Abstract
Objective—To determine hemodynamic effects of 3 concentrations of sevoflurane in cats.
Animals—6 cats.
Procedure—Cats were anesthetized with sevoflurane in oxygen. After instruments were inserted, endtidal sevoflurane concentration was set at 1.25, 1.5, or 1.75 times the individual minimum alveolar concentration (MAC), which was determined in another study. Twenty-five minutes were allowed after each change of concentration. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, oxygen saturation, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured for each sevoflurane concentration before and during noxious stimulation. Arterial and mixed-venous bicarbonate concentrations, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, PaO2, mixed-venous partial pressure of oxygen (Pv–O2), oxygen delivery, oxygen consumption, oxygen-extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. Spontaneous and mechanical ventilations were studied during separate experiments.
Results—Mode of ventilation did not significantly influence any of the variables examined. Therefore, data from both ventilation modes were pooled for analysis. Mean arterial pressure, cardiac index, stroke index, rate-pressure product, left ventricular stroke work index, arterial and mixed-venous pH, PaO2, and oxygen delivery decreased, whereas PaCO2, Pva–O2, and mixed-venous partial pressure of CO2 increased significantly with increasing doses of sevoflurane. Noxious stimulation caused a significant increase in most cardiovascular variables.
Conclusions and Clinical Relevance—Sevoflurane induces dose-dependent cardiovascular depression in cats that is mainly attributable to myocardial depression. ( Am J Vet Res 2004;65:20–25)
