Showing papers in "Anesthesiology in 1980"
565 citations
TL;DR: Differences in anesthetic potencies, intraoperative effects, analgesia, physical side effects, incidences and types of postanesthetic emergence phenomena, and anesthetic preferences among the optical isomers of ketamine are disclosed.
Abstract: To assess the intraoperative and postoperative effects of the optical isomers of ketamine. compared with the racemic mixture as sole anesthetics, equianesthetic doses of racemic ketamine (RK), 2 mg/kg, (+)ketamine (PK), 1 mg/kg, and (−)ketamine (MK), 3 mg/kg, were administered intravenously in a ran
383 citations
TL;DR: That both the ventilatory and mouth occlusion pressure responses to CO2 are equally depressed by intravenous injections of midazolam and of diazepam at equipotent doses suggests a direct depression of the central respiratory drive by these drugs.
Abstract: The purpose of this study was to examine the respiratory depression produced by diazepam and by midazolam. Ventilatory and mouth occlusion pressure responses to CO2 were measured in eight healthy volunteers before and after the intravenous administration of 0.3 mg/kg of diazepam and 0.15 mg/kg of midazolam. The mean ventilatory response to CO2 (mean +/- SEM) decreased after administration of diazepam or midazolam from 2.0 +/- 0.2 to 1.3 +/- 0.1 1.min-1/torr or from 2.1 +/- 0.2 to 1.4 +/- 0.1 1.min-1/torr, respectively. In the same volunteers, the mouth occlusion pressure responses decreased from 0.54 +/- 0.05 to 0.30 +/- 0.04 cm H2O/torr after midazolam and from 0.67 +/- 0.12 to 0.28 +/- 0.07 cm H2O/torr after diazepam. When compared with the control slopes of the ventilatory and mouth occlusion pressure responses, the drug slopes were significantly different. Respiration was similarly depressed after diazepam and after midazolam. That both the ventilatory and mouth occlusion pressure responses to CO2 are equally depressed by intravenous injections of midazolam and of diazepam at equipotent doses suggests a direct depression of the central respiratory drive by these drugs.
258 citations
238 citations
TL;DR: A new Neurologic and Adaptive Capacity Score (NACS) for full-term neonates is described and compared with the Scanlon Early Neonatal Neurobehavioral Scale (ENNS), the most widely used test for evaluating effects of obstetric medication on the neonate.
Abstract: A variety of examinations are currently available for evaluating the neurobehavior of the newborn. These exams are often difficult and time-consuming to perform, require extensive training of the examiners, and produce results that may be difficult to interpret. The authors describe a new Neurologic and Adaptive Capacity Score (NACS) for full-term neonates and compare it with the Scanlon Early Neonatal Neurobehavioral Scale (ENNS), the most widely used test for evaluating effects of obstetric medication on the neonate. The NACS was designed as a screening test to detect central nervous system depression from drugs and also to differentiate these effects from those found after birth trauma and perinatal asphyxia. The NACS is based on 20 criteria, each of which is given a score of 0, 1, or 2. These criteria assess five general areas: 1) adaptive capacity; 2) passive tone; 3) active tone; 4) primary reflexes; and 5) alertness, crying, and motor activity (general observations). In contrast to the ENNS, the NACS places more emphasis on motor tone, avoids the use of noxious stimuli (pinprick, repeated Moro examinations), takes half the time to perform, and provides for any given baby a single number that immediately identifies a depressed or vigorous neonate.
218 citations
205 citations
TL;DR: Variability in analgesic responses to intramuscularly administered meperidine has been related to variable and unpredictable blood concentrations after injection, and correlations were found between MCP and neuroticism and extroversion scores from a personality inventory and physical variables.
Abstract: Variability in analgesic responses to intramuscularly administered meperidine has been related to variable and unpredictable blood concentrations after injection. However, the contribution of variability in the relationship between blood concentration and effect has not been examined. The present study was designed to determine the relationship between blood meperidine concentrations and analgesic effects in nine patients during the first two postoperative days. Pain was estimated by subjective bioassay. The blood concentration-effect curves were steep, with a difference of as little as 0.05 microgram/ml between the mean concentrations associated with severe pain and those associated with effective analgesia. Each curve had two inflection points: the maximum concentration still associated with severe pain (MCP) (0.41 microgram/ml, SD = 0.17, n = 76) and the minimum effective analgesic concentration (MEAC) (0.46 microgram/ml, SD = 0.18, n = 19). Interpatient variability of MEAC was appreciable (coefficient of variation = 39 percent) and intrapatient variability was also detected. Variable pain control following intermittent intramuscular injections was shown to be due not only to variation in absorption, as reported previously, but also to variation in the blood meperidine concentration-analgesic response relationships. However, correlations were found between MCP and neuroticism and extroversion scores from a personality inventory and physical variables. Thus, equations that allow prediction of an individual's MCP were derived by multivariable regression. A blood meperidine concentration of 0.7 microgram/ml would be expected to provide freedom from severe pain in approximately 95 per cent of cases. An intravenous infusion regimen for achieving and maintaining this concentration is described.
201 citations
TL;DR: Findings indicate that local anesthetic agents are similar to other biological stress modalities in terms of their differential effects on nerve fibers of various sizes and conduction velocities, i.e., the large fast-conducting fibers are more susceptible to conduction blockade than are the smaller, slower- Conducting fibers.
Abstract: The differential sensitivities of mammalian nerve fibers to various local anesthetic agents were investigated. Lidocaine, tetracaine, etidocaine, and bupivacaine demonstrated a consistent pattern of conduction blockade in which the large fast-conducting A fibers were blocked at the lowest drug concentration, the intermediate B fibers were blocked at a higher drug concentration, and the smallest, slowest-conducting C fibers required the highest drug concentration for conduction blockade. A comparison of procaine, chloroprocaine, cocaine, tetrodotoxin and saxitoxin on B and C fibers showed similar effects. These findings indicate that local anesthetic agents are similar to other biological stress modalities in terms of their differential effects on nerve fibers of various sizes and conduction velocities, i.e., the large fast-conducting fibers are more susceptible to conduction blockade than are the smaller, slower-conducting fibers. Discrepancies between results of this study and previous reports in the literature are discussed.
162 citations
TL;DR: The scoring system may be clinically useful in the preoperative evaluation and postoperative care of the patient with myasthenia gravis and serves as an aid to the physician in identifying those able to tolerate early tracheal extubation.
Abstract: In order to determine predictors for the postoperative need of mechanical ventilation in patients with myasthenia gravis undergoing thymectomy, the authors retrospectively applied multivariate discriminant analysis to preoperative physical, historical, and laboratory data of 24 myasthenic patients. They identified four risk factors--duration of myasthenia, respiratory disease, pyridostigmine dosage, and vital capacity--that allowed prediction of which patients would need postoperative mechanical ventilation and which could readily have their tracheas extubated. The four factors were weighted according to their respective importance in making this prediction and combined to form a preoperative scoring system. Using the resultant scores for each patient, the authors correctly predicted ventilatory need in 91 per cent of the patients, and only conservative errors (predicting the need for ventilatory support) were made. Traditionally used criteria for evaluating myasthenic patients were poorer predictors than the four factors identified by the authors. The scoring system may be clinically useful in the preoperative evaluation and postoperative care of the patient with myasthenia gravis, for its identifies important variables in the evaluation of the myasthenic patient and serves as an aid to the physician in identifying those able to tolerate early tracheal extubation.
160 citations
TL;DR: In experiments examining "cerebral protective effects" of therapies during brain hypoxia-ischemia, stringent control of body temperature is necessary and a possible clinical benefit resulting from modest reduction in body temperature in patients with marginal cerebral oxygenation is suggested.
Abstract: Male Wistar rats with unilateral carotid ligation were exposed to arterial hypoxia (PaO2 20-23 torr for 20 min) while body temperature was controlled at 37 degrees C, 36 degrees C, or 34 degrees C. Brain cortical concentrations of ATP, phosphocreatine (PCr) and lactate were measured microfluorometrically. Normothermic hypoxic rats had severe metabolic changes with low brain ATP and extremely high brain lactate. When rectal temperature was controlled at 36 degrees C during hypoxia, brain ATP was not different from that observed in normothermic, normoxic rats, and brain lactate was significantly lower than during normothermic hypoxia. At 34 degrees C, brain lactate was even less, but still three times higher than that observed in normothermic normoxic rats. PCr was significantly higher following hypoxia at 34 degrees C than at 37 degrees C. In part, this latter finding may reflect preservation of intracellular pH at 34 degrees C. A decrease of body temperature of 1-3 degrees C can minimize or prevent brain energy failure during hypoxia as well as decrease the magnitude of brain tissue acidosis. Thus, in experiments examining "cerebral protective effects" of therapies during brain hypoxia-ischemia, stringent control of body temperature is necessary. Furthermore, a possible clinical benefit resulting from modest reduction in body temperature in patients with marginal cerebral oxygenation is suggested.
157 citations
TL;DR: With rewarming, cardiovascular collapse with severe tissue hypoxia and acidosis developed; CBF became grossly inadequate, resulting in depletion of brain energy stores, and VO2 continued to decrease, and at 24 hours values were 7 and 28 per cent of control, respectively.
Abstract: The authors had previously observed a deleterious cerebrovascular effect of prolonged hypothermia in primates and cats. In this study they examined the systemic as well as cerebral hemodynamic and metabolic effects of 24 hours of hypothermia in the dog. With decreases in temperature to 29 C, cardiac
TL;DR: There was no significant difference between the groups in times spent in the intensive care unit, hemodynamic performances, or plasma norepinephrine levels; however, the patients whose tracheas were extubated early received less morphine and diazepam and suffered significantly less cardiopulmonary morbidity.
Abstract: Sequelae of early versus late extubation of the trachea in patients following coronary-artery bypass grafting were compared prospectively in 38 patients randomly assigned to one of the two groups. The times to extubation were 2 +/- 2 and 18 +/- 3 hours after operation for the two groups. Comparisons were made between groups for the following five variables: time spent in the intensive care unit; drug utilization in the intensive care unit; cardiopulmonary morbidity; hemodynamic performance; patient stress (plasma norepinephrine levels). The anesthetic technique consisted of induction with thiopental, nitrous oxide, and halothane, followed by maintenance with nitrous oxide and halothane. Pancuronium was the only muscle relaxant administered. Patients whose tracheas were extubated early had muscle relaxants reversed prior to the application of extubation criteria. There was no significant difference between the groups in times spent in the intensive care unit, hemodynamic performances, or plasma norepinephrine levels; however, the patients whose tracheas were extubated early received less morphine and diazepam and suffered significantly less cardiopulmonary morbidity.
TL;DR: To determine the effects of tidal volume (VT) and positive end-expiratory pressure (PEEP) on pulmonary oxygen exchange during endobronchial (one-lung) anesthesia, the authors studied the effects at 8 and 16 per cent total lung capacity, at zero end- Expiratory Pressure (ZEEP), and at 10 c.
Abstract: To determine the effects of tidal volume (VT) and positive end-expiratory pressure (PEEP) on pulmonary oxygen exchange during endobronchial (one-lung) anesthesia, the authors studied the effects of VT at 8 and 16 per cent total lung capacity (TLC), at zero end-expiratory pressure (ZEEP), and at 10 cmH2O PEEP in 16 patients in the lateral position. Anesthesia was maintained with halothane and oxygen. During two-lung ventilation (FIO2 0.99), mean PaO2 and physiologic shunt (Qs/Qt) were 421 +/- 12 mmHg and 0.22 +/- 0.02, respectively. During one-lung ventilation, PaO2 decreased and venous admixture (or Qs/Qt) increased in every patient. The magnitude of this decrease correlated directly with preoperative forced expiratory volume in one second (FEV1) (r = 0.66, P less than 0.005). A VT of 16 per cent of TLC at ZEEP resulted in the highest mean PaO2 (210 +/- 30 mmHg) and lowest Qs/Qt (0.35 +/- 0.02), probably as a result of end-inspiratory alveolar recruitment with the least pulmonary blood flow redistribution. When 10 cmH2O PEEP was applied during 16 per cent TLC ventilation, mean PaO2 decreased from 210 +/- 35 to 162 +/- 25 mmHg (P less than 0.05). PEEP did not significantly affect PaO2 during 8 per cent TLC ventilation. At both levels of VT, PEEP reduced mean Qt by approximatley 10 per cent (P less than 0.01) and increased compliance (P less than 0.01). However, PEEP did not significantly affect mean Qs/Qt or mean arterial or pulmonary arterial pressures at either level of VT. There was considerable variation in PaO2 and Qs/Qt among patients.
TL;DR: In the presence of myocardial infarction, epidural blockade had less effect on systemic pressure and left ventricular filling pressure was decreased, and sympathetic blockade redistributed coronary blood flow, favoring the endocardium in both the normal and the infarcted heart.
Abstract: The effects of reversible sympathetic neural blockade of the canine myocardium under control conditions and in the presence of decreased coronary blood flow and after myocardial infarction were investigated in 17 dogs. A multiple-microsphere technique was used to measure distribution of blood flow in the myocardium. Epidural blockade was associated with the following changes in the ratio of endocardial to epicardial blood flow: under control conditions, no change; after 50 per cent decrease in coronary flow, 18 per cent increase in endocardial/epicardial ratio; after myocardial infarction at unrestricted coronary flow, 43 per cent ratio increase; after myocardial infarction and 50 per cent decrease in coronary flow, 76 per cent increase of endocardial/epicardial ratio. These effects appear to be independent of systemic factors, and may result from alterations in tone of transmural resistance vessels. In addition, cervicothoracic epidural blockade resulted in a decrease in systemic pressure and an increase in coronary vascular resistance as myocardial oxygen demand decreased. When systemic pressure was restored these effects were abolished. In the presence of myocardial infarction, epidural blockade had less effect on systemic pressure and left ventricular filling pressure was decreased. With decreased coronary flow, sympathetic blockade redistributed coronary blood flow, favoring sympathetic blockade redistributed coronary blood flow, favoring the endocardium in both the normal and the infarcted heart.
TL;DR: An alternative index, the development of CO2 retention at constant alveolar ventilation, more reliably identified patients in whom severe VA/Q inequality developed during inhalational anesthesia.
Abstract: The development of impairment of pulmonary gas exchange during inhalational anesthesia was studied in ten patients (ages 52–75 years) by use of the multiple-inert-gas elimination method. Preoperative pulmonary function tests indicated a wide range of abnormal pulmonary function. Control gas-exchange studies with the subjects awake (supine position) demonstrated modest increases in pulmonary ventilation-blood flow (VA/Q) distribution in all subjects (mean log SD = 0.96), but the shunt was minimal (mean 1.3 per cent). Inhalational anesthesia was either 1) halo-thane, 0.4 per cent (end-tidal) in N2O, 50–60 per cent, balance oxygen, for eight subjects, or 2) halothane, 0.6 per cent, in nitrogen, 50–60 per cent, balance oxygen, for two subjects. Striking increases in retention of the least soluble tracer gases (SF6, and ethane) were seen in all patients after a minimum of 35 min of anesthesia, during mechanical ventilation with both anesthetic regimens. This was due to one of three different patterns of responses. Three subjects showed primarily increased intrapulmonary shunt (mean shunt = 23 per cent of cardiac output). Three subjects showed primarily increases in low-VA/Q units (mean = 32 per cent of cardiac output), with little or no shunt, while the remaining four had both intrapulmonary shunt and units of low VA/Q. Arterial blood PO2 measurements suggested substantially greater impairment of oxygenation when the pattern of response was primarily an increase in shunt. This difference was accentuated by the concentrating effect of N2O uptake on alveolar PO2 in low-VA/Q units. As a consequence, arterial blood PO2 values grossly underestimated the VA/Q inequality in patients in whom low-VA/Q regions developed. An alternative index, the development of CO2 retention at constant alveolar ventilation, more reliably identified patients in whom severe VA/Q inequality developed during inhalational anesthesia.
TL;DR: The results suggest that analgesia induced by nitrous oxide may be partly related to the opiate receptor-endorphin system in man.
Abstract: The possible reversal of nitrous oxide analgesia by naloxone was investigated. Two studies were conducted in 21 healthy male subjects, who responded to ischemic pain produced by tourniquet applied to the upper arm for 15 min, while breathing air or nitrous oxide, 33 per cent. Using a double-blind procedure, the subjects received intravenous injections of naloxone and saline solution on different days. In eight subjects, naloxone, 8 mg, administered without nitrous oxide, had no effect on pain report. However, unlike saline solution, naloxone, 8 mg, decreased significantly the analgesia induced by nitrous oxide. In 13 subjects, naloxone, 4 mg, also decreased significantly the effect of nitrous oxide analgesia in comparison with saline solution. Naloxone showed its reversal effect mainly on sensory response rating obtained during the painful stages of ischemia, between 11 and 15 min. The results suggest that analgesia induced by nitrous oxide may be partly related to the opiate receptor--endorphin system in man.
TL;DR: This study has defined subclasses of patients with coronary-artery disease for whom pulmonary arterial pressure monitoring is indicated prior to, during, and following coronary-artersy surgery.
Abstract: To delineate the indications for pulmonary arterial pressure monitoring, the relationship between central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) was examined in 30 patients with coronary-artery disease and ventricular dysfunction (ejection fractions ranging from 0.26 to 0.84) prior to, during, and after coronary-artery surgery. For each patient, 30 simultaneous measurements of CVP and PCWP were made during a 36-hour period that included the awake state, the anesthetized state with and without surgery, before and after pericardiotomy, before and after cardiopulmonary bypass, and one, four, eight, and 24 hours after operation. At each point, changes in filling pressures were acutely induced by changing body position to alter venous return. The CVPs ranged from 0 to 19 torr, and the PCWPs from 0 to 31 torr. The CVP and the PCWP correlated well (r = 0.89) during all measurement periods for patients who had ejection fractions greater than 0.50 without angiographically demonstrable ventricular dyssynergy preoperatively. Changes in CVP (delta CVP) and PCWP (delta PCWP) over the 35-hour period also correlated well (r = 0.94). Normality (abnormality) of the CVP was predictive of normality (abnormality) of the PCWP for more than 96 per cent of the 450 data points. On the other hand, for patients with ejection fractions less than 0.40 or with hyssynergy, the CVP did not correlate with the PCWP (r = 0.24), and delta CVP did not correlate with delta PCWP (r = 0.04). Normality (abnormality) of the CVP was predictive of normality (abnormality) of the PCWP for less than 62 per cent of the 450 data points. This study has defined subclasses of patients with coronary-artery disease for whom pulmonary arterial pressure monitoring is indicated prior to, during, and following coronary-artery surgery.
TL;DR: The authors believe that monitoring of PAP for detection and treatment of air embolism is justified during seated neurosurgical procedures.
Abstract: The use of pulmonary arterial pressure (PAP) monitoring was compared with precordial Doppler ultrasound monitoring and continuous infrared end-tidal CO2 fraction (FETCO2) analysis for detection and treatment of venous air embolism in 52 consecutive patients undergoing neurosurgical procedures in the seated position. Doppler air sounds were identified 44 times during 20 operations. During 12 operations there were 17 episodes of Doppler air sounds associated with increased PAP (mean increase = 13 ± 2.8 torr SE, P
TL;DR: The log-probit curve yields results that are not statistically significantly different from those of the linear regression method, and is a better fit to the data at the clinically important extremes (85–99 per cent) of the response scale.
Abstract: This study was done to demonstrate the validity of the log-probit method of analyzing dose–response data and to test the accuracy of the incremental dose method for generating dose–response data for pancuronium and d-tubocurarine. During balanced general anesthesia, cumulative dose–response data were obtained from ten patients each for pancuronium and d-tubocurarine. Dose–response data were also obtained using a single bolus injection method in 46 patients given pancuronium and 27 patients given d-tubocurarine. Evoked thumb adduction response was measured using an FT-10 force-displacement transducer and recorded on a Grass®-7 polygraph. Dose–response data were plotted on log-probit paper and analyzed by the Litchfield-Wilcoxon approximation method to determine mean ED50 and ED95 for each muscle relaxant. The dose–response data were also plotted on arithmetic scales and analyzed by the linear regression method to determine ED50 and ED95. These results were compared with those obtained by use of the log-probit method. The validity of the incremental dose method of obtaining dose–response curves was determined by comparison with the dose–response curves obtained using the conventional single bolus injection method. For each neuromuscular relaxant studied, the mean dose–response curve obtained by the cumulative dose method was not statistically significantly different from the bolus method dose–response curve. Comparing methods of analysis, the log-probit method yields results that are statistically not different from those obtained by use of conventional linear regression analysis. The log-probit plot is a simple, accurate, appropriate approach for analyzing neuromuscular relaxant dose–response data. The log-probit curve yields results that are not statistically significantly different from those of the linear regression method, and is a better fit to the data at the clinically important extremes (85–99 per cent) of the response scale. For pancuronium and d-tubocurarine, the incremental dose method is efficient and accurate for generating dose–response curves.
TL;DR: The results imply that the protective effect of barbiturates under such conditions is unrelated to inhibition of lipid peroxidation, and suggest that instead they may act by other mechanisms.
Abstract: The protective effect of barbiturates in cerebral ischemia has been proposed to be related to inhibition of lipid peroxidation. The present in-vitro study was undertaken to test the efficiencies of different barbiturates to inhibit peroxidative reactions in brain tissue, and to compare their effects with established free radical scavengers (chlorpromazine and promethazine). Cortical homogenates, prepared from decapitated rats, were incubated at 37 C with 5 per cent O2 (in N2) in the presence of ferrous sulfate (0.01 mM) and ascorbic acid (0.25 mM). During incubation there was extensive lipid peroxidation in the tissue, as evidenced by appreciable production of thiobarbituric acid-reactive material (TBAR), 1.2 μmol malondialdehyde g−1 cortex in one hour. Thiopental (1.0 mM) caused a 96 per cent inhibition of TBAR production, while other barbiturates (in the same concentrations) had only small (methohexital) or no (pentobarbital and phenobarbital) inhibitory effect. The inhibition of TBAR production by 1.0 mM thiopental was similar to that found with 1.0 mM chlorpromazine or 0.1 mM promethazine. The inhibitory effect of thiopental on lipid peroxidation was confirmed by analysis of fatty acids and phospholipids. Thiopental prevented the peroxidative degradation of polyenoic (20:4, 22:6) fatty acids and of ethanolamine phosphoglyceride that otherwise occurred during incubation. The marked differences between the tested barbiturates with respect to their abilities to inhibit lipid peroxidation in vitro are at variance with the fact that all of these barbiturates have been reported to protect the ischemic brain in various situations in vivo. The results imply that the protective effect of barbiturates under such conditions is unrelated to inhibition of lipid peroxidation, and suggest that instead they may act by other mechanisms.