Professional Documents
Culture Documents
Worldwide Statistics
Each year:
> 4 million patients are admitted
with unstable angina and acute MI
> 900,000 patients undergo PTCA
with or without stent
Myocardial Ischemia
Spectrum of presentation
silent ischemia
exertion-induced angina
unstable angina
acute myocardial infarction
ACS
Risk stratification
Risk of death
Directed therapy
Aspirin
Indications Administer to all patients
with ACS, particularly reperfusion
candidates
Give as soon as possible
Nitroglycerine
Indications
Chest pain of suspected cardiac origin
Unstable angina
Complications of AMI, including
congestive heart failure, left ventricular
failure
Hypertensive crisis or urgency with
chest pain
Nitroglycerin
Indications
Morphine Sulfate
Indications
Chest pain and anxiety associated with
AMI or cardiac ischemia
Acute cardiogenic pulmonary edema (if
blood pressure is adequate)
Morphine Sulfate
Indications
To reduce pain of ischemia
To reduce anxiety
To reduce extension of ischemia by
reducing
oxygen demands
Morphine Sulfate
Precautions (Watch Out!)
Administer slowly and titrate to effect
May compromise respiration; therefore
use with caution in acute pulmonary
edema
Causes hypotension in volume-depleted
patients
ST elevation or new or
presumably new LBBB:
strongly suspicious for
injury
ST-elevation AMI
ST depression or dynamic
T-wave inversion:
strongly suspicious
for ischemia
High-risk unstable angina/
nonST-elevation AMI
Nondiagnostic ECG:
absence of changes
in ST segment or
T waves
Intermediate/low-risk
unstable angina
ST Elevation
27
Recognition
of AMI
Know what to look
for
ST elevation >1 mm
3 contiguous leads
J point plus
0.04 second
PR baseline
ST-segment deviation
= 4.5 mm
28
ST Elevation
Baseline
Ischemiatall or inverted T wave (infarct),
ST segment may be depressed (angina)
Injuryelevated ST segment, T wave
may invert
Infarction (Acute)abnormal Q wave,
ST segment may be elevated and T wave
may be inverted
Infarction (Age Unknown)abnormal Q wave,
ST segment and T wave returned to normal
29
Beta Blockers
Indications (When & Why?)
To reduce myocardial ischemia and
damage in AMI patients with elevated
heart rates, blood pressure, or both
Blocks catecholamines from binding to
-adrenergic receptors
Reduces HR, BP, myocardial contractility
Decreases AV nodal conduction
Decreases incidence of primary VF
Heparin
Indications (When & Why?)
For use in ACS patients with Non Q wave
MI or unstable angina
Inhibits thrombin generation by factor
Xa inhibition and also inhibit thrombin
indirectly by formation of a complex
with antithrombin III
Fibrinolytics
Indications (When & Why?)
For AMI in adults
ST elevation or new or presumably new
LBBB; strongly suspicious for injury
Time of onset of symptoms < 12 hours
Fibrinolytics
Indications (When & Why?)
For Acute Ischemic Stroke
Sudden onset of focal neurologic deficits or
alterations in consciousness
Absence of subarachnoid or intracerebral
hemorrhage
Alteplase can be started in less than 3 hours
of symptom onset
ACE Inhibitors
Indications (When & Why?)
Reduce mortality & improve LV
dysfunction in post AMI patients
Help prevent adverse LV remodeling,
delay progression of heart failure, and
decrease sudden death & recurrent MI
ACE Inhibitors
Indications (When & Why?)
Suspected MI & ST elevation in 2 or
more anterior leads
Hypertension
Clinical signs of AMI with LV dysfunction
LV ejection fraction <40%
ACE Inhibitors
Indications (When & Why?)
Generally not started in the ED but
within first 24 hours after:
Fibrinolytic therapy has been completed
Blood pressure has stabilized
Definition
Otherwise know as heart attack
An MI occurs when there is a diminished
blood supply to the heart which leads to
myocardial cell damage and ischemia.
Contractile function stops in the necrotic
areas of the heart.
Ischemia usually occurs due to blockage
of the coronary vessels.
MI Classifications
MIs can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
Transmural and Subendocardial
Diagnostic
ST elevations (STEMI) and non ST
elevations (NSTEMI).
Epidemiology
MIs are the leading cause of death in the
United States, affecting one in five men
and one in six women.
450,000 people in the US die from
coronary disease each year.
Incidence rates increase with age as do
mortality rates due to infarction.
Epidemiology
The survival rate for those hospitalized
due to MI has reached approximately
95%.
This is the result of the advancements
made in modern medical technology.
Risk Factors
The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
Age
Gender
Family history
Risk Factors
Modifiable
Smoking
Diabetes Control
Hypertension
Hyperlipidemia
Obesity
Physical Inactivity
Smoking
Tobacco use increases the risk of
coronary artery disease two to six times
more than non smokers.
Nicotine increases platelet thrombus
adhesion and vessel
inflammation.
Hyperlipidemia
Elevated levels of cholesterol, LDLs or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
Almost 50% of the U.S.
population has some
form of dyslipidemia.
Pathophysiology
Ischemia develops when there is an
increased demand for oxygen or a
decreased supply of oxygen.
Ischemia can develop within 10 seconds
and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply.
Pathophysiology
As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.
Severity of the MI depends on three
factors.
Level of occlusion
Length of time of occlusion
Presence or absence of collateral circulation
Chest Pain
The most common initial manifestation is
chest pain or discomfort.
This is not relieved by rest, position
change or nitrate administration.
Pain is described by heaviness, pressure,
fullness and crushing sensation.
Not everyone experiences this sensation.
Chest Pain
Cardiovascular Changes
Urine output will decrease
Lung sounds will change to crackles
Jugular veins may become distended and
have obvious pulsations.
Diagnostics
After collecting patient health history, a
series of EKGs should be taken to rule
out or confirm MI.
12 lead EKGs can help to distinguish
between ST-elevation MIs and Non-STelevation MIs.
Angina
Stable
Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
Chest pain caused by the 4 Es.
Pain is usually relieved with rest, pain
meds and nitrates.
Variable/Prinzmetal/Spasm
Transient ischemia that occurs
unpredictably and almost always at rest.
Pain is caused by vasospasm of the
arteries.
ST segment elevations will be noted.
Unstable
Chest pain at rest or with exercise and
tends to last greater than 15 minutes.
This results in reversible myocardial
ischemia but is a sign that an infarct is
soon to come.
EKG will reveal ST segment depression
and T wave inversion.
STEMI
ST segment elevations
T wave changes
Q wave development
Enzyme elevations
Reciprocals
NSTEMI
ST segment depressions
T wave changes
No Q wave development
Mild enzyme elevations
No reciprocals
Phases of a STEMI
Hyperacute Phase
Occurs within the first few hours of MI onset.
Leads facing the infarcted surface: ST
segment elevation.
Leads facing the uninjured surface: ST
segment depression (reciprocals)
T waves become tall, widened and might be
taller than the R wave.
Phases of a STEMI
Fully Evolved Phase
Q wave development
ST elevation
T waves start to become inverted in leads
facing the injury.
Phases of a STEMI
Resolution phase
Weeks after there will be a gradual return of
ST segments to baseline.
T waves will gradually return to normal but are
the last to change back.
CPK
Creatine Phosphokinase
Begin to rise 3 to 12 hours after acute MI.
Peak in 24 hours
Return to normal in 2 to 3 days
Troponin
Myocardial muscle protein released into
circulation after injury.
These are highly specific indicators of MI.
Troponin rises quickly like CK but will
continue to stay elevated for 2 weeks.
Myoglobin-lacks cardiac specificity.
Treatment Options
The immediate goal for any acute MI is to
restore normal coronary blood flow to
vessels and salvage myocardium.
There are a variety of medical and
medicinal therapies to treat an MI.
Morphine
Oxygen
Nitroglycerin
Aspirin
Fibrinolytic Therapy
Indicated for patients with STEMI MIs.
Should be given within 12 hours of
symptom onset.
Fibrinolytics will break down clots found
within the vessles
Contraindications: post op surgical
patients, history of hemorrhagic stroke,
ulcer disease, pregnancy, ect.
Cardiac Catheterization
A diagnostic angiography which includes
angioplasty and possible stenting.
Performed by an interventional
cardiologist with a cardiac surgeon on
stand by.
Percutaneous procedure through the
femoral or brachial artery.
Cardiac Catheterization
Upon arrival to the cath lab all actue MI
patients will receive:
A bolus dose of plavix
IV Integrelin
Heparin dose either subcu or IV drip
Angiomax : a DTI may be substituted for
heparin and integrelin.
HANDLING
SUDDEN CARDIAC ARREST
Heart Attack
Heart Attack
The
heart
muscle
contracts
in response to electrical
stimulus generated by
the
hearts pacemaker Cells
with the result of a
pulse,
blood pressure, breathing
& other
circulation.
signs
of
Ventricular
Fibrillation
Causes :
Coronary artery disease
Acute coronary syndromes
Electrocution.
Drug toxicity and sensitivity
Asphyxia
Drowning
Blunt force trauma to the chest.
of
Low LVEF.
Cardiomyopathy
Long QT Syndrome.
Treatment
Chain of Survival
Early access.
Early CPR.
Early defibrillation.
Early advanced life support.
(BCLS).
*
A for Airway.
B for Breathing.
C for Circulation.
* Finger
sweep.
* Jaw Thrust.
Breathing
* Feel - carotids
Cardiac compressions
Anterior lateral
Guidelines 2000
For communities :
3-5 minutes, preferably less than 3
minutes.
For hospitals :
less than 3 minutes.
Safety First
Types of AEDs
Semi Automatic : Analyses patients rhythm and
advises if
rhythm needs a shock. Operator has to press shock
button
to deliver the shock.
TYPES OF AEDs
TYPES OF AEDs
ON/OFF
VF / Pulseless VT
VF / Pulseless VT
Epinephrine 1 mg IV push, repeat every 3 to 5 minutes
or
Vasopressin 40 U IV, single dose, 1 time only
Consider antiarrhythmics:
Amiodarone (llb for persistent or recurrent VF/pulseless VT)
Lidocaine (Indeterminate for persistent or recurrent VF/pulseless VT)
Magnesium (llb if known hypomagnesemic state)
Procainamide (Indeterminate for persistent VF/pulseless VT;
llb for recurrent VF/pulseless VT)
Resume attempts to defibrillate
Epinephrine
Indications (When & Why?)
Increases:
Heart rate
Force of contraction
Conduction velocity
Peripheral vasoconstriction
Bronchial dilation
VF / Pulseless VT
Vasopressin
Indications (When & Why?)
Used to clamp down on vessels
Improves perfusion of heart, lungs, and
brain
No direct effects on heart
VF / Pulseless VT
Amiodarone
Indications (When & Why?)
Powerful antiarrhythmic with substantial
toxicity, especially in the long term
Has effects on sodium & potassium
VF / Pulseless VT
Lidocaine
Indications (When & Why?)
Depresses automaticity
Depresses excitability
Raises ventricular fibrillation threshold
Decreases ventricular irritability
VF / Pulseless VT
Magnesium Sulfate
Indications (When & Why?)
Cardiac arrest associated with torsades
de pointes or suspected
hypomagnesemic state
Refractory VF
VF with history of ETOH abuse
Life-threatening ventricular arrhythmias
due to digitalis toxicity, tricyclic
overdose
VF / Pulseless VT
Procainamide
Indications (When & Why?)
Recurrent VF
Depresses automaticity
Depresses excitability
Raises ventricular fibrillation threshold
Decreases ventricular irritability
VF / Pulseless VT
PEA
PEA
Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes
Atropine Sulfate
Indications (When & Why?)
Should only be used for bradycardia
Relative or Absolute
Asystole
Asystole
Transcutaneous pacing:
If considered, perform immediately
Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes
Atropine 1 mg IV,
repeat every 3 to 5 minutes
up to a total of 0.04 mg/kg
Asystole persists
Withhold or cease resuscitation efforts?
Consider quality of resuscitation?
Atypical clinical features present?
Support for cease-efforts protocols in place?
Cardiac
Emergencies and
CPR
Introduction
Basic Life Support needed for patient whose
breathing or heart has stopped
Ventilations are given to oxygenate blood
when breathing is inadequate or has stopped
If heart has stopped, chest compressions are
given to circulate blood to vital organs
Ventilation combined with chest
compressions is called cardiopulmonary
resuscitation (CPR)
CPR is commonly given to patients in cardiac
arrest as a result of heart attack
Circulatory System:
Emergencies
Any condition that affects respiration
Reduces ability to deliver oxygen
Severe bleeding
Shock
Stroke
Reduces blood flow to brain
Heart conditions
Reduce tissue oxygenation
Circulatory System:
Emergencies continued
Heart attack
Can lead to cardiac arrest
Ventricular fibrillation
Heart muscle flutters rather than
pumping blood
Cardiopulmonary
Resuscitation (CPR)
CPR helps keep patient alive by circulating
some oxygenated blood to vital organs
Ventilations move oxygen into lungs where
it is picked up by blood
Compressions on sternum increase
pressure inside chest, moving some blood
to brain/other tissues
Cardiopulmonary
Resuscitation (CPR) continued
Blood circulation resulting from chest
compressions not as strong as circulation
from heartbeat
Can help keep brain/other tissues alive
until normal heart rhythm restored
Cardiopulmonary
Resuscitation (CPR) continued
Often electric shock from AED is needed to
restore a heartbeatand CPR can keep
patient viable until then
CPR should be started as soon as possible
In some instances, the heart may start
again spontaneously with CPR
General Technique of
CPR
If unresponsive, not breathing, and no
pulse, start chest compressions
Find the correct hand position
Two hands for adults
One or 2 hands for child
Two fingers for infant
Single-Rescuer CPR
1. Check patients responsiveness,
open airway, and determine that
patient is not breathing adequately
2. Give 2 ventilations, each lasting 1
second
3. Determine victim has no pulse
Single-Rescuer CPR
2. Give 2
ventilations, each
lasting 1 second
3. Determine victim
has no pulse
Chest Compressions
Alert
Be careful with
your hand position
For adults/children,
keep your fingers
off patients chest
Do not give
compressions over
bottom tip of
breastbone
Chest Compressions
Alert
When
compressing,
keep elbows
straight and
hands in contact
with patients
chest at all times
Chest Compressions
Alert
Compress chest
hard and fast, but
let chest recoil
completely
between
compressions.
Minimize amount
of time used giving
ventilations
between sets of
compressions.
Chest Compressions:
Bradycardia in Child
Infant or child being given rescue
breaths or oxygen may have a pulse
but still inadequate perfusion
If pulse < 60 beats/minute and infant
or child has signs of poor perfusion,
provide CPR
Two-Rescuer CPR
Performed in cycles of 30:2 for adult
(15:2 for infant or child)
One rescuer provides breaths, second
rescuer gives chest compressions
Rescuers switch positions every 2
minutes
Change done after full CPR cycle
Accomplish change in < 5 seconds
Two-Rescuer CPR
continued
If AED present, one rescuer gives
CPR while the other sets up unit
If unit advises CPR, rescuers give
CPR together
Third rescuer can apply cricoid
pressure
Two-Rescuer CPR
continued
If you are assisting another trained rescuer
who places an advanced airway:
Chest compressions given continually
No pauses for ventilations
Give ventilations at rate of 8 10
breaths/ minute
Differences in Two-Rescuer
Training
If First Responder started CPR, arriving
second rescuer may have a higher level of
training
Rescuer with greater training determines
how CPR should best be continued
Skill:
CPR For Adult
or Child
(Two Rescuers)
Two-Rescuer CPR:
Infants
Skill:
CPR: Infants
Two Rescuers
Rescuer 1 checks
ABCs. Rescuer 2
locates site for
chest
compressions.
If no pulse, rescuer
2 gives 15 chest
compressions.