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- normal QT = < 440ms (two large squares) – prolonged QT > 450ms
- produces prolonged ventricular repolarisation -> predisposes to malignant ventricular arrhythmias
- 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: QTc >440ms (11 small squares or T wave after half the R-R distance)
- ECHO: structural heart disease
- treat cause
- avoidance of increased sympathetic tone
- cardiac pacing
- Torsades des pointes
- Ventricular Fibrillation (VF)
Calculating the QTc Interval
QTc = QT/ V(R-R interval in secs)
Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation.
- 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.)