant illness or injury will need rapid transport and treatment after initial stabilization and basic decontamination is carried out. In virtually all cases, patients with serious trauma or medical illness can be quickly stripped and flushed with water prior to delivery to prehospital health providers outside the hot zone. This is true even in cold or inclement weather. If this cannot be performed because of acute lifethreatening conditions or other circumstances, then the vehicle must be protected and those providing care during transport and driving the vehicle must be properly fitted and trained with the appropriate level of specialized protective gear. However, every effort should be made to decontaminate the victim at the scene if the means to do so are available. In those jurisdictions where a prehospital provider might be placed in such a situation without assistance from a properly trained hazmat specialist, advance arrangements for additional training and protective equipment should be made.
Victim and Response Personnel Followup

The names, addresses, and telephone numbers of all personnel and victims who have been or may have been exposed at a haz-mat scene should be recorded for future notification if it is subsequently determined that medical evaluation or treatment is required.
Prehospital Decontamination
Unprotected EMS responders must advise on and observe the decontamination procedures from a distance to ensure that they are properly carried out. They should practice with the local haz-mat team to become familiar with the steps involved. If there is any doubt about the potential for secondary contamination, decontaminate the victim. A contaminated appendage can be washed without wetting the whole body if that is the only part contaminated. Clothing
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NOTE: This document is designed to address the most common types of chemicals found. Please refer to your individual departments resources (Cameo, Tomes, Toxicology manuals) for clinical management of these and other medical emergencies. Also consider contacting the Poison Control Center for South Florida at: FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. Flush exposed skin with water spray. If clothing has been soaked by acid or acid spray, remove and doublebag clothing and flush skin for 1 2 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.
PREHOSPITAL MANAGEMENT ACIDS & ACID MISTS (NOT Including Hydrofluoric Acid) FORMS:
Gas, liquid (variable concentrations), mixtures with water, and aerosolized dusts. 1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing and circulation). Reevaluate airway, intubating the trachea if victim has developed severe respiratory distress. Provide highflow oxygen by mask. Attach cardiac monitor. 3. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing, strider or coughing. 4. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 1015 minutes or until symptoms of pain or irritation have resolved. 5. Victims with minimal or quickly resolving symptoms probably do not require immediate evaluation in the emergency department. However, remember that with certain acids and lowsolubility gases (e.g., fuming nitric acid forming nitrogen oxides) pulmonary edema may occur after a delay of 1224 hours. 6. Ingestion: DO NOT induce vomiting. Immediately dilute with 1 glass of water or milk. FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222
BACKGROUND:
Acids act as direct irritants and corrosive agents to skin and moist mucosal membranes. Severe burns may result. Generally, these substances have very good warning properties. Even fairly low airborne concentrations of acid mists or vapors produce rapid onset of eye, nose and throat irritation. Inhalation of higher concentrations can produce cough, strider, wheezing, chemical pneumonia or noncardiogenic pulmonary edema. Occasionally, pulmonary edema may be delayed for several hours, especially with lowsolubility gases such as nitrogen oxides (given off by nitric acid). Ingestion of acids can result in severe injury to the airway, esophagus and stomach.
POTENTIAL FOR SECONDARY CONTAMINATION:

Small amounts of acid mists can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. However, clothing which has become soaked with concentrated acid may be corrosive to rescuers. Once the victim has been stripped and flushed with water, there is no significant risk of secondary contamination. Decontamination is not necessary for victims with inhalation exposure only.
PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA:

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus particularly if mists or vapors are present. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor.
PREHOSPITAL MANAGEMENT
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize
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Haz-Mat Guidelines
Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed. 3. If clothing has been soaked by liquid ammonia, remove and doublebag. Flush skin with water spray for 1 2 minutes. Remove contacts and irrigate exposed eyes if symptomatic.
PREHOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION:

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective a equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary 2. Evaluate ABCs (airway, breathing, and circulation). Watch for signs of airway closure and laryngeal edema, such as hoarseness, strider, or retractions. Administer oxygen by mask. Bronchodilators maybe helpful for wheezing. Intubate if patient manifests severe respiratory distress from pulmonary edema or upper airway swelling. Obtain arterial blood gases and chest xray if respiratory distress is present. If respiratory distress is present or if exposed to low solubility gases such as nitrogen oxides, admit and observe 24 to 48 hours for possible delayed onset of pulmonary edema. Severe upper airway edema may necessitate endotracheal intubation or cricothyrotomy. Aerosolized bronchodilators (e.g., Albuterol) may be helpful for victims with wheezing. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, or Morgan Lens, for at least 1015 minutes or until symptoms of pain or irritation have resolved. Victims with minimal or quickly resolving symptoms after brief inhalation exposure probably do not require immediate evaluation in the emergency department. Ingestion: DO NOT induce vomiting. Immediately dilute with 1 glass of water or milk. FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222
AMMONIA (LIQUID AND GAS) FORMS:

Gas (anhydrous) and liquid (aqueous solutions, variable concentrations). NOTE: Liquefied compressed gas may produce cryogenic (freezing) hazard as it is released into the atmosphere.
BACKGROUND:
Ammonia (NH3) is a direct irritant and alkaline corrosive agent to moist mucous membranes and, to a lesser extent, to intact skin. Ammonia has very good warning properties. Even fairly low airborne concentrations produce rapid onset of eye, nose and throat irritation. Higher concentrations can produce cough, strider, wheezing, chemical pneumonia or non cardiogenic pulmonary edema. The onset of pulmonary edema is usually rapid but may occasionally be delayed for 1224 hours. Ingestion of concentrated ammonia solutions (e.g., > 5%) may cause serious corrosive injury to the esophagus and stomach.

Small amounts of ammonia vapor can be trapped in clothing after an overwhelming exposure but are usually not sufficient to create a hazard for health care personnel away from the scene. However, clothing which has become soaked with concentrated liquid ammonia may be corrosive to rescuers. Once the victim has been stripped and flushed with water, there is no significant risk of secondary contamination.

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir device or manually triggered oxygen powered breathing device, if possible and practical.
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be H-5
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caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 been stripped and flushed with water, there is no significant risk of secondary contamination.

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus particularly if mists or vapors are present. Silicone breathing apparatus masks may not protect rescuers for some blister agents due to chemical incompatibility. Approved butyl rubber masks are prefered. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. Flush exposed skin with water spray. If clothing has been soaked by acid or acid spray, remove and doublebag clothing and flush skin for 1 2 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.
BLISTER AGENTS FORMS:

There are two agents referred to as blister agents, mustard agents and lewsite. Sulfur mustard agents are colorless when pure, but typically are a yellow to brown oily liquid with a slight mustard to garlic odor. Nitrogen mustards can be colorless to pale yellow with a fishy, musty, fruity, or butter almond odor. Lewsites are an oily, colorless liquid while pure, but is amber to black when impure. The lewsites may have the odor of geraniums or garlic-like. These agents produce vapors, but may be dispersed in a gas, aerosol, or liquid form.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. Assistance from the local haz-mat team or your Regional Poison Control Center should be requested to verify that decontaminaiton efforts are sufficent. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing and circulation). Reevaluate airway, intubating the trachea if victim has developed severe respiratory distress. Provide highflow oxygen by mask. Attach cardiac monitor. 3. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing, strider or coughing. 4. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 1015 minutes or until symptoms of pain or irritation have resolved. FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222
BACKGROUND:
Blister agents are considered to be a chemical warfare agent. In the form of gas or liquid, blister agents affect the skin, eyes, lungs, and gastro-intestinal tract. Internal organs may also be affected as vapors are taken up in the circulatory system and transported throughout the body. The effects of blister agents may not be immediate. Though Lewsite effects are immediate, pateints exposed to mustard agents do not show signs or symptoms for 2 to 24 hours after exposure. Signs of blister agents include reddening and blistering of effected tissue. Mild exposure may result in tearing, inflammation of the skin, irritation of mucious membrane, hoarseness, coughing and sneezing. Severe exposures which are incapacitating may include loss of sight, formation of blisters on the skin, nausea, vomiting and diarrhea, with severe respiratory distress. If inhaled, burns may cause swelling of the airway and bronchiole passagesand patients may present with non-cardiogenic pulmonary edema.

Small amounts of liquid can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. However, clothing which has become soaked with blister agents may be corrosive to rescuers. Once the victim has H-6
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Haz-Mat Guidelines PREHOSPITAL MANAGEMENT

Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Treat burns per Burn protocol. Consider pain management as appropriate. Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed.
PATIENT MANAGEMENT IN THE HOT ZONE! DECON AREA:

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical 3. If clothing has been soaked by hypochlorite solution, remove and doublebag. Flush skin with water spray for 1 2 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing, and circulation). Reevaluate airway, intubating the trachea if victim has developed severe respiratory distress due to upper airway swelling or pulmonary edema. Continue to provide high flow oxygen by mask. Attach cardiac monitor. 3. Aerosolized bronchodilators (e.g., Albuterol) may be helpful for victims with wheezing. 4. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, or Morgan Lens, for at least 1030 minutes or until symptoms of pain or irrigation have resolved. 5. Victims with minimal or quickly resolving symptoms probably do not require immediate evaluation in the emergency department. Those with persistent cough, wheezing, or altered mental status should receive urgent medical evaluation. 6. Ingestion: DO NOT induce vomiting. Immediately dilute with 1 glass of water or milk.
CHLORINE GAS FORMS:

Gas (anhydrous) or liquid (aqueous chlorine) are usually in the form of hypochlorite, variable concentrations. The liquid hypochlorite solutions are very unstable and react with acids to release chlorine gas. NOTE: Liquefied compressed gas may produce cryogenic (freezing) hazard as it is released into the atmosphere.
BACKGROUND:
Chlorine is a highly irritating gas, which rapidly forms hydrochloric acid after contact with moist mucous membranes in the upper airway and in the lungs. Symptoms occur rapidly and provide good warning properties for exposure. Low concentrations produce eye, nose and throat irritation. Higher concentrations produce cough, wheezing, choking, chemical pneumonitis, or pulmonary edema. Ingestion of concentrated hypochlorite solutions can cause serious corrosive esophageal or stomach injury.

Small amounts of chlorine gas can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. However, clothing which has become soaked with concentrated hypochlorite solution may be corrosive to rescuers and may offgas chlorine. Once the victim has been stripped and flushed with water, there is no significant risk of secondary contamination. Decontamination is not necessary after simple inhalation exposure.
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minH-7
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utes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 to remove themselves from the tot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. If clothing has been soaked by solid or liquid CN containing material, remove and doublebag clothing. Flush skin with water spray for 12 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing, and circulation). Reevaluate airway, intubating the trachea if victim is unconscious or has developed severe respiratory distress. Continue to provide high flow oxygen by mask. Attach cardiac monitor. Consider use of sodium thiosulfate IV. 3. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 20 minutes or until symptoms of pain or irrigation have resolved.
CYANIDE FORMS:
Gas (hydrogen cyanide), liquid (solutions of cyanide salts), and solid (cyanide salts). Hydrogen cyanide gas may be formed when acid is added to a cyanide salt or a nitrile.
BACKGROUND:
Cyanide (CN) is an extremely toxic compound, which is widely used in industry in a variety of forms (gas, liquid, solid). CN gas (HCN) is a major toxic component in cases of smoke inhalation. CN produces toxicity by interfering with cellular metabolism. Secondarily, CN can interfere with the transmission of oxygen. Symptoms and signs include headache, dizziness, vomiting, tachypnea, tachycardia, and coma. There may be a distinctive odor (bitter almonds) on the victims clothing or breath. Death can occur within minutes of exposure. If exposure is by inhalation of CN gas, peak toxic effects are seen within minutes, but after ingestion of a CN salt, effects may be delayed until the CN is absorbed from the stomach.
Note: Rapid intervention is imperative to a positive outcome. This can be done be early recognition and having properly trained personnel and specialized medication available. Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. If patient is unconscious but still breathing, administer Amyl Nitrite inhalant, allowing patient to inhale Amyl Nitrite for 20-30 seconds per minute. If patient is not breathing, intubate and place perles in the BVM reservoir and ventilate. Administer 100% supplemental O2. Establish IV - with Normal Saline

If the exposure was by inhalation of HCN gas, there is not little risk of secondary exposure to rescuers. Victims whose clothing is contaminated with HCN solution can secondarily contaminate rescuers by direct contact or through off-gassing. Victims who have ingested CN solutions pose the greatest risk to responders, if regurgetaiton occurs.

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed
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Haz-Mat Guidelines
Sodium Nitrite 10ml of a 3% solution IV over 2 minutes. (Pediatric dose is .33 ml/kg of a 3% solution over 10 minutes). Sodium Thiosulfate 50 ml of a 25% solution over 10 minutes. (Pediatric dose is 1.65ml up to 50 ml over 10 minutes). Do not administer Sodium Thiosulfate in Hydrogen Sulfide poisoning). Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 potential for secondary contamination is low and decontamination is not required. Liquid formulation of ETO may be absorbed by clothing, shoes, and boots from which it can off gas. Remove and throw out grossly contaminated clothing, shoes and boots.

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. Remove exposed individual from source of contamination. Remove grossly contaminated clothing, shoes and boots and throw out. Flush the skin with water spray vigorously for at least 15 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.
ETHYLENE OXIDE (ETO, EO) FORMS:

Liquid and gas. Used to produce ethylene glycol for antifreeze products, sterilize food, fumigate books, dental, pharmaceutical, medical and scientific equipment and supplies, and, in health care facilities, to gas sterilize equipment. ETO in its pure form is extremely flammable, explosive and toxic. Inhalation or direct contact by dermal exposure should be avoided. ETO is a colorless gas with an etherlike (sweetish) odor that is readily detected at first; however, continued exposure results in olfactory fatigue.
BACKGROUND:
ETO in a gaseous form can enter the body through the lungs, skin or eyes. Shortterm exposure can cause irritation to eyes, nose, throat and lungs. Even brief skin contact with liquid ETO can cause edema and erythema with progression to blister formation in 612 hours. Acute exposure to several hundred ppm can lead to nausea, vomiting, olfactory fatigue, nervous system injury and respiratory distress. Prolonged breathing of these high concentrations can cause dizziness, weakness, chest pain and pulmonary edema. Symptoms after mild exposure usually clear within a few hours. However, onset of pulmonary edema may be delayed up to 24 hours. Symptoms usually clear without residual within hours after termination of exposure. The material is a known sensitizer and has produced allergic and anaphylactic reactions. Peripheral neuropathy has been infrequently observed. Cancer and adverse reproductive effects, including spontaneous abortions among female hospital workers, have been reported in various studies but longterm effects are not completely known.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing, and circulation). Quickly establish airway, and stabilize C spine if trauma if suspected. Administer supplemental oxygen as soon as it is practical. 3. Give bronchodilators if significant wheezing is present. 4. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 1015 minutes or until symptoms of pain or irrigation have resolved. 5. Victims with minimal or quickly resolving symptoms may not require hospital emergency department evaluation.

Following inhalation exposure to ETO gas ONLY, the
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon
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process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. If the victim has been soaked by formalin solution, remove and double bag clothing and flush skin for 1 2 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. 2. Evaluate and support ABCs (airway, breathing, and circulation). Reevaluate the airway, intubating the trachea if victim has developed severe respiratory distress due to upper airway swelling or pulmonary edema. Continue to provide supplemental oxygen. Attach cardiac monitor. 3. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing. 4. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, or Morgan Lens, for at least 20 minutes or until symptoms of pain or irrigation have resolved. 5. Victims with minimal or quickly resolving symptoms of eye and throat irritation do not require immediate evaluation in the emergency department. Those with persistent cough, wheezing, or altered mental status should receive urgent medical evaluation. 6. Ingestion: DO NOT induce vomiting. Immediately dilute with 1 glass of water or milk.
FORMALDEHYDE FORMS:
Formaldehyde is a gas. Formalin is an aqueous solution, usually about 35% formaldehyde that may also contain 5-15% methanol.
BACKGROUND:
Formaldehyde is a gas with a pungent odor used widely in paper processing, wood products, preform insulation, carpeting, furniture, and fabrics. It is a highly water soluble gas with toxicity beginning at very low levels of exposure. Inhalation of high concentrations can cause severe coughing, wheezing, and noncardiogenic pulmonary edema. Skin and eye irritation may occur, and direct contact with concentrated aqueous solutions can cause burns. Ingestion of Formalin may cause corrosive injury of the esophagus and stomach, and absorption of the formaldehyde and methanol can cause metabolic acidosis and blindness due to metabolism to formic acid. Formaldehyde is a known animal and suspected human carcinogen.

Victims who have inhaled formaldehyde gas are not contaminating to others and do not require decontamination. Victims whose clothing or skin is soaked with formalin solution may offgas formalin and methanol, but once the clothing has been removed and the skin flushed with water, there is no significant risk of secondary contamination of rescuers outside of the hot zone, even if the characteristic residual odor of formaldehyde is still detectable.
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be

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Haz-Mat Guidelines
caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. EKG Monitoring Establish IV - with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. Remove and doublebag clothing. Flush skin with water spray for 1 2 minutes with water spray. Remove contact lenses and irrigate exposed eyes if symptomatic.

1. If victim is NOT decontaminated and responder is properly trained, don appropriate agentspecific protective equipment and selfcontained breathing apparatus. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local haz-mat team or your Regional Poison Control Center. If victim is decontaminated, don appropriate protective equipment consistent with risk of secondary contamination. If available, magnesium sulfate solution (Epsom salt) or lime water (calcium hydroxide) is effective irrigating solutions. Also, magnesium containing antacids such a Maalox or Mylanta can be applied topically. 2. Evaluate and support ABCs (airway, breathing, and circulation). Reevaluate airway, intubating the trachea if victim is unconscious or has developed severe respiratory distress due to upper airway swelling or pulmonary edema. Continue to provide highflow oxygen by mask. Attach cardiac monitor. 3. Provide continuous cardiac monitoring to look for QT interval prolongation, which is an early sign of hypocalemia. a. Treat tetany or cardiac arrest with IV 5 cc calcium chloride 10% (or 10 cc calcium gluconate 10%). b. Consider prophylactic calcium for victims with high concentration (1020%) exposure to greater than 35% body surface area. 4. Ingestion: DO NOT induce vomiting immediately dilute with 1 glass of water or milk. If available, give magnesium or calciumcontaining antacid (both will bind fluoride). 5. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 1015 minutes or until symptoms of pain or irrigation have resolved.
HYDROFLUORIC ACID FORMS:

Gas, liquid (variable concentrations), and fluoride salts in the presence of acids may generate toxic quantities of hydrogen fluoride.
BACKGROUND:
Hydrofluoric acid (HF) produces toxicity quite distinct from other mineral acids. The acid moiety (hydrogen ion) is relatively unimportant, producing little burning sensation on initial contact. In contrast, the highly toxic fluoride ion has the ability to penetrate tissue and produce indolent ulceration or bony destruction. Solutions of greater than 1020% are particularly destructive. Solutions of greater than 60% concentration can cause significant respiratory exposures. As well inhalation may cause eye, nose and throat irritation, cough, tracheal bronchitis, and delayed onset pulmonary edema. Ingestion may produce severe corrosive burns of the esophagus and stomach. Systemic absorption of fluoride (i.e. from a burn or after ingestion) may result in severe hypocalemia, hypomagnesia, and hyperkalemia, resulting in tetany and cardiac arrest.

Until the soaked clothing has been removed and the affected body part has been flushed, there is some hazard to treating health care personnel, depending on the concentration. Following basic decontamination, there is usually no significant risk of secondary contamination.
PATIENT MANAGEMENT IN THE HOT ZONE DECON AREA:

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed
Decontaminate May need to continue to flush skin and/or eyes even after patient has gone through a formal decon 03/01/05 H - 11

process. All areas need to be flushed minimum of 20 minutes. Use of the Morgan Lens for flushing the eyes is recommended. Individuals must be trained in the use of this device. Severe injury or permanent damage may be caused from improper use. Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, intubate early. Administer 100 % O2. Inhalation Injury Mix 6 cc of Normal Saline with 3 cc of 10% Calcium Gluconate and nebulize. EKG Monitoring Establish IV - with Normal Saline Eye Injury from Hydrofluoric Acid Apply 1-2 drops of Tetracaine to eye. Prepare an eye wash solution by mixing Calcium Gluconate (10%) 50ml in NS 500ml. Apply eyewash solution by using a Morgan Theraputic Lens. Burns to skin After flushing with copious amounts of water, prepare a skin gel by mixing Calcium Gluconate (10%) 10ml into a 2-ounce tube of KY jelly (making a 2.5% gel). CPAP for Pulmonary Edema (Non Cardiogenic Shock - do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222 pesticides inhibit the enzyme cholinesterase, resulting in buildup of excessive acetylcholine. Signs and symptoms include hypersalivation, sweating, bronchospasm, abdominal cramps, diarrhea, muscle weakness, small pupils, twitching and seizures. Death is due to respiratory muscle paralysis. For certain organophosphates, if victim survives the acute poisoning, they may develop delayed onset peripheral neuropathy. Nonspecific symptoms such as upper respiratory irritation, dizziness, nausea and headache after inhalation exposure may be due to the solvent vehicle (e.g. xylene) and not due to cholinesterase inhibition. Potential toxicity of the solvent vehicle should always be considered.

Many organophosphates are wellabsorbed through intact skin, and thus may pose a serious hazard to rescuers or health care personnel. If rescuers begin to exibit signs and symptoms of OP poisoning, they should immediately administer a Mark I auto-injector to prevent becoming incapacitated. Rescuers who have been treated with Atropine may be able to continue working, but must be closely monitored for heat stress. Water decontamination may be insufficient to remove oily compounds.

1. Rescuers should don agentspecific protective clothing and gloves, and selfcontained breathing apparatus. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. 2.Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing and consider high flow supplemental oxygen by bag valve mask with reservoir, if possible and practical. 3. Remove and doublebag clothing. Flush skin with water spray for 1 2 minutes. Remove contact lenses and irrigate exposed eyes if symptomatic.
NERVE AGENTS (GA, GB, GD, GF, VX) FORMS:

All nerve agents in the pure form are a colorless liquid. The vapor pressure of these agents varies widley. These agents may be dispersed through the use of solvents to increase vapor pressure, or explosive devices to atomize the material. Nerve agents can pose an exposure risk through all routes.
(See Organophospate Poisoning) FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222
TRIAGE
Red (Highest Priority)- An individual who is convulsing or who is postictal, who is not breathing or is having breathing difficulties, or who has a combination of two or more organ systems affected (respiratory effects, gastrointestinal effects, skeletal muscular twitching or weakness, disturbances in level of consciousness). These persons require antidotes immediately to save their lives. Included in this category are casualties with no respiratory or cardiac activity, if resources are available to provide appropriate immediate care. Yellow (Medium Priority)- An individual who suspects he has had or has had liquid agent on his skin, but who has no
PESTICIDES ORGANOPHOSPHATES FORMS:

The typical way organophosphates are found is either in a liquid (usually solution with xylene or other organic solvent) or solid (wettable powder) state which may be inhaled in an aerosol form or as a component of smoke.
BACKGROUND:
Organophosphate pesticides are widely used in home gardening and commercial agriculture. A variety of products are available, with widely varying potencies. Organophosphate H - 12
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Haz-Mat Guidelines
FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 2221222
effects. This patient must be kept under observation for at least 18 hours. An individual who was given 4 mg. or more of atropine, and who is recovering from the effects of both the agent and the antidote. Green (Low Priority)- An individual who is able to walk and talk after a vapor exposure. Some miosis without other effects. Individuals may only need monitoring for at least one hour.
UNKNOWN MATERIAL FORMS:

This section assumes that a victim has been exposed to a hazardous material, which cannot be identified in the form of a gas or vapor, liquid, or solid/dust.
Decontaminate Prioritize and Vitalize Airway Management If airway is compromised by secretions or is rapidly closing, atropine administration should be given immediately. The administration of atropine will aid the intubation efforts. Administer 100 % O2. When intubated, maintain 5cm of H2O PEEP. Brochoconstriction may prevent intubation efforts and should be treated with an initial dosage of Atropine. Atropine may be given via ET tube. EKG Monitoring Establish IV - with Normal Saline Atropine - 2mg (>9 y.o.), 1mg (2-9 y.o.), .5mg (0-2 y.o.) every 5 minutes if IV, or 10 to 15 if IM until SLUDGE symptoms are relieved. Atropine administration in a hypoxic patient may precipitate Ventricular Fibrillation If the patient is hypoxic, the initial dosage of atropine must be given IM to prevent ventricular fibrillation. (pts heart rate may be >60/min. Though the patients heart rate is one indicator to determine if the patient needs more atropine, the patients respiratory effort is a better indicator to determine if sufficent atropine has been administered.) Pralidoxime - (2-Pam) 1 gram diluted in 20 mL of Sterile Water mixed in 100 ml normal saline and given IVP over 20-30 minutes. 600 mg IM may be used if no IV access is available. IV administration may cause prolonged marked hypertension if given too rapidly. Labetolol may be indicated if hypertension persists for more than 20 minutes. The pediatric dosage for Pralidoxime is 15mg/kg. Dosages may be repeated every 15 minutes until signs/ symptoms are eliminated. Diazepam 5-10 mg for seizures. May substitute Lorazapam (Ativan) 1-2 mg for Diazepam. CPAP for Pulmonary Edema (do not use Furosemide) Mark-1, CANA or Atrox Auto-Injector kit is the preferred method of administration. They can be self administered through an IM route and are designed to be re-administered PRN.The Mark I kit contains two auto-injectors, one Atropine (2 mg) and one Pralidoxime (600 mg). Atrox autoinjectors area available in multiple dose ranges based on patients age. These units are available in 0.5mg, 1.0 mg, or 2.0 mg dosages. CANA auto-injectors contain 10 mg of Valium for the treatment of seizures in a severely exposed victim.
BACKGROUND:
Every attempt should be made to identify the substance involved using placards, shipping papers, or other means. However, if such identification is impossible, responders should make worst-case assumptions about the material. Rescuers should assume that the material might be: a. Poisonous by inhalation, ingestion, and cutaneous absorption; b. Corrosive (either acidic or alkaline); c. Lipid soluble, and therefore able to penetrate certain types of protective clothing and protective gear, and able to be absorbed through intact skin; d. Oily and persistent on skin and clothing, and therefore difficult to decontaminate; and, e. Reactive and likely to give rise to irritant or poisonous gases on contact with water or heat.

Victims contaminated with an unknown liquid or solid/dust material should be assumed to be carrying a risk of secondary contamination. If the victims only exposure, was to small amounts of gas or vapor, the risk of secondary contamination to health care personnel away from, the scene is probably very small. Theoretically, small amounts of gas might be trapped in a victims clothing. In such a situation once the clothing had been removed and double bagged, the risk to rescuers would be minimal. However, if the exposure involved an aerosol which might condense on a victims skin or clothing, there would be a potential for secondary contamination until decontamination had been carried out. For exposures involving direct contact with an unknown liquid or solid material or dust, rescuers should assume that the victim poses a risk of secondary contamination until decontaminated. When in doubt, decontaminate the victim.

1. In general, until the possibility of fire, explosion, or serious reactivity has been ruled out, rescuers will not enter the Hot Zone. Once entry appears to be
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feasible, rescuers should don fully encapsulated protective clothing and gloves capable of withstanding both corrosives and hydrocarbon solvents, and selfcontained breathing apparatus. 2. Quickly evaluate and support ABCs. Stabilize the spine (if trauma suspected), establish airway and breathing, and consider high flow supplemental oxygen by bag naive mask with reservoir, if possible and practical. 3. Remove and double bag clothing. Flush skin with water spray for 1 2 minutes. If the victim complains of eye irritation, have the victim remove contact lenses if able to do so. Irrigate exposed eyes if symptomatic. REGIONAL POISON CONTROL CENTER AT: (800) 2221222
PRE-HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION:

1. If victim is NOT decontaminated and responder is properly trained, don protective equipment (self contained breathing apparatus) capable of withstanding brief exposure to both corrosives and hydrocarbon solvents. Activate basic decontamination protocol. If these requirements cannot be met, request assistance from the local hazmat team or your Regional Poison Control Center. In addition, wash oily contaminated areas, including skin or hair, with soap and/or shampoo. 2. Reevaluate airway, intubating the trachea if victim is unconscious or has developed severe respiratory distress. Continue to provide highflow oxygen by mask. Attach cardiac monitor. 3. Support BP if needed, with IV crystalloid solutions. Treat bradycardia with Atropine or other modality appropriate to the patients clinical status. 4. Consider aerosolized bronchodilators if significant wheezing is present. 5. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing, for at least 1015 minutes or until symptoms of pain or irritation have resolved. 6. Even if significant ingestion is suspected, do not induce vomiting. Instead, if the victim is conscious and able to protect the airway, immediately dilute with 1 glass of water and give activated charcoal 60 100 grams if available. Do NOT give activated charcoal if a corrosive is suspected. 7. Continue to irrigate injured eyes or exposed areas of skin for at least 15 to 20 minutes if the victim continues to complain of discomfort. 8. Treat seizures with Diazepam (Valium): 5 10 mg IV for an adult; and 1 2 mg IV for children or Ativan (Lorazepam): 5 - 10 mg IV for an adult; and 0.1 mg/kg over 2-5 minutes. FOR ADVICE ON CLINICAL MANAGEMENT, CALL YOUR H - 14 03/01/05
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H - 15
Appendix A
APPENDIX A
ACLS Quickie
All patients:
Vitalize/Prioritize Oxygen/Airway EKG Monitored 12 Lead EKG V4R if any ST elevation in leads II, III, aVF
Asystole
Think 6 Hs & 6 Ts (See table A) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.0mg 1:10,000 IVP/IO q 3-5 minutes Atropine 1.0mg IV/IO q 3-5 minutes to max of 3.0mg (0.03-0.04mg/kg)
**CPRInterventionCPR pattern (Minimize interruptions in CPR)** Bradycardia

Atropine 0.5mg IV/IO q 3-5 minutes to max of 3.0mg (0.03-0.04mg/kg) Transcutaneous Pacing Dopamine 5-20 ug/kg/min Epinephrine 2-10ug/min
Pulseless Electrical Activity

Think 6 Hs & 6 Ts (See table A) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.0mg 1:10,000 IVP/IO q 3-5 minutes Atropine 1.0mg IV/IO q 3-5 minutes to max of 3.0mg (0.03-0.04mg/kg)
**CPRInterventionCPR pattern (Minimize interruptions in CPR)** Ventricular Fibrillation (VF) / Pulseless Ventricular Tachycardia (PVT)
Think 6 Hs & 6 Ts (See Table A) Witnessed Arrest - Immediate defibrillation (See table B) Unwitnessed Arrest CPR for 5 cycles / 2 minutes, then defibrillation (See table B) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.0mg 1:10,000 IVP/IO q 3-5 minutes Amiodarone 300mg IV/IO, repeat 150mg IV/IO in 5 minutes OR Lidocaine 1.0-1.5mg/kg IV/IO to max 3mg/kg Magnesium Sulfate 1-2g diluted in 10cc over 2 minutes for torsades de pointes Sodium Bicarb. 1meq/kg IV/IO
**CPRInterventionCPR pattern (Minimize interruptions in CPR)**
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AA- 1
Tachycardia (Wide Complex = QRS > 0.12 seconds)

Unstable (Serious Signs and Symptoms) Ventricular rate > 150 BPM Immediate synchronized cardioversion (See page C-3 & Table B) Regular Rhythm: (V-Tach or Uncertain Rhythm) Amiodarone 150mg IV/IO over 10 minutes, repeat as needed to max 2.2g in 24 hours OR Lidocaine 0.5 - 0.75mg/kg IV/IO, repeat 0.5 - 0.75mg/kg to max of 3mg/kg Prepare for synchronized Cardioversion (See page C-3 & Table B) If SVT with aberrancy: Adenosine 6mg IVP/IO, 12mg IVP/IO, 12mg IVP/IO Irregular Rhythm: (Polymorphic VT) Unstable - Defibrillate (See Table B) Amiodarone 150mg IV/IO over 10 minutes, repeat as needed to max 2.2g in 24 hours Lidocaine 0.5 - 0.75mg/kg IV/IO, repeat 0.5 - 0.75mg/kg to max of 3mg/kg Magnesium Sulfate 1-2g IV diluted in 10cc over 2 minutes for Torsades de Pointes
Tachycardia (Narrow Complex = QRS < 0.12 seconds)

Unstable (Serious Signs and Symptoms) Immediate synchronized cardioversion (See page C-3 & Table B) Regular Rhythm: Attempt vagal maneuvers Adenosine 6mg IVP/IO, 12mg IVP/IO, 12mg IVP/IO Cardizem 0.25mg/kg IV/IO over 2 minutes, may repeat in 15 minutes at 0.35mg/kg IV/IO over 2 minutes Irregular Rhythm: (Probable A-Fib, A-Flutter or M.A.T.) Cardizem 0.25mg/kg IV/IO over 2 minutes, may repeat in 15 minutes at 0.35mg/kg IV/IO over 2 minutes
Table A
6 Hs 6 Ts Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia Hydrogen Ion (acidosis) Hyper/Hypokalemia Hypoglycemia Tamponade Tension pneumothorax Thrombosis-Coronary Thrombosis-Pulmonary Toxins Trauma (Hypovolemia)
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AA-2
Appendix A
Table B
Adult Electrical Therapy
Defibrillation: Biphasic rectilinear waveform Initial = 120j (i.e. Zoll, Phillips) Subsequent = 120j or higher Biphasic truncated exponential waveform Initial = 150j (i.e. Medtronics) Subsequent = 150j or higher Monophasic waveform Initial = 360j Subsequent = 360j Cardioversion: (Narrow Complex Tachycardia) Monophasic (A-Flutter or Re-entry SVT) Initial = 50j Subsequent =100j, 200j, 300j, 360j Monophasic (A-Fib) Initial = 100j Subsequent = 200j, 300j, 360j Biphasic Initial = 100j Subsequent = 120j, 150j, 200j Cardioversion: (Wide Complex Tachycardia) Monophasic Initial = 100j Subsequent = 200j, 300j, 360j Biphasic Initial = 100j Subsequent 120j, 150j, 200j
Pediatric Electrical Therapy

Defibrillation: Monophasic / Biphasic Initial = 2j/kg Subsequent = 4j/kg, 4j/kg Cardioversion Monophasic / Biphasic Initial = 0.5j/kg 1.0j/kg Subsequent = 2j/kg
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AA- 3
Appendix B
APPENDIX B
Guide to the Hospitals in the Operating Region
BREVARD COUNTY
Holmes Regional Medical Center 1350 South Hickory St 1000 36th Street 13695 U.S. Highway One Melbourne, FL 32901 Vero Beach, FL 32960 Sebastian, FL 32958 800-541-1928 772 5674311 772 5893186 772 2235995 772 2235721 941 7632151 407-841-5111 561 7377733 561 3957100 561 8426141 561 9657300 561 4984440 561 9966571 561 6555511 561 7444460 561 6221411 561 9677800 561 7983300 561 8446300 561 882-8262 561 7988500 561 4888000 772 3354000 772 4614000
***
INDIAN RIVER COUNTY

Indian River Memorial Hospital Sebastian River Medical Center
MARTIN COUNTY
Martin Memorial Medical Center Martin Memorial Hospital South 300 Southeast Hospital Avenue Stuart, FL 34994 2100 Southeast Salerno Road Stuart, FL 34997 1796 Highway 441 North 1414 Kuhl Avenue 2815 South Seacrest Boulevard 800 Meadows Road 2201 45th Street 5301 South Congress Avenue 5352 Linton Boulevard 1201 South Main Street 1300 North Flagler Drive 1210 South Old Dixie Highway 3360 Burns Road 2829 10th Avenue 13001 Southern Boulevard 901 45th Street 7305 N. Military Trail 10101 Forest Hill Boulevard 21644 State Road Seven Okeechobee, FL 34972 Orlando, FL 32806 Boyton Beach, FL 33435 Boca Raton, FL 33486 West Palm Beach, FL 33407 Atlantis, FL 33462 Delray Beach, FL 33484 Belle Glade, FL 33430 West Palm Beach, FL 33401 Jupiter, FL 33458 Palm Beach Gardens, FL 33410 Lake Worth, FL 33461 Loxahatchee, FL 33470 West Palm Beach, FL 33407 West Palm Beach, Fl 33410 West Palm Beach, FL 33414 Boca Raton, FL 33428
OKEECHOBEE COUNTY
Columbia Raulerson Hospital
ORANGE COUNTY
Orlando Region Medical Center
***
PALM BEACH COUNTY

Bethesda Memorial Hospital Boca Raton Community Hospital Columbia Hospital Columbia JFK Medical Center Delray Medical Center Glades General Hospital Good Samaritan Hospital Jupiter Medical Center Palm Beach Gardens Medical Center Palm Beach Regional Hospital Palms West Hospital St. Marys Medical Center VA Medical Center Wellington Regional Medical Center West Boca Medical Center
***
***
ST. LUCIE COUNTY

Columbia Medical Center Port St. Lucie Lawnwood Regional Medical Center 1800 Southeast Tiffany Avenue Port St. Lucie, FL 34952 1700 South 23rd Street Port St. Lucie, FL 34950
*** Area Trauma Centers
Poison Control Center
1-800-282-3171
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AB-1
Appendix C
APPENDIX C
TRAUMA TRANSPORT PROTOCOLS
AC-1
Wong-Baker FACES Pain Scale
Instructions
Explain to the patient that each face is for a person who feels happy because they have no pain (hurt) or sad because they have some or a lot of pain. Face 0 is very happy because they do not hurt at all Face 1 hurts just a little bit Face 2 hurts a little more Face 3 hurts even more Face 4 hurts a whole lot more Face 5 hurts as much as you can imagine, although you do not have to be crying to feel this bad Ask the patient to choose the face that best describes how he/she is feeling
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AD-2
Appendix E
PREHOSPITAL FIBRINOLYTIC CHECKLIST

Inclusion Criteria
1. Is the patient 18 years of age or older? 2. Ischemic discomfort present for greater than 20 minutes but less than 12 hours? YES NO YES NO
APPENDIX E
3. ST segment elevation >1mm in 2 or more anatomically contiguous limb leads or ST YES NO segment elevation >2 mm in 2 or more anatomically contiguous precordial leads (V1V6) or new or presumably new LBBB?
INCLUSION / EXCLUSION CHECKLIST

Note: Any YES answer to the questions listed below will EXCLUDE the patient from the administration of a fibrinolytic medication. 1. History of stroke or TIA at any time. 2. Brain tumor, AVM (arterialvenous malformation), or cerebral aneurysm. 3. Any major surgery, trauma (including CPR for greater than 2 minutes), or any type of internal bleeding or hemorrhage within the past 4 weeks (e.g. black tarry stools or vomiting blood). 4. Hypertension at the time of presentation that exceeds 180 systolic or 110 diastolic. 5. Patient in cardiogenic shock (systolic BP<90 mm Hg) or the patient is intubated. 6. Hemophilia or any known bleeding disorder. YES NO YES NO YES NO
YES NO YES NO YES NO
7. Radiating pain through to the upper back characterized as a ripping or tearing pain YES NO accompanied by unequal blood pressures or distal pulses when comparing the right and left arms (suggestive of a Dissecting Aortic Aneurysm). 8. Use of cocaine or other amphetamines within the past 3 days. 9. Pregnancy. YES NO YES NO
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AE-1
Cincinatti Stroke Scale

Facial Droop
Action: Have the patient show their teeth or smile Normal: Both sides of the face move equally well Abnormal: One side of the face does not move as well as the other side.
Arm Drift
Action: Have the patient close their eyes and hold both arms out Normal: Both arms move the same or both arms do not move at all Abnormal: One arm does not move or one arm drifts down compared to the other
Speech
Action: Have the patient say: You cant teach an old dog new tricks Normal: Patient uses correct words with no slurring Abnormal: Patient slurs words, uses inappropriate words, or is unable to speak Interpretation: If any one of these 3 signs fall into the Abnormal category, the probability of a stroke is 72%.
01/09/06
AE-2
Appendix F
APPENDIX F
HELICOPTER ACTIVATION CRITERIA
The guidelines for helicopter response include but are not limited to the following:
Trauma patients that meet the trauma scorecard methodology and criteria as set forth by your agency. Scene to trauma center by ground transport is greater than 20 minutes. Trauma Alert with scene extrication time greater than 15 minutes. Ground response to specific scenes greater than 15 minutes Mass Casualty Incidents evacuations (MCI) To augment or expedite pre-hospital transport, transport patient upon request by a provider. Inter-Facility Transfers (IFT) when rapid transport is deemed medically necessary. For the critically ill patients requiring specialized services and facilities located in other areas.
Example: Pediatrics, Obstetrics, burn unit, cardiac cath labs etc.
Stroke and Cardiac Alert patients located in areas that would otherwise be outside the three hour window of
opportunity for thrombolitic therapy.
03/01/05
AF-1
Appendix G
APPENDIX G
TASER INJURIES
Caution Most injuries from a taser devise are the result of secondary injuries such as from a fall. The electrical current is considered safe with an output of 1.76 Joules per pulse. Due to the nature of these incidents, EMS personnel do not medically clear persons in police custody who were subdued with a tazer. EMS providers should always err on the side of caution and recommend transport of these patients.
Basic Life Support Confirm that law enforcement has disconnected the wires from the hand held unit Oxygen / Airway Spinal Immobilize, if indicated Secure the taser prongs in place as an impaled object if not already removed by law enforcement. Do not remove the prongs unless they interfere with critical life care measures Advanced Life Support 12 lead EKG monitor V4R should be evaluated if any ST elevation in leads II, III or aVF IV 0.9 % NaCl Treat underlying conditions, as needed (cardiac arrhythmias, altered mental status, etc.)
02/15/06
AG-1
02/15/06
AG-2
Lillian Avner, D.O. Medical Director
July 1, 2009 Martin County Fire Rescue 800 SE Monterey Road Stuart, Florida 34994 Chief Wouters, As the Medical Director for Martin County Fire Rescue, I would like to have the following changes made to the Emergency Guidelines as they pertain to Martin County. The administration of Cardizem (Diltiazem) is referenced in the current protocols on pages D-9 and C-6 as being administered by infusion over 2 minutes. To reduce side effects of Cardizem, infusion rates should be slowed to have all infusion administered over 5 minutes. If you have any questions or concerns, please contact me at your convenience.
Sincerely,
Lillian Avner, D.O. Medical Director Martin County Fire Rescue

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Emergency Medicical Guidelines

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PREFACE

Emergency Medical Guidelines

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

RATIONALE OF EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

GENERAL MEDICAL ................................................................ E3

HAZARDOUS MATERIALS MANAGEMENT....................... E58

TOXICOLOGY ........................................................................... E60

Procedural Guidelines ...................................... P1

MEDICATION AND FLUID ADMINISTRATION ................. P33

GENERAL ................................................................................. P55

IMMOBILIZATION .................................................................. P64

MULTIPLE CASUALTY INCIDENTS .................................... P74

Treatment Guidelines ...................................... M1

TRAUMA / ENVIRONMENTAL ................................................ T1

Drug Reference ................................................ D1

Haz-Mat Guidelines ......................................... H1

Appendix A ..................................................... AA1

Appendix B ..................................................... AB1

Appendix C ..................................................... AC1

Appendix D ..................................................... AD1

Appendix E ..................................................... AE1

Appendix F ..................................................... AF1

EMERGENCY MEDICAL GUIDELINES

PRIORITY TWOSERIOUS (SECONDARY)

PRIORITY THREEMINOR OR STABLE CONDITION

GENERAL MEDICAL ABDOMINAL AORTIC ANEURYSMS

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

ALTERED LEVEL OF CONSCIOUSNESS/ ALCOHOLISM

Glascow Coma Scale

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) / CHRONIC BRONCHITIS / EMPHYSEMA

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

EMERGENCY MEDICAL GUIDELINES

DO NOT RESUSCITATE ORDER (DNRO)

EMERGENCY MEDICAL GUIDELINES

HIGH RISK PREGNANCY

EMERGENCY MEDICAL GUIDELINES

PREGNANCY INDUCED HYPERTENSION

PROBLEMS WITH THE SECOND STAGE OF LABOR/THIRD TRIMESTER BLEEDING

EMERGENCY MEDICAL GUIDELINES

POTENTIAL FOR COMPLICATIONS

PREMEDICATION PATIENT ASSESSMENT

UNDERSTANDING THE PATIENTS NEEDS

EMERGENCY MEDICAL GUIDELINES

DEALING WITH THE VIOLENT PATIENT

DEALING WITH THE SUICIDAL PATIENT

DEALING WITH THE ACUTE PSYCHOTIC PATIENT

FOR A PATIENT WITH A SCHIZOPHRENIC REACTION:

FOR A PATIENT WHOS PARANOID:

ONCE RESTRAINED, ALWAYS RESTRAINED

EMERGENCY MEDICAL GUIDELINES

USE OF LEATHER RESTRAINTS

Adverse effects include interactions with other

PRECAUTIONS Patient dosing is very variable. More medication

RAPID SEQUENCE INTUBATION (RSI)

CARE FOR THE PARALYZED PATIENT