Comparison of the cardiorespiratory effects of a combination of ketamine and propofol, propofol alone, or a combination of ketamine and diazepam before and after induction of anesthesia in dogs sedated with acepromazine and oxymorphone

Natalia Henao-Guerrero Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Carolina H. Riccó Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

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Abstract

Objective—To evaluate the cardiorespiratory effects of IV administration of propofol (4 mg/kg), ketamine hydrochloride and propofol (2 mg/kg each; K-P), or ketamine hydrochloride (5 mg/kg) and diazepam (0.2 mg/kg; K-D) before and after induction of anesthesia (IoA) in dogs sedated with acepromazine maleate and oxymorphone hydrochloride.

Animals—10 healthy adult Beagles.

Procedures—Each dog was randomly allocated to receive 2 of 3 treatments (1-week interval). For instrumentation prior to each treatment, each dog was anesthetized with isoflurane. After full recovery, acepromazine (0.02 mg/kg) and oxymorphone (0.05 mg/kg) were administered IV. Fifteen minutes later (before IoA), each dog received treatment IV with propofol, K-P, or K-D. Cardiorespiratory and arterial blood gas variables were assessed before, immediately after, and 5 minutes after IoA.

Results—Compared with findings before IoA, dogs receiving the K-P or K-D treatment had increased cardiac output, oxygen delivery, and heart rate 5 minutes after IoA; K-P administration did not change mean arterial blood pressure or stroke volume and decreased systemic vascular resistance. Propofol decreased mean arterial blood pressure and systemic vascular resistance immediately after IoA but did not change heart rate, cardiac output, or oxygen delivery. All treatments caused some degree of apnea, hypoventilation, and hypoxemia (Pao2 < 80 mm Hg).

Conclusions and Clinical Relevance—In dogs, K-P treatment maintained mean arterial blood pressure better than propofol alone and increased heart rate, cardiac output, or oxygen delivery, as did the K-D treatment. Supplemental 100% oxygen should be provided during IoA with all 3 treatments.

Abstract

Objective—To evaluate the cardiorespiratory effects of IV administration of propofol (4 mg/kg), ketamine hydrochloride and propofol (2 mg/kg each; K-P), or ketamine hydrochloride (5 mg/kg) and diazepam (0.2 mg/kg; K-D) before and after induction of anesthesia (IoA) in dogs sedated with acepromazine maleate and oxymorphone hydrochloride.

Animals—10 healthy adult Beagles.

Procedures—Each dog was randomly allocated to receive 2 of 3 treatments (1-week interval). For instrumentation prior to each treatment, each dog was anesthetized with isoflurane. After full recovery, acepromazine (0.02 mg/kg) and oxymorphone (0.05 mg/kg) were administered IV. Fifteen minutes later (before IoA), each dog received treatment IV with propofol, K-P, or K-D. Cardiorespiratory and arterial blood gas variables were assessed before, immediately after, and 5 minutes after IoA.

Results—Compared with findings before IoA, dogs receiving the K-P or K-D treatment had increased cardiac output, oxygen delivery, and heart rate 5 minutes after IoA; K-P administration did not change mean arterial blood pressure or stroke volume and decreased systemic vascular resistance. Propofol decreased mean arterial blood pressure and systemic vascular resistance immediately after IoA but did not change heart rate, cardiac output, or oxygen delivery. All treatments caused some degree of apnea, hypoventilation, and hypoxemia (Pao2 < 80 mm Hg).

Conclusions and Clinical Relevance—In dogs, K-P treatment maintained mean arterial blood pressure better than propofol alone and increased heart rate, cardiac output, or oxygen delivery, as did the K-D treatment. Supplemental 100% oxygen should be provided during IoA with all 3 treatments.

Contributor Notes

Supported in part by an internal grant provided by the Virginia-Maryland Regional College of Veterinary Medicine, Helen and Frank Spurr Research Fund.

Presented in poster form at the Association of Veterinary Anaesthetists Spring Meeting, Bari, Italy, April 2011, and in abstract form at the 17th Annual International Veterinary Emergency and Critical Care Symposium, Nashville, Tenn, September 2011.

The authors thank Dr. Stephen Werre for statistical support and Dana Calicott for technical support.

Address correspondence to Dr. Henao-Guerrero (nguerrer@vt.edu).
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