long QT syndrome
After each heartbeat the heart muscle must “reset” electrically before it can beat again — a recovery phase called repolarization. In long QT syndrome this reset takes too long, leaving the heart in a vulnerable state for an extended window. Imagine a runner who needs an unusually long pause between strides; if pushed at the wrong moment, the rhythm can stumble into chaos.
The lengthened recovery shows up on the ECG as a prolonged QT interval, corrected for heart rate as the QTc. The danger is a specific, dramatic ventricular tachycardia called torsades de pointes, which can cause fainting and sometimes degenerate into ventricular fibrillation and sudden death. Triggers vary by type and include exertion, swimming, emotional shock or sudden loud noises.
Long QT can be inherited through faulty ion-channel genes or acquired from medicines (some antibiotics, antipsychotics and antiarrhythmics) and low blood potassium or magnesium. Management combines avoiding QT-prolonging drugs and triggers, correcting electrolytes, beta-blockers for many inherited forms, and an implantable defibrillator for those at highest risk.
A teenager faints during swimming; her ECG shows a markedly prolonged QTc and genetic testing confirms inherited long QT syndrome, after which she avoids triggering drugs and starts a beta-blocker.
Exertion- or swimming-triggered fainting in a young person should prompt a look at the QTc.
Because many common drugs prolong the QT interval, checking the QTc before and after starting them — and avoiding combinations — is a routine safety step, especially when potassium or magnesium is low.