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- Author or Editor: Ann M. Hess x
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Abstract
OBJECTIVE
To evaluate the sedative and cardiopulmonary effects of various combinations of acepromazine, dexmedetomidine, hydromorphone, and glycopyrrolate, followed by anesthetic induction with propofol and maintenance with isoflurane in healthy dogs.
ANIMALS
6 healthy adult female Beagles.
PROCEDURES
Dogs were instrumented for hemodynamic measurements while anesthetized with isoflurane. Two hours after recovery, dogs received 1 of 4 IM combinations in a crossover design with 1 week between treatments: hydromorphone (0.1 mg/kg) and acepromazine (0.005 mg/kg; HA); hydromorphone and dexmedetomidine (0.0025 mg/kg; HD); hydromorphone, acepromazine, and dexmedetomidine (HAD); and hydromorphone, acepromazine, dexmedetomidine, and glycopyrrolate (0.02 mg/kg; HADG). Sedation was scored after 30 minutes. Physiologic variables and cardiac index were measured after sedation, after anesthetic induction with propofol, and every 15 minutes during maintenance of anesthesia with isoflurane for 60 minutes (target expired concentration at 760 mm Hg, 1.3%).
RESULTS
Sedation scores were not significantly different among treatments. Mean ± SD cardiac index was significantly higher for the HA (202 ± 45 mL/min/kg) and HADG (185 ± 59 mL/min/kg) treatments than for the HD (88 ± 31 mL/min/kg) and HAD (103 ± 25 mL/min/kg) treatments after sedation and through the first 15 minutes of isoflurane anesthesia. No ventricular arrhythmias were noted with any treatment.
CLINICAL RELEVANCE
In healthy dogs, IM administration of HADG before propofol and isoflurane anesthesia provided acceptable cardiopulmonary function with no adverse effects. This combination should be considered for routine anesthetic premedication in healthy dogs.
Abstract
OBJECTIVE
To determine if tissue oxygen saturation (StO2) correlates with oxygen delivery (DO2) and/or cardiac output (CO) in a canine hemorrhagic shock model.
ANIMALS
8 healthy purpose-bred dogs.
METHODS
Dogs were anesthetized, and hemorrhagic shock was induced by withdrawing up to 60% of total blood volume, targeting a mean arterial pressure (MAP) of 40 mm Hg. The withdrawn blood was returned to the patient in 2 equal aliquots. Data was collected at 4 time points: 10 minutes after MAP was stabilized under anesthesia (time point [TP]-1), 10 minutes after up to 60% of blood volume was removed to target a MAP of 40 mm Hg (TP2), 10 minutes after the return of 50% of shed blood (TP3), and 10 minutes after the return of the remaining 50% of shed blood (TP4). Total blood volume withdrawn, StO2, CO, heart rate, and MAP were recorded, and DO2 was calculated at each TP.
RESULTS
Mean StO2 significantly decreased between TP1 (77.8% [± 9.54]) and TP2 (44.8% [± 19.5]; P < .001 vs TP1). Mean StO2 increased to 63.1% (± 9.85) at TP3, but remained significantly lower compared to TP1 (P = .002). There was no difference between mean StO2 at TP4 (82.5% [± 12.6]) versus TP1 (P = .466). StO2 has a strong, positive correlation to both CO (r = 0.80; P < .001) and DO2 (r = 0.75; P < .001).
CLINICAL RELEVANCE
A decrease in StO2 may be used in conjunction with physical examination findings and diagnostic parameters to support a diagnosis of shock. The return of shed blood was correlated with increases in StO2, DO2, and CO, suggesting that StO2 may be used as a marker of adequate resuscitation.
