Polymorphic ventricular tachycardia is classically described as a rhythm of ectopic ventricular origin that is characterized by an irregular cadence and a constantly changing morphologic picture, amplitude, and polarity of the complexes (Figure 33-1). The complexes are wide, as you would expect for a ventricular rhythm, and typically appear to twist and turn along a central axis. The rhythm is typically triggered by a premature ventricular contraction (PVC) that occurs along the relative refractory period of the previous complex. The QT interval of the baseline rhythm is normal in polymorphic VTach.
Figure 33-1 A patient with a normal QT interval has a premature ventricular contraction that triggers a run of polymorphic ventricular tachycardia. Note the rapid rates of the tachycardia and the lack of distinction between the components of the ventricular complexes. Finally, note that the amplitude of the complexes is constantly changing in each grouping as the polarity of the complexes changes from negative to positive (represented by the blue and pink arrows). This reversal of polarity on the same strip is virtually pathognomonic for this type of arrhythmia.
Typically, the usual rates occur between 200 and 250 beats per minute (BPM). The ventricular rates, however, can be anywhere from 150 to 300 BPM (in very rare cases, there have even been cases with rates as slow as 100 BPM). The very rapid rate associated with polymorphic VTach tends to blur the distinction between the QRS waves, the ST segments, and T waves, and the complexes take on an appearance similar to ventricular flutter. Unlike ventricular flutter, however, the morphology of the complexes is constantly changing, almost on a beat-to-beat basis, due to a constant reversal of the polarity of the rhythm from positive to negative.
The changing polarity of the complexes appears to occur periodically, creating a grouped appearance in the rhythm. The groupings are composed of anywhere from 5 to 20 complexes on average. The number of groupings, however, depends on the duration of the arrhythmia.
Polymorphic VTach demonstrates a close relationship to the patient’s underlying heart rate when the patient is not in tachycardia. Many patients develop the arrhythmia during periods of bradycardia or severe atrioventricular (AV) block. On the other hand, drugs that speed the underlying heart rate can prevent the formation of the arrhythmia.
The rhythm is typically seen in patients undergoing an acute myocardial infarction (AMI) or severe ischemia. The development of this electrocardiographic arrhythmia in a patient with a normal QT interval should prompt a search for an AMI, ischemia, or silent ischemia. If ischemia or infarct is ruled out as a cause, further evaluation to isolate a cause should follow the differential diagnosis that is described in the section on torsade de pointes.
Hemodynamic instability and consequences of low cardiac output are more frequent in polymorphic VTach compared with monomorphic VTach. A large part of the reason lies in the faster rates seen with polymorphic VTach. The rhythm is usually self-limiting, but can break down into ventricular fibrillation and can cause sudden death.
Management strategies are identical to those used in monomorphic VTach. Remember, electrical cardioversion or defibrillation should be your first-line response to a significantly hemodynamically compromised patient with this arrhythmia.
