Circulatory dynamics during surface-induced hypothermia under halothane-ether azeotrope anesthesia.
Circulatory dynamics during surface- induced deep hypothermia using the halothane-diethyl ether azeotrope in 100% oxygen (O2) without circulatory arrest and 95% O2 and 5% carbon dioxide (CO2) with and without 60 minutes of arrest were evaluated in 15 adult mongrel dogs. Mean arterial pressure was lower in animals given 5% CO2 than in animals given 100% O2 during cooling. Cardiac output in the 5% CO2 groups increased until 30 degrees C cooling and then gradually decreased to 29% of control at 20 degrees C. Cardiac output in the 100% O2 group progressively decreased to 16% of control at 20 degrees C cooling and was 51 to 77% of the output in the 5% CO2 animals at comparable temperatures throughout the hypothermia procedure. The differences in cardiac output were attributed primarily to changes in stroke volume since heart rates were not significantly different. These changes were probably secondary to differences in systemic vascular resistance, which had increased sixfold in the animals given 100% O2 and had only doubled in the 5% CO2 groups at 20 degrees C during cooling. Hemodynamic variables in animals given 5% CO2 did not reveal significant differences in arrested versus nonarrested animals during early rewarming. However, with further warming, cardiac output, stroke volume, left ventricular stroke work, and mean pulmonary arterial and pulmonary artery wedge pressures were lower, and systemic and pulmonary vascular resistances were higher in the arrest group. We conclude that the improved results with halothane-diethyl ether azeotrope in 95% O2 and 5% CO2 during surface hypothermia are due to a greater cardiac output and reduced peripheral vascular resistance.[1]References
- Circulatory dynamics during surface-induced hypothermia under halothane-ether azeotrope anesthesia. Haneda, K., Sands, M.P., Thomas, R., Merrick, S.H., Hessel, E.A., Dillard, D.H. Ann. Thorac. Surg. (1982) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
