Key result
Reduction in temperature to 27 degrees C magnified the shortening of action potential duration (143 ms vs 18 ms at 37 degrees C) when pacing cycle length was reduced from 2000 to 500 ms.
Absolute Event Rate: 143% vs 18%
Reduction in temperature magnifies cycle length dependent changes in action potential duration, which may indicate a greater dispersion of premature action potential durations during hypothermia and predispose to hypothermia-induced arrhythmias.
Hypothermia may heighten arrhythmia risk via magnified APD shortening; leaves open translation from animal data to clinical practice.
OBJECTIVE: The aim was to investigate the effects of temperature on cycle length dependent changes of action potential duration and on restitution of action potential duration. METHODS: Guinea pig papillary muscle action potentials were recorded using conventional microelectrode techniques. Action potential duration was measured at cycle lengths ranging from 500 to 2000 ms at both 27 degrees C and 37 degrees C. Restitution of action potential duration was determined by introducing an extra stimulus at progressively longer diastolic intervals from 40 to 9000 ms at pacing cycle lengths of 500, 1000, and 2000 ms. RESULTS: At 37 degrees C, action potential duration measured at 90% of repolarisation (APD90) during continuous pacing and the maximum value of APD90 achieved during restitution (APD90pl) decreased by 18(SEM 6) ms (n = 7) and 24(7) ms (n = 6), respectively, when pacing cycle length was reduced from 2000 to 500 ms. At 27 degrees C, the magnitude of the shortening of APD90 and APD90pl observed when pacing cycle length was similarly reduced was greater than at 37 degrees C, ie, 143(21) ms (n = 6) and 115(11) ms (n = 6), respectively. Thus the relation for restitution of action potential duration shifted downwards with reduction in pacing cycle length, and the magnitude of this shift was greater at 27 degrees C than at 37 degrees C. The difference between APD90 at the shortest diastolic interval (40 ms) and at diastolic interval of 100 ms (range of premature action potential durations) was much greater at 27 degrees C than at 37 degrees C at all three pacing cycle lengths. CONCLUSIONS: Reduction in temperature magnifies the cycle length dependent changes in action potential duration both during abrupt changes in cycle length, as with an extra stimulus, and during changes of steady state cycle length. This may indicate a greater dispersion of premature action potential durations during hypothermia, and hence predispose to hypothermia induced arrhythmias.
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Bjørnstad et al. (1993) studied this question. Temperature reduction (27 degrees C) vs. 37 degrees C was evaluated on Change in action potential duration (APD90) when pacing cycle length was reduced from 2000 to 500 ms. Reduction in temperature to 27 degrees C magnified the shortening of action potential duration (143 ms vs 18 ms at 37 degrees C) when pacing cycle length was reduced from 2000 to 500 ms.
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