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

Abstract

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.

Introduction

Acepromazine is a phenothiazine widely used in veterinary medicine to provide mild-to-moderate sedation in dogs (Stepien et al., 1995, Monteiro et al., 2008, Monteiro et al., 2009). Furthermore, acepromazine has anti-arrhythmogenic action (Dyson & Pettifer 1997) and reduces the minimum alveolar concentration of inhalation agents in dogs (Heard et al., 1986, Webb and O`Brien, 1988).

Although widely used, acepromazine decreases systemic arterial pressure by as much as 20% in healthy dogs (Popovic et al., 1972, Turner et al., 1974, Monteiro et al., 2008, Monteiro et al., 2009). A proposed mechanism of action is α₁-adrenergic receptor blockade decreasing systemic vascular resistance (SVR) (Ludders et al. 1983). This was not confirmed by hemodynamic monitoring in early studies; however, Stepien et al. (1995) administered acepromazine (0.1mg kg^–1) intravenously (IV) to conscious dogs and documented no change in SVR and, therefore, attributed the decrease in blood pressure to a reduction in cardiac output (CO).

The objective of this study was to evaluate the relationship between the administration of progressively increasing doses of acepromazine and hemodynamic, respiratory and sedative effects in conscious dogs. The hypothesis was that acepromazine would cause dose-dependent depression in cardiovascular variables and sedation.