Basic Cardiac Dysrhythmias

Ventricular Rhythms and Atrio-

Ventricular Blocks
 Ventricular Escape Rhythm

Rate: Below 60 bpm Regularity: Regular

P Wave Morphology: No P wave present
PR Interval: Immeasurable
QRS Duration and Morphology: Greater than 120ms
(0.12 seconds), Uniform Morphology
QT Interval: The QRS complex is often difficult to
discern from the T wave, if measurable the QT
Interval will be less than the preceding R-R
Interval.
 Ventricular Escape Rhythm
Causes: The Purkinje fibers are the last line of
defense as a pacing site. This rhythm is protective
in conditions of failure of the SA and AV nodes.
Common causes are ischemia or infarction, severe
acid-base disturbances, Cardiomyopathy, and
Digitalis Toxicity.
Do not give antiarrhythmic: Suppression of
Ventricular Escape Rhythm will leave the patient
without a protective inherent pacemaker and
should be avoided.
Treatment entails Transcutaneous Pacing and
Dopamnine or Epinephrine infusion. Atropine less
effective.
 Accelerated Idioventricular Rhythm

Accelerated from 60-100 bpm.

Enhanced Autorhythmicity of the Ventricular
Tissue common during an MI and reperfusion.
Usually transient and without hemodynamic
compromise.
Premature Ventricular Complexes (PVCs)
 PVCs

By definition, PVCs are early beats

that come from the ventricle.
PVCs make the Ventricular Rhythm
Irregular.
They can occur as individual complexes, pairs,
triplets, and in patterns such as bigeminy,
trigeminy, quadrageminy, and can come from one
focus or multiple foci.
PVCs are wide and bizarre.
 PVCs

Causes: Frequent causes of PVCs include

stimulants like caffeine and cocaine, alcohol,
hypoxia, acid-base imbalances, electrolyte
disturbances MI, CHF, Myocarditis, Valve
Disease and re-perfusion.
PVCs are precursor complexes to Ventricular
Tachycardia and Ventricular Fibrillation.
 PVCs

Treatment: Focused on the correction of the underlying

cause, i.e. correcting electrolytes, hypoxia etc.
Treatment of PVCs is limited to those that produce
severe symptoms, or those that fall on the downslope
of the T wave and cause triplets of runs of PVCs.
Medications given to suppress ventricular ectopy
(lidocaine, procainamide, amiodarone, sotalol) also
suppress protective ventricular escape rhythms, and
have a pro-arrhythmic properties.
Treatment is a cost-benefit analysis
Ventricular Tachycardia
 Ventricular Tachycardia

Rate: 140-250bpm
Regularity: Regular
P Wave Morphology: No Discernable P waves
PR Interval: Immeasurable
QRS Duration and Morphology: QRS Duration
is Greater Than 120ms (0.12seconds),
morphology can be identical or vary.
QT Interval: Most Often Immeasurable.
There is a sub-catogory of VT know as
polymorphic, prolonged QT, Ventricular
Tachycardia, based on the QT of the
underlying rhythm.
 Ventricular Tachycardia

Causes: MI, CHF, Cardiomyopathy,

Electrolyte Disturbances, Acid Base
Imbalances, R on T Phenomena,
Direct stimulation of the Myocardium
Concerns: Patients response to VT varies
tremendously. Patient response can vary
from being asymptomatic to being
pulseless. VT is a destructive rhythm
that can deteriorate to Ventricular
Fibrillation and death rapidly.
 Ventricular Tachycardia
Treatment Groups:
1) Pulseless Ventricular Tachycardia
Defibrillate following treatment for
Ventricular fibrillation
2) Pulse Present with Serious Signs and
Symptoms
Synchronized Cardioversion
3) Pulse Present without Serious S & S
Time for Medication Trials
 Defibrillation

Goal: Spontaneous Depolarization of a critical

mass of cardiac cells to disrupt the erratic and
fast rhythm, so the conduction system can
restore normal function.
Does not take into consideration the patients
rhythm, as it is not pulse producing.
Indications: VF, Pulseless VT
 Ventricular Tachycardia
Medications: Any of the following antiarrhythmic medications
1. Amiodarone 150mg IV over 10 minutes ( may repeat)
2. Lidocaine 0.5-0.75mg/kg IV push (may repeat)
3. Procainamide 20-50mg/min (max 17mg/ kg) stop if
arrhythmia suppressed, hypotension, QRS duration increases
> 50% AVOID if patient presents with prolonged QT or CHF
Follow with a continuous medication infusion

4. If refractory to above medications Sotalol 100mg (1.5mg/kg)

over 5 minutes AVOID if patient presents with prolonged QT
IF at anytime the patient becomes unstable: CARDIOVERT
Torsades de Pointes:
Magnesium Sulfate 1-2gm IV over 5-60 min.
 Ventricular Fibrillation

Rate: Immeasurable Regularity: Chaotic

P Wave Morphology and AV Ratio: Chaotic
PR Interval: Immeasurable
QRS Duration and Morphology: Absent
QT Interval: Absent
 VF
Treatment: What is in the Guidelines?
(CPR, Defib, CPR, Defib, CPR &Drug, Defib, CPR &Drug,
Defib ) is this true?
Initiate CPR as soon as pulselessness is established
Defibrillate as soon as available
Medications:
1. Epinephrine 1mg IVP
CPR and Defibrillation
2. Anti-arrhythmic medications
Amiodarone 300mg IV/IO push
or
Lidocaine 1-1.5mg/kg IV/IO push
CPR and Defibrillation
 Asystole

Rate: None Regularity: None

P Wave Morphology and AV Ratio: None
PR Interval: None
QRS Duration and Morphology: None
QT Interval: None
 Asystole

Causes: Untreated VT, or VF, Electrocution,

profound Electrolyte or Acid-Base Imbalance,
MI
Medications for the treatment of asystole are not
rhythm specific, and do not improve survival
to discharge.
Check to make sure the patient does not have a
Do Not Resuscitate order
 Asystole

Treatment:
CPR as soon as pulselessness is established
1) Epinephrine 1mg IVP q3-5 min or
Vasopressin 40 units IV/IO to replace first
or second dose of epinephrine?! Is this still
valid?

Consider Early Termination of Efforts

 Pulseless Electrical Activity (PEA)

Any rhythm except Asystole, VF,

and VT
(as they have their own algorithms)
There is a disassociation with the electrical and
the mechanical functions of the heart (It used to
be called electromechanical dissociation).
Always answer the question:
Is there a pulse with this rhythm?
 PEA

General Treatment:
CPR as soon as pulselessness is established.
Endotracheal Intubation (better airway)
Large Bore IV Access (better for circulation)
1) Epinephrine 1mg IVP q 3-5 min or
Vasopressin 40 units IV/IO

Plus, think about the 6 Hs and 6 Ts

 PEA

Hypoxia Intubate and administer 100% 02

Hypovolemia Administer large volumes of IVF
Hydrogen Ion(Acidosis) Fluid Resus. CPR
Hypo/hyperthermia- Active cooling, warming
Hypo/hyperglycemia- correct glucose level
Hypo/hyper-electrolytes- follow rapid
chemistries to correct imbalance
 PEA

Tablet (Overdose)- Specific Antidote

Tension Pneumothorax- Needle Decompression
Tamponade, Pericardial- Pericardialcentesis
Thrombus, Coronary- Emergent Cath, Heparin
Thrombus, Pulmonary- Heparin, Thoracic
Surgery
Trauma- Specific Treatment
 1 Degree AV Block
st

1st Degree AV Block is a delay in conduction above to bundle

branches that can occur with several underlying rhythms.
Regularity: Regular
P Wave Morphology and AV Ratio: Uniform P waves, 1:1Ratio
PR Interval: Consistent Long PR Interval, Greater than 200ms
(0.2 seconds)
QRS Duration and Morphology: Less than 120ms
(0.12seconds).
QT Interval: Less than the preceding R-R Interval
 1st Degree AV Block

Causes: Cardiomyopathy, Ischemia or Injury to

the AV node, Valvular Disorders, Digitalis
Toxicity, Mechanical Injury to the AV node or
Junctional Tissue
Concerns: No major concerns, although watch
for progression to further block development.
Treatments: Not Required.
 2nd Degree AV Block (Mobitz I)
(Wenckebach)

Rate: Depends on Underlying SA node Rhythm and pattern of block

Regularity: Regular Atrial Rate, Ventricular Rhythm Irregular.
P Wave Morphology and AV Ratio: Uniform P wave Morphology, some P
waves do not have associated QRS complexes, AV Ratio > 1:1
PR Interval: Progressively Prolonged PR Intervals, until P wave does not
have associated QRS complex
QRS Duration and Morphology: Less than 120ms (0.12seconds).
QT Interval: Less than the preceding R-R Interval
 Wenckebach

Causes: Inferior MI, Cardiomyopathies, Digitalis

Toxicity, Valvular Disease
Concerns: Hemodynamic threat is based on Heart Rate,
thus individual symptoms vary. Watch for
progression of block.
Treatment is based on symptoms of bradycardia,
includes the use of transcutaneous pacing, atropine,
and dopamine and epinephrine infusions.
Permanent pacemaker placement may be indicated if
Wenckebach persists.
 2nd Degree AV Block (Mobitz II)
(Classic)

Rate: Usually Slow, Depending on SA node Rate.

Regularity: Makes Ventricular Rhythm Irregular the majority of the time.
Occasionally can be in a pattern when Ventricular Rhythm is Regular
P Wave Morphology and AV Ratio: Identical P wave Morphology, AV Ratio
>1:1PR Interval: Consistently Long PR Intervals, Some P wave have no
associated QRS complexes
QRS Duration and Morphology: Less than 120ms (0.12seconds).
QT Interval: Less than the preceding R-R Interval
 2nd Degree AV Block (Mobitz II)
(Classic)
Causes: Worsening Ischemia or Injury to the AV
node or Junctional Tissue by Injury or Ischemia,
Cardiomyopathy or Valve Disease, or Digitalis
Toxicity
Concerns: More of a concern, as Bradycardia is
Common, and patients often progress to Complete
Heart Block
Treatments: The treatment for all bradycardias is based
on the presence of symptoms. Transcutaneous pacing
may be superior to Atropine.
 3rd Degree AV Block
(Complete Heart Block)

Rate: Usually Slow Regularity: Both Atrial and Ventricular Rhythms

are Regular
P Wave Morphology and AV Ratio: P wave morphology is Identical, P
waves and QRS complexes do not correlate, making the AV ratio
>1:1PR Interval: Not Measurable, P waves do not have correlated QRS
complexes
QRS Duration and Morphology: QRS duration can be narrow or wide.
(Complete Heart Block is essentially the SA node providing stimulation of
atrial depolarization, and a lower pacer site providing stimulation of
ventricular depolarization at the same time)
QT Interval: Less than the preceding RR Interval
 Complete Heart Block

Causes: Untreated Digitalis Toxicity, Worsening Ischemia or

Injury, Cardiomyopathy, Valvular Disease, Mechanical
Trauma to the AV Node
Concerns: Hemodynamic Compromise can occur because of a
slow heart rate and the loss of atrioventricular synchrony.
CHB is a common PEA, is there a pulse with this rhythm?
Treatments: Includes transcutaneous pacing, atropine, and the
use of dopamine or epinephrine drips. Transcutaneous Pacing
is the first choice for CHB as there no communication between
the SA node and the Ventricle, therefore speeding up SA node
rate will not be beneficial, and has been known to further slow
down ventricular response.