Cardiovascular effects of a ketamine-medetomidine combination that produces deep sedation in Yucatan mini swine.

Seven chronically instrumented Yucatan minipigs were deeply sedated with the combination of ketamine (10 mg/kg), a dissociative anesthetic, and medetomidine (0.2 mg/kg), an alpha 2-adrenoceptor agonist used as an animal sedative in Europe. Both drugs were drawn in the same syringe and administered in the left atrium via a previously inserted permanent catheter. As a result, hypertension (mean arterial pressure from 116 +/- 12 mmHg to 142 +/- 18 mmHg) occurred and was followed by bradycardia (from 107 +/- 22 bpm to 71 +/- 9 bpm). Concomitantly, both the rate of increase in ventricular pressure (48%) and ventricular wall thickening fraction (37%) decreased, thus indicating some worsening of left ventricular function. Further, systemic vascular resistance increased (290%) resulting in a reduction in cardiac output from 0.4 +/- 0.3 l/minute. Also, left ventricular end diastolic pressure initially increased (maximum 10.2 +/- 10.8 mmHg) but returned to the control level in 5 minutes. In spite of an increase in respiratory frequency (3x), PaCO2 increased and PaO2 and pH declined. Rectal temperature decreased from 38.4 +/- 0.9 to 36.0 +/- 0.8 degrees C. All of these changes were transient and returned to control levels during the follow-up period (2 hours). However, epinephrine concentration was exceptionally decreased by the drugs and stayed under the detection limit (20 pg/kg) for the entire time, whereas norepinephrine was undetectable for 10 minutes postadministration. Ketamine-medetomidine, administered in a dose that produced deep sedation, induced marked but reversible changes in most of the cardiovascular variables; there were no pedal or palpebral reflexes for 30 minutes.