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Canadian Journal of Anesthesia, Vol 45, 373-376, Copyright © 1998 by Canadian Anesthesiologists' Society
ARTICLES |
M Miyabe, S Takahashi, S Sato and H Toyooka
Department of Anesthesiology, University of Tsukuba, Japan. miyabe@igaku.md.tsukuba.ac.jp
PURPOSE: Apnea is one of the potential complications during anaesthesia. If sympathetic nerve activity is blocked by epidural anaesthesia, circulatory responses to apnea might change. Our objective was to assess the potential modifying effects of epidural anaesthesia on the cardiovascular responses to apnea in the animals. METHODS: Twenty rabbits anaesthetised with pentobarbital (25 mg.kg-1 i.v., 8 mg.kg-1.hr-1) and pacuronium bromide (0.2 mg.kg-1.hr-1 i.v.) were randomly assigned to one of two groups: control (n = 10) and epidural (n = 10). In the control group, 0.6 ml saline, and in the epidural group, 0.6 ml lidocaine 1% was injected into the epidural space respectively. After mechanical ventilation with FIO2 0.4, apnea was induced by disconnecting the anaesthetic circuit from the endotracheal tube, and mean arterial pressure (MAP), heart rate (HR), and time to cardiac arrest were measured. RESULTS: Before apnea MAP was lower in the epidural than in the control group (73 +/- 10 vs 91 +/- 10 mmHg, P < 0.05). Heart rate was not different between groups (264 +/- 36 vs 266 +/- 24 bpm). Mean arterial pressure increased in the control group after apnea, but not in the epidural group. The time to cardiac arrest was less in the epidural group than in the control group (420 +/- 67 vs 520 +/- 61 sec, P < 0.05). Heart rate decreased markedly after apnea in the control group whereas it decreased gradually in the epidural group. CONCLUSION: Thoracic epidural anaesthesia attenuated cardiovascular response to apnea and reduced the time to cardiac arrest.
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