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- Author or Editor: Peter Hellyer x
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Summary
Effects of endotoxemia on left ventricular contractility and systemic hemodynamics were determined in pentobarbital-anesthetized swine. A multielectrode conductance (volume) catheter and a high-fidelity pressure transducer catheter were passed retrograde into the left ventricle to continuously measure pressure and volume. End-systolic pressure-volume relationships were determined during transient (8 to 10 s) caudal vena caval balloon occlusion. Lactated Ringer's solution was administered at a rate sufficient to maintain left ventricular end-diastolic pressure ≥ 6 mm of Hg. Following baseline measurements, Escherichia coli endotoxin (055-B5) was infused iv at 2.5 μg/kg of body weight/h for 3 hours. Left ventricular end-systolic elastance (Ees), the slope of the end-systolic pressure-volume relationship; end-systolic elastance normalized for left ventricular end-diastolic volume (Ees norm); the rate of increase of left ventricular pressure (dP/dtmax); and preload recruitable stroke work (prsw, stroke work-to-end-diastolic volume relationship) did not change in endotoxemic swine, compared with baseline measurements or with values from control (physiologic saline solution-treated) swine. Left ventricular pressures and volumes had marked pig-to-pig variability in the control and endotoxin-treated groups. Determination of Ees, Ees norm, and prsw was further confounded by development of frequent premature ventricular contractions during caudal vena caval balloon occlusion. Endotoxin significantly (P < 0.05) decreased left ventricular end-diastolic pressure, compared with that in control swine, and significantly (P < 0.01) decreased left ventricular end-diastolic volume, compared with baseline. Endotoxin decreased cardiac index and arterial blood pressure, whereas heart rate, central venous pressure, and mean pulmonary arterial pressure increased. Endotoxin did not decrease myocardial contractility, as measured by Ees, Ees norm dP/dtmax, or prsw in anesthetized swine.
Summary
We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [mac]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered iv. Five minutes later, dobutamine infusion was started at dosage of 2.5 μg/kg/min, iv. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 μg/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (add) in saline-treated horses (mean ± sem, add = 105.6 ± 16.3 μg/kg) and atropimzed horses (add = 36.2 ± 8.7 μg/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (hr) or systolic (sap), diastolic (dap), or mean (map) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the add. These results indicate that atropine may lower the arrhythmogenic threshold for dobutamine in halothane-anesthetized horses.
Abstract
Objective—To determine whether infusion of xylazine and ketamine or xylazine and propofol after sevoflurane administration in horses would improve the quality of recovery from anesthesia.
Animals—6 healthy adult horses.
Procedures—For each horse, anesthesia was induced by administration of xylazine, diazepam, and ketamine and maintained with sevoflurane for approximately 90 minutes (of which the last 60 minutes were under steady-state conditions) 3 times at 1-week intervals. For 1 anesthetic episode, each horse was allowed to recover from sevoflurane anesthesia; for the other 2 episodes, xylazine and ketamine or xylazine and propofol were infused for 30 or 15 minutes, respectively, after termination of sevoflurane administration. Selected cardiopulmonary variables were measured during anesthesia and recovery. Recovery events were monitored and subjectively scored.
Results—Cardiopulmonary variables differed minimally among treatments, although the xylazine-propofol infusion was associated with greater respiratory depression than was the xylazine-ketamine infusion. Interval from discontinuation of sevoflurane or infusion administration to standing did not differ significantly among treatments, but the number of attempts required to stand successfully was significantly lower after xylazine-propofol infusion, compared with the number of attempts after sevoflurane alone. Scores for recovery from anesthesia were significantly lower (ie, better recovery) after either infusion, compared with scores for sevoflurane administration alone.
Conclusions and Clinical Relevance—Xylazine-ketamine or xylazine-propofol infusion significantly improved quality of recovery from sevoflurane anesthesia in horses. Xylazine-ketamine or xylazine-propofol infusions may be of benefit during recovery from sevoflurane anesthesia in horses for which a smooth recovery is particularly critical. However, oxygenation and ventilation should be monitored carefully.
Abstract
Objective—To measure cardiac output in healthy female anesthetized dogs by use of lithium dilution cardiac output and determine whether changes in mean arterial pressure were caused by changes in cardiac output or systemic vascular resistance.
Design—Prospective clinical study.
Animals—20 healthy female dogs.
Procedure—Dogs were anesthetized for ovariohysterectomy. Ten dogs breathed spontaneously throughout anesthesia, and 10 dogs received intermittent positive-pressure ventilation. Cardiovascular and respiratory measurements, including lithium dilution cardiac output, were performed during anesthesia and surgery.
Results—Mean arterial pressure and systemic vascular resistance index were low after induction of anesthesia and just prior to surgery and increased significantly after surgery began. Cardiac index (cardiac output indexed to body surface area) did not change significantly throughout anesthesia and surgery.
Conclusions and Clinical Relevance—Results provide baseline data for cardiac output and cardiac index measurements during clinical anesthesia and surgery in dogs. Changes in mean arterial pressure do not necessarily reflect corresponding changes in cardiac index. (J Am Vet Med Assoc 2005;227:1419–1423)
