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Q1: What is shown in fig 1 (see p 539), and what is its significance?
Figure 1 shows a prolonged QT interval (corrected QT 520 milliseconds) and macroscopic T wave alternans. T wave alternans is defined as a beat to beat variation in the amplitude or polarity of the T wave. Macroscopic T wave alternans is a predictor of malignant ventricular arrhythmias.1 Microvolt T wave alternans is a validated predictor of mortality and morbidity in a variety of patient groups.1 This ECG anomaly is seen with both transient physiological stress (for example, exercise), and with pathological stress such as electrolyte abnormalities and myocardial ischaemia. Indeed, revascularisation in ischaemia has even been shown to reduce the incidence of T wave alternans.1 It has also been documented in association with the long QT and Brugada syndromes.2
T wave alternans on a millivolt scale visible to the naked eye (macroscopic T wave alternans) is predominantly a subject for individual case reports. It is often a precursor to the subsequent development of torsades de pointes (polymorphic ventricular tachycardia). Regardless of amplitude, T wave alternans should be regarded as a warning of malignant arrhythmias.
Q2: What is the arrhythmia in fig 2 (see p 539)?
The upper trace in fig 2 is lead II from a conventional electrocardiographic recording. It shows macroscopic T wave alternans in the first four beats degenerating into torsades de pointes (polymorphic VT). In comparison with fig 1, the QT interval is yet further prolonged. The lower trace shows loss of the arterial pressure waveform.
Q3: What was the procedure used to treat the patient in fig 3 (see p 539)?
Figure 3 shows a ventricular paced rhythm. Torsades de pointes in this patient was treated by ventricular overdrive pacing. The patient was given verapamil to ensure his own rhythm was slower than that delivered by the temporary pacing wire. In addition, the patient received intravenous magnesium sulphate to correct the hypomagnesaemia.
T wave alternans is uncommon and often overlooked except when it is of a large (millivolt) amplitude such as in this case. Its mechanism demonstrates modern electrophysiological understanding of the basis of arrhythmia generation.
Many arrhythmias occur as a result of re-entry circuits. A re-entry circuit occurs when a depolarising wave travels in a circle from myocyte to myocyte. Each myocyte becomes refractory for a short time to further depolarisation as the ion channels in the cell membrane are reset. By the time the wave comes full circle, however, the first myocyte is no longer refractory and is able allow the circus movement to continue round the circuit indefinitely.
Such circuits depend on heterogeneity of repolarisation. Normally the myocardium depolarises rapidly and synchronously which is represented on the ECG by the narrow QRS complex. The myocardium is then refractory until ventricular repolarisation is completed. Repolarisation is slower and more heterogeneous than depolarisation and hence the T wave appears as broad deflection on the ECG. The more heterogeneous the repolarisation, the greater the chance that part of the myocardium will no longer be refractory should an ectopic beat occur, and hence allow a re-entry circuit to be established.
Heterogeneity of repolarisation is formally known as transmural dispersion of repolarisation (TDR). Increased TDR occurs with electrolyte abnormalities (for example, hypokalaemia, hypomagnesaemia), with intrinsic abnormalities of the ion channels due to genetic mutations (the congenital long QT syndromes), and as an effect of drug therapy (antiarrhythmics, β-agonists, erythromycin, etc).3
Increased TDR manifests on the surface electrocardiogram as alteration in the timing and amplitude of the T wave. This is the mechanism of both T wave alternans and the better known prolonged QT interval. Interestingly, while T wave alternans is always associated with increased TDR, long QT intervals may be found with a normal distribution of repolarisation. A long QT interval may occur when the whole myocardium repolarises late but synchronously (small TDR) or when just part of the myocardium lags behind repolarisation of the rest (large TDR). Drugs such as amiodarone prolong the action potential, and hence the QT interval, yet decrease the TDR.
This patient had two separate factors operating to increase the TDR. Firstly he had a low serum magnesium concentration which like abnormalities in potassium and calcium is known to alter the dynamics of repolarisation of the myocardium. Secondly, he was on nebulised β2-agonists (salbutamol), and given 1:1000 adrenaline during the cardiac arrest. The dispersion in the rate of repolarisation is therefore increased.
Just as the T waves represent myocardial repolarisation, T wave alternans is the correlate of increased variation in the rate of repolarisation.4 Sometimes the myocytes repolarise synchronously and sometimes less so; sometimes the wave of repolarisation is in one direction, and sometimes the other. It is an early warning sign of re-entry circuits and ventricular arrhythmias and in particular torsades de pointes. Although T wave alternans is a rare electrocardiographic sign, when present it should be treated with suitable respect.
Macroscopic T wave alternans and recurrent torsades de pointes.