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 language | English |
|---|---|
| Pages (from-to) | 590-596 |
| Number of pages | 7 |
| Journal | Anesthesia and Analgesia |
| Volume | 73 |
| Issue number | 5 |
| Publication status | Published - Jan 1 1991 |
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All Science Journal Classification (ASJC) codes
- Anesthesiology and Pain Medicine
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Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia. / Sato, M.; Hoka, S.; Arimura, H.; Ono, K.; Yoshitake, J.
In: Anesthesia and Analgesia, Vol. 73, No. 5, 01.01.1991, p. 590-596.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia
AU - Sato, M.
AU - Hoka, S.
AU - Arimura, H.
AU - Ono, K.
AU - Yoshitake, J.
PY - 1991/1/1
Y1 - 1991/1/1
N2 - 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.
AB - 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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M3 - Article
C2 - 1952140
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VL - 73
SP - 590
EP - 596
JO - Anesthesia and Analgesia
JF - Anesthesia and Analgesia
SN - 0003-2999
IS - 5
ER -