Total body hypothermia increases dispersion of ventricular repolarization

J. Jason Sims, Stevin A. Dubin, John R Vender, Allison W. Miller, Michael R. Ujhelyi

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
JournalCritical Care Medicine
Volume27
Issue number1 SUPPL.
StatePublished - Dec 1 1999

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Hypothermia
Ventricular Fibrillation
Action Potentials
Collapse Therapy
Induced Hypothermia
Control Groups
Ice
Cardiac Arrhythmias
Shock
Swine
Hot Temperature
Oxygen
Glucose
Temperature
Water
Incidence

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Jason Sims, J., Dubin, S. A., Vender, J. R., Miller, A. W., & Ujhelyi, M. R. (1999). Total body hypothermia increases dispersion of ventricular repolarization. Critical Care Medicine, 27(1 SUPPL.).

Total body hypothermia increases dispersion of ventricular repolarization. / Jason Sims, J.; Dubin, Stevin A.; Vender, John R; Miller, Allison W.; Ujhelyi, Michael R.

In: Critical Care Medicine, Vol. 27, No. 1 SUPPL., 01.12.1999.

Research output: Contribution to journalArticle

Jason Sims, J, Dubin, SA, Vender, JR, Miller, AW & Ujhelyi, MR 1999, 'Total body hypothermia increases dispersion of ventricular repolarization', Critical Care Medicine, vol. 27, no. 1 SUPPL..
Jason Sims J, Dubin SA, Vender JR, Miller AW, Ujhelyi MR. Total body hypothermia increases dispersion of ventricular repolarization. Critical Care Medicine. 1999 Dec 1;27(1 SUPPL.).
Jason Sims, J. ; Dubin, Stevin A. ; Vender, John R ; Miller, Allison W. ; Ujhelyi, Michael R. / Total body hypothermia increases dispersion of ventricular repolarization. In: Critical Care Medicine. 1999 ; Vol. 27, No. 1 SUPPL.
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abstract = "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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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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