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1. Premature ventricular complexes (PVCs)
2. Aberrancy vs. ventricular ectopy
3. Ventricular tachycardia
4. Differential diagnosis of wide QRS tachycardias
5. Accelerated ventricular rhythms
6. Idioventricular rhythm
7. Ventricular Parasystole

1. Premature Ventricular Complexes (PVCs)

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 PVCs may be unifocal (see above), multifocal (see below) or multiformed. Multifocal PVCs have different sites of origin, which means their coupling intervals (measured from the previous QRS complexes) are usually different. Multiformed PVCs usually have the same coupling intervals (because they originate in the same ectopic site but their conduction through the ventricles differ. Multiformed PVCs are common in digitalis intoxication.

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 PVCs may occur as isolated single events or as couplets, triplets, and salvos (4-6 PVCs in a row), also called brief ventricular tachycardias.

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 PVCs may occur early in the cycle (R-on-T phenomenon), after the T wave (as seen above), or late in the cycle - often fusing with the next QRS (fusion beat). R-on-T PVCs may be especially dangerous in an acute ischemic situation, because the ventricles may be more vulnerable to ventricular tachycardia or fibrillation. Examples are seen below.

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In the above example, "late" (end-diastolic) PVCs are illustrated with varying degrees of fusion. For fusion to occur the sinus P wave must have made it to the ventricles to start the activation sequence, but before ventricular activation is completed the "late" PVC occurs. The resultant QRS looks a bit like the normal QRS, and a bit like the PVC; i.e., a fusion QRS.

 The events following a PVC are of interest. Usually a PVC is followed by a complete compensatory pause because the sinus node timing is not interrupted; one sinus P wave isn't able to reach the ventricles because they are still refractory from the PVC; the following sinus impulse occurs on time based on the sinus rate. In contrast, PACs are usually followed by an incomplete pause because the PAC usually enters the sinus node and resets its timing; this enables the following sinus P wave to appear earlier than expected. These concepts are illustrated below.

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 Not all PVCs are followed by a pause. If a PVC occurs early enough (especially if the heart rate is slow), it may appear sandwiched in between two normal beats. This is called an interpolated PVC. The sinus impulse following the PVC may be conducted with a longer PR interval because of retrograde concealed conduction by the PVC into the AV junction slowing subsequent conduction of the sinus impulse.

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 Finally a PVC may retrogradely capture the atrium, reset the sinus node, and be followed by an incomplete pause. Often the retrograde P wave can be seen on the ECG, hiding in the ST-T wave of the PVC.

 The most unusual post-PVC event is when retrograde activation of the AV junction re-enters the ventricles as a ventricular echo. This is illustrated below. The "ladder" diagram below the ECG helps us understand the mechanism. The P wave following the PVC is the sinus P wave, but the PR interval is too short for it to have caused the next QRS. (Remember, the PR interval following an interpolated PVC is usually longer than normal, not shorter!).

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 PVCs usually stick out like "sore thumbs", because they are bizarre in appearance compared to the normal complexes. However, not all premature sore thumbs are PVCs. In the example below 2 PACs are seen, #1 with a normal QRS, and #2 with RBBB aberrancy - which looks like a sore thumb. The challenge, therefore, is to recognize sore thumbs for what they are, and that's the next topic for discussion!

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2. Aberrancy vs. Ventricular Ectopy

A most important question

 Aberrant Ventricular Conduction: defined as the intermittent abnormal intraventricular conduction of a supraventricular impulse. The phenomenon comes about because of unequal refractoriness of the bundle branches and critical prematurity of a supraventricular impulse (see diagram of "Three Fates of PACs"). With such critical prematurity, the supraventricular impulse encounters one bundle branch (or fascicle) which is responsive, and the other which is refractory, and is consequently conducted with a bundle branch block or fascicular block pattern.

 ECG clues to the differential diagnosis of wide QRS premature beats:

 Preceding ectopic P wave (i.e., the P' of the PAC) usually hidden in the ST-T wave of the previous beat favors aberrant ventricular conduction. In the ECG below note the arrow pointing at a premature P wave in the ST-T segment. The QRS has a RBBB morphology.

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 Analyze the compensatory pause: A complete pause favors ventricular ectopy (i.e., no resetting of the sinus pacemaker; next sinus impulse comes on time). An incomplete pause favors aberration (i.e., because supraventricular prematures are more likely to reset the sinus node's timing). Be aware of exceptions to this simple rule because PVCs can activate the atria retrogradely and reset the sinus node (incomplete pause), and PACs can fail to reset the sinus node (complete pause).

 Long-Short Rule (Ashman Phenomenon): The earlier in the cycle a PAC occurs and the longer the preceding cycle, the more likely the PAC will be conducted with aberration (see diagram "The Three Fates of PACs"). This is because the refractory period of the ventricular conduction system is proportional to cycle length or heart rate; the longer the cycle length or slower the heart rate, the longer the recovery time of the conduction system. In most individuals the right bundle normally recovers more slowly than the left bundle, and a critically timed PAC is therefore more likely to conduct with RBBB than with LBBB. In diseased hearts, however, LBBB aberrancy is also seen. Dr. Richard Ashman and colleagues first described this in 1947 in patients with atrial fibrillation. He noted that the QRS complexes ending a short RR interval were often of a RBBB pattern if the preceding RR interval was long. (That's all it takes to get your name attached to a phenomenon; you must publish!).

 Analyze the QRS morphology of the funny-looking beat. This is one of the most rewarding of the clinical clues, especially if lead V1 (or the MCL1 monitored lead in intensive care units) is used. Since aberrancy is almost always in the form of a bundle branch block morphology, V1 is the best lead for differentiating RBBB from LBBB; RBBB creates a positive deflection, and LBBB, a negative deflection. Therefore, the first order of business is to identify the direction of QRS forces in V1.

If the QRS in V1 is mostly positive the following possibilities exist:

 rsR' or rSR' QRS morphologies suggests RBBB aberrancy >90% of the time!

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Note the rsR' morphology of PAC #2!

 monophasic R waves or R waves with a notch or slur on the downstroke of the R waves suggests ventricular ectopy > 90% of the time (see below)!

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 monophasic R wave with a notch or slur on the upstroke of R wave: 50-50 possibility or either!

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In the above ECG the premature wide QRS is an aberrantly conducted PAC because of the easily seen preceding P wave. The QRS morphology could be either!

 qR morphology suggests ventricular ectopy unless a previous anteroseptal MI or unless the patient's normal V1 QRS complex has a QS morphology (i.e., no initial r-wave)!



If the QRS in V1 is mostly negative the following possibilities exist:

 Rapid downstroke of the S wave with or without a preceding "thin" r wave suggests LBBB aberrancy almost always!

 Fat" r wave (0.04s) or notch/slur on downstroke of S wave or >0.06s delay from QRS onset to nadir of S wave almost always suggests ventricular ectopy!

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In the above ECG the wide premature QRS is a PVC because of the >0.06s delay from onset of the QRS to the nadir of the S wave (approximately 0.08s).

Another QRS morphology clue from Lead V6:

 If the wide QRS morphology is predominately negative in direction in lead V6, then it's most likely ventricular ectopy (assuming V6 is accurately placed in mid axillary line)!



 The timing of the premature wide QRS complex is also important because aberrantly conducted QRS complexes only occur early in the cardiac cycle during the refractory period of one of the conduction branches. Therefore, late premature wide QRS complexes (after the T wave, for example) are most often ventricular ectopic in origin.

3. Ventricular Tachycardia

 Descriptors to consider when considering ventricular tachycardia:

 Sustained (lasting >30 sec) vs. nonsustained

 Monomorphic (uniform morphology) vs. polymorphic vs. Torsade-de-pointes

 Torsade-de-pointes: a polymorphic ventricular tachycardia associated with the long-QT syndromes characterized by phasic variations in the polarity of the QRS complexes around the baseline. Ventricular rate is often >200bpm and ventricular fibrillation is a consequence.

 Presence of AV dissociation (independent atrial activity) vs. retrograde atrial capture

 Presence of fusion QRS complexes (Dressler beats) which occur when supraventricular beats (usually sinus) get into the ventricles during the ectopic activation sequence.

 Differential Diagnosis: just as for single premature funny-looking beats, not all wide QRS tachycardias are ventricular in origin (i.e., they may be supraventricular tachycardias with bundle branch block or WPW preexcitation)!

4. Differential Diagnosis of Wide QRS Tachycardias

 Although this is an ECG tutorial, let's not forget some simple bedside clues to ventricular tachycardia:

 Advanced heart disease (e.g., coronary heart disease) statistically favors ventricular tachycardia

 Cannon 'a' waves in the jugular venous pulse suggests ventricular tachycardia with AV dissociation. Under these circumstances atrial contractions may occur when the tricuspid valve is still closed which leads to the giant retrograde pulsations seen in the JV pulse. With AV dissociation these giant a-waves occur irregularly.

 Variable intensity of the S1 heart sound at the apex (mitral closure); again this is seen when there is AV dissociation resulting in varying position of the mitral valve leaflets depending on the timing of atrial and ventricular systole.

 If the patient is hemodynamically unstable, think ventricular tachycardia and act accordingly!



 ECG Clues:

 Regularity of the rhythm: If the wide QRS tachycardia is sustained and monomorphic, then the rhythm is usually regular (i.e., RR intervals equal); an irregularly-irregular rhythm suggests atrial fibrillation with aberration or with WPW preexcitation.

 A-V Dissociation strongly suggests ventricular tachycardia! Unfortunately AV dissociation only occurs in approximately 50% of ventricular tachycardias (the other 50% have retrograde atrial capture or "V-A association"). Of the patients with AV dissociation, it is only easily recognized if the rate of tachycardia is <150 bpm. Faster heart rates make it difficult to visualize dissociated P waves.

 Fusion beats or captures often occur when there is AV dissociation and this also strongly suggests a ventricular origin for the wide QRS tachycardia.

 QRS morphology in lead V1 or V6 as described above for single premature funny looking beats is often the best clue to the origin, so go back and check out the clues! Also consider a few other morphology clues:

 Bizarre frontal-plane QRS axis (i.e. from +150 degrees to -90 degrees or NW quadrant) suggests ventricular tachycardia

 QRS morphology similar to previously seen PVCs suggests ventricular tachycardia

 If all the QRS complexes from V1 to V6 are in the same direction (positive or negative), ventricular tachycardia is likely

 Especially wide QRS complexes (>0.16s) suggests ventricular tachycardia

 Also consider the following Four-step Algorithm reported by Brugada et al, Circulation 1991;83:1649:

Step 1: Absence of RS complex in all leads V1-V6?
Yes: Dx is ventricular tachycardia!

Step 2: No: Is interval from beginning of R wave to nadir of S wave >0.1s in any RS lead?
Yes: Dx is ventricular tachycardia!

Step 3: No: Are AV dissociation, fusions, or captures seen?
Yes: Dx is ventricular tachycardia!

Step 4: No: Are there morphology criteria for VT present both in leads V1 and V6?
Yes: Dx is ventricular tachycardia!

NO: Diagnosis is supraventricular tachycardia with aberration!

5. Accelerated Ventricular Rhythms

(see ECG below)

 An "active" ventricular rhythm due to enhanced automaticity of a ventricular pacemaker (reperfusion after thrombolytic therapy is a common causal factor).

 Ventricular rate 60-100 bpm (anything faster would be ventricular tachycardia)

 Sometimes called isochronic ventricular rhythm because the ventricular rate is close to underlying sinus rate

 May begin and end with fusion beats (ventricular activation partly due to the normal sinus activation of the ventricles and partly from the ectopic focus).

 Usually benign, short lasting, and not requiring of therapy.

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6. Idioventricular Rhythm

 A "passive" escape rhythm that occurs by default whenever higher-lever pacemakers in AV junction or sinus node fail to control ventricular activation.

 Escape rate is usually 30-50 bpm (i.e., slower than a junctional escape rhythm).

 Seen most often in complete AV block with AV dissociation or in other bradycardic conditions.

7. Ventricular Parasystole

 Non-fixed coupled PVCs where the inter-ectopic intervals (i.e., timing between PVCs) are some multiple (i.e., 1x, 2x, 3x, . . . etc.) of the basic rate of the parasystolic focus

 PVCs have uniform morphology unless fusion beats occur

 Usually entrance block is present around the ectopic focus, which means that the primary rhythm (e.g., sinus rhythm) is unable to enter the ectopic site and reset its timing.

 May also see exit block; i.e., the output from the ectopic site may occasionally be blocked (i.e., no PVC when one is expected).

 Fusion beats are common when ectopic site fires while ventricles are already being activated from primary pacemaker

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 Parasystolic rhythms may also be seen in the atria and AV junction

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