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Effects of Augmenting Cardiac Contractility, Preload, and Heart Rate on Cardiac Output During Enflurane Anesthesia
Author(s) -
Michiko Sato,
Sumio Hoka,
Hiroyuki Arimura,
Koichi Ono,
J Yoshitake
Publication year - 1991
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/00000539-199111000-00014
Subject(s) - medicine , preload , enflurane , contractility , cardiac output , anesthesia , heart rate , cardiology , hemodynamics , blood pressure , isoflurane
Changes in cardiac output in response to augmenting cardiac contractility, preload, and heart rate during enflurane anesthesia were examined in 12 open-chested dogs. Cardiac contractility was assessed by the slope of the end-systolic pressure-volume relation (Emax). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) was administered to augment cardiac contractility. Autologous blood (5.0 and 10 mL/kg) was infused to increase preload. Atrial pacing was used to increase the heart rate by about 30%. Cardiac output decreased from 96 +/- 4 (0% enflurane) (mean +/- SE) to 73 +/- 5 (1.7% enflurane) and to 46 +/- 7 mL.kg-1.min-1 (3.4% enflurane), concomitantly with decreases in Emax from 6.0 +/- 1.2 (0% enflurane) to 4.5 +/- 1.2 (1.7% enflurane) and to 2.5 +/- 0.5 mm Hg/mL (3.4% enflurane). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) increased Emax from 69% +/- 7% (compared to 0% enflurane with no dobutamine) to 139% +/- 15%, 167% +/- 25%, and 183% +/- 35% at 1.7% enflurane, and from 43% +/- 8% to 78% +/- 7%, 137% +/- 20%, and 157% +/- 22% at 3.4% enflurane, respectively. The decreases in cardiac output by 1.7% and 3.4% enflurane were reversed by the intravenous administration of 3 micrograms.kg-1.min-1 of dobutamine. Cardiac output was significantly increased by administration of 10 mL/kg of autologous blood at 1.7% enflurane, but did not significantly increase at 3.4% enflurane. Increasing the heart rate did not significantly increase cardiac output at 1.7% and 3.4% enflurane. The results of this study suggest that increasing cardiac contractility is the most effective therapeutic means of reversing circulatory depression during enflurane anesthesia.

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