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32 Cards in this Set

  • Front
  • Back
Define Automaticity
Intrinsic property of specialized, pacemaker cells that dictates that they will spontaneously depolarize to a threshold voltage in a rhythmic, repeated fashion.

Rate at which the tissue reaches threshold (slope of Na+ influx in phase 4 depol) determines its sponteneous rhythm

--SA node fastest(60-100 bpm)
--AV node (50 bpm)
--Purkinje fibers (40 bpm)
Define Escape Beat
As a result of automaticity, tissue in a subsidiary pacemaker fires to depolarize the heart when a pacemaker fails

EBs are LATE (not pre-mature!) beats, occurring later than the regular pacemaker would have

EBs TERMINATE A PAUSE caused by a slowed sinus rhythem (return of HR after brief flatline)- EBs = good!

EBs prevent asystole and prevent the HR from becoming too slow when SA node firing is impaired

--Hierarchical order of EBs

--Slower than the usual beat
Junctional Escape Beats
JUNCTIONAL ESCAPE BEATS: Protective back-up mech that maintains a heart rate and CO when SA node or AV node conduction fail (asystole)

Arise from the AV node or proximal bundle of His

SLOW and LATE w/ 40-60 bpm

-No P waves evident b/c impulse originates below atria
-normal QRS b/c still using Purkinje system
Aberrant conduction
ABERRANT CONDUCTION: Rate related impairment of conduction down one of the bundle branches

Results from differential recovery (refractory period) of the two bundle branches

Follows a premature stimulus

Mimics a premature ventricular beat

RBBB with wide QRS
--> RV depol occurs via slow cell to cell conduction
--> INCONSISTENT pattern since right bundle is functional
Reentry Tachycardia
1) Requires specific substrates
-Dual pathway (functional or anatomic division in conduction system)
-Region of slowed conduction
-Region of unidirectional block

2) Allows establishment of sustained tachycardia

3) Occurs at any level of the conduction system, or myocardium

REENTRY TACHYCARDIA: usually follows a premature stimulus from coming from above

A circus movement of the wave front causes depolarization of the distal tissues each time the circuit is completed

*Macroreentry- large circuit involving considerable area (atrial flutter)
*Microreentry - small circuit (ventricular tachy)
Abnormalities of electrical function can produce clinical sequelae in two ways:
Remember: CO = SV x HR

CO FALLS if the heart goes
--TOO FAST (too little time in diastole, SV falls) or
--TOO SLOW (SV can only become so large, so CO falls d/t fall in HR)

*CO can be maintained between HR of 40-160bpm, but will fall if the rate is higher or lower
Ventricular Escape Beat
Widened QRS complex b/c NOT using the purkinje system, conduction is occurring cell-to-cell (slower)
- No P wave
- comes late
Escape beat
Escape beat:

--no P wave

--delayed QRS wave b/c ventricular contraction is d/t AV node which takes longer to reach threshold

--AV node has shallower phase 4 and will take longer to depolarize ventricles
Aberrant conduction
Aberrant conduction:

--Right bundle branch depolarizes slower than left.

--Small segment time when LBB is in relative refractory period and the RBB is in an absolute refractory period

--If an early beat occurs at this time the ECG will look like a RBBB where every beat appears wide
Fusion beat
Fusion beat:

Ventricular depolarization resulting from impulses that originated at two different sites.

WPW syndrome: fusion of impulses from AV node and from the ectopic tissue.
Compensatory pause
Compensatory pause:

--Defining marker for PVC

--Found when sinus rhythm is uninterrupted by the PVC

--The P wave that occurs during or immediately following PVC is NOT conducted, creating a pause

--After an irregular beat there is a pause before the next beat so that the rhythm remains the same as it was before the irregular beat
SA node dysrythmias
Sinus tachycardia:
Sinus tachycardia:

--MC dysrythmia

--Caused by fever, anemia or exercise

--innappropriate sinus tachycardia: the SA node is set too fast, which results in heart dilation

--Can lead to CHF, but can be reversible with treatment
SA node dysrythmias
Sinus bradycardia:
Sinus bradycardia:

Often occurs in a person in very good shape with a distensible heart (ie marathon runner)

These hearts have a high SV and so the heart does not need to increase HR to maintain CO.

Also seen in
-patients on beta-blockers
-elderly patients
SA node dysrythmias
Premature atrial contractions (PAC):
Premature atrial contractions (PAC):

--Area in the atria which depolarizes spontaneously, sends a second wave front through the atria that results in an irregular p wave.

--After irregular beat, the SA node is reset

--The next beat occurs at a regular sinus cycle rate with no compensatory pause.

--Early p wave, an irregular p shape, and the next beat occurring in sinus rhythm.
Atrial flutter:
Atrial flutter:
-Irritable focus of atrial automaticity fire a PAC

-Circus rhythm of atrial depolerization

-Only some P waves make it through AV node b/c the circus cycle is so fast

-Produces a "sawtooth atrial wave" on ECG

-AV node able to maintain HR consistent with life
Carotid massage: A-Flutter vs. A-Fib
Carotid massage: vagally-med slowing of AV conductioon

In A-flutter: causes an incremental drop in ventricular response (QRS)(ie 1:3--> 1:4, thus slow the rate of depolarization)

In A-fib: causes a gradual slowing of ventricular response
Atrial Fibrillation:
600-1000/min to AV node
Atrial Fibrillation:
“Electrical anarchy” where every atrial cell depolarizes independently

No True P waves, just a wavering baseline

Underlying pathology - always dilated atria!!

Irregularly, irregular ventricular response rhythm (random AV nodal conduc, not in a set pattern like A-flutter)

No two QRS complexes occur at the same distance from each other on ECG

Disorganized contraction, thrombi, emboli likely

Increased O2 demand
Atrioventricular Block:
Atrioventricular Block:

--AV node receives signals from above that it can’t handle.

--There is normal SA node rhythm.
Three classes of AV Block:
Three classes of AV Block:

1st degree- all beats conduct through AV node from the SA node, so every P wave will occur
--> However the conduction is slowed there is a long PR interval

2nd degree- only some beats make it through the AV node

3rd degree- no beats make it through
Type I Mobitz AV Block:
Lesion above bundle of His
Type I Mobitz AV Block:

SA node functions normally

PR intervals progressively prolonged

Predictable Pattern

P wave not follwed by QRS
PR interval- Progressively longer, then drops a QRS

Tx: generally, nothing
Dysrhythmia meds aren’t used anymore
Type I Mobitz AV Block:
Rule regarding the increment change in the PR interval:
Type I Mobitz AV Block:
The change in PR length between the first two beats of the set is the greatest.
Length of time b/w the first two QRS peaks is greatest.
R-R interval becomes shorter between beats
Type II Mobitz AV Block:
Lesion below bundle of HIS
Type II Mobitz AV Block:

Dropped P waves with no pattern

More dangerous than Type I b/c more likely to lead to total heard block

Unpredictable, follows no particular pattern

Low CO, so syncope (faint)

Tx: Kill the AV node with heat and put in a pacemaker
No meds
3rd degree AV block:
3rd degree AV block:

Atrium is beating regularly, but the ventricle is NOT beating with the same rhythm

Ventricular escape rhythms rescue ventricular depolerization

The two chambers are uncoordinated
AV Nodal Dysrhythmias:
AV nodal (junctional) premature beats:
AV nodal (junctional) premature beats:

AV node phase 4 is faster than SA node

Causes a premature, narrow QRS w/o P wave before it

WPW Pre-Excitation Syndrome
Conduction from the SA node and an anatomical bypass tract, but AV node conducts the signal slower

The same signal goes through the AV node and then through the His-Purkinje system, overtaking the signal that went through the bypass tract.

Produces Fusion beat:
1. short PR (bypass tract conducts faster in atria)
2. delta wave (first wide portion of the QRS complex.)
3. wide QRS

Tx: catheter to burn the bypass tract with high frequency energy.
Two possible scenarios:
Short PR makes WPW a good setup for reentry tachycardia:
Short PR makes WPW a good setup for reentry tachycardia:

1. Premature beat from the SA node could go through the AV node and then pass retrograde back through the bypass tract, causing a narrow QRS complex.

2.The beat could pass through the bypass tract and then retrograde through the AV node, causing a wide QRS complex b/c the signal doesn’t travel through the His-Purkinje fibers.
AV nodal reentry tachycardia (microreentry tachycardia):
AV nodal reentry tachycardia (microreentry tachycardia):

MC AV rhythm disturbance

Functional divide of AV node: one side has longer refractory period than the other, setting up a reentry circuit

a PAC conducts down fast portion of the AV node and then retrograde up the slow

Narrow QRS, w/ NO delta wave

Signal can be inverted, but it’s usually incorporated into the QRS


Always supraventricular

AV nodal tachy = junctional tachycardia.
Premature Ventricular Contractions:
Premature Ventricular Contractions:

Similar to PAC’s, but with a compensatory pause

Everyone has these, which is fine in normal hearts, problematic in diseased hearts esp. when accompanies by ischemia

Accelerated phase 4 in the ventricular tissue, but NOT in the His-Purkinje system.

Early, wide QRS
Next P wave comes right when it should since SA node not reset

Compensatory pause b/w the crazy beat and the next, normal one
PVC Categories:
PVC Categories:
1. PVC
2. Couplet- 2 PVC’s in a row
3. Triplet/ventricular tachycardia- 3 PVC’s in a row: “3-beat run of ventricular tach”
(monomorphic, polymorphic)
4. Bigeminy- every other beat is a PVC
5. Trigeminy- every third beat is a PVC
Monomorphic Ventricular Tachycardia
Ventricular Tachycardia:

3+ PVC’s in a row - classified as monophoric if
all the beats are arising from the same location
Polymorphic Ventricular Tachycardia
Torsades-de-pointe (turning on point):

Wide QRS that gets bigger, then smaller, then bigger, then smaller, etc.

Always assoc. w/ QT prolongation

Life threatening and should be treated aggressively
Ventricular Fibrillation

Ischemic event -> fibrillation -> no CO -> die

You lose all coordinated contraction in fibrillation, meaning you can’t pump CO needed to survive

Incompatible with life, defibrillation must be proptly carried out

This is the rhythm in most terminal events

This is the putative cause of most cases of sudden cardiac death

May result following period of v-tach or spontaneously