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- Author or Editor: Bruno H. Pypendop x
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Abstract
Objective—To characterize the cardiovascular effects of romifidine at doses ranging from 5 to 100 µg/kg of body weight, IV.
Animals—25 clinically normal male Beagles.
Procedure—Romifidine was administered IV at a dose of 5, 10, 25, 50, or 100 µg/kg (n = 5/group). Heart rate, arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, body temperature, cardiac output, and PCV were measured immediately prior to and at selected times after romifidine administration. Cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, and left and right ventricular stroke work indices were calculated. Degree of sedation was assessed by an observer who was blinded to the dose administered.
Results—Romifidine induced a decrease in heart rate, pulmonary arterial pressure, rate-pressure product, cardiac index, and right ventricular stroke work index and an increase in central venous pressure, pulmonary capillary wedge pressure, and systemic vascular resistance index. In dogs given romifidine at a dose of 25, 50, or 100 µg/kg, an initial increase followed by a prolonged decrease in arterial pressure was observed. Arterial pressure immediately decreased in dogs given romifidine at a dose of 5 or 10 µg/kg.
Conclusion and Clinical Relevance—Results suggest that IV administration of romifidine induces dose-dependent cardiovascular changes in dogs. However, the 2 lowest doses (5 and 10 µg/kg) induced less cardiovascular depression, and doses ≥ 25 µg/kg induced similar cardiovascular changes, suggesting that there may be a ceiling on the cardiovascular effects of romifidine. (Am J Vet Res 2001; 62:490–495)
Abstract
Objective—To determine hemodynamic effects of 3 concentrations of sevoflurane in cats.
Animals—6 cats.
Procedure—Cats were anesthetized with sevoflurane in oxygen. After instruments were inserted, endtidal sevoflurane concentration was set at 1.25, 1.5, or 1.75 times the individual minimum alveolar concentration (MAC), which was determined in another study. Twenty-five minutes were allowed after each change of concentration. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, oxygen saturation, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured for each sevoflurane concentration before and during noxious stimulation. Arterial and mixed-venous bicarbonate concentrations, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, PaO2, mixed-venous partial pressure of oxygen (Pv–O2), oxygen delivery, oxygen consumption, oxygen-extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. Spontaneous and mechanical ventilations were studied during separate experiments.
Results—Mode of ventilation did not significantly influence any of the variables examined. Therefore, data from both ventilation modes were pooled for analysis. Mean arterial pressure, cardiac index, stroke index, rate-pressure product, left ventricular stroke work index, arterial and mixed-venous pH, PaO2, and oxygen delivery decreased, whereas PaCO2, Pva–O2, and mixed-venous partial pressure of CO2 increased significantly with increasing doses of sevoflurane. Noxious stimulation caused a significant increase in most cardiovascular variables.
Conclusions and Clinical Relevance—Sevoflurane induces dose-dependent cardiovascular depression in cats that is mainly attributable to myocardial depression. ( Am J Vet Res 2004;65:20–25)
Abstract
Objective—To determine the hemodynamic effects of lidocaine (administered IV to achieve 6 plasma concentrations) in isoflurane-anesthetized cats.
Animals—6 cats.
Procedure—Cats were anesthetized with isoflurane in oxygen (end-tidal isoflurane concentration set at 1.25 times the predetermined individual minimum alveolar concentration). Lidocaine was administered IV to each cat to achieve target pseudo–steady-state plasma concentrations of 0, 3, 5, 7, 9, and 11 µg/mL, and isoflurane concentration was reduced to an equipotent concentration. At each plasma lidocaine concentration, cardiovascular and blood gas variables; PCV; and plasma total protein, lactate, lidocaine, and monoethylglycinexylidide concentrations were measured in cats before and during noxious stimulation. Derived variables were calculated.
Results—In isoflurane-anesthetized cats, heart rate, cardiac index, stroke index, right ventricular stroke work index, plasma total protein concentration, mixed-venous PO2 and hemoglobin oxygen saturation, arterial and mixed-venous bicarbonate concentrations, and oxygen delivery were significantly lower during lidocaine administration, compared with values determined without lidocaine administration. Mean arterial pressure, central venous pressure, pulmonary artery pressure, systemic and pulmonary vascular resistance indices, PCV, arterial and mixed-venous hemoglobin concentrations, plasma lactate concentration, arterial oxygen concentration, and oxygen extraction ratio were significantly higher during administration of lidocaine, compared with values determined without lidocaine administration. Noxious stimulation did not significantly affect most variables.
Conclusions and Clinical Relevance—In isofluraneanesthetized cats, although IV administration of lidocaine significantly decreased inhalant requirements, it appeared to be associated with greater cardiovascular depression than an equipotent dose of isoflurane alone. Administration of lidocaine to reduce isoflurane requirements is not recommended in cats. (Am J Vet Res 2005;66:661–668)
Abstract
Objective—To determine the pharmacokinetics of ketamine and norketamine in isoflurane-anesthetized dogs.
Animals—6 dogs.
Procedure—The minimum alveolar concentration (MAC) of isoflurane was determined in each dog. Isoflurane concentration was then set at 0.75 times the individual's MAC, and ketamine (3 mg/kg) was administered IV. Blood samples were collected at various times following ketamine administration. Blood was immediately centrifuged, and the plasma separated and frozen until analyzed. Ketamine and norketamine concentrations were measured in the plasma samples by use of liquid chromatography–mass spectrometry. Ketamine concentration-time data were fitted to compartment models. Norketamine concentration-time data were examined by use of noncompartmental analysis.
Results—The MAC of isoflurane was 1.43 ± 0.18% (mean ± SD). A 2-compartment model best described the disposition of ketamine. The apparent volume of distribution of the central compartment, the apparent volume of distribution at steady state, and the clearance were 371.3 ± 162 mL/kg, 4,060.3 ± 2,405.7 mL/kg, and 58.2 ± 17.3 mL/min/kg, respectively. Norketamine rapidly appeared in plasma following ketamine administration and had a terminal half-life of 63.6 ± 23.9 minutes. A large variability in plasma concentrations, and therefore pharmacokinetic parameters, was observed among dogs for ketamine and norketamine.
Conclusions and Clinical Relevance—In isoflurane-anesthetized dogs, a high variability in the disposition of ketamine appears to exist among individuals. The disposition of ketamine may be difficult to predict in clinical patients. (Am J Vet Res 2005;66:2034–2038)
Abstract
Objective—To determine whether the variability of cardiorespiratory measurements is smaller when administering desflurane at a multiple of the individual's minimum alveolar concentration (MAC) or at a predetermined, identical concentration in all subjects.
Animals—10 dogs.
Procedures—Desflurane was administered at 1.5 times the individual's MAC (iMAC) and 1.5 times the group's MAC (gMAC). The order of concentrations was randomly selected. Heart rate, respiratory rate, arterial blood pressure, central venous pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, arterial and mixed-venous blood gas tensions and pH, and cardiac output were measured. The desflurane concentration required to achieve a mean arterial pressure (MAP) of 60 mm Hg was then determined. Finally, the desflurane concentration required to achieve an end-tidal PCO2 of 55 mm Hg was measured.
Results—Variances when administering 1.5 iMAC or 1.5 gMAC were not significantly different for any variable studied. Differences between the MAC multiples needed to reach an MAP of 60 mm Hg and the mean of the sample were significantly larger when gMAC was used, compared with iMAC, indicating that a multiple of iMAC better predicted the concentration resulting in a MAP of 60 mm Hg.
Conclusions and Clinical Relevance—Results suggest that, in a small group of dogs, variability in cardiorespiratory measurements among dogs is unlikely to differ whether an inhalant anesthetic is administered at a multiple of the iMAC in each dog or at an identical gMAC in all dogs.
Abstract
Objective—To characterize the pharmacokinetics of dexmedetomidine after IV administration of a bolus to conscious healthy cats.
Animals—5 healthy adult spayed female cats.
Procedures—Dexmedetomidine was administered IV as a bolus at 3 doses (5, 20, or 50 μg/kg) on separate days in a random order. Blood samples were collected immediately before and at various times for 8 hours after drug administration. Plasma dexmedetomidine concentrations were determined with liquid chromatography–mass spectrometry. Compartment models were fitted to the concentration-time data by means of nonlinear regression.
Results—A 2-compartment model best fit the concentration-time data after administration of 5 μg/kg, whereas a 3-compartment model best fit the data after administration of 20 and 50 μg/kg. The median volume of distribution at steady-state and terminal half-life were 371 mL/kg (range, 266 to 435 mL/kg) and 31.8 minutes (range, 30.3 to 39.7 minutes), respectively, after administration of 5 μg/kg; 545 mL/kg (range, 445 to 998 mL/kg) and 56.3 minutes (range, 39.3 to 68.9 minutes), respectively, after administration of 20 μg/kg; and 750 mL/kg (range, 514 to 938 mL/kg) and 75.3 minutes (range, 52.2 to 223.3 minutes), respectively, after administration of 50 μg/kg.
Conclusions and Clinical Relevance—The pharmacokinetics of dexmedetomidine was characterized by a small volume of distribution and moderate clearance and had minimal dose dependence within the range of doses evaluated. These data will help clinicians design dosing regimens once effective plasma concentrations are established.
Abstract
Objective—To characterize the relationship between plasma dexmedetomidine concentration and the temperature difference between the thermal threshold and skin temperature (ΔT) and between plasma dexmedetomidine concentration and sedation score in healthy cats.
Animals—5 healthy adult spayed female cats.
Procedures—Cats received IV administrations of saline (0.9% NaCl) solution, dexmedetomidine (5, 20, or 50 μg/kg), or acepromazine (0.1 mg/kg). Blood samples were collected and thermal threshold and sedation score were determined before and at various times up to 8 hours after drug administration. In addition, cats received an IV infusion of dexmedetomidine that targeted a concentration achieving 99% of the maximum effect on ΔT.
Results—No change in ΔT over time was found for the saline solution and acepromazine treatments; ΔT increased for 45 minutes when cats received dexmedetomidine at 5 and 20 μg/kg and for 180 minutes when cats received dexmedetomidine at 50 μg/kg. No change in sedation score over time was found for saline solution. Sedation score increased for 120 minutes after cats received acepromazine and for 60, 120, and 180 minutes after cats received dexmedetomidine at 5, 20, and 50 μg/kg, respectively. The plasma dexmedetomidine concentration–effect relationships for the effect on ΔT and sedation score were almost identical. The plasma dexmedetomidine concentration after infusion was lower than targeted, and ΔT was not significantly affected.
Conclusions and Clinical Relevance—Dexmedetomidine administration to cats resulted in thermal analgesia and also profound sedation. These data may be useful for predicting the course of thermal analgesia and sedation after dexmedetomidine administration to cats.
Abstract
OBJECTIVE
To determine whether isoflurane-anesthetized cats with demonstrated resistance to the immobilizing effects of fentanyl would exhibit naltrexone-reversible sparing of the minimum alveolar concentration (MAC) of isoflurane when fentanyl was coadministered with the centrally acting catecholamine receptor antagonist acepromazine.
ANIMALS
5 healthy male purpose-bred cats.
PROCEDURES
Anesthesia was induced and maintained with isoflurane in oxygen. Baseline isoflurane MAC was measured by use of a standard tail clamp stimulus and bracketing study design. Afterward, fentanyl was administered IV to achieve a plasma concentration of 100 ng/mL by means of target-controlled infusion, and isoflurane MAC was remeasured. Next, acepromazine maleate (0.1 mg/kg) was administered IV, and isoflurane MAC was remeasured. Finally, isoflurane concentration was equilibrated at 70% of the baseline MAC. Movement of cats in response to tail clamping was tested before and after IV bolus administration of naltrexone. Physiologic responses were compared among treatment conditions.
RESULTS
Isoflurane MAC did not differ significantly between baseline and fentanyl infusion (mean ± SD, 1.944 ± 0.111% and 1.982 ± 0.126%, respectively). Acepromazine with fentanyl significantly decreased isoflurane MAC to 1.002 ± 0.056% of 1 atm pressure. When isoflurane was increased to 70% of the baseline MAC, no cats moved in response to tail clamping before naltrexone administration, but all cats moved after naltrexone administration.
CONCLUSIONS AND CLINICAL RELEVANCE
Acepromazine caused fentanyl to decrease the isoflurane MAC in cats that otherwise did not exhibit altered isoflurane requirements with fentanyl alone. Results suggested that opioid-mediated increases in brain catecholamine concentrations in cats counteract the opioid MAC-sparing effect.
Abstract
Objective—To compare effects of isoflurane and propofol on the cystometrogram and urethral pressure profile (UPP) in healthy female cats.
Animals—6 healthy female cats.
Procedures—Cats were anesthetized, and a consistent plane of anesthesia was maintained with low and high doses of isoflurane and propofol. A 6-F double-lumen urinary catheter was placed aseptically in the urethra for cystometrogram and UPP measurements. Threshold pressure and volume were recorded for cystometrograms. Maximum urethral pressure for smooth and skeletal muscle portions of the urethra, maximum urethral closure pressure, and functional profile length were measured during each UPP measurement. Heart rate and respiratory rate were recorded.
Results—Cats anesthetized with the low dose of propofol had consistent detrusor reflexes, compared with results for the other anesthetics. Mean ± SD threshold pressure, volume per unit of body weight, and compliance were 75.7 ± 16.3 cm H2O, 8.3 ± 3.2 mL/kg, and 0.5 ± 0.4 mL/cm H2O, respectively, for low-dose propofol. Anesthesia with either dose of propofol caused a significantly higher percentage change in heart rate during the cystometrogram, compared with results for anesthesia with isoflurane. Maximal urethral pressure in the area corresponding to skeletal muscle and the maximum urethral closure pressure were significantly higher for the low dose of propofol, compared with results for the high dose of propofol.
Conclusions and Clinical Relevance—The low-dose propofol regimen was the easiest to titrate and maintain and yielded diagnostic-quality detrusor reflexes in all 6 cats. Anesthetic depth should be titrated appropriately when performing urodynamic procedures.
Abstract
Objective—To qualitatively and quantitatively evaluate the characteristics of desflurane with regard to the induction of and recovery from anesthesia in cats.
Animals—6 cats.
Procedure—Anesthesia was induced and maintained with desflurane in oxygen. Individual minimum alveolar concentration (MAC) values were determined; anesthesia was maintained at 1.25 × MAC for a total anesthesia time (including MAC determination) of 5 hours. Cats were allowed to recover from anesthesia. Induction and recovery periods were video recorded and later scored by use of a grading scale from 0 to 100 (100 being the best outcome). Timing of events was recorded.
Results—The MAC of desflurane was 10.27 ± 1.06%, and mean dose was 5.6 ± 0.2 MAC-hours. Times to loss of coordination, recumbency, and endotracheal intubation were 1.3 ± 0.4, 2.3 ± 0.3, and 6.4 ± 1.1 minutes, respectively. Median score for quality of anesthetic induction was 93 (range, 91 to 94). Times to first movement, extubation, standing, and ability to jump and land with coordination were 2.8 ± 1.0, 3.8 ± 0.5, 14.3 ± 3.9, and 26.4 ± 5.1 minutes, respectively. Alveolar washout of desflurane was rapid. Median score for quality of anesthetic recovery was 94 (range, 86 to 96).
Conclusions and Clinical Relevance—Desflurane was associated with rapid induction of and recovery from anesthesia in cats; assessors rated the overall quality of induction and recovery as excellent. Results appear to support the use of desflurane for induction and maintenance of anesthesia in healthy cats. (Am J Vet Res 2004;65:748–751)
