Cardiopulmonary effects of a halothane/oxygen combination in hypovolemic cats.

The cardiopulmonary effects of a halothane/oxygen combination were studied in eight cats subjected to a 25% whole blood volume loss. Test parameters included cardiac output measured via thermodilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and blood gas analysis. Values for cardiac index, stroke volume and systemic vascular resistance were calculated from these data. Posthemorrhage cardiac output, cardiac index, stroke volume and measurements of arterial blood pressure were significantly decreased (p less than 0.05). Heart rate remained unchanged. Following induction of halothane anesthesia the above parameters experienced a further significant decline (p less than 0.05) from their immediate preanesthetic (i.e. posthemorrhage) values. Heart rate also significantly decreased (p less than 0.05). Thirty minutes following the cessation of halothane anesthesia these values returned to near-hemorrhage levels, being above their respective preanesthetic values. Systemic vascular resistance initially rose, peaking ten minutes into halothane anesthesia, before gradually falling to prehemorrhage values at the end of halothane anesthesia. Following hemorrhage, respiratory rate demonstrated a transient increase, associated with an arterial CO2 tension fall, before returning to initial values at the preanesthetic time. During halothane anesthesia respiratory rate remained unchanged whereas arterial CO2 tension rose significantly (p less than 0.05) and pH declined slightly from preanesthetic readings. These returned to prehemorrhage values 30 minutes following the cessation of halothane anesthesia.     

Cardiopulmonary effects of a halothane/oxygen combination in healthy cats.

The effects of a halothane/oxygen combination on the cardiopulmonary function of 11 healthy cats were studied. Test parameters included cardiac output, measured via thermo-dilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and blood gas analysis. Values for systemic vascular resistance, cardiac index and stroke volume were calculated from these data. Cardiac output, cardiac index, heart rate, stroke volume, arterial blood pressure (systolic, diastolic and mean) and arterial blood pH were significantly decreased (p less than 0.001). Respiratory rate was also significantly decreased (p less than 0.007) with arterial CO2 tension being significantly increased (p less than 0.001). Statistically significant changes, where seen, persisted for the duration of the anesthetic period. Arterial O2 tension and systemic vascular resistance remained unchanged. All parameters returned to near pretest values within 30 minutes following cessation of halothane anesthesia.     

Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane, and enflurane

The cardiopulmonary effects of sevoflurane (mean, 2·6, 3·8–3·9 and 5·2 per cent) were compared with those of halothane (1·2, 1·8 and 2·4 per cent), enflurane (2·4, 3·6 and 4·8 per cent) and isoflurane (1·6, 2·4 and 3·2–3·3 per cent) at end-tidal concentrations equivalent to 1, 1·5 and 2 minimal alveolar concentrations (macs) during spontaneous or controlled ventilation (sv or cv) in 57 cats. Cats were assigned to four groups of nine animals each in sv trial and four groups of five or six animals each in cv trial. During sv, respiration rate was decreased by sevoflurane and isoflurane at 2 mac and by enflurane at each mac multiple when compared with control values, whereas halothane increased respiration rate at 2 mac. The degree of hypercapnia and acidosis induced by sevoflurane was not different from that induced by isoflurane and was less than that induced by halothane at 1 to 1·5 mac or enflurane at 2 mac. During sv and cv, four anaesthetics decreased heart rate at 2 mac when compared with control values, but there was no significant difference between anaesthetics. Sevoflurane, like halothane and isoflurane, induced hypotension at 2 mac when compared with 1 mac.     

Cardiopulmonary and behavioral effects of fentanyl-droperidol in cats

The combination of the narcotic fentanyl (0.4 mg/ml) and the tranquilizer droperidol (20 mg/ml) was injected into 12 healthy adult cats at a rate of 1 ml/9 kg of body weight, sc. Arterial blood pressure, heart rate, respiratory frequency, PaCO2, and PaO2, arterial pH (pHa), and rectal temperature were measured before and 30, 60, 90, and 120 minutes after injection of fentanyl-droperidol. Respiratory frequency was decreased significantly (P less than 0.05) and heart rate increased significantly (P less than 0.05) at all measurement intervals after drug administration. Observed decrements in arterial blood pressure were not significant. Arterial PO2, PCO2, and pH did not change significantly. A significant (P less than 0.05) decrease in body temperature was measured 90 minutes after drug administration. All cats were calm, tractable, and frequently assumed lateral recumbency after administration of fentanyl-droperidol. This maximal tranquil state was determined to be 30 to 60 minutes after drug administration.     

Hepatic effects of halothane and isoflurane anesthesia in goats

OBJECTIVE: To determine hepatic effects of halothane and isoflurane anesthesia in young healthy goats. DESIGN: Randomized prospective clinical trial. ANIMALS: 24 healthy 9-month-old female goats. PROCEDURE: Goats were sedated with xylazine hydrochloride and ketamine hydrochloride and anesthetized with halothane (n = 12) or isoflurane (12) while undergoing tendon surgery. End-tidal halothane and isoflurane concentrations were maintained at 0.9 and 1.2 times the minimal alveolar concentrations, respectively, and ventilation was controlled. Venous blood samples were collected approximately 15 minutes after xylazine was administered and 24 and 48 hours after anesthesia, and serum aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT) activities and bilirubin concentration were measured. Goats were euthanatized 25 or 62 days after anesthesia, and postmortem liver specimens were submitted for histologic examination. RESULTS: All goats recovered from anesthesia and survived until euthanasia. Serum SDH, GGT, and ALP activities and bilirubin concentration did not increase after anesthesia, but serum AST activity was significantly increased. However, serum hepatic enzyme activities were within reference limits at all times in all except 1 goat in which serum AST activity was high 24 and 48 hours after anesthesia. This goat had been anesthetized with halothane and had the longest duration of anesthesia. No clinically important abnormalities were seen on histologic examination of liver specimens. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that use of halothane or isoflurane for anesthesia in young healthy goats is unlikely to cause hepatic injury.     

Cardiopulmonary effects of three different anaesthesia protocols in cats.

To develop an alternative anaesthetic regimen for cats with cardiomyopathy, the cardiopulmonary effects of three different premedication-induction protocols, followed by one hour maintenance with isoflurane in oxygen: air were evaluated in six cats. Group I: acepromazine (10 microg/kg) + buprenorphine (10 microg/kg) IM, etomidate (1-2 mg/kg) IV induction. Group II: midazolam (1 mg/kg) + ketamine (10 mg/kg) IM induction. Group III: medetomidine (1.5 mg/m2 body surface) IM, propofol (1-2 mg/kg) IV induction. Heart rate, arterial blood pressure, arterial blood gases, respiration rate, and temperature were recorded for the duration of the experiment. In group I the sedative effect after premedication was limited. In the other groups the level of sedation was sufficient. In all groups premedication resulted in a reduced blood pressure which decreased further immediately following induction. The reduction in mean arterial pressure (MAP) reached statistical significance in group I (142+/-22 to 81+/-14 mmHg) and group II (153+/-28 to 98+/-20 mmHg) but not in group III (165+/-24 to 134+/-29 mmHg). Despite the decrease in blood pressure, MAP was judged to have remained within an acceptable range in all groups. During maintenance of anaesthesia, heart rate decreased significantly in group III (from 165+/-24 to 125+/-10 b.p.m. at t=80 min). During anaesthesia the PCO2 and PO2 values increased significantly in all groups. On the basis of the results, the combination acepromazine-buprenorphine is preferred because heart rate, MAP, and respiration are acceptable, it has a limited sedative effect but recovery is smooth.     

Cardiopulmonary effects of prolonged anesthesia via propofol-medetomidine infusion in ponies

OBJECTIVE: To determine cardiopulmonary effects of total IV anesthesia with propofol and medetomidine in ponies and effect of atipamezole on recovery. ANIMALS: 10 ponies. PROCEDURE: After sedation was induced by IV administration of medetomidine (7 microg/kg of body weight), anesthesia was induced by IV administration of propofol 12 mg/kg) and maintained for 4 hours with infusions of medetomidine (3.5 microg/kg per hour) and propofol 10.07 to 0.11 mg/kg per minute). Spontaneous respiration was supplemented with oxygen. Cardiopulmonary measurements and blood concentrations of propofol were determined during anesthesia. Five ponies received atipamezole (60 microg/kg) during recovery. RESULTS: During anesthesia, mean cardiac index and heart rate increased significantly until 150 minutes, then decreased until cessation of anesthesia. Mean arterial pressure and systemic vascular resistance index increased significantly between 150 minutes and 4 hours. In 4 ponies, PaO2 decreased to < 60 mm Hg. Mean blood propofol concentrations from 20 minutes after induction onwards ranged from 2.3 to 3.5 microg/ml. Recoveries were without complications and were complete within 28 minutes with atipamezole administration and 39 minutes without atipamezole administration. CONCLUSIONS AND CLINICAL RELEVANCE: During total IV anesthesia of long duration with medetomidine-propofol, cardiovascular function is comparable to or better than under inhalation anesthesia. This technique may prove suitable in equids in which prompt recovery is essential; however, in some animals severe hypoxia may develop and oxygen supplementation may be necessary.     

Cardiopulmonary effects of using carbon dioxide for laparoscopic surgery in cats

The cardiopulmonary effects of capnoperitoneum were investigated in 8 spontaneously breathing, young adult female cats undergoing laparoscopic pancreatic biopsy (intra-abdominal pressure 12 mmHg). Cats were premedicated with acepromazine and hydromorphone, induced with ketamine and diazepam, and maintained using an end-tidal isoflurane concentration of 1.13% in 100% oxygen. Direct systemic arterial blood pressure, heart and respiratory rates, end-tidal carbon dioxide (CO(2)), and isoflurane were recorded every 5 min before insufflation (baseline), during insufflation of the abdomen with CO(2), and following desufflation. Arterial blood samples were drawn at baseline, at 10 and 30 min of insufflation, and 5 min after desufflation for blood gases. The significant findings (P < 0.05) were as follows: insufflation produced an increase in heart rate (5 to 15 min and at 30 min), mean arterial blood pressure (25 to 30 min), and diastolic arterial blood pressure (10 to 30 min). After desufflation, respiratory rate increased for 15 min. The changes were within physiologically acceptable limits in these healthy, anesthetized cats despite no artificial maintenance of minute ventilation.     

Cardiopulmonary and acid-base effects of desflurane and sevoflurane in spontaneously breathing cats

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO2), arterial blood pH (pH), arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. Anesthesia was induced with propofol (8+/-2.3mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test (P<0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO2 increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20-T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously.     

Cardiopulmonary effects of a ketamine/acepromazine combination in hypovolemic cats.

The cardiopulmonary effects of a ketamine/ acepromazine combination was studied in ten cats subjected to a 25% whole blood volume loss. Test parameters included cardiac output, measured via thermodilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and blood gas analysis. Values for cardiac index, stroke volume and systemic vascular resistance were calculated from these data. Posthemorrhage, cardiac output, cardiac index, stroke volume, heart rate and measurements of arterial blood pressure were significantly decreased (p less than 0.05). Following the induction of ketamine/ acepromazine anesthesia, cardiac output, cardiac index, stroke volume and heart rate showed mild but statistically insignificant declines and were above their respective posthemorrhage values 120 min into ketamine/ acepromazine anesthesia. Measurements of arterial blood pressure showed further declines from their respective posthemorrhage values that were statistically significant (p less than 0.05). Following hemorrhage, respiratory rate increased significantly (p less than 0.05), associated with a fall in arterial CO2 tension. During ketamine/ acepromazine anesthesia, respiratory rate showed a dramatic and significant decline (p less than 0.05) with arterial CO2 tension rising to prehemorrhage values. Systemic vascular resistance, arterial O2 tension and pH remained essentially unchanged throughout the experimental period.     

Immediate and long-term effects of halothane anesthesia on equine platelet function

The acute and long-term quantitative and qualitative effects of halothane anesthesia on equine platelet performance were studied in fourteen horses. Horses were anesthetized with only halothane in O2 for about 8.0 MAC hours. Platelet numbers declined during the anesthetic period but returned to normal within 24 h. Platelet aggregation was significantly diminished during the anesthetic period and for up to 4 days after anesthesia. A period of hyperaggregability occurred at the 7th day.     

Cardiopulmonary effects of a ketamine hydrochloride/acepromazine combination in healthy cats.

The effect of a ketamine hydrochloride/acepromazine combination on the cardiopulmonary function of 11 healthy cats was studied. Test parameters included cardiac output, measured by thermodilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and arterial blood gas analysis. Values for systemic vascular resistance, cardiac index and stroke volume were calculated. The cardiac output, cardiac index, stroke volume, arterial blood pressure and arterial blood pH decreased significantly (p less than 0.006). The arterial CO2 increased significantly (p less than 0.006). All changes occurred during the five to 45 minute postinduction time period. The heart rate, respiratory rate, arterial O2 and systemic vascular resistance were not significantly altered. The anesthetic regime maintained an adequate plane of surgical anesthesia for 30-45 minutes.     

Arrhythmogenicity of dopamine and its effects on hemodynamics in dogs under halothane anesthesia

The arrhythmogenicity of dopamine, its effects on cardiac function, hemodynamics, and diuresis under halothane anesthesia were evaluated in dogs. The induction time of arrhythemias and the effect of arrhythmias on cardiac function, hemodynamics, and diuresis were determined after infusion of dopamine for 30-min period at increasing doses of 3, 5, 7, 10, and 15 micrograms/kg/min. The results were as follows. 1. Arrhythmia induction percentage was 28.6% at 5 micrograms/kg/mn, 42.9% at 7 micrograms/kg/min, 25% at 10 micrograms/kg/min, and 41.7% at 15 micrograms/kg/min. The induction time of arrhythemias (sec) was 459 at 5 micrograms/kg/min, 332 at 7 micrograms/kg/min, 152 at 10 micrograms/kg/min, and 279 at 15 micrograms/kg/min. No arrhythmias were present at 3 micrograms/kg/min. 2. Heart rate and myocardial oxygen consumption was increased in the arrhythmia-induced group compared to the non-arrhythmia-induced group. 3. Myocardial contractility, mean aortic pressure, mean pulmonary arterial pressure, and diuresis increased dose-dependently in the non-arrhythmia-induced group; however, these measures were increased in the arrhythmia-induced group without regard to dose.     

Cardiopulmonary effects of romifidine and detomidine used as premedicants for ketamine/halothane anaesthesia in ponies

The cardiopulmonary effects of romifidine at 80 microg/kg (R80) or 120 pg/kg (R120), and detomidine at 20 pg/kg (D20) when used as premedicants for ketamine/halothane anaesthesia were investigated in six ponies. Using a blinded crossover design, acepromazine (0-04 mg/kg) was administered followed by the alpha-2 agonist. Anaesthesia was induced with ketamine at 2.2 mg/kg and maintained with halothane (expired concentration 1.0 per cent) in oxygen for three hours. During anaesthesia, arterial blood pressure, cardiac index, PaO2 and PmvO2 decreased, and systemic vascular resistance and PaCO2 increased. The cardiac indices for R80, R120 and D20 were, respectively, 39, 39 and 32 ml/kg/minute at 30 minutes and 29, 29 and 26 ml/kg/minute at 180 minutes. The alpha-2 agonists had similar cardiovascular effects, but PaO2 was significantly lower with R120. The quality of anaesthesia was similar in all three groups.     

Comparison of the hemodynamic effects of halothane alone and halothane combined with epidurally administered morphine for anesthesia in ventilated dogs

The hemodynamic effects of 1.5 minimal alveolar concentration of halothane alone (1.6% end-tidal) and 1.5 minimal alveolar concentration of halothane (1.1% end-tidal concentration) combined with epidurally administered morphine were compared during controlled ventilation in 10 dogs used on 2 occasions and randomly allocated to 2 groups. Arterial blood pressure, cardiac index, stroke volume, left ventricular work, and pulmonary arterial pressure were significantly (P less than 0.05) higher in dogs of the morphine-treated group before administration of morphine. After epidural administration of morphine (0.1 mg/kg of body weight diluted in 0.26 ml of saline solution/kg), hemodynamic changes were not observed, and the aforementioned variables remained significantly (P less than 0.05) higher than values in dogs of the halothane only group. Compared with halothane (1.6%) alone, the reduction in halothane end-tidal concentration (1.1%) associated with epidurally administered morphine is beneficial in maintaining hemodynamic function.     

Hepatic necrosis following halothane anesthesia in goats

One goat anesthetized with thiamylal sodium, xylazine, and halothane for repair of an abominal hernia, and 7 of 29 goats similarly anesthetized for an experiment unrelated to considerations of anesthesia, developed signs of hepatic failure within 24 hours of anesthesia. Affected goats had high values for serum aspartate transaminase and serum total bilirubin by 12 to 24 hours after induction of anesthesia. Necropsy of the 8 affected goats revealed centrilobular to massive hepatic necrosis (8 of 8), brain lesions consistent with hepatic encephalopathy (3 of 4), and acute renal tubular necrosis (6 of 6). Two unaffected goats had no hepatic necrosis. Causes of hepatic necrosis other than those related to anesthesia (eg, infectious agents, toxins) were ruled out by lack of supporting necropsy findings or were considered unlikely because of lack of opportunity for exposure. Hepatic lesions in these goats closely resembled those described in human beings with halothane-associated hepatic injury, although in both species these lesions are nonspecific at the gross and light microscopic levels. The pathogenesis of halothane-associated hepatic injury in goats, as in human beings, remains to be determined.