Why Bradycardia Induces Polymorphic Ventricular Tachycardia
Bradycardia triggers polymorphic ventricular tachycardia (specifically torsades de pointes) by creating pauses in cardiac rhythm that prolong ventricular repolarization, increase QT interval dispersion, and generate early afterdepolarizations that serve as the substrate for reentrant arrhythmias. 1
Electrophysiologic Mechanism
The relationship between bradycardia and polymorphic VT is fundamentally linked to abnormal repolarization:
- Slow heart rates prolong the action potential duration, which increases the QT interval and creates heterogeneity in ventricular repolarization across different myocardial regions 1
- Pauses in rhythm are particularly dangerous because they allow for maximal prolongation of repolarization and create the electrical substrate for triggered activity 1
- Early afterdepolarizations (EADs) occur during the prolonged repolarization phase, serving as the trigger that initiates the polymorphic VT 2
Clinical Context: Torsades de Pointes
This mechanism is most clinically relevant in torsades de pointes, the classic form of pause-dependent polymorphic VT:
- The American Heart Association explicitly recognizes that polymorphic VT can be "precipitated by pauses in rhythm" when associated with acquired long QT syndrome 1
- The pattern is typically: bradycardia → pause → QT prolongation → premature ventricular contraction → torsades de pointes 1, 3
- This is why pacing or isoproterenol (which increases heart rate) are recommended treatments - they eliminate the bradycardia and pauses that perpetuate the arrhythmia 1, 3
Treatment Implications Based on Mechanism
Understanding this mechanism directly guides emergency therapy:
- For bradycardia-associated polymorphic VT with long QT, temporary overdrive pacing at 90-110 bpm is recommended to prevent the pauses that trigger the arrhythmia 1, 3
- IV isoproterenol may be considered when pacing is not immediately available, as it increases heart rate and shortens the QT interval 1
- IV magnesium sulfate (1-2g) should be administered regardless of serum levels, as it stabilizes the myocardial membrane and reduces early afterdepolarizations 1, 4, 3
Critical Distinction: Not All Polymorphic VT is Bradycardia-Dependent
A common pitfall is assuming all polymorphic VT is related to bradycardia and long QT - this is incorrect and dangerous:
- Polymorphic VT without QT prolongation is most commonly caused by acute myocardial ischemia, not bradycardia, and requires completely different management (beta-blockers, revascularization) 1, 5
- In ischemic polymorphic VT, the mechanism is abnormal repolarization from injured myocardium, not pause-dependent triggered activity 5
- Isoproterenol and pacing (appropriate for bradycardia-induced torsades) would be inappropriate and potentially harmful in ischemic polymorphic VT 1
Specific High-Risk Scenarios
Certain clinical situations create the perfect storm for bradycardia-induced polymorphic VT:
- Drug-induced QT prolongation combined with bradycardia (from beta-blockers, calcium channel blockers, or high vagal tone) creates maximal risk 1, 3
- Electrolyte depletion (hypokalemia, hypomagnesemia) amplifies the effect of bradycardia on repolarization abnormalities 1
- Congenital long QT syndrome patients are particularly vulnerable when bradycardia occurs, though beta-blockers remain the mainstay of chronic therapy 1
Practical Recognition at the Bedside
Look for the characteristic "short-long-short" sequence on telemetry: a premature beat, followed by a compensatory pause (bradycardia), followed by another premature beat that initiates torsades 1, 6. This pattern confirms the pause-dependent mechanism and indicates that rate acceleration (pacing or isoproterenol) is the appropriate intervention 1, 3.