Hemodynamic effects of incremental doses of acepromazine in isoflurane-anesthetized dogs.

OBJECTIVE: To evaluate the effects of incremental doses of acepromazine on hemodynamics in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: Healthy, adult, mixed-breed dogs (two male and four female) weighing 16.8 ± 5.1 kg (mean ± standard deviation). METHODS: Dogs were anesthetized with propofol (7 mg kg-1) intravenously (IV) and isoflurane. Thermodilution and arterial catheters were placed for hemodynamic monitoring and arterial blood sampling for blood gas analysis. Baseline measurements were performed with stable expired concentration of isoflurane (Fe'Iso) at 1.8%. Each dog was then administered four incremental acepromazine injections (10, 15, 25 and 50 µg kg-1) IV, and measurements were repeated 20 minutes after each acepromazine injection with Fe'Iso decreased to 1.2%. The four acepromazine injections resulted in cumulative doses of 10, 25, 50 and 100 µg kg-1 (time points ACP10, ACP25, ACP50 and ACP100, respectively). RESULTS: Compared with baseline, cardiac index (CI) increased significantly by 34%, whereas systemic vascular resistance index (SVRI) decreased by 25% at ACP50 and ACP100. Arterial oxygen content (CaO2) was significantly lower than baseline after all acepromazine injections (maximum decreases of 11%) and was lower at ACP50 and ACP100 than at ACP10. No significant change was found in heart rate, stroke index, oxygen delivery index and systolic, mean and diastolic blood pressures. Hypotension (mean arterial pressure < 60 mmHg) was observed in one dog at baseline, ACP10, ACP25 and ACP100, and in two dogs at ACP50. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with isoflurane alone, anesthesia with acepromazine-isoflurane resulted in increased CI and decreased SVRI and CaO2 values. These effects were dose-related, being more pronounced at ACP50 and ACP100. Under the conditions of this study, acepromazine administration did not change blood pressure.

Hemodynamic, respiratory and sedative effects of progressively increasing doses of acepromazine in conscious dogs.

OBJECTIVE: To evaluate the effects of progressively increasing doses of acepromazine on cardiopulmonary variables and sedation in conscious dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: A group of six healthy, adult, mixed-breed dogs weighing 16.5 ± 5.0 kg (mean ± standard deviation). METHODS: Dogs were instrumented with thermodilution and arterial catheters for evaluation of hemodynamics and arterial blood gases. On a single occasion, acepromazine was administered intravenously to each dog at 10, 15, 25 and 50 µg kg-1 at 20 minute intervals, resulting in cumulative acepromazine doses of 10 µg kg-1 (ACP10), 25 µg kg-1 (ACP25), 50 µg kg-1 (ACP50) and 100 µg kg-1 (ACP100). Hemodynamic data and sedation scores were recorded before (baseline) and 20 minutes after each acepromazine dose. RESULTS: Compared with baseline, all acepromazine doses significantly decreased stroke index (SI), mean arterial pressure (MAP) and arterial oxygen content (CaO2) with maximum decreases of 16%, 17% and 21%, respectively. Cardiac index (CI) decreased by up to 19% but not significantly. Decreases of 26-38% were recorded for oxygen delivery index (DO2I), with significant differences for ACP50 and ACP100. Systemic vascular resistance index (SVRI) and heart rate did not change significantly. No significant difference was found among acepromazine doses for hemodynamic data. After ACP10, mild sedation was observed in five/six dogs and moderate sedation in one/six dogs, whereas after ACP25, ACP50 and ACP100, moderate sedation was observed in five/six or six/six dogs. CONCLUSIONS AND CLINICAL RELEVANCE: In conscious dogs, acepromazine decreased MAP, SI, CaO2 and DO2I, but no significant dose effect was detected. SVRI was not significantly changed, suggesting that the reduction in MAP resulted from decreased CI. The ACP25, ACP50 and ACP100 doses resulted in moderate sedation in most dogs; ACP10 resulted in only mild sedation.