Cardiology · Arrhythmias
The facts most likely to be tested
Torsades de Pointes is a polymorphic ventricular tachycardia characterized by a twisting of the QRS complexes around the isoelectric line.
The hallmark ECG finding is a prolonged QT interval (typically >500 ms) preceding the onset of the arrhythmia.
First-line treatment for a hemodynamically unstable patient is immediate unsynchronized defibrillation.
First-line treatment for a hemodynamically stable patient is intravenous magnesium sulfate.
Acquired Torsades is most commonly caused by electrolyte disturbances (hypokalemia, hypomagnesemia) or QT-prolonging medications.
Common offending drug classes include antiarrhythmics (Class IA and III), macrolides, fluoroquinolones, and antipsychotics.
Congenital Long QT syndrome is often associated with autosomal dominant (Romano-Ward) or autosomal recessive (Jervell and Lange-Nielsen) inheritance patterns.
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A 62-year-old woman is brought to the emergency department after a syncopal episode. She has a history of depression and was recently started on levofloxacin for a urinary tract infection. Her physical examination reveals a regular pulse of 110/min and a blood pressure of 95/60 mmHg. An ECG shows a prolonged QT interval and a polymorphic ventricular tachycardia with a twisting appearance of the QRS complexes.
What is the most appropriate initial pharmacologic treatment for this patient?
Intravenous magnesium sulfate
The patient is hemodynamically stable with Torsades de Pointes induced by a QT-prolonging antibiotic; therefore, intravenous magnesium sulfate is the treatment of choice to stabilize the cardiac membrane.
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Etiology / Epidemiology
Occurs in patients with prolonged QT interval due to electrolyte disturbances or QT-prolonging medications.
Clinical Manifestations
Polymorphic ventricular tachycardia with twisting of the points; presents as syncope or sudden cardiac death.
Diagnosis
ECG shows polymorphic QRS complexes with a QTc > 500 ms.
Treatment
Magnesium sulfate is the first-line treatment; avoid antiarrhythmics that prolong QT.
Prognosis
High risk of progression to ventricular fibrillation; requires immediate correction of underlying triggers.
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Epidemiology & Etiology
Commonly triggered by hypokalemia, hypomagnesemia, or hypocalcemia. Iatrogenic causes include macrolides, fluoroquinolones, and antipsychotics. Patients with congenital long QT syndrome are at highest risk.
Pertinent Anatomy
Involves the ventricular myocardium and the His-Purkinje system. Repolarization abnormalities lead to early afterdepolarizations that trigger re-entrant circuits.
Pathophysiology
Delayed repolarization allows for early afterdepolarizations (EADs) during phase 3 of the action potential. These EADs trigger a polymorphic ventricular tachycardia that appears to twist around the isoelectric line. If persistent, the rhythm degenerates into ventricular fibrillation.
Clinical Manifestations
Patients typically present with syncope, palpitations, or seizure-like activity due to cerebral hypoperfusion. The twisting of the points appearance on ECG is pathognomonic. Sudden cardiac arrest is a frequent initial presentation in undiagnosed cases.
Diagnosis
ECG is the gold standard. Look for a QTc > 500 ms and polymorphic QRS complexes that change amplitude and polarity. Always calculate the QTc using Bazett's formula.
Treatment
Administer IV magnesium sulfate (2g bolus) immediately, even if serum magnesium is normal. If hemodynamically unstable, perform unsynchronized cardioversion. Do not use Class IA, IC, or III antiarrhythmics as they further prolong the QT interval.
Prognosis
High risk of ventricular fibrillation and death if untreated. Requires continuous cardiac monitoring and aggressive electrolyte repletion to prevent recurrence.
Differential Diagnosis
Ventricular Tachycardia: Monomorphic QRS complexes
Ventricular Fibrillation: Chaotic, irregular rhythm without distinct QRS
Brugada Syndrome: ST elevation in V1-V3 with RBBB pattern
Hyperkalemia: Peaked T waves and widened QRS
Wolff-Parkinson-White: Delta wave and short PR interval