CARDIOPULMONARY EFFECTS OF HALOTHANE IN HYPOVOLEMIC DOGS

Citation
Pj. Pascoe et al., CARDIOPULMONARY EFFECTS OF HALOTHANE IN HYPOVOLEMIC DOGS, American journal of veterinary research, 55(1), 1994, pp. 121-126
Citations number
32
Categorie Soggetti
Veterinary Sciences
ISSN journal
00029645
Volume
55
Issue
1
Year of publication
1994
Pages
121 - 126
Database
ISI
SICI code
0002-9645(1994)55:1<121:CEOHIH>2.0.ZU;2-T
Abstract
Cardiopulmonary effects of halothane administration were studied in hy povolemic dogs. Baseline cardiopulmonary data were recorded from consc ious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was ac hieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by fu rther removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 +/- 0.02% was maintained, and cardiopulmonary effects were measur ed 3, 15, 30, and 60 minutes later. After blood withdraw-al and prior to halothane administration, systemic vascular resistance index, oxyge n extraction, and base deficit increased. Compared with baseline value s, these variables were decreased: mean arterial pressure, mean pulmon ary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous o xygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after in tubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean ar terial pressure and arterial and venous pH decreased, compared with va lues measured immediately prior to halothane administration. Fifteen m inutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and ven ous pH remained decreased. At 60 minutes, mean pulmonary arterial pres sure and pulmonary arterial occlusion pressure were increased and mixe d venous pH was decreased, compared with values measured before haloth ane administration. Results of this, study indicated that induction of anesthesia with halothane and maintenance at an end-tidal halothane c oncentration of 1.13% induced significant changes in blood pressure, w ith minimal effects on cardiac output and pulmonary function, when adm inistered to hypovolemic dogs.