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Lesson V (cont) Ventricular Arrhythmias
Frank G. Yanowitz, MD
Associate Professor of Medicine
University of Utah School of Medicine
Return to the beginning of Lesson V
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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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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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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!
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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!
If the QRS in V1 is mostly negative the following possibilities exist:
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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:
Descriptors to consider when considering ventricular tachycardia:
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)!
Although this is an ECG tutorial, let's not forget some simple bedside clues to ventricular tachycardia:
ECG Clues:
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!
(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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A "passive" escape rhythm that occurs by default whenever higher-lever pacemakers in AV junction or sinus node fail to control ventricular activation.
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
Return to the beginning of Lesson V Go back to supraventricular arrhythmias
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