The ECG on admission to the coronary care unit showed sinus rhythm, QT prolongation and disappearance of previous ST depression. It was mentioned that the patient was under continuous cardiac monitoring during his stay on the surgical ward. Review of these tracings (Fig. 1), corresponding with extremity leads II and III, demonstrated the occurrence of torsade de pointes (TdP). At first, a typical short–long–short sequence of R-R cycles is seen, consisting of a premature ventricular extrasystole (VES), followed by a compensatory pause and another VES which, because of the underlying long QT, does not have the short coupling interval typical of idiopathic ventricular fibrillation. This initiates a polymorphic ventricular tachycardia at a rate of approximately 240 beats/min (Fig. 1, arrow), which finally degenerates into ventricular fibrillation (VF; Fig. 1, dotted arrow). After DC shock by the resuscitation team (Fig. 1, single arrowhead), there is a short period of asystole with a few non-captured pacemaker spikes (Fig. 1, striped arrows), followed by the onset of atrial fibrillation (Fig. 1, double arrowhead), resulting in haemodynamic recovery. At the time of his collapse, the patient was receiving treatment with fluconazole and haloperidol, both known to cause QT prolongation. After these medications were stopped, the QT interval normalised and the patient made a full recovery.
Fig. 1
Cardiac tracings whilst the patient was on the ward, corresponding with leads II and III. A short–long–short sequence of R-R cycles initiates TdP (arrow) which degenerates into VF (dotted arrow), terminated by DC shock (single arrowhead). A brief period of asystole (striped arrow) is followed by the onset of atrial fibrillation (double arrowhead), resulting in restoration of cardiac output