Cardiac electrophysiology during hypothermia. Implications for medical treatment.

Reduction in body temperature induces characteristic electrophysiological and mechanical alterations of the heart. The heart rate is markedly reduced. Myocardial conduction is slowed, partly due to reduced rate of depolarization of the action potential, and is reflected by widening of the QRS-complex in the ECG. There is also a fall in resting membrane potential. Action potential duration and refractory period are markedly lengthened during hypothermia, attributed to delayed repolarization. This is reflected by increased QT-time in the ECG. Since action potential duration changes significantly even after as small temperature changes as 1 to 2 degrees C, nonuniform cooling or rewarming of the heart may cause significant dispersion of conduction, action potential duration and refractoriness in the myocardium. This dispersion may cause unidirectional block, hence creating a substrate for reentry atrial and ventricular arrhythmias, and may be an important mechanism for explaining the hypothermia-associated arrhythmias. Class III antiarrhythmic drugs such as d-sotalol lengthen long action potentials at low temperatures to a greater extent than the shorter action potentials at higher temperatures. This may further increase dispersion and thereby the tendency towards arrhythmias. Sotalol as an example, shows that some antiarrhythmic drugs may have increased arrhythmogenic effect and should probably be contraindicated during hypothermia.