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Background
- I) Definition
Torsades de Pointes (TdP) is a specific form of polymorphic ventricular tachycardia (VT) characterized by a distinctive twisting morphology of the QRS complexes around the isoelectric line on ECG. It is closely associated with a prolonged QT interval and typically presents with syncope, seizures, or sudden cardiac arrest. TdP may be self-terminating or degenerate into ventricular fibrillation, leading to sudden cardiac death if not promptly treated.
- II) Classification/Types
By Etiology:
- Congenital TdP: Resulting from inherited long QT syndromes (LQT1, LQT2, LQT3)
- Acquired TdP: Most commonly drug-induced or due to electrolyte disturbances
By Clinical Context:
- Pause-dependent TdP: Occurs after a long RR interval or post-premature beat pause (common in bradycardia or AV block)
- Adrenergic TdP: Triggered by increased sympathetic activity (seen in congenital LQTS, especially LQT1)
Pathophysiology
TdP arises from early afterdepolarizations (EADs) during phase 2 or 3 of the cardiac action potential, which occur due to prolonged repolarization. These EADs can trigger premature ventricular contractions in a myocardium with heterogenous refractoriness, leading to a reentrant polymorphic VT. Prolonged QT, bradycardia, and pauses increase the susceptibility. The arrhythmia is potentiated by hypokalemia, hypomagnesemia, and drugs that block potassium channels (especially I<sub>Kr</sub>).
Epidemiology
- More common in females due to longer baseline QT intervals
- Incidence increases with QT-prolonging drugs or electrolyte imbalances
- Responsible for a subset of cases of sudden cardiac death and syncope
- Seen in both hospital and outpatient settings, especially in polypharmacy patients
Etiology
- I) Causes
Acquired (Most common):
- QT-prolonging drugs:
- Antiarrhythmics: quinidine, sotalol, amiodarone
- Antipsychotics: haloperidol, ziprasidone
- Antibiotics: macrolides, fluoroquinolones
- Antidepressants: TCAs, SSRIs
- Electrolyte disturbances:
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
- Starvation, anorexia nervosa
- Severe bradycardia or AV block
- Organophosphate poisoning
Congenital:
- Long QT syndromes (LQTS types 1–3)
- Jervell-Lange-Nielsen syndrome (with deafness)
- Andersen-Tawil syndrome (includes periodic paralysis)
- II) Risk Factors
- Female sex
- Bradycardia
- Structural heart disease
- Electrolyte abnormalities
- Renal insufficiency
- Polypharmacy with QT-prolonging agents
- Family history of sudden cardiac death
Clinical Presentation
- I) History (Symptoms)
- Sudden, transient syncope
- Palpitations
- Lightheadedness or near-syncope
- Seizure-like activity (due to cerebral hypoperfusion)
- Sudden cardiac arrest (if progression to VF)
- II) Physical Exam (Signs)
- May be normal between episodes
- Hypotension or pulselessness during sustained arrhythmia
- Irregular pulse, bradycardia (pause-dependent TdP)
- Signs of underlying illness (malnutrition, intoxication, bradyarrhythmias)
Differential Diagnosis (DDx)
- Polymorphic VT without QT prolongation (e.g., ischemia-induced VT)
- Ventricular fibrillation
- Monomorphic VT
- Seizure disorder (in misdiagnosed TdP syncope)
- AV block with ventricular escape rhythm
Diagnostic Tests
Initial Work-Up
- 12-lead ECG: Prolonged QTc (>460 ms in women, >440 ms in men); polymorphic VT with twisting QRS complexes
- Serum electrolytes: Potassium, magnesium, calcium
- Drug screen: Identify QT-prolonging agents
- Cardiac enzymes: Rule out ischemia if suspected
- Echocardiogram: Evaluate for structural disease
- Genetic testing: If congenital LQTS suspected
- Ambulatory monitoring: If episodes are transient and undocumented
Treatment
- I) Initial Management
Unstable or pulseless TdP:
- Immediate defibrillation
Stable TdP with sustained rhythm:
- IV magnesium sulfate 2 g over 1–2 minutes (even if serum Mg is normal)
- Temporary pacing to increase HR if bradycardia-related
- Isoproterenol infusion to increase heart rate (in congenital or pause-dependent TdP)
- Stop QT-prolonging medications
- Correct electrolyte abnormalities (K+ >4.5 mEq/L, Mg >2 mg/dL)
- II) Medications
Drug Class | Examples | Notes |
Magnesium sulfate | IV magnesium sulfate | First-line for acute management |
Beta-blockers | Nadolol, Propranolol | Used in congenital LQTS (especially LQT1, LQT2) |
Potassium | Oral/IV | Maintain K+ at high-normal levels |
Isoproterenol | IV infusion | Used in bradycardia-dependent TdP or congenital LQTS |
Antiarrhythmics | Avoid unless necessary | Amiodarone may worsen QT; use caution |
Device Therapy
- Temporary pacing: Overdrive pacing (rate 90–110 bpm) for pause-dependent TdP
- Implantable Cardioverter-Defibrillator (ICD): For survivors of cardiac arrest or high-risk congenital LQTS
Consults/Referrals
- Cardiology: All TdP patients for QTc evaluation and risk stratification
- Electrophysiology: For device therapy (ICD, pacing) or refractory cases
- Genetics: For inherited LQTS syndromes
- Pharmacy: Medication review to avoid QT-prolonging interactions
Patient Education, Screening, Vaccines
Education
- Avoid QT-prolonging drugs (patients should carry a list)
- Recognize symptoms of arrhythmia (syncope, palpitations)
- Importance of medication adherence (especially beta-blockers in LQTS)
- Family screening if congenital LQTS diagnosed
- Wear medical alert ID
Screening/Prevention
- Routine ECG in high-risk patients (e.g., polypharmacy, bradycardia)
- Screen first-degree relatives in congenital LQTS
- Electrolyte monitoring during illness or diuretic use
Vaccinations
- No TdP-specific vaccine
- Routine influenza and pneumococcal vaccines for those with structural heart disease or ICD
Follow-Up
Short-Term
- Monitor ECG for QTc normalization
- Daily electrolytes until stabilized
- Continuous telemetry in hospitalized patients
- Review all medications for QT risk
Long-Term
- Periodic ECG to monitor QT interval
- Beta-blocker therapy in congenital LQTS
- ICD follow-up if placed
- Genetic counseling and family screening
- Avoidance of QT-prolonging agents and high-risk scenarios (e.g., fasting, dehydration)
Prognosis
- Excellent with early recognition and treatment of reversible causes
- Recurrent risk high if underlying etiology (e.g., drugs, electrolytes) not corrected
- Congenital LQTS: Variable prognosis depending on subtype; beta-blockers and ICDs improve survival
- Untreated TdP may progress to VF and death
