Intraoperative detection of changes in left ventricular segmental wall motion by transesophageal two-dimensional echocardiography.
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Biomedical subjects
Publications and source records attributed to M K Cahalan.
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When the aorta must be temporarily occluded at the suprarenal or supraceliac levels during surgery, the resulting large increase in afterload may make the myocardium ischemic, even though systemic and pulmonary artery pressures and cardiac output are maintained at normal levels. These traditional indices of myocardial well-being do not appear to be sufficiently sensitive, since cardiac complications are still the most frequent cause of perioperative death and morbidity after aortic reconstruction. To evaluate two-dimensional transesophageal echocardiography as a monitor of myocardial well-being, we studied 24 American Society of Anesthesiologists physical status class III or IV adult patients who were undergoing aortic reconstruction and occlusion at the supraceliac (n = 12), suprarenal-infraceliac (n = 6), or infrarenal (n = 6) level. In addition to traditional monitors, we used a gastroscope tipped with a special 3.5 MHz two-dimensional echocardiographic transducer (Diasonics) that was placed in the esophagus to give a cross-sectional view of the left ventricle through the base of the papillary muscles. The hemodynamic effects of clamping the aorta were managed by administration of vasodilating drugs, anesthetics, and fluids to keep systemic and pulmonary arterial pressures normal. Occlusion at the supraceliac level caused major increases in left ventricular end-systolic and end-diastolic areas, decreases in ejection fraction, and frequent wall motion abnormalities; these changes were not detected by conventional monitoring devices. Occlusion at the suprarenal-infraceliac level caused similar but smaller changes, and occlusion at the infrarenal level caused only minimal cardiovascular effects. We conclude that the two-dimensional transesophageal echocardiogram offers promise as an intraoperative monitoring device.
To determine whether brief periods of hypoxia could produce hepatic injury, we pretreated Sprague-Dawley rats with phenobarbital, deprived them of food for 24 hr, and then exposed them to various hypoxic mixtures of nitrogen and oxygen for various lengths of time. Rats exposed to 6% oxygen for 15 or more minutes had centrilobular injury, the severity of which was directly related to the length of exposure (r = 0.71). Extrapolation of these data indicated that no injury would occur if exposures were less than 5 min. Experiments using lower concentrations of oxygen did not reveal hepatic injury, probably because death of the animals occurred before the appearance of detectable injury of the liver. Feeding animals before imposition of hypoxia markedly decreased the risk of hepatic injury. Whether patients who are deprived of food preoperatively and whose liver enzymes are induced incur an increased risk of hepatic injury from brief periods of hypoxia remains to be determined.
We speculated that the inhibitory effect of isoflurane on the metabolism of halothane might reduce hepatic injury produced by halothane. To test this hypothesis we pretreated male rats with phenobarbital and 24 hr later exposed them to one of three types of anesthesia. One group of rats was anesthetized with 0.6 MAC isoflurane in 21-25% oxygen for 20 min, followed by exposure to 0.3 MAC isoflurane and 0.3 MAC halothane either in 9% oxygen for 46 min (n = 5) or in 12% oxygen for 60 min (n = 11). A second group of rats received 0.3 MAC halothane in 9% oxygen for either 46 min (n = 12) or in 12% oxygen for 60 min (n = 10). The third group received 0.3 MAC isoflurane in 9% oxygen for either 46 min (n = 12) or for 120 min (n = 8). The rats were killed 24 hr after the exposures and liver slides prepared. Histologic examination revealed that rats treated with isoflurane plus halothane, or with halothane alone showed a significant hepatic injury (P less than 0.005) when compared with those treated with isoflurane. Thus isoflurane failed to protect the liver from halothane-induced injury.
Anesthetic hepatotoxicity was tested under various conditions of hypoxia in rats pretreated with phenobarbital. Administration of 0.3 MAC halothane or fentanyl in 9% oxygen (fractional concentration of inspired oxygen = 0.09) for 46 min produced centrilobular hepatic injury in all rats (P less than 0.001 vs all other groups). Isoflurane, nitrous oxide, and thiopental at 0.3 MAC did not produce hepatic injury greater than that produced in control rats given 9% oxygen, nor was significant injury produced in control phenobarbital-pretreated rats who breathed 6 or 7.5% oxygen for 46 min. With an inspired oxygen concentration of 7.5%, hepatic injury occurred after exposure to 92.5% nitrous oxide (P less than 0.05), but not after enflurane, isoflurane, or thiopental. When hypoxia associated with 9% oxygen was extended to 2 hr, 91% nitrous oxide produced significant injury (P less than 0.001 compared with the controls), while enflurane, isoflurane, and thiopental did not. These and previous results suggest that all anesthetics can produce liver injury in the hypoxic rat model and that the ranking of hepatotoxicity (most to least) may be halothane, fentanyl, nitrous oxide, enflurane = isoflurane = thiopental.
Vecuronium is a new nondepolarizing muscle relaxant which has been shown to cause no significant cardiovascular effects. Utilizing invasive monitoring in patients undergoing coronary artery bypass grafting, the authors compared the cardiovascular effects of vecuronium (0.28 mg/kg) in seven anesthetized patients with those of pancuronium (0.1 mg/kg) in five anesthetized patients. This dose of pancuronium represents three times its ED90 (dose producing a 90% depression of evoked twitch tension), while the vecuronium dose represents twelve times its ED90. This relatively large dose of vecuronium was chosen deliberately in an attempt to manifest any possible cardiovascular effects. Following administration of vecuronium, cardiac output increased 9% and systemic vascular resistance decreased 12%, while pancuronium produced a significantly greater 17% increase in cardiac output without change in systemic vascular resistance. Heart rate and systemic mean arterial pressure did not change following vecuronium, while increasing 22% and 24%, respectively, following pancuronium. The authors conclude that large doses of vecuronium have minimal cardiovascular effects and thus offer an advantage over pancuronium in patients anesthetized for coronary artery surgery.
To establish criteria for administration of the optimal dose of alpha-adrenergic receptor blocking drugs, we studied cardiac performance and tissue oxygen tension in three patients who underwent excision of pheochromocytoma. Subcutaneous oxygen tension was measured by the method of Niinikoski and Hunt. Cardiac function was assessed by thermodilution cardiac output, systemic and pulmonary arterial blood pressures, and continuous two-dimensional transesophageal echocardiography of a cross section of the left ventricle at the level of the papillary muscles. Despite large changes in cardiac output and systemic, pulmonary, and wedge pressures, intraoperative tissue oxygen tensions and ejection fractions remained normal (even at times of peak catecholamine excretion and very abnormal wedge pressures). Studies of healthy animals that received no alpha-adrenergic receptor blocking drugs showed major decrements of tissue oxygen in response to modest doses of epinephrine. We conclude that progressive administration of alpha-adrenergic receptor blocking drugs does not absolutely protect the patient from major changes in blood pressure during operation for pheochromocytoma, but that cardiac performance and oxygen supply to the tissues are unimpaired.
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The authors describe a noninvasive method of estimating the kinetic constants that characterize metabolism of inhaled anesthetics in humans. Ten healthy male volunteers breathed subanesthetic concentrations of halothane and isoflurane in a fixed inspired ratio of 20:1. Isoflurane served as a marker that identified changes in uptake in nonmetabolizing depots. Each study progressed through nine 30-min levels (numbered 0-8). At each level, inspired concentrations of both halothane and isoflurane were doubled, and alveolar concentrations and uptakes were determined. Clearance (uptake/alveolar concentration) of isoflurane remained constant over a range of concentrations of 0.00006 to 0.008%. In contrast, clearance of halothane decreased as the alveolar concentration increased from 0.0007 to 0.13%. On this basis, the authors assumed that the clearance of halothane was a combination of linear clearance to depots and saturable metabolism, the former proportional to the clearance of isoflurane, and the latter attributable to a Michaelis-Menten process. Applying such a model to halothane, they estimated the mean (+/- SE) Vmax (the composite maximum rate of metabolism) to be 0.79 +/- 0.09 ml . min-1 . individual-1, and the Km (the composite concentration at which half-saturation of enzymes occurs) to be 0.029 +/- 0.003%. This model provides a significantly better data fit than that provided by two simpler submodels, one of which assumes that all clearance is linear, and the other of which allows a part of clearance to be saturable but ignores the isoflurane marker data. The value of 0.029% for Km indicates that a wide range of clinical anesthetic concentrations will produce similar rates of metabolism; that metabolism will proceed at near maximum rates during the first several minutes of recovery; and that most metabolism probably occurs after, rather than during, anesthesia.
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