Torsades de Pointes (TdP)- Pathogenesis and Clinical Findings

Torsades de Pointes (TdP): Pathogenesis and Clinical Findings
Drugs (e.g. Class 1A [quinidine], Class III [sotalol,
amiodarone], TCAs, erythromycin, quinolones, anti-histamines)
Sinus bradycardia, AV block
Metabolic abnormality (hypo K+/Ca2+/Mg2+)
Primary heart disease: ischemic, congestive heart failure, cardiomyopathy
Acquired long QT syndrome
Congenital long QT syndrome
↓ repolarizing current/ ­ depolarizing current in cardiomyocytes
Mutated cardiac ion channels
Author: Nicola Adderley Reviewers: Luke Gagnon Emily Ryznar *Saman Rezazadeh *George Veenhuyzen MD at time of publication*
↓ repolarizing current in cardiomyocytes
­ QTc interval
Prolonged ventricular action potential duration
Early after depolarization (EAD) triggering PVC
Torsades de Pointes
Illustrated changes to action potential:
Normal cardiac action potential
Abbreviations: TCAs: tricyclic antidepressants AV: atrioventricular QTc: QT interval, corrected for heart rate
PVC: premature ventricular contraction
VF: ventricular fibrillation
SR: sinus rhythm
Polymorphic ventricular tachycardia initiated by PVC in the setting of QT interval prolongation and maintained by functional re-entry
Non-sustained TdP
Asymptomatic, palpitations, syncope (length-dependent)
Illustrated changes to ECG Strip:
Sinus rhythm restored
Degeneration to VF
Sudden cardiac death
Prolonged repolarization
Triggered beat (PVC)
A. Prolonged QT interval B. PVC
C. PVC triggers TdP
D. Non-sustained TdP
E. Return to SR
Sign/Symptom/Lab Finding
Published March 10, 2019 on