Cardiopulmonary effects of anesthesia induced and maintained with isoflurane in cats.

OBJECTIVE: To determine the cardiopulmonary effects of anesthesia induced and maintained with isoflurane (ISO) in cats. ANIMALS: 8 healthy cats between 1 and 5 years old. PROCEDURE: Anesthesia was induced with ISO in oxygen. Two anesthetic depths were maintained in each cat; mean alveolar concentrations (MAC) were 1.3 and 2.0 times MAC. Ventilation was either spontaneous or controlled. Each cat received each treatment combination according to a Latin square design. Cardiopulmonary measurements were made after 20 minutes of constant conditions with each combination of anesthetic depth and ventilatory mode. RESULTS: Cardiac index was not different between ISO doses, but 2.0 MAC ISO reduced arterial blood pressure and total peripheral resistance. Cardiac index and systolic arterial blood pressure were reduced by controlled ventilation. The PaCO2 and pulmonary artery pressure were highest in association with 2.0 MAC ISO during spontaneous ventilation. Changes in pHa were attributable to changes in PaCO2. CONCLUSIONS: 2.0 MAC ISO causes hypotension and hypercapnia; however, cardiac index is maintained. Hypercapnia may be abolished with controlled ventilation, but at the expense of reduced cardiac index. 1.3 MAC ISO results in minimal cardiopulmonary depression, especially when healthy cats are allowed to breathe spontaneously. CLINICAL RELEVANCE: Hypoventilation associated with untoward physiologic responses to 2.0 MAC may be overcome with controlled ventilation, but results in marked reduction in cardiovascular performance; thus, use of 2.0 MAC ISO should be avoided in cats.

Cardiopulmonary effects of desflurane in cats.

OBJECTIVE: To evaluate the cardiopulmonary effects of 2 anesthetic planes of desflurane (DES) during spontaneous ventilation (SV) and controlled ventilation (CV) in cats. DESIGN: Repeated Latin square. ANIMALS: Eight healthy adult cats. PROCEDURE: Each cat received 1.3 times the minimum alveolar concentration (MAC) of DES and 1.7 MAC of DES in oxygen during CV and SV. The data were analyzed as a repeated measures design. Heart rate, cardiac output, arterial blood pressure, pulmonary artery pressure, respiratory rate, PaO2, PaCO2, pHa, PCV, and serum total protein concentration were measured during each treatment. Stroke volume, cardiac index, total peripheral resistance, and oxygen consumption were calculated. RESULTS: Cardiac index and stroke volume were not different between 1.3 and 1.7 MAC of DES, but CV decreased cardiac index and stroke volume (P < 0.05). Systolic arterial pressure was decreased during 1.7 MAC of DES and during CV. Mean arterial blood pressure was decreased at 1.7 MAC during CV, but not SV. The PaCO2 was higher at 1.7 MAC than at 1.3 MAC during SV. Spontaneously ventilating cats at 1.7 MAC had higher pulmonary artery pressures than other treatments. The PCV was decreased during CV. CONCLUSION: 1.7 MAC of DES causes decreased systolic and mean arterial pressures and marked hypercapnia, but cardiac index is not affected. The hypercapnia is probably responsible for the increased pulmonary artery pressures in the spontaneously ventilating cats during 1.7 MAC. Hypercapnia can be corrected by CV but this reduces cardiac output.

Cardiovascular effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane in experimentally induced hypothyroidism in dogs.

This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (Q), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentration were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and PACO2 maintained between 38 to 42 mm Hg. Isoflurane caused significant (P < .05) dose-dependent reduction in Q, SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower Q, SV, SAP, and MAP PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in Q, SV, and arterial pressure.

The minimum alveolar concentration of desflurane in cats.

Eight adult cats, 4 male and 4 female, (3.5 +/- 0.9 [SD] kg) were used to determine the minimum alveolar concentration (MAC) of desflurane. Desflurane (DES) anesthesia was induced in a 20 L chamber with an oxygen inflow of 10 L/min and the DES vaporizer set at 18%. After 3.5 +/- 0.5 min, the cats were removed from the chamber and anesthesia was maintained via mask (14% DES, 3L/min O2) until successful intubation. Anesthesia was maintained with DES in oxygen at a flow of at least 200 mL/kg/min through a nonrebreathing circuit. The time from the start of induction to completion of intubation was 6.2 +/- 1.1 min. Esophageal temperature was maintained between 37.8 degrees C and 38.6 degrees C. Hand-collected end-tidal gas samples were obtained from a catheter positioned inside the lumen of the endotracheal tube. Inspired and end-tidal DES concentrations were measured with a Biochem 8100 anesthetic agent monitor that was calibrated with known gas standards and modified to accept hand-collected samples. A constant alveolar concentration of DES was maintained for at least 15 minutes, then a clamp was applied to the tail and the cat observed for gross purposeful movement. The end-tidal DES was then increased (if a positive response) or decreased (if a negative response) by 20% and the test repeated after 15 minutes of constant conditions. The final iteration was 10%. The MAC of DES in these cats was 9.79 +/- 0.70 vol %. The FA/FI ratio for desflurane was always greater than 0.97.

Gastric myoelectric and motor activity in dogs after isoflurane anesthesia.

To characterize the effects of isoflurane on gastric motility, gastric electrical and contractile activities were assessed in six healthy adult dogs before and after recovery from anesthesia. Baseline recordings (fasting and fed state) were obtained in unanesthestized dogs 8 days after implantation of serosal electrodes and strain-gauge force transducers. After an overnight fast, dogs were anesthetized with 1.3 minimum alveolar concentration (MAC) isoflurane for 4.5 hours (approximately 6 MAC hours). No other anesthetic or sedative drugs were administered. During anesthesia, ventilation was mechanically controlled to maintain arterial carbon dioxide tension at 36 +/- 4 mm Hg. Gastric electrical and contractile activities (fasting and fed state) were recorded again 18 hours after recovery from isoflurane anesthesia. Recordings were analyzed to determine gastric slow-wave frequency, presence of slow-wave dysrhythmias, slow-wave propagation velocity, coupling of contractions to slow waves, a motility index based on relative contractile amplitudes, and onset and duration of contractions after a standardized meal. The only variable that was significantly decreased 18 hours after 6 MAC hours of isoflurane anesthesia was the gastric motility index during fasting-state phase III. This decrease was not apparent in the fed-state test periods. Our results suggest that, with the exception of gastric motility index during fasting-state phase III, variables for gastric electrical and contractile activities in dogs are unaffected by isoflurane 18 hours after anesthesia.

Modification of a nonrebreathing circuit adapter to prevent barotrauma in anesthetized patients.

Barotrauma, pneumothorax, and pneumomediastinum occurred in two anesthetized cats in which the waste gas outlet of a nonrebreathing circuit was occluded. To prevent any similar cases of barotrauma, we have modified our nonrebreathing circuit adapters by inserting a 15 cm H2O PEEP valve into the gas pathway of the nonrebreathing circuit adapter. This PEEP valve prevents the circuit and airway pressures from exceeding 15 cm H2O if the pop-off valve of the nonrebreathing circuit adapter is inadvertently left closed.

Cardiopulmonary effects of three prolonged periods of isoflurane anesthesia in an adult elephant.

An adult 3,500-kg female African elephant was anesthetized 3 times for treatment of subcutaneous fistulas over the lateral aspect of each cubitus (anesthesia 1 and 2) and for repair of a fractured tusk (anesthesia 3). Lateral recumbency and anesthesia were achieved with etorphine (anesthesia 1 and 2) or etorphine and azaperone (anesthesia 3). The elephant's trachea was intubated and anesthesia was maintained by use of isoflurane and oxygen delivered via 2 standard large animal anesthesia machines joined in parallel. The range of total recumbency time was 2.4 to 3.3 hours. Breathing and heart rates, systemic arterial pressure, rectal temperature, PaO2, pH, and end-tidal gases were monitored. After administration of etorphine, measurements were made while the air-breathing elephant was recumbent, then every 5 minutes (cardiovascular) or 15 minutes (blood gases) after commencement of administration of isoflurane and oxygen. Tachycardia and hypertension were detected after administration of etorphine, but heart rate and systemic arterial pressure decreased to within normal ranges after administration of isoflurane and oxygen. The elephant remained well oxygenated while anesthetized and breathing a high oxygen mixture. The elephant had an uneventful recovery from each anesthesia.

Cardiopulmonary effects of positioning pregnant cows in dorsal recumbency during the third trimester.

The uterine hemodynamic response to maternal positioning in dorsal recombency was evaluated in 7 conscious pregnant cows during the third trimester. Anesthetic or sedative drugs were not administered. Uterine artery flow was measured, using a previously implanted ultrasonic flow probe. Catheters implanted in the uterine artery and vein were used for measurement of blood pressure and for blood sample collections. Heart rate, systemic arterial pressure, uterine arterial blood flow, arterial and venous oxygen and carbon dioxide tensions, and pH were measured in cows in standing position. Cows were cast with ropes and positioned in dorsal recumbency, then measurements were repeated at 15 and 30 minutes. Compared with standing measurements, dorsal recumbency caused 50% increase in heart rate and 44% increase in arterial blood pressure. Uterine artery flow did not change significantly. Despite increased ventilation, arterial oxygenation was reduced during dorsal recombency. There were minimal differences between measurements at 15 and 30 minutes of dorsal recumbency.

Cardiopulmonary and behavioral responses to computer-driven infusion of detomidine in standing horses.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1. (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [loge detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [loge detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). (ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical and haematological changes following prolonged halothane anaesthesia in horses.

Six healthy horses were anaesthetised with halothane (1.2 times the horse minimal alveolar concentration) in oxygen for more than 12 hours. Serum bilirubin, aspartate aminotransferase, alkaline phosphatase and L-iditol dehydrogenase values were significantly (P < 0.05) increased for up to nine days after anaesthesia. These changes suggest an anaesthesia related liver dysfunction. Creatine kinase increased to an average of more than 1400 IU litre-1 24 hours after anaesthesia and this change is indicative of muscle cell disruption. Renal-associated biochemical results, (that is serum creatinine and inorganic phosphate concentrations) were significantly increased transiently and are indicative of reduced renal function during and immediately after anaesthesia. Plasma concentrations of eicosanoids (6-keto-PGF1a, PGF2a, PGE and thromboxane) following anaesthesia were not different from preanaesthetic values. The magnitude of liver and muscle cell related increases in serum enzyme activities resulting from prolonged halothane anaesthesia was in excess of that previously reported for anaesthesia of shorter duration.

Circulatory and respiratory responses of spontaneously breathing, laterally recumbent horses to 12 hours of halothane anesthesia.

Cardiovascular and respiratory changes that accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2 and PaCO2 did not significantly change during the 12 hours of study, PVO2 increased significantly (P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time (significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-keto-prostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Evaluation of the Doppler ultrasonic method of measuring systolic arterial blood pressure in cats.

The accuracy of the Doppler technique for indirect systolic blood pressure measurement was assessed in 16 anesthetized cats. Eight cats were anesthetized with isoflurane and 8 were anesthetized with halothane. Anesthetic depth and mode of ventilation were varied to obtain a wide range of arterial blood pressure. A Doppler transducer was placed on the palmer surface of the left forelimb over the common digital branch of the radial artery to detect blood flow, and a blood pressure monitoring cuff with a width 37% the limb circumference was placed half way between the elbow and the carpus. To enable direct arterial pressure measurements, the left femoral artery was catheterized and the blood pressure waveforms recorded simultaneously. Systolic blood pressure measured by use of the Doppler ultrasonic technique was significantly lower than that obtained from the femoral artery catheter. Using linear regression, we determined a clinically useful calibration adjustment for Doppler indirect blood pressure measurement in cats: femoral systolic pressure = Doppler systolic pressure + 14 mm of Hg.

Cardiopulmonary responses to experimentally induced gastric dilatation in isoflurane-anesthetized dogs.

Gastric dilatation was experimentally induced in 6 anesthetized dogs maintained with constant-dose isoflurane in oxygen. An intragastric balloon was used to distend the stomach with a constant 30 mm of Hg pressure for 3.5 hours. The PaCO2 was maintained between 35 and 45 mm of Hg, using intermittent positive-pressure ventilation. Cardiopulmonary measurements prior to stomach distension (baseline) were compared with measurements taken during 0.1, 0.5, 1.0, 1.5, 2.5, and 3.5 hours of stomach distension by analyzing the change from baseline in a randomized-block analysis with each dog as a block. After distending the stomach, cardiac index increased (P less than 0.01) from 1.5 to 3.5 hours. Stroke volume did not change, thus the increase in the cardiac index was attributable to an increase in heart rate. During inflation, increases were observed in systemic arterial, pulmonary arterial, and right atrial pressure. Respiratory frequency was unchanged; however, to maintain PaCO2 constant, it was necessary to progressively increase peak airway pressure. Although PaO2 tended to decrease during gastric dilation, the dogs were never hypoxemic. These results indicate that when our methods are used to maintain a constant anesthetic dose of isoflurane in oxygen, an observed increase in cardiovascular performance is expected. This differs from other studies in anesthetized dogs that have shown reduction in cardiovascular performance following gastric dilatation.

The case for nonrebreathing circuits for very small animals.

The advantages of using modern nonrebreathing systems in very small patients far outweighs the few disadvantages. Their use results in more precise control of anesthetic depth, better ventilation and gas exchange, and a lower incidence of mechanical problems.

Thermodilution estimation of cardiac output at high flows in anesthetized horses.

The purpose of this study was to compare the thermodilution technique for estimation of cardiac output with the indocyanine green dye dilution technique at flows between 10 and 39 L/min in halothane-anesthetized horses. The estimation of area of dye dilution cardiac output curves was made by using the fore-'n-aft (FA) triangle method. This shorthand technique was compared with logarithmic exponential extrapolation and summation (extrapolated area), using 64 cardiac output curves. Then, 256 simultaneous thermodilution measurements were compared with dye dilution measurements calculated by use of the FA technique. Forty milliliters of iced 0.9% NaCl solution containing 15 mg of indocyanine green dye was used as the indicator. This was delivered in less than 1 second to the right atrium, using a power injector. A thermistor positioned in the pulmonary artery detected the thermal indicator. Blood was withdrawn from the carotid artery through a densitometer cuvette to measure the dye concentration. The FA estimations of area were higher than those determined by use of extrapolated area. A multiplicative adjustment of 0.837 was estimated. On average, thermodilution estimates of cardiac output exceeded the adjusted FA determinations. Using a weighted linear regression, we determined the following calibration adjustment: thermal dilution cardiac output/1.048 = indocyanine green dye dilution cardiac output.

General anesthesia for horses with specific problems.

We have discussed anesthetic techniques, special considerations, and expected complications involved in anesthetizing horses for abdominal, orthopedic, and head and neck surgery, and myelography and have described expected physiologic dysfunction that may require changes in anesthetic technique or supportive measures. The objective is high-quality patient care and reduction in anesthesia-related morbidity and death.

Effect of body posture on cardiopulmonary function in horses during five hours of constant-dose halothane anesthesia.

Cardiovascular and respiratory functions were serially characterized in 7 healthy, spontaneously breathing, adult horses (from which food had been withheld) during 5 hours of constant 1.06% alveolar halothane (end-expired halothane concentration of 1.06%; equivalent to 1.2 times the minimal alveolar anesthetic concentration for horses). To enable comparison of temporal results in relation to 2 body postures, horses were studied in lateral recumbency (LR) and dorsal recumbency (DR) on separate occasions. Temporal changes in results of measures of circulation previously reported from this laboratory for horses in LR were confirmed (ie, a time-related increase in systemic arterial blood pressure, cardiac output, stroke volume, and PCV). During DR, systemic arterial blood pressure was initially significantly (P less than 0.05) greater and pulmonary artery pressure less than results at comparable periods during LR. Differences ceased to exist with duration of anesthesia. Except for a greater heart rate at hour 5 of DR, no other significant differences in circulation were found between LR and DR. In general, except for PaO2, measures of ventilation did not change with time in either LR or DR. The PaO2 was significantly greater during LR, compared with DR, but the average did not change significantly with time in either body posture.

Cardiopulmonary effects of ephedrine in halothane-anesthetized horses.

The cardiopulmonary effects of intravenous (i.v.) administration of the sympathomimetic drug ephedrine during two different levels of halothane anesthesia [end-tidal concentration of 1.37% (light anesthesia) and 2.1% (deep anesthesia)] were studied in eight horses. Anesthesia was induced and maintained using only halothane in O2. Ventilation was controlled to maintain a Paco2 of 38-42 mmHg. Following instrumentation and stabilization of the horse at the halothane concentration being studied, baseline measurements of cardiac output (Q), arterial blood pressure (AP), pulmonary artery pressure, heart rate, Pao2, Paco2 and pH were made. Ephedrine was then administered (0.06 mg/kg i.v.) and these measurements repeated at 10, 20, 30, 45 and 60 min after injection. At both doses of halothane there was a significant (P less than 0.05) increase in Q, stroke volume (SV), and systolic AP following ephedrine administration. In addition, at 2.1% halothane, ephedrine administration resulted in a significant (P less than 0.05) increase in mean AP and Pao2 and a decrease in total peripheral resistance. The increase in systolic AP, Q, and SV was significantly (P less than 0.05) greater at 2.1% halothane than at 1.37% halothane. Ephedrine administration to horses during both light and deep halothane anesthesia results in an increase in AP that is due to an increase in Q and SV.