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Summary

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered iv to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.

Free access
in American Journal of Veterinary Research

Summary

Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 ± 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration. Results of this study indicated that induction of anesthesia with halothane and maintenance at an end-tidal halothane concentration of 1.13% induced significant changes in blood pressure, with minimal effects on cardiac output and pulmonary function, when administered to hypovolemic dogs.

Free access
in American Journal of Veterinary Research

Summary

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered iv to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.

Free access
in American Journal of Veterinary Research

SUMMARY

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered iv to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine fluid retention, glomerular filtration rate, and urine output in dogs anesthetized for a surgical orthopedic procedure.

Animals—23 dogs treated with a tibial plateau leveling osteotomy.

Procedures—12 dogs were used as a control group. Cardiac output was measured in 5 dogs, and 6 dogs received carprofen for at least 14 days. Dogs received oxymorphone, atropine, propofol, and isoflurane for anesthesia (duration, 4 hours). Urine and blood samples were obtained for analysis every 30 minutes. Lactated Ringer's solution was administered at 10 mL/kg/h. Urine output was measured and glomerular filtration rate was estimated. Fluid retention was measured by use of body weight, fluid balance, and bioimpedance spectroscopy.

Results—No difference was found among control, cardiac output, or carprofen groups, so data were combined. Median urine output and glomerular filtration rate were 0.46 mL/kg/h and 1.84 mL/kg/min. Dogs retained a large amount of fluids during anesthesia, as indicated by increased body weight, positive fluid balance, increased total body water volume, and increased extracellular fluid volume. The PCV, total protein concentration, and esophageal temperature decreased in a linear manner.

Conclusions and Clinical Relevance—Dogs anesthetized for a tibial plateau leveling osteotomy retained a large amount of fluids, had low urinary output, and had decreased PCV, total protein concentration, and esophageal temperature. Evaluation of urine output alone in anesthetized dogs may not be an adequate indicator of fluid balance.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To describe the pharmacokinetics of lidocaine and its active metabolite, monoethylglycinexylidide (MEGX), after IV administration of a single bolus of lidocaine in cats that were awake in phase 1 and anesthetized with isoflurane in phase 2 of the study.

Animals—8 healthy adult cats.

Procedure—During phase 1, cats were administered lidocaine (2 mg/kg, IV) as a bolus injection (time 0). During phase 2, cats were anesthetized with isoflurane and maintained at 0.75 times the minimum alveolar concentration of isoflurane for each specific cat. After a 15-minute equilibration period, lidocaine (2 mg/kg, IV) was administered as a bolus injection to each cat (time 0). In both phases, plasma concentrations of lidocaine and MEGX were measured at various time points by use of liquid chromatography-mass spectrometry.

Results—Anesthesia with isoflurane significantly decreased the volume of the central compartment, clearance, and elimination half-life of lidocaine and significantly increased the extrapolated plasma drug concentration at time 0, compared with values for awake cats. Pharmacokinetics of MEGX were also changed by isoflurane-induced anesthesia because the maximum observed plasma concentration (Cmax), area under the concentration-time curve extrapolated to infinity, and time to Cmax were significantly higher in anesthetized cats, compared with values for awake cats.

Conclusions and Clinical Relevance—Pharmacokinetics of lidocaine and MEGX were substantially altered in cats anesthetized by use of isoflurane. When pharmacokinetic variables are used to determine loading and infusion doses in awake or anesthetized cats, they should be measured in cats that are awake or anesthetized, respectively. (Am J Vet Res 2005;66:1162–1166)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the pharmacokinetics of dexmedetomidine administered as a short-duration IV infusion in isoflurane-anesthetized cats.

Animals—6 healthy adult domestic female cats.

Procedures—Dexmedetomidine hydrochloride was injected IV (10 μg/kg over 5 minutes [rate, 2 μg/kg/min]) in isoflurane-anesthetized cats. Blood samples were obtained immediately prior to and at 1, 2, 5, 6, 7, 10, 15, 30, 60, 90, 120, 240, and 480 minutes following the start of the IV infusion. Collected blood samples were transferred to tubes containing EDTA, immediately placed on ice, and then centrifuged at 3,901 × g for 10 minutes at 4°C. The plasma was harvested and stored at −20°C until analyzed. Plasma dexmedetomidine concentrations were determined by means of liquid chromatography–mass spectrometry. Dexmedetomidine plasma concentration-time data were fitted to compartmental models.

Results—A 2-compartment model with input in and elimination from the central compartment best described the disposition of dexmedetomidine administered via short-duration IV infusion in isoflurane-anesthetized cats. Weighted mean ± SEM apparent volume of distribution of the central compartment and apparent volume of distribution at steady-state were 402 ± 47 mL/kg and 1,701 ± 200 mL/kg, respectively; clearance and terminal half-life (harmonic mean ± jackknife pseudo-SD) were 6.3 ± 2.8 mL/min/kg and 198 ± 75 minutes, respectively. The area under the plasma concentration curve and maximal plasma concentration were 1,061 ± 292 min•ng/mL and 17.6 ± 1.8 ng/mL, respectively.

Conclusions and Clinical Relevance—Disposition of dexmedetomidine administered via short-duration IV infusion in isoflurane-anesthetized cats was characterized by a moderate clearance and a long terminal half-life.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine cardiopulmonary effects of incremental doses of dopamine and phenylephrine during isoflurane-induced hypotension in cats with hypertrophic cardiomyopathy (HCM).

Animals—6 adult cats with severe naturally occurring HCM.

Procedures—Each cat was anesthetized twice (once for dopamine treatment and once for phenylephrine treatment; treatment order was randomized). Hypotension was induced by increasing isoflurane concentration. Cardiopulmonary data, including measurement of plasma concentration of cardiac troponin I (cTnI), were obtained before anesthesia, 20 minutes after onset of hypotension, and 20 minutes after each incremental infusion of dopamine (2.5, 5, and 10 μg/kg/min) or phenylephrine (0.25, 0.5, and 1 μg/kg/min).

Results—Mean ± SD end-tidal isoflurane concentration for dopamine and phenylephrine was 2.44 ± 0.05% and 2.48 ± 0.04%, respectively. Cardiac index and tissue oxygen delivery were significantly increased after administration of dopamine, compared with results after administration of phenylephrine. Systemic vascular resistance index was significantly increased after administration of phenylephrine, compared with results after administration of dopamine. Oxygen consumption remained unchanged for both treatments. Systemic and pulmonary arterial blood pressures were increased after administration of both dopamine and phenylephrine. Acid-base status and blood lactate concentration did not change and were not different between treatments. The cTnI concentration increased during anesthesia and infusion of dopamine and phenylephrine but did not differ significantly between treatments.

Conclusions and Clinical Relevance—Dopamine and phenylephrine induced dose-dependent increases in systemic and pulmonary blood pressure, but only dopamine resulted in increased cardiac output. Hypotension and infusions of dopamine and phenylephrine caused significant increases in cTnI concentrations.

Full access
in American Journal of Veterinary Research