Hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats

Bruno H Pypendop, Linda S Barter, Peter J Pascoe, M. G. Ranasinghe, Kirby Pasloske

Research output: Contribution to journalArticle

Abstract

Objective: To characterize the hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats. Study design: Experimental study. Animals: A group of six adult healthy male neutered cats. Methods: Cats were anesthetized with desflurane in oxygen for instrumentation. Catheters were placed in a medial saphenous vein for drug administration and in a carotid artery for arterial blood pressure measurement and blood collection. A thermodilution catheter was placed in the pulmonary artery via an introducer placed in a jugular vein for measurement of central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and core body temperature, and for sampling mixed venous blood. A lead II electrocardiogram was connected. Desflurane administration was discontinued and a target-controlled infusion system was used to administer alfaxalone to reach six plasma alfaxalone concentrations ranging from 1.0 to 30.4 mg L−1, with 7.6 mg L−1 considered a clinical concentration for anesthesia. Cardiovascular measurements were recorded, and arterial and mixed-venous blood samples were collected for blood-gas analysis and plasma alfaxalone concentration measurement at each target concentration. Data were analyzed using a repeated-measures analysis of variance and Dunnett's test for comparisons to the lowest target concentration. Significance was set at p < 0.05. Results: Mean ± standard deviation plasma alfaxalone concentrations were 0.73 ± 0.32, 1.42 ± 0.41, 3.44 ± 0.40, 6.56 ± 0.43, 18.88 ± 6.81 and 49.47 ± 5.50 mg L−1 for the 1, 1.9, 3.8, 7.6, 15.2, and 30.4 mg L−1 target concentrations, respectively. PaCO2 increased with increasing target plasma alfaxalone concentrations and was 69.4 ± 14.2 mmHg (9.3 ± 1.9 kPa) at the 30.4 mg L−1 target. Some cardiovascular variables were statistically significantly affected by increasing target plasma alfaxalone concentrations. Conclusion and clinical relevance: Within the plasma concentration range studied, alfaxalone caused hypoventilation, but the cardiovascular effects were of small clinical significance.

Original languageEnglish (US)
JournalVeterinary Anaesthesia and Analgesia
DOIs
StatePublished - Jan 1 2019

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hemodynamics
pulmonary artery
Cats
Hemodynamics
cats
catheters
blood
saphenous vein
Pulmonary Artery
carotid arteries
electrocardiography
jugular vein
blood gases
instrumentation
cardiac output
body temperature
blood pressure
anesthesia
Catheters
analysis of variance

Keywords

  • alfaxalone
  • cardiovascular
  • cats

ASJC Scopus subject areas

  • veterinary(all)

Cite this

@article{1bfa212f809241c5b9de85195d2ef80b,
title = "Hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats",
abstract = "Objective: To characterize the hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats. Study design: Experimental study. Animals: A group of six adult healthy male neutered cats. Methods: Cats were anesthetized with desflurane in oxygen for instrumentation. Catheters were placed in a medial saphenous vein for drug administration and in a carotid artery for arterial blood pressure measurement and blood collection. A thermodilution catheter was placed in the pulmonary artery via an introducer placed in a jugular vein for measurement of central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and core body temperature, and for sampling mixed venous blood. A lead II electrocardiogram was connected. Desflurane administration was discontinued and a target-controlled infusion system was used to administer alfaxalone to reach six plasma alfaxalone concentrations ranging from 1.0 to 30.4 mg L−1, with 7.6 mg L−1 considered a clinical concentration for anesthesia. Cardiovascular measurements were recorded, and arterial and mixed-venous blood samples were collected for blood-gas analysis and plasma alfaxalone concentration measurement at each target concentration. Data were analyzed using a repeated-measures analysis of variance and Dunnett's test for comparisons to the lowest target concentration. Significance was set at p < 0.05. Results: Mean ± standard deviation plasma alfaxalone concentrations were 0.73 ± 0.32, 1.42 ± 0.41, 3.44 ± 0.40, 6.56 ± 0.43, 18.88 ± 6.81 and 49.47 ± 5.50 mg L−1 for the 1, 1.9, 3.8, 7.6, 15.2, and 30.4 mg L−1 target concentrations, respectively. PaCO2 increased with increasing target plasma alfaxalone concentrations and was 69.4 ± 14.2 mmHg (9.3 ± 1.9 kPa) at the 30.4 mg L−1 target. Some cardiovascular variables were statistically significantly affected by increasing target plasma alfaxalone concentrations. Conclusion and clinical relevance: Within the plasma concentration range studied, alfaxalone caused hypoventilation, but the cardiovascular effects were of small clinical significance.",
keywords = "alfaxalone, cardiovascular, cats",
author = "Pypendop, {Bruno H} and Barter, {Linda S} and Pascoe, {Peter J} and Ranasinghe, {M. G.} and Kirby Pasloske",
year = "2019",
month = "1",
day = "1",
doi = "10.1016/j.vaa.2019.05.004",
language = "English (US)",
journal = "Veterinary Anaesthesia and Analgesia",
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T1 - Hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats

AU - Pypendop, Bruno H

AU - Barter, Linda S

AU - Pascoe, Peter J

AU - Ranasinghe, M. G.

AU - Pasloske, Kirby

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Objective: To characterize the hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats. Study design: Experimental study. Animals: A group of six adult healthy male neutered cats. Methods: Cats were anesthetized with desflurane in oxygen for instrumentation. Catheters were placed in a medial saphenous vein for drug administration and in a carotid artery for arterial blood pressure measurement and blood collection. A thermodilution catheter was placed in the pulmonary artery via an introducer placed in a jugular vein for measurement of central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and core body temperature, and for sampling mixed venous blood. A lead II electrocardiogram was connected. Desflurane administration was discontinued and a target-controlled infusion system was used to administer alfaxalone to reach six plasma alfaxalone concentrations ranging from 1.0 to 30.4 mg L−1, with 7.6 mg L−1 considered a clinical concentration for anesthesia. Cardiovascular measurements were recorded, and arterial and mixed-venous blood samples were collected for blood-gas analysis and plasma alfaxalone concentration measurement at each target concentration. Data were analyzed using a repeated-measures analysis of variance and Dunnett's test for comparisons to the lowest target concentration. Significance was set at p < 0.05. Results: Mean ± standard deviation plasma alfaxalone concentrations were 0.73 ± 0.32, 1.42 ± 0.41, 3.44 ± 0.40, 6.56 ± 0.43, 18.88 ± 6.81 and 49.47 ± 5.50 mg L−1 for the 1, 1.9, 3.8, 7.6, 15.2, and 30.4 mg L−1 target concentrations, respectively. PaCO2 increased with increasing target plasma alfaxalone concentrations and was 69.4 ± 14.2 mmHg (9.3 ± 1.9 kPa) at the 30.4 mg L−1 target. Some cardiovascular variables were statistically significantly affected by increasing target plasma alfaxalone concentrations. Conclusion and clinical relevance: Within the plasma concentration range studied, alfaxalone caused hypoventilation, but the cardiovascular effects were of small clinical significance.

AB - Objective: To characterize the hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats. Study design: Experimental study. Animals: A group of six adult healthy male neutered cats. Methods: Cats were anesthetized with desflurane in oxygen for instrumentation. Catheters were placed in a medial saphenous vein for drug administration and in a carotid artery for arterial blood pressure measurement and blood collection. A thermodilution catheter was placed in the pulmonary artery via an introducer placed in a jugular vein for measurement of central venous pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and core body temperature, and for sampling mixed venous blood. A lead II electrocardiogram was connected. Desflurane administration was discontinued and a target-controlled infusion system was used to administer alfaxalone to reach six plasma alfaxalone concentrations ranging from 1.0 to 30.4 mg L−1, with 7.6 mg L−1 considered a clinical concentration for anesthesia. Cardiovascular measurements were recorded, and arterial and mixed-venous blood samples were collected for blood-gas analysis and plasma alfaxalone concentration measurement at each target concentration. Data were analyzed using a repeated-measures analysis of variance and Dunnett's test for comparisons to the lowest target concentration. Significance was set at p < 0.05. Results: Mean ± standard deviation plasma alfaxalone concentrations were 0.73 ± 0.32, 1.42 ± 0.41, 3.44 ± 0.40, 6.56 ± 0.43, 18.88 ± 6.81 and 49.47 ± 5.50 mg L−1 for the 1, 1.9, 3.8, 7.6, 15.2, and 30.4 mg L−1 target concentrations, respectively. PaCO2 increased with increasing target plasma alfaxalone concentrations and was 69.4 ± 14.2 mmHg (9.3 ± 1.9 kPa) at the 30.4 mg L−1 target. Some cardiovascular variables were statistically significantly affected by increasing target plasma alfaxalone concentrations. Conclusion and clinical relevance: Within the plasma concentration range studied, alfaxalone caused hypoventilation, but the cardiovascular effects were of small clinical significance.

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