Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia

M. Sato, Sumio Hoka, H. Arimura, K. Ono, J. Yoshitake

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Abstract

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 (E(max)). Dobutamine (3, 6, and 9 μg·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 E(max) 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 μg·kg-1·min-1) increased E(max) 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 μg·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.

Original languageEnglish
Pages (from-to)590-596
Number of pages7
JournalAnesthesia and Analgesia
Volume73
Issue number5
Publication statusPublished - Jan 1 1991

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Enflurane
Cardiac Output
Anesthesia
Heart Rate
Dobutamine

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia. / Sato, M.; Hoka, Sumio; Arimura, H.; Ono, K.; Yoshitake, J.

In: Anesthesia and Analgesia, Vol. 73, No. 5, 01.01.1991, p. 590-596.

Research output: Contribution to journalArticle

Sato, M, Hoka, S, Arimura, H, Ono, K & Yoshitake, J 1991, 'Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia', Anesthesia and Analgesia, vol. 73, no. 5, pp. 590-596.
Sato, M. ; Hoka, Sumio ; Arimura, H. ; Ono, K. ; Yoshitake, J. / Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia. In: Anesthesia and Analgesia. 1991 ; Vol. 73, No. 5. pp. 590-596.
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abstract = "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 (E(max)). Dobutamine (3, 6, and 9 μg·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 E(max) 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 μg·kg-1·min-1) increased E(max) 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 μg·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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