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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Cardiac electrophysiology during hypothermia. Implications for medical treatment. 181 84

To investigate whether changes in temperature influence the electrophysiologic effects of the class III antiarrhythmic agent d-sotalol, we studied its effects on propranolol-pretreated guinea pig papillary muscles at temperatures ranging from 37 degrees to 27 degrees C by means of conventional microelectrode techniques. We also examined the rate-dependent effect of d-sotalol at 37 degrees and 27 degrees C. Before the addition of d-sotalol, reducing the temperature from 37 degrees to 27 degrees C increased the action potential duration recorded at 50% repolarization (APD50) from 112 +/- 7 msec to 271 +/- 15 msec and action potential duration recorded at 90% repolarization (APD90) from 136 +/- 7 msec to 325 +/- 10 msec. d-Sotalol (50 mumol/L) lengthened APD50 and APD90 to a greater degree at low temperatures. Thus at 37 degrees C d-sotalol lengthened APD50 and APD90 by 12 +/- 6 msec and 19 +/- 5 msec, and at 27 degrees C by 37 +/- 5 msec and 52 +/- 7 msec, respectively. d-Sotalol produced its greatest effect on APD at long pacing cycle lengths, thus demonstrating reverse dependence. This rate-dependent effect was more marked at 27 degrees C than at 37 degrees C. The greater effect of d-sotalol on APD at long pacing cycle lengths may be explained by the modulated receptor hypothesis, assuming that the drug has a higher affinity for closed potassium channels. Such a mechanism may also explain the accentuated class III antiarrhythmic action of d-sotalol observed during hypothermia.
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PMID:Class III antiarrhythmic action of d-sotalol during hypothermia. 201 75