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Abstract

Objective—To determine the cardiovascular effects of dopamine and dobutamine infusions during nor-movolemia, hypovolemia (HV) through blood loss of 10 mL/kg (HV10), further loss to 25 mL/kg (HV25), and volume replacement (VR) in isoflurane-anesthetized dogs.

Animals—7 healthy young dogs.

Procedures—Dogs were anesthetized with isoflurane 2 times (3 weeks apart). Cardiovascular measurements were obtained for each volume state. The cardiac index (CI) determined by the lithium dilution technique was compared with CI assessed by the arterial pulse contour technique. At each volume state, random treatment with dobutamine or dopamine was assessed (CI by the arterial pulse contour technique). Ten-minute treatments with 3 and6 μg of dobutamine/kg/min or 7 and 14 μg of dopamine/kg/min (low and high doses, respectively) were administered sequentially. Differences from baseline were determined for volume, drug, and dose effects.

Results—Significant proportional changes in blood pressure (BP), stroke index (SI), and CI were evident with changes in volume state. Systemic vascular resistance (SVR) decreased after VR. Dobutamine induced little change in BP; increased heart rate (HR), SI, and CI; and decreased SVR (high dose). Dopamine increased BP and SI, did not change CI, and increased SVR (high dose). The arterial pulse contour technique underestimated changes in CI associated with volume changes.

Conclusions and Clinical Relevance—Isoflurane eliminates clinically obvious compensatory increases in HR during HV. Dopamine is suitable for temporary management of blood loss in isoflurane-anesthetized dogs. Dobutamine increased CI without an associated improvement in BP. The arterial pulse contour monitor should be recalibrated when volume status changes.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare induction with hydromorphone and diazepam (HydroD) or oxymorphone and diazepam (OxyD) followed by maintenance with isoflurane in dogs with induced hypovolemia.

Animals—6 healthy mixed-breed dogs.

Procedure—The study used a crossover design. Measurements were obtained in normovolemic dogs during isoflurane. Hypovolemia was induced (blood loss of 30 mL/kg) and measurements repeated following recovery from anesthesia, after HydroD (hydromorphone, 0.1 mg/kg; diazepam, 0.2 mg/kg; IV) or OxyD (oxymorphone, 0.05 mg/kg; diazepam, 0.2 mg/kg; IV), after another dose of the same opioid, during administration of isoflurane (end-tidal concentration, 0.9%), and after glycopyrrolate (0.01 mg/kg, IV). Significant changes were identified.

Results—Induction effect was evident within 1 minute. All dogs were intubated after the second dose of opioid. No significant differences were found between inductions. The HydroD decreased heart rate (mean ± SEM, –41 ± 9.8 beats/min), whereas both inductions increased stroke index (0.4 ± 0.09 mL/kg/beat) and caused moderate respiratory depression. Cardiac index was decreased (±30.2 ± 6.04 mL/kg/min) and there was minor metabolic acidosis during isoflurane following HydroD, compared with values for anesthetized normovolemic dogs. Glycopyrrolate increased heart rate (50 ± 8.6 beats/min) and decreased systolic blood pressure (–23.2 ± 4.87 mm Hg) in dogs induced with HydroD and decreased stroke index (–0.3 ± 0.08 mL/kg/beat) for both inductions.

Conclusions and Clinical Relevance—Similar effects were detected after administration of HydroD or OxyD in hypovolemic dogs. Either combination should be safe for use in hypovolemic dogs. Administration of glycopyrrolate was not beneficial. (Am J Vet Res 2005;66:1227–1237)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether administration of the nonsteroidal anti-inflammatory drugs meloxicam or carprofen to healthy dogs that were subsequently anesthetized and subjected to painful electrical stimulation has adverse effects on renal function as measured by glomerular filtration rate (GFR) and evaluation of serum concentrations of urea and creatinine.

Animals—6 male and 6 female healthy young-adult Beagles.

Procedure—A study was conducted in accordance with a randomized crossover Latin-square design. One of 3 treatments (saline [0.9% NaCl] solution, 0.2 mg of meloxicam/kg, or 4.0 mg of carprofen/kg) was administered IV 1 hour before anesthesia was induced by use of drugs in accordance with a standard anesthetic protocol (butorphanol tartrate and acepromazine maleate as preanesthetic medications, ketamine hydrochloride and diazepam for induction, and maintenance with isoflurane). Anesthetized dogs were subjected to intermittent electrical stimulation for 30 minutes. Direct, mean arterial blood pressure; heart rate; and respiratory rate were monitored. End-tidal isoflurane concentration was maintained at 1.5 times the minimum alveolar concentration. The GFR, as measured by plasma clearance of 99mTc-diethylenetriaminepentaacetic acid, and serum concentrations of serum and creatinine were determined 24 hours after induction of anesthesia.

Results—Neither meloxicam nor carprofen significantly affected GFR or serum concentrations of urea and creatinine, compared with values for the saline treatment.

Conclusions and Clinical Relevance—When administered 1 hour before onset of anesthesia and painful electrical stimulation, meloxicam or carprofen did not cause clinically important alterations of renal function in young healthy dogs. (Am J Vet Res 2004;65:1384–1390)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the cardiac anesthetic index (CAI) of isoflurane in green iguanas and whether butorphanol affected the CAI.

Design—Prospective randomized controlled trial.

Animals—7 healthy mature iguanas.

Procedure—In 5 iguanas, CAI was determined after induction of anesthesia with isoflurane alone, and in 5 iguanas, CAI was determined after induction of anesthesia with isoflurane and IM administration of butorphanol (1 mg/kg [0.45 mg/lb]). Three iguanas underwent both treatments. Animals were equilibrated for 20 minutes at 1.5 times the minimum alveolar concentration (MAC) of isoflurane and observed for evidence of cardiovascular arrest. If there was no evidence of cardiovascular arrest, end-tidal isoflurane concentration was increased by 20%, and animals were allowed to equilibrate for another 20 minutes. This process was repeated until cardiovascular arrest occurred or vaporizer output could no longer be consistently increased. The CAI was calculated by dividing the highest end-tidal isoflurane concentration by the MAC.

Results—None of the iguanas developed cardiovascular arrest and all survived. Mean ± SD highest endtidal isoflurane concentration during anesthesia with isoflurane alone (9.2 ± 0.60%) was not significantly different from mean concentration during anesthesia with isoflurane and butorphanol (9.0 ± 0.43%). The CAI was > 4.32.

Conclusions and Clinical Relevance—Results suggest that the CAI of isoflurane in green iguanas is > 4.32 and not affected by administration of butorphanol. Isoflurane appears to be a safe anesthetic in green iguanas. (J Am Vet Med Assoc 2003;222: 1565–1568)

Restricted access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine minimum alveolar concentration (MAC) of isoflurane in green iguanas and effects of butorphanol on MAC.

Design—Prospective randomized trial.

Animals—10 healthy mature iguanas.

Procedure—In each iguana, MAC was measured 3 times: twice after induction of anesthesia with isoflurane and once after induction of anesthesia with isoflurane and IM administration of butorphanol (1 mg/kg [0.45 mg/lb]). A blood sample was collected from the tail vein for blood-gas analysis at the beginning and end of the anesthetic period. The MAC was determined with a standard bracketing technique; an electrical current was used as the supramaximal stimulus. Animals were artificially ventilated with a ventilator set to deliver a tidal volume of 30 mL/kg (14 mL/lb) at a rate of 4 breaths/min.

Results—Mean ± SD MAC values during the 3 trials (2 without and 1 with butorphanol) were 2.0 ± 0.6, 2.1 ± 0.6, and 1.7 ± 0.7%, respectively, which were not significantly different from each other. Heart rate and end-tidal partial pressure of CO2 were also not significantly different among the 3 trials. Mean ± SD heart rate was 48 ± 10 beats/min; mean end-tidal partial pressure of CO2 was 22 ± 10 mm Hg. There were no significant differences in blood-gas values for samples obtained at the beginning versus the end of the anesthetic period.

Conclusions and Clinical Relevance—Results suggest that the MAC of isoflurane in green iguanas is 2.1% and that butorphanol does not have any significant isoflurane-sparing effects. (J Am Vet Med Assoc 2003;222:1559–1564)

Restricted access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate the dose-related cardiovascular and urine output (UrO) effects of dopamine hydrochloride and dobutamine hydrochloride, administered individually and in combination at various ratios, and identify individual doses that achieve target mean arterial blood pressure (MAP; 70 mm Hg) and cardiac index (CI; 150 mL/kg/min) in dogs during deep isoflurane anesthesia.

Animals—10 young clinically normal dogs.

Procedures—Following isoflurane equilibration at a baseline MAP of 50 mm Hg on 3 occasions, dogs randomly received IV administration of dopamine (3, 7, 10, 15, and 20 μg/kg/min), dobutamine (1, 2, 4, 6, and 8 μg/kg/min), and dopamine-dobutamine combinations (3.5:1, 3.5:4, 7:2, 14:1, and 14:4 μg/kg/min) in a crossover study. Selected cardiovascular and UrO effects were determined following 20-minute infusions at each dose.

Results—Dopamine caused significant dose-dependent responses and achieved target MAP and CI at 7 μg/kg/min; dobutamine at 2 μg/kg/min significantly affected only CI values. At any dose, dopamine significantly affected UrO, whereas dobutamine did not. Target MAP and CI values were achieved with a dopamine-dobutamine combination at 7:2 μg/kg/min; a dopamine-related dose response for MAP and dopamine- and dobutamine-related dose responses for CI were identified. Changes in UrO were associated with dopamine only.

Conclusions and Clinical Relevance—In isoflurane-anesthetized dogs, a guideline dose for dopamine of 7 μg/kg/min is suggested; dobutamine alone did not improve MAP. Data regarding cardiovascular and UrO effects indicated that the combination of dopamine and dobutamine did not provide greater benefit than use of dopamine alone in dogs.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the cardiopulmonary effects of anesthetic induction with thiopental, propofol, or ketamine hydrochloride and diazepam in dogs sedated with medetomidine and hydromorphone.

Animals—6 healthy adult dogs.

Procedures—Dogs received 3 induction regimens in a randomized crossover study. Twenty minutes after sedation with medetomidine (10 μg/kg, IV) and hydromorphone (0.05 mg/kg, IV), anesthesia was induced with ketamine-diazepam, propofol, or thiopental and then maintained with isoflurane in oxygen. Measurements were obtained prior to sedation (baseline), 10 minutes after administration of preanesthetic medications, after induction before receiving oxygen, and after the start of isoflurane-oxygen administration.

Results—Doses required for induction were 1.25 mg of ketamine/kg with 0.0625 mg of diazepam/kg, 1 mg of propofol/kg, and 2.5 mg of thiopental/kg. After administration of preanesthetic medications, heart rate (HR), cardiac index, and PaO 2 values were significantly lower and mean arterial blood pressure, central venous pressure, and PaCO 2 values were significantly higher than baseline values for all regimens. After induction of anesthesia, compared with postsedation values, HR was greater for ketamine-diazepam and thiopental regimens, whereas PaCO 2 tension was greater and stroke index values were lower for all regimens. After induction, PaO 2 values were significantly lower and HR and cardiac index values significantly higher for the ketamine-diazepam regimen, compared with values for the propofol and thiopental regimens.

Conclusions and Clinical Relevance—Medetomidine and hydromorphone caused dramatic hemodynamic alterations, and at the doses used, the 3 induction regimens did not induce important additional cardiovascular alterations. However, administration of supplemental oxygen is recommended.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To assess agreement between arterial pressure waveform–derived cardiac output (PCO) and lithium dilution cardiac output (LiDCO) systems in measurements of various levels of cardiac output (CO) induced by changes in anesthetic depth and administration of inotropic drugs in dogs.

Animals—6 healthy dogs.

Procedure—Dogs were anesthetized on 2 occasions separated by at least 5 days. Inotropic drug administration (dopamine or dobutamine) was randomly assigned in a crossover manner. Following initial calibration of PCO measurements with a LiDCO measurement, 4 randomly assigned treatments were administered to vary CO; subsequently, concurrent pairs of PCO and LiDCO measurements were obtained. Treatments included a light plane of anesthesia, deep plane of anesthesia, continuous infusion of an inotropic drug (rate adjusted to achieve a mean arterial pressure of 65 to 80 mm Hg), and continuous infusion of an inotropic drug (7 µg/kg/min).

Results—Significant differences in PCO and LiDCO measurements were found during deep planes of anesthesia and with dopamine infusions but not during the light plane of anesthesia or with dobutamine infusions. The PCO system provided higher CO measurements than the LiDCO system during deep planes of anesthesia but lower CO measurements during dopamine infusions.

Conclusions and Clinical Relevance—The PCO system tracked changes in CO in a similar direction as the LiDCO system. The PCO system provided better agreement with LiDCO measurements over time when hemodynamic conditions were similar to those during initial calibration. Recalibration of the PCO system is recommended when hemodynamic conditions or pressure waveforms are altered appreciably. (Am J Vet Res 2005;66:1430–1436)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine minimum alveolar concentration (MAC) of isoflurane in mechanically ventilated Dumeril monitors (Varanus dumerili).

Design—Prospective study.

Animals—10 healthy adult Dumeril monitors.

Procedure—Anesthesia was induced with isoflurane in oxygen delivered through a face mask. Monitors were endotracheally intubated, and end-tidal and inspired isoflurane concentrations were continuously measured. After equilibration at an end-tidal-toinspired isoflurane concentration ratio of > 0.9 for 20 minutes, an electrical stimulus (50 Hz, 50 V) was delivered to the ventral aspect of the tail for up to 1 minute and the monitor was observed for purposeful movement. End-tidal isoflurane concentration was then decreased by 10%, and equilibration and stimulation were repeated. The MAC was calculated as the mean of the lowest end-tidal isoflurane concentration that prevented positive response and the highest concentration that allowed response. A blood sample for blood gas analysis was collected from the tail vein at the beginning and end of the anesthetic period.

Results—Mean ± SD MAC of isoflurane was 1.54 ± 0.17%. Mean heart rates at the upper and lower MAC values were 32.4 ± 3 beats/min and 34 ± 4.5 beats/min, respectively. During the experiment, Paco2 decreased significantly from 43.1 mm Hg to 27.9 mm Hg and blood pH and HCO3 concentration increased significantly from 7.33 to 7.64 and from 25.3 to 32.9 mmol/L, respectively.

Conclusions and Clinical Relevance—The MAC of isoflurane in Dumeril monitors was similar to that reported in mammals but lower than values reported in other reptiles. This difference may be reflective of the more advanced cardiovascular physiologic features of monitor lizards. (J Am Vet Med Assoc 2005; 226:1098–1101)

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine the minimum alveolar concentration (MAC) of sevoflurane and assess the sevoflurane-sparing effect of coadministration of nitrous oxide in mechanically ventilated Dumeril monitors (Varanus dumerili).

Design—Prospective crossover study.

Animals—10 healthy adult Dumeril monitors.

Procedure—Anesthesia was induced with sevoflurane in 100% oxygen or sevoflurane in 66% nitrous oxide (N2O) with 34% oxygen, delivered through a face mask. Monitors were endotracheally intubated, and end-tidal and inspired isoflurane concentrations were measured continuously; MAC was determined by use of a standard bracketing technique. An electrical stimulus (50 Hz, 50 V) was delivered to the ventral aspect of the tail as the supramaximal stimulus. A blood sample for blood gas analyses was collected from the ventral coccygeal vessels at the beginning and end of the anesthetic period. An interval of at least 7 days was allowed to elapse between treatments.

Results—The MAC ± SDs of sevoflurane in oxygen and with N2O were 2.51 ± 0.46% and 1.83 ± 0.33%, respectively. There was a significant difference between the 2 treatments, and the mean MAC-reducing effect of N2O was 26.4 ± 11.4%. Assuming simple linear additivity of sevoflurane and N2O, the MAC for N2O was estimated to be 244%. No significant differences in blood gas values—with the predictable exception of oxygen pressure—were detected between the 2 groups.

Conclusions and Clinical Relevance—The MAC of sevoflurane in Dumeril monitors is similar to that reported for other species. The addition of N2O significantly decreased the MAC of sevoflurane in this species. (J Am Vet Med Assoc 2005;227:575–578)

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in Journal of the American Veterinary Medical Association