Long QT Syndrome

Last Updated on by FRCEM Intermediate

Overview

  • normal QT = < 440ms (two large squares) – prolonged QT > 450ms
  • produces prolonged ventricular repolarisation -> predisposes to malignant ventricular arrhythmias

Causes

  • drugs: amiodarone, TCA’s, many antibiotics, fluconazole, erythromycin, metoclopramide, quinidine, haloperidol, droperidol, methadone, ondansetron, SSRI’s
  • genetic: cardiac ion channel mutation (Na+, K+)
  • myocardial disease: MI, RF, 3rd degree HB, cardiomyopathy
  • electrolytes: low Ca2+, low K+, low Mg2+

ECG

  • ECG: QTc >440ms (11 small squares or T wave after half the R-R distance)
  • ECHO: structural heart disease

Treatment

  • treat cause
  • beta-blockade
  • avoidance of increased sympathetic tone
  • cardiac pacing
  • ICD

Complications

  • Torsades des pointes
  • Ventricular Fibrillation (VF)

Calculating the QTc Interval

Bazett’s formula
QTc = QT/ V(R-R interval in secs)
= 320/
= 320/0.77
= 457

Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation.

Clinical Significance

  • TdP is often short lived and self terminating, however can be associated with hemodynamic instability and collapse. TdP may also degenerate into ventricular fibrillation (VF).
  • QT prolongation may occur secondary to multiple drug effects, electrolyte abnormalities and medical conditions; these may combine to produce TdP, e.g. hypokalaemia may precipitate TdP in a patient with congenital long QT syndrome.
  • Recognition of TdP and the risk of TdP allows the instigation of specific management strategies (e.g. magnesium, isoprenaline, overdrive pacing, etc.)

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