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 language | English (US) |
|---|---|
| Journal | Veterinary Anaesthesia and Analgesia |
| DOIs | |
| State | Published - Jan 1 2019 |
Fingerprint
Keywords
- alfaxalone
- cardiovascular
- cats
ASJC Scopus subject areas
- veterinary(all)
Cite this
Hemodynamic effects of subclinical, clinical and supraclinical plasma alfaxalone concentrations in cats. / Pypendop, Bruno H; Barter, Linda S; Pascoe, Peter J; Ranasinghe, M. G.; Pasloske, Kirby.
In: Veterinary Anaesthesia and Analgesia, 01.01.2019.Research output: Contribution to journal › Article
}
TY - JOUR
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.
KW - alfaxalone
KW - cardiovascular
KW - cats
UR - http://www.scopus.com/inward/record.url?scp=85068556274&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85068556274&partnerID=8YFLogxK
U2 - 10.1016/j.vaa.2019.05.004
DO - 10.1016/j.vaa.2019.05.004
M3 - Article
JO - Veterinary Anaesthesia and Analgesia
JF - Veterinary Anaesthesia and Analgesia
SN - 1467-2987
ER -