Etiology
Pathophysiology
- A specific form of Polymorphic Ventricular Tachycardia occurring in the context of a prolonged QT interval.
- Characterized by QRS complexes that “twist” around the isoelectric line (Torsades de pointes = twisting of the points).
- Mechanism: Prolonged repolarization leads to Early Afterdepolarizations (EADs), triggering re-entrant circuits.
- Can progress to Ventricular Fibrillation (VF) and sudden cardiac death (SCD).
Clinical features
- Often asymptomatic
- Cardiovascular features
- Palpitations
- Tachycardia (HR ≥100/min; typically regular)
- Chest pain/pressure
- Dyspnea, orthopnea
- Symptoms of reduced cardiac output
- Dizziness
- Hypotension
- Syncope
- Cardiogenic shock and loss of consciousness
- Cardiac arrest
Diagnostics
- Polymorphic VT with QRS complexes that typically appear to twist around the isoelectric line, usually in self-limiting bursts
- Often preceded by bigeminy and followed by several premature ventricular contractions
- R-on-T phenomenon may also be seen.
Treatment
- Hemodynamically Unstable (Shock, unconscious, pulseless):
- Immediate unsynchronized cardioversion (defibrillation) & CPR per ACLS protocol.
- Hemodynamically Stable:
- First-line: IV Magnesium Sulfate (give even if serum Mg2+ is normal). c
- Acts as a natural Ca2+ channel blocker. Decreases inward Ca2+ influx → Suppresses Early Afterdepolarizations (EADs) → Terminates TdP.
- Refractory / Recurrent / Bradycardia-induced:
- Transvenous overdrive pacing OR Isoproterenol infusion (↑ HR shortens the QT interval, terminating the arrhythmia).
- Underlying Cause Correction:
- D/C all QT-prolonging meds immediately.
- Replete K+ to > 4.0 mEq/L and Mg2+ to > 2.0 mg/dL.
- Long-Term (Congenital Long QT):
- Beta-blockers (propranolol, nadolol) to blunt sympathetic tone.
- Implantable Cardioverter-Defibrillator (ICD) if recurrent syncope or prior cardiac arrest.