TY - JOUR
T1 - Total body hypothermia increases dispersion of ventricular repolarization
AU - Jason Sims, J.
AU - Dubin, Stevin A.
AU - Vender, John
AU - Miller, Allison W.
AU - Ujhelyi, Michael R.
PY - 1999
Y1 - 1999
N2 - Background: Total body hypothermia is used to slow metabolic processes, thereby reducing oxygen and glucose utilization during surgery. However, ventricular fibrillation (VF) with subsequent circulatory collapse limits this therapy. We hypothesize that hypothermia may promote VF by increasing dispersion of ventricular repolarization, a known proarrhythmic condition. Methods: 17 swine were randomized to a hypothermia group (n=8) or a control group (n=9). Action potential duration at 90% repolarization was measured at 6 ventricular sites using monophasic action potential probes. Dispersion of repolarization was calculated as the maximum difference between the 6 sites. Effective refractory periods at 2 myocardial sites, and paced QRS duration were also measured. Electrophysiologic parameters were determined at baseline (normothermia=38°-40°C) and during treatment with total body hypothermia (30°C) or no temperature change for control. Hypothermia was induced by circulating ice water through anterior and posterior surgical thermal blankets. Results: The graph below represents the mean±SEM of dispersion of repolarization (*=p=0.002). Hypothermia significantly lengthened repolarization at each myocardial site by an average of 11±0.6% (data not shown). However, hypothermia also increased dispersion of repolarization by 87% (see graph). Similar to repolarization, refractoriness was increased by 9.5±0.5%. As expected, hypothermia also decreased global conduction as measured by paced QRS duration (88±2ms to 111±4ms, p=0.002). These changes were associated with an increase in the incidence of pacing induced VF, from 0% at baseline to 100% during hypothermia. Electrophysiologic parameters did not change in the control group. Conclusions: Hypothermia may promote VF by increasing dispersion of ventricular repolarization. Dispersion of repolarization in conjunction with slow conduction would provide an excellent substrate for reentrant arrhythmias.
AB - Background: Total body hypothermia is used to slow metabolic processes, thereby reducing oxygen and glucose utilization during surgery. However, ventricular fibrillation (VF) with subsequent circulatory collapse limits this therapy. We hypothesize that hypothermia may promote VF by increasing dispersion of ventricular repolarization, a known proarrhythmic condition. Methods: 17 swine were randomized to a hypothermia group (n=8) or a control group (n=9). Action potential duration at 90% repolarization was measured at 6 ventricular sites using monophasic action potential probes. Dispersion of repolarization was calculated as the maximum difference between the 6 sites. Effective refractory periods at 2 myocardial sites, and paced QRS duration were also measured. Electrophysiologic parameters were determined at baseline (normothermia=38°-40°C) and during treatment with total body hypothermia (30°C) or no temperature change for control. Hypothermia was induced by circulating ice water through anterior and posterior surgical thermal blankets. Results: The graph below represents the mean±SEM of dispersion of repolarization (*=p=0.002). Hypothermia significantly lengthened repolarization at each myocardial site by an average of 11±0.6% (data not shown). However, hypothermia also increased dispersion of repolarization by 87% (see graph). Similar to repolarization, refractoriness was increased by 9.5±0.5%. As expected, hypothermia also decreased global conduction as measured by paced QRS duration (88±2ms to 111±4ms, p=0.002). These changes were associated with an increase in the incidence of pacing induced VF, from 0% at baseline to 100% during hypothermia. Electrophysiologic parameters did not change in the control group. Conclusions: Hypothermia may promote VF by increasing dispersion of ventricular repolarization. Dispersion of repolarization in conjunction with slow conduction would provide an excellent substrate for reentrant arrhythmias.
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M3 - Article
AN - SCOPUS:33750804716
SN - 0090-3493
VL - 27
SP - A108
JO - Critical care medicine
JF - Critical care medicine
IS - 1 SUPPL.
ER -