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Defibrillation energy requirements and electrical heterogeneity during total body hypothermia

  • M. R. Ujhelyi(corresponding author)
    ,
  • J. J. Sims
    ,
  • S. A. Dubin
    ,
  • ,
  • A. W. Miller
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Abstract

Objective: Determine the effects of hypothermia on defibrillation energy requirements and cardiac electrophysiology. Design: Prospective randomized acute intervention trial. Setting: Medical center animal laboratory. Subjects: Fifteen domestic farm swine. Interventions: Swine were randomized to a hypothermia group (n = 8) or a control group (n = 7). All animals were instrumented with a transvenous defibrillation system connected to a defibrillator that delivers a biphasic-truncated waveform. Values for defibrillation energy requirements were measured at baseline (normothermia, 38-40°C) and during treatment with total body hypothermia (30°C) or no temperature change (sham). Hypothermia was induced by circulating ice-water through anterior and posterior surgical thermal blankets. Measurements and Main Results: Defibrillation energy requirement values at 20%, 50%, and 80% were determined by using an up/down method. In the hypothermia group, defibrillation energy requirement values at baseline did not significantly change during hypothermia (defibrillation energy requirements 50% = 14 ± 2 J vs. 15 ± 2 J, respectively). Similarly, the defibrillation energy requirement values in the control group did not change from baseline to sham phase (defibrillation energy requirements 50% = 12 ± 1 J vs. 13 ± 1 J, respectively). Hypothermia profoundly affected cardiac electrophysiology, decreasing ventricular fibrillation threshold by 72%, conduction velocity by 25% (p < .01), and tissue excitability, while it prolonged ventricular repolarization and refractoriness by 7.5% to 15%, respectively (p < .05). Conclusions: Total body cooling to 30°C was highly arrhythmogenic, although this unstable electrophysiological state did not alter ventricular defibrillation energy requirements. These data suggest that hypothermia may be used to slow metabolic processes without concern over the ability to successfully defibrillate and treat hypothermia-induced arrhythmias.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1006-1011 (6 pages)

Journal (Volume, Issue Number)

Critical care medicine (Volume 29, Issue 5)

Publication milestones

  • Published - 2001

Publication status

Published - 2001

ISSN

0090-3493

Publication IDs

  • Scopus: 0035011544
  • PubMed: 11378613

Publication metrics

Metrics

Scopus
citations
SciVal
citations
39
Fractional count
1
Fractional count
0.20
Fractional count
4
Fractional count
0.80
Fractional count
1
Fractional count
1
SciVal
FWCI
0.45
SciVal
Author count
5
SciVal
Paper percentile
82

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Citation count
47
Captures
24

Funding Details

Supported, in part, by a Grant-in-Aid from the American Heart Association Southeast Affiliate; by the American Foundation for Pharmaceutical Education (to MRU); by the American College of Clinical Pharmacy (to JJS); and by Guidant (St. Paul, MN), which provided defibrillation equipment.
FundersFunding numbers
ACCP
-
AFPE
-
American Heart Association Southeast Affiliate
-