Hemodynamic effects of sevoflurane in cats

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, end-tidal 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 (PVO2), 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, PVO2, 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.     

Comparison of sevoflurane and isoflurane in domestic ferrets (Mustela putorius furo)

Isoflurane anesthesia is commonly used in ferrets for routine examinations and diagnostics. Sevoflurane is now being used as well, but there have been no studies to date directly comparing these agents in domestic ferrets. A prospective study was designed to evaluate the quality and speed of anesthetic induction and recovery using isoflurane and sevoflurane in ferrets. In addition effects on heart rate, blood pressure and packed cell volume were also recorded. No significant differences were noted between anesthetic agents.     

Anesthetic indices of sevoflurane and isoflurane in unpremedicated dogs

OBJECTIVE: To compare the anesthetic index of sevoflurane with that of isoflurane in unpremedicated dogs. DESIGN: Randomized complete-block crossover design. ANIMALS: 8 healthy adult dogs. PROCEDURE: Anesthesia was induced by administering sevoflurane or isoflurane through a face mask. Time to intubation was recorded. After induction of anesthesia, minimal alveolar concentration (MAC) was determined with a tail clamp method while dogs were mechanically ventilated. Apneic concentration was determined while dogs were breathing spontaneously by increasing the anesthetic concentration until dogs became apneic. Anesthetic index was calculated as apneic concentration divided by MAC. RESULTS: Anesthetic index of sevoflurane (mean +/- SEM, 3.45 +/- 0.22) was significantly higher than that of isoflurane (2.61 +/- 0.14). No clinically important differences in heart rate; systolic, mean, and diastolic blood pressures; oxygen saturation; and respiratory rate were detected when dogs were anesthetized with sevoflurane versus isoflurane. There was a significant linear trend toward lower values for end-tidal partial pressure of carbon dioxide during anesthesia with sevoflurane, compared with isoflurane, at increasing equipotent anesthetic doses. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that sevoflurane has a higher anesthetic index in dogs than isoflurane. Sevoflurane and isoflurane caused similar dose-related cardiovascular depression, but although both agents caused dose-related respiratory depression, sevoflurane caused less respiratory depression at higher equipotent anesthetic doses.     

Cardiovascular and Pulmonary Effects of Sevoflurane Anesthesia in Horses

The effects of 1.0, 1.5, and 2.0 minimum alveolar concentration (MAC) of sevoflurane on hemodynamic, pulmonary and blood chemistry variables were measured during spontaneous and controlled ventilation in healthy horses. Sevoflurane was the only anesthetic drug administered to the horses. In a dose-dependent manner, sevoflurane significantly decreased ( P <.05) mean arterial blood pressure, cardiac output, and stroke volume. There was a progressive decrease in peripheral vascular resistance and an increase in heart rate as the concentration of sevoflurane was increased, but the differences were not significant. During spontaneous ventilation there was a dose-dependent decrease in respiratory rate that caused a decrease in the minute volume. As the dose of sevoflurane increased, the arterial carbon dioxide tension also increased ( P <.05). All blood chemistries remained within normal limits. Recovery from anesthesia was without incident. In conclusion, sevoflurane induces a dose-dependent decrease in hemodynamic variables and pulmonary function in horses that is not greatly different from that of other approved inhalant anesthetics.     

Determination of the minimum anesthetic concentration and cardiovascular dose response for sevoflurane in chickens during controlled ventilation

OBJECTIVE: To determine the minimum anesthetic concentration for sevoflurane and effects of various multiples of minimum anesthetic concentration on arterial pressure and heart rate during controlled ventilation in chickens. STUDY DESIGN: Prospective experimental study. ANIMALS: Seven healthy chickens, 6 to 8 months old, weighing 1.6 to 3.4 kg. METHODS: A rebreathing, semiclosed anesthetic circuit was used. Anesthesia was induced by mask with sevoflurane in oxygen. Each chicken was endotracheally intubated, then controlled ventilation was started and the end-tidal CO2 partial pressure was maintained at 30 to 40 mm Hg. Body temperature was maintained at 39.5 degrees to 41.0 degrees C. The inspired and end-tidal sevoflurane concentration were monitored with a multigas monitor. Minimum anesthetic concentration was determined as the minimal end-tidal sevoflurane concentration which prevented gross purposeful movement in response to clamping a toe for 1 minute. After the determination, the cardiovascular effects of sevoflurane at 1.0, 1.5, and 2.0 times the minimum anesthetic concentration were determined. RESULTS: The minimum anesthetic concentration for sevoflurane was 2.21% + 0.32% (mean +/- SD). Mean arterial pressure and heart rate at minimum anesthetic concentration were 84 +/- 13 mm Hg and 150 +/- 58 beats/min, respectively. There was a dose-dependent decrease in arterial pressure. The heart rate did not change significantly over the range 1 to 2 x minimum anesthetic concentration. No cardiac arrhythmias developed throughout the experiments. CONCLUSIONS AND CLINICAL RELEVANCE: The minimum anesthetic concentration for sevoflurane in chickens was within the range of minimum alveolar concentration reported in mammals. When the concentration of sevoflurane is increased during controlled ventilation in chickens, decrease in arterial pressure should be expected.     

Hemodynamic effects of sevoflurane in spontaneously breathing cats

Sevoflurane has recently been introduced in feline anesthesia. However, its cardiovascular effects have not, to our knowledge, been reported in this species. Six healthy cats, aged 1.81 ± 0.31 years (mean ± SEM) and weighing 3.47 ± 0.11 kg, were studied. Anesthesia was induced and maintained with sevoflurane in oxygen. Body temperature was maintained between 38.5 and 39.55 °C. After instrumentation, end‐tidal sevoflurane concentration was randomly set at 1.25, 1.5, and 1.75 times the individual minimum alveolar concentration (MAC), determined in a previous study, according to a Latin Square Design. Thirty minutes of stabilization was allowed after each change of concentration. ECG and heart rate, systemic and pulmonary arterial pressures, central venous pressure (CVP), and core body temperature were continuously monitored and recorded. Inspired and end‐tidal oxygen, carbon dioxide, and sevoflurane concentrations were measured using a Raman spectrometer, calibrated every 80 minutes with three calibration gases of known sevoflurane concentration (1, 2, and 5%). Moreover, at selected times, pulmonary artery occlusion pressure and cardiac output (thermodilution) were measured, and arterial and mixed venous blood samples were collected for pH and blood gas analysis, hemoglobin concentration, hemoglobin oxygen saturation, packed cell volume (PCV) and total protein determination, and lactate concentration measurement. Cardiac index (CI), stroke index (SI), systemic and pulmonary vascular resistance indices, rate‐pressure product, left and right ventricular stroke work indices (LVSWI and RVSWI, respectively), arterial and mixed venous oxygen contents, oxygen delivery, oxygen consumption, and oxygen utilization ratio were calculated. Data were analyzed by a Repeated Measure Latin Square Design followed by a Tukey's test for 2 × 2 comparisons. Arterial pH significantly decreased from 7.40 ± 0.05 to 7.29 ± 0.07 with the administration of increasing concentrations of sevoflurane. Similarly, LVSWI decreased from 3.72 ± 0.60 to 2.60 ± 0.46 g m^?2. Mean arterial pressure, PaO₂, mixed venous pH, CI, SI, and oxygen delivery tended to decrease dose‐dependently, whereas CVP, PaCO₂, Pv CO₂, PCV, and arterial and mixed venous hemoglobin concentrations tended to increase dose‐dependently with the administration of sevoflurane. However, these trends did not reach statistical significance, possibly because of the limited number of animals studied. Sevoflurane seemed to induce dose‐dependent cardiovascular depression in cats.     

新型吸入麻醉剂-七氟醚的研究进展II.兽医药效学

新型吸入麻醉剂七氟醚在犬、猫、马、鼠的 MAC分别为 2 .1 0～ 2 .36 ,2 .5 8,2 .31 ,2 .40～ 2 .5 0 Vol%。像异氟醚那样 ,七氟醚可降低脑血管阻力、脑代谢率、脑耗氧量、心肌收缩功能和血压。七氟醚可引起猫惊厥。虽然猪的心跳在七氟醚麻醉下维持稳定 ,但研究表明犬的心率则升高。七氟醚麻醉下引起心律失常的肾上腺素剂量与异氟醚相似 ,但大大高于氟烷或安氟醚。七氟醚对呼吸道的刺激性明显低于其他吸入麻醉剂。尚未见其肝肾毒性。七氟醚已向理想的吸入麻醉剂方向迈出了更进一步     

Anesthetic and cardiovascular effects of balanced anesthesia using constant rate infusion of midazolam-ketamine-medetomidine with inhalation of oxygen-sevoflurane (MKM-OS anesthesia) in horses

The anesthetic sparring and cardiovascular effects produced by midazolam 0.8 mg/ml-ketamine 40 mg/ml-medetomidine 0.05 mg/ml (0.025 ml/kg/hr) drug infusion during sevoflurane in oxygen (MKM-OS) anesthesia was determined in healthy horses. The anesthetic sparring effects of MKM-OS were assessed in 6 healthy thoroughbred horses in which the right carotid artery was surgically relocated to a subcutaneous position. All horses were intubated and ventilated with oxygen using intermittent positive pressure ventilation (IPPV). The end-tidal concentration of sevoflurane (ET(SEV)) required to maintain surgical anesthesia was approximately 1.7%. Heart rate and mean arterial blood pressure averaged 23-41 beats/min and 70-112 mmHg, respectively. All horses stood between 23-44 min after the cessation of all anesthetic drugs. The cardiovascular effects of MKM-OS anesthesia were evaluated in 5 healthy thoroughbred horses ventilated using IPPV. Anesthesia was maintained for 4 hr at an ET(SEV) of 1.7%. Each horse was studied during left lateral (LR) and dorsal recumbency (DR) with a minimum interval between evaluations of 1 month. Cardiac output and cardiac index were maintained between 70-80% of baseline values during LR and 65-70% of baseline values during DR. Stroke volume was maintained between 75-85% of baseline values during LR and 60-70% of baseline values during DR. Systemic vascular resistance was not different from baseline values regardless of position. MKM-OS anesthesia may be useful for prolonged equine surgery because of its minimal cardiovascular depression in both of lateral and dorsal recumbency.     

新型吸入麻醉剂－七氟醚的研究进展II. 兽医药效学

新型吸入麻醉剂七氟醚在犬、猫、马、鼠的MAC分别为2.10～2.36, 2.58, 2.31, 2.40～2.50 Vol％。像异氟醚那样，七氟醚可降低脑血管阻力、脑代谢率、脑耗氧量、心肌收缩功能和血压。七氟醚可引起猫惊厥。虽然猪的心跳在七氟醚麻醉下维持稳定，但研究表明犬的心率则升高。七氟醚麻醉下引起心律失常的肾上腺素剂量与异氟醚相似，但大大高于氟烷或安氟醚。七氟醚对呼吸道的刺激性明显低于其他吸入麻醉剂。尚未见其肝肾毒性。七氟醚已向理想的吸入麻醉剂方向迈出了更进一步。     

Sevoflurane anesthesia in desert tortoises (Gopherus agassizii).

The effects of sevoflurane on anesthesia induction, recovery, ventricular pressures, heart rate, ventricular pH, blood gas values, and electrolytes were evaluated in desert tortoises (Gopherus agassizii). Tortoises were orotracheally intubated while awake and ventilated manually with 3-7% sevoflurane in oxygen (1 L/min) to achieve desired expired sevoflurane concentrations. Data, consisting of induction time, recovery time, systolic, diastolic, and mean ventricular pressures, heart rate, ventricular pH, blood gas values, and electrolytes, were collected prior to anesthesia and sequentially at 2.50% and 3.75% expired sevoflurane as measured at the junction of the endotracheal tube and the breathing circuit. Blood pressure was measured and blood samples were collected through a 25-ga needle passed through a cardiac access port that was placed while the tortoises were in dorsal recumbency. Mean (+/-SE) induction time was 2.55+/-0.55 min, recovery time was 27.58+/-7.55 min, and duration of anesthesia was 105+/-12 min. Mean (+/-SD) values for systolic, diastolic, and mean ventricular pressures in awake tortoises were 28+/-3 mm Hg, 22+/-2 mm Hg, and 24+/-2 mm Hg, respectively. Sevoflurane (2.5% expired) significantly decreased systolic (14+/-3 mm Hg), diastolic (12+/-1 mm Hg), and mean (13+/-1 mm Hg) ventricular pressures compared with those of awake tortoises. Ventricular pressures did not decrease further with increasing depth of anesthesia. Heart rate (32+/-4 beats/min) did not change significantly under sevoflurane anesthesia. Sevoflurane administration increased ventricular PO2 but did not change Na+, K+, or iCa++ concentrations. Sevoflurane appears to provide safe and effective anesthesia with rapid induction and recovery.     

Effects of propofol-sevoflurane anesthesia on the maternal and fetal hemodynamics blood gases, and uterine activity in pregnant goats

To determine the effects of propofol and sevoflurane on hemodynamics, acid-base balance and uterine activity in pregnant animals, a prospective experimental study was designed by use of ten pregnant goats. Propofol was intravenously administered at a bolus dose of 5 mg/kg and then infused a rate of 0.3 mg/kg/min for 5 min. Following the induction, the animals were incrementally inhaled 2.7 and 4.1% of end-tidal concentration of sevoflurane each for 30 min, and then recovered. The maternal and fetal heart rate (HR), arterial blood pressure (BP) and acid-base balance, the intrauterine pressure (IUP), and the uterine blood flow (UBF) were measured. Following the pre-anesthetic data, the parameters were measured 7 times throughout the anesthetic and recovering periods. The propofol infusion induced 1.37 times of HR increase and produced decrease in PO(2) and a relevant metabolic acidemia in the mother, with no effect in the fetus. Sevoflurane reduced BP in the fetus from 30 (2.7%) to 60 (4.1%) min of inhalation. The uterine contractions disappeared throughout sevoflurane inhalation, and then recurred within 15 min after the cessation of sevoflurane. Propofol injection increases HR, and induces a moderate hypoxemia and metabolic acidemia associated with the suppressed ventilation for pregnant goats, with less effect on the fetal hemodinamics. Sevoflurane causes minimal change in maternal hemodynamics, but induces significant hypotension in the fetus and reduction of uterine activity. These data may be useful in making anesthetic choices combined with analgesia for Caesarian section in goats.     

Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs.

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.     

Cardiovascular effects of sevoflurane in Holstein calves

Objective The purpose of this study was to determine the cardiovascular effects of sevoflurane in calves. Study design Prospective experimental study. Animals Six, healthy, 8–12‐week‐old Holstein calves weighing 80 ± 4.5 (mean ± SEM) kg were studied. Methods Anesthesia was induced by face‐mask administration of 7% sevoflurane in O₂. Calves tracheae were intubated, placed in right lateral recumbency, and maintained with 3.7% end‐tidal concentration sevoflurane for 30 minutes to allow catheterization of the auricular artery and placement of a Swan‐Ganz thermodilution catheter into the pulmonary artery. After instrumentation, administration of sevoflurane was temporarily discontinued until mean arterial pressure was > 100 mm Hg. Baseline values were recorded and the vaporizer output increased to administer 3.7% end‐tidal sevoflurane concentration. Ventilation was controlled to maintain normocapnia. The following were recorded at 5, 10, 15, 30 and 45 minutes after collection of baseline data and expressed as the mean value (± SEM): direct systolic, diastolic, and mean arterial blood pressures; cardiac output; mean pulmonary arterial pressure; pulmonary arterial occlusion pressure, heart rate; and pulmonary arterial temperature. Cardiac index and systemic and pulmonary vascular resistance values were calculated using standard formulae. Arterial blood gases were analyzed at baseline, and at 15 and 45 minutes. Differences from baseline values were determined using one‐way analysis of variance for repeated measures with post‐hoc differences between mean values identified using Dunnet's test (p < 0.05). Results Mean time from beginning sevoflurane administration to intubation of the trachea was 224 ± 9 seconds. The mean end‐tidal sevoflurane concentration at baseline was 0.7 (± 0.11)%. Sevoflurane anesthesia was associated with decreased arterial blood pressure at all sampling times. Mean arterial blood pressure decreased from a baseline value of 112 ± 7 mm Hg to a minimum value of 88 ± 4 mm Hg at 5 minutes. Compared with baseline, arterial pH was decreased at 15 minutes. Pulmonary arterial blood temperature was decreased at 15, 30 and 45 minutes. Arterial CO₂ tension increased from a baseline value of 43 ± 3 to 54 ± 4 mm Hg (5.7 ± 0.4 to 7.2 ± 0.3 kPa) at 15 minutes. Mean pulmonary arterial pressure was increased at 30 and 45 minutes. Pulmonary arterial occlusion pressure increased from a baseline value of 18 ± 2 to 23 ± 2 mm Hg at 45 minutes. There were no significant changes in other measured variables. All calves recovered from anesthesia uneventfully. Conclusion We conclude that sevoflurane for induction and maintenance of anesthesia was effective and reliable in these calves and that neither hypotension nor decreased cardiac output was a clinical concern. Clinical relevance Use of sevoflurane for mask induction and maintenance of anesthesia in young calves is a suitable alternative to injectable and other inhalant anesthetics.     

Low flow anaesthesia with isoflurane and sevoflurane in the dog

The aim of the present study was to compare the safety and efficacy of sevoflurane and isoflurane during low flow anaesthesia (fresh gas flow (FGF) 14 ml/kg/min) as well as to compare the consumption of both anaesthetics. Data were gathered from 60 dogs assigned for surgery under general anaesthesia with an expected duration of 75 minutes or longer. All dogs were induced with 0.6 mg/kg (maximum 25 mg) l-methadone and 1 mg/kg (maximum 25 mg) diazepam i.v.. Anaesthesia was maintained with isoflurane (group 1) or sevoflurane (group 2) in a mixture with 50% O2 and 50% N2O as carrier gases, under controlled ventilation. Monitoring included electrocardiogram, body temperature, the temperature of in- and exspired gases, arterial oxygen saturation, arterial blood pressure as well as a continuous monitoring of inhaled and exhaled gas concentrations (O2, N2O, CO2, isoflurane, sevoflurane). The consumption of isoflurane and sevoflurane as well as the dogs' recovery times were evaluated for both groups. In all groups the inspired oxygen concentrations ranged above the minimum value of 30 Vol% during low flow anaesthesia, with an arterial oxygen saturation above 97%. End tidal concentration of CO2, heart rate and arterial blood pressure were within the physiological ranges and showed no differences between the two groups. Recovery time was significantly shorter after sevoflurane compared to isoflurane anaesthesia, whilst the consumption of sevoflurane was higher than that of isoflurane. Sevoflurane appears to be as clinically safe as isoflurane in low flow anaesthesia. Even considering that sevoflurane is more expensive than isoflurane, the use of the low flow technique decreases the cost of anaesthesia due to the reduced volatile anaesthetic consumption.     

Comparison of the effect of propofol and sevoflurane on the urethral pressure profile in healthy female dogs

OBJECTIVE: To compare the effects of propofol and sevoflurane on the urethral pressure profile in female dogs. ANIMALS: 10 healthy female dogs. PROCEDURE: Urethral pressure profilometry was performed in awake dogs, during anesthesia with sevoflurane at 1.5, 2.0, and 3.0% end-tidal concentration, and during infusion of propofol at rates of 0.4, 0.8, and 1.2 mg/kg/min. A consistent plane of anesthesia was maintained for each anesthetic protocol. Maximum urethral pressure, maximum urethral closure pressure, functional profile length, and functional area were measured. RESULTS: Mean maximum urethral closure pressure of awake dogs was not significantly different than that of dogs anesthetized with propofol at all infusion rates or with sevoflurane at 1.5 and 2.0% end-tidal concentration. Functional area in awake dogs was significantly higher than in anesthetized dogs. Functional area of dogs during anesthesia with sevoflurane at 3.0% end-tidal concentration was significantly lower than functional area for other anesthetic protocols. Individual differences in the magnitude of effects of propofol and sevoflurane on urethral pressures were observed. CONCLUSIONS AND CLINICAL RELEVANCE: Sevoflurane is an alternative to propofol for anesthesia in female dogs undergoing urethral pressure profilometry. Use of these anesthetics at appropriate administration rates should reliably distinguish normal from abnormal maximum urethral closure pressures and functional areas. Titration of anesthetic depth is a critical component of urodynamic testing.     

Anesthetic potency and cardiopulmonary effects of sevoflurane in goats: comparison with isoflurane and halothane.

The anesthetic potency and cardiopulmonary effects of sevoflurane were compared with those of isoflurane and halothane in goats. The (mean +/- SD) minimal alveolar concentration (MAC) was 0.96 +/- 0.12% for halothane, 1.29 +/- 0.11% for isoflurane, and 2.33 +/- 0.15% for sevoflurane. Cardiopulmonary effects of sevoflurane, halothane and isoflurane were examined at end-tidal concentrations equivalent to 1, 1.5 and 2 MAC during either spontaneous or controlled ventilation (SV or CV). During SV, there were no significant differences in respiration rate, tidal volume and minute ventilation between anesthetics. Dose-dependent decreases in both tidal volume and minute ventilation induced by halothane were greater than those by either sevoflurane or isoflurane. Hypercapnia and acidosis induced by sevoflurane were not significantly different from those by either isoflurane or halothane at 1 and 1.5 MAC, but were less than those by halothane at 2 MAC. There was no significant difference in heart rate between anesthetics during SV and CV. During SV, all anesthetics induced dose-dependent decreases in arterial pressure, rate pressure product, systemic vascular resistance, left ventricular minute work index and left ventricular stroke work index. Systemic vascular resistance with isoflurane at 2 MAC was lower than that with sevoflurane. During CV, sevoflurane induced dose-dependent circulatory depression (decreases in arterial pressure, cardiac index, rate pressure product, systemic vascular resistance, left ventricular minute work index and right ventricular minute work index), similar to isoflurane. Halothane did not significantly alter systemic vascular resistance from 1 to 2 MAC.     

Determination of the minimum anesthetic concentration of sevoflurane in thick-billed parrots (Rhynchopsitta pachyrhyncha)

Objective-To determine the minimum anesthetic concentration (MAC) of sevoflurane in thick-billed parrots (Rhynchopsitta pachyrhyncha) and compare MAC obtained via mechanical and electrical stimulation. Animals-15 healthy thick-billed parrots. Procedures-Anesthesia was induced in each parrot by administration of sevoflurane in oxygen. An end-tidal sevoflurane concentration of 2.5% was established in the first bird. Fifteen minutes was allowed for equilibration. Then, 2 types of noxious stimulation (mechanical and electrical) were applied; stimuli were separated by 15 minutes. Responses to stimuli were graded as positive or negative. For a positive or negative response to a stimulus, the target end-tidal sevoflurane concentration of the subsequent bird was increased or decreased by 10%, respectively. The MAC was calculated as the mean end-tidal sevoflurane concentration during crossover events, defined as instances in which independent pairs of birds evaluated in succession had opposite responses. A quantal method was used to determine sevoflurane MAC. Physiologic variables and arterial blood gas values were also measured. Results-Via quantal analysis, mean sevoflurane MAC in thick-billed parrots determined with mechanical stimulation was 2.35% (90% fiducial interval, 1.32% to 2.66%), which differed significantly from the mean sevoflurane MAC determined with electrical stimulation, which was 4.24% (90% fiducial interval, 3.61% to 8.71%). Conclusions and Clinical Relevance-Sevoflurane MAC in thick-billed parrots determined by mechanical stimulation was similar to values determined in chickens and mammals. Sevoflurane MAC determined by electrical stimulation was significantly higher, which suggested that the 2 types of stimulation did not induce similar results in thick-billed parrots.     

Cardiovascular effects of tramadol in dogs anesthetized with sevoflurane

Cardiovascular effects of tramadol were evaluated in dogs anesthetized with sevoflurane. Six beagle dogs were anesthetized twice at 7 days interval. The minimum alveolar concentration (MAC) of sevoflurane was earlier determined in each dog. The dogs were then anesthetized with sevoflurane at 1.3 times of predetermined individual MAC and cardiovascular parameters were evaluated before (baseline) and after an intravenous injection of tramadol (4 mg/kg). The administration of tramadol produced a transient and mild increase in arterial blood pressure (ABP) (P=0.004) with prolonged increase in systemic vascular resistance (SVR) (P<0.0001). Compared with baseline value, mean ABP increased significantly at 5 min (119% of baseline value, P=0.003), 10 min (113%, P=0.027), and 15 min (111%, P=0.022). SVR also increased significantly at 5 min (128%, P<0.0001), 10 min (121%, P=0.026), 30 min (114%, P=0.025), 45 min (113%, P=0.025) and 60 min (112%, P=0.048). Plasma concentrations of tramadol were weakly correlated with the percentage changes in mean ABP (r=0.642, P<0.0001) and SVR (r=0.646, P<0.0001). There was no significant change in heart rate, cardiac output, cardiac index, stroke volume, pulmonary arterial pressure, right atrial pressure and pulmonary capillary wedge pressure. In conclusion, the administration of tramadol produces a prolonged peripheral vascular constriction in dogs anesthetized with sevoflurane, which is accompanied with a transient and mild increase in arterial blood pressure. It also indicated that the degree of vasoconstriction might depend on the plasma concentration of tramadol.     

Cardiovascular effects of propofol alone and in combination with ketamine for total intravenous anesthesia in cats

OBJECTIVE: To compare cardiovascular effects of equipotent infusion doses of propofol alone and in combination with ketamine administered with and without noxious stimulation in cats. ANIMALS: 6 cats. PROCEDURE: Cats were anesthetized with propofol (loading dose, 6.6 mg/kg; constant rate infusion [CRI], 0.22 mg/kg/min) and instrumented for blood collection and measurement of blood pressures and cardiac output. Cats were maintained at this CRI for a further 60 minutes, and blood samples and measurements were taken. A noxious stimulus was applied for 5 minutes, and blood samples and measurements were obtained. Propofol concentration was decreased to 0.14 mg/kg/min, and ketamine (loading dose, 2 mg/kg; CRI, 23 microg/kg/min) was administered. After a further 60 minutes, blood samples and measurements were taken. A second 5-minute noxious stimulus was applied, and blood samples and measurements were obtained. RESULTS: Mean arterial pressure, central venous pressure, pulmonary arterial occlusion pressure, stroke index, cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, oxygen delivery index, oxygen consumption index, oxygen utilization ratio, partial pressure of oxygen in mixed venous blood, pH of arterial blood, PaCO2, arterial bicarbonate concentration, and base deficit values collected during propofol were not changed by the addition of ketamine and reduction of propofol. Compared with propofol, ketamine and reduction of propofol significantly increased mean pulmonary arterial pressure and venous admixture and significantly decreased PaO2. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of propofol by CRI for maintenance of anesthesia induced stable hemodynamics and could prove to be clinically useful in cats.     

The influence of ventilation mode (spontaneous ventilation, IPPV and PEEP) on cardiopulmonary parameters in sevoflurane anaesthetized dogs

The purpose of this study was to investigate the cardiopulmonary influences of sevoflurane in oxygen at two anaesthetic concentrations (1.5 and 2 MAC) during spontaneous and controlled ventilation in dogs. After premedication with fentany-droperidol (5 microg/kg and 0.25 mg/kg intramuscularly) and induction with propofol (6 mg/kg intravenously) six dogs were anaesthetized for 3 h. Three types of ventilation were compared: spontaneous ventilation (SpV), intermittent positive pressure ventilation (IPPV), and positive end expiratory pressure ventilation (PEEP, 5 cm H2O). Heart rate, haemoglobin oxygen saturation, arterial blood pressures, right atrial and pulmonary arterial pressures, pulmonary capillary wedge pressure and cardiac output were measured. End tidal CO2%, inspiratory oxygen fraction, respiration rate and tidal volume were recorded using a multi-gas analyser and a respirometer. Acid-base and blood gas analyses were performed. Cardiac index, stroke volume, stroke index, systemic and pulmonary vascular resistance, left and right ventricular stroke work index were calculated. Increasing the MAC value during sevoflurane anaesthesia with spontaneous ventilation induced a marked cardiopulmonary depression; on the other hand, heart rate increased significantly, but the increases were not clinically relevant. The influences of artificial respiration on cardiopulmonary parameters during 1.5 MAC sevoflurane anaesthesia were minimal. In contrast, PEEP ventilation during 2 MAC concentration had more pronounced negative influences, especially on right cardiac parameters. In conclusion, at 1.5 MAC, a surgical anaesthesia level, sevoflurane can be used safely in healthy dogs during spontaneous and controlled ventilation (IPPV and PEEP of 5 cm H2O).