The anesthesiologist outside the operating room: a new and exciting opportunity.
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Biomedical subjects
Publications and source records attributed to L J Saidman.
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Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 min and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 +/- 9.1 micrograms X kg-1), followed by a continuous infusion at 10-20 micrograms X kg-1 X hr-1 (total dose 63.6 +/- 10.1 micrograms X kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 +/- 1.55 ms preinduction versus 22.18 +/- 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 +/- 1.30 microV preinduction versus 1.31 +/- 0.74 microV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t = 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be misinterpreted as neurologic injury in evolution.
A computerized signal processing technique that removes low-frequency respiratory variation from pulmonary artery pressure and other central vascular pressure measurements, and produces a waveform devoid of respiratory artifact, has been developed. This technique has been integrated into a portable bedside monitor. The authors tested the technique in critically ill patients, and found that, compared to physician readings of conventional strip charts, it proved to be a very convenient and accurate method of determining pulmonary artery pressures continuously, regardless of ventilation.
We have pharmacodynamically modeled the relationship between the thiopental serum concentration and its effects on the electroencephalogram (EEG). Power spectral analysis was used to calculate the spectral edge, a measure of the underlying EEG frequency that characterizes the progressive slowing of the EEG induced by thiopental. Eight male volunteer subjects had venous thiopental serum concentrations measured, and 10 surgical patients had arterial serum concentrations measured. Thiopental was infused at a rate of 75 to 150 mg/min until a burst suppression EEG pattern was evident. Frequent blood samples were obtained during and after the infusion for measurement of serum thiopental concentrations, and the EEG was recorded for subsequent off-line power spectral analysis to calculate the spectral edge. With venous blood sampling, it was not possible to demonstrate significant hysteresis between the thiopental serum concentration and the spectral edge, allowing thiopental concentrations to be directly related to the spectral edge. With arterial blood sampling, significant hysteresis was present, requiring an effect compartment to relate concentration to effect. The half-time for equilibration (mean +/- SD) between concentration and response for the arterial data was 1.2 +/- 0.30 min. This value for Keo is consistent with known values for cerebral blood flow and thiopental brain: blood partition coefficient. Arterial-venous concentration differences cause the apparent lack of hysteresis with venous blood sampling. An inhibitory sigmoid Emax pharmacodynamic model optimally characterized the relationship between thiopental concentrations and the spectral edge. This model allows estimation of the thiopental serum concentration that causes one-half of the maximal EEG slowing (IC50), which is a measure of an individual's sensitivity to thiopental. Except for the hysteresis, there was no statistical difference in the parameters of the inhibitory sigmoid Emax pharmacodynamic model when venous and arterial blood samplings were compared. Arterial blood sampling offers some distinct advantages when pharmacodynamically modeling continuous, rapidly changing measures of drug effect, such as the EEG.
Experience at our institution with drug dependence among anesthesia residents, coupled with a lack of published data, prompted us to survey US anesthesia training programs. Two hundred eighty-nine programs were surveyed, 247 (85.5%) responded, and 184 (74%) of these programs had at least one suspected incident of drug dependence to report. Three hundred thirty-four confirmed persons were reported, including a substantial number of instructors. Meperidine and fentanyl were the most frequently mentioned drugs. Behavior changes were frequently noted by staff personnel, and in general such changes led directly to detection. After confirmation of abuse, the majority of impaired anesthetists were referred for psychiatric care, with few in need of actual detoxification. Detailed follow-up was available for about 40% of the total; 71 persons were offered a return to their original place of employment, while 30 persons died of drug overdose. Chemical impairment may be more common than usually thought in anesthesia, perhaps in part because of drug availability.
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Six pentobarbital-anesthetized dogs were prepared with endobronchial tubes and electromagnetic flow probes. The effects of changing inspired oxygen concentrations (FIO2 = 1, 0.21, 0.15, 0.1, 0.075, 0.05, and 0) were tested on test segments of different size corresponding to left lower lobe, left upper lobe-lingula, left lung, right lung, right lung plus left lower lobe, right lung plus left upper lobe-lingula, and whole lung. In each test the rest of the lung received oxygen. Hypoxic pulmonary vasoconstriction is demonstrated by both diversion of blood flow away from hypoxic test segments and by increased perfusion pressure. Flow diversion (FD%) decreases with the size of the hypoxic test segment (%QSN) from a maximum of 75% for very small segments to zero when the whole lung is hypoxic. FD% increases linearly as alveolar oxygen tension (PAO2) of the test segment is decreased in the range of 130--28 Torr. When mixed venous oxygen tension (PVO2) is less than 45 Torr FD% is reduced. These relationships are described by FD% = [74.99 - 0.0778 (%QSN) - 0.00661 (%QSN)2] [1.268 - 0.0096 (PAO2)] [0.47 + 0.012 (PVO2)], with r = 0.92 and standard error for prediction of 8.4%. Pulmonary perfusion pressure changes (PPH/PPN) increase with the size of the hypoxic test segments from 0 with very small segments to approximately 2.2 for the hypoxic whole lung. For all test segments PPH/PPN increases linearly with PAO2. These relationships are described by PPH/PPN = 1 + [0.0043 (%QSN) + 0.000072 (%QSN)2] [1.234 - 0.0096 (PAO2)], with r = 0.91 and standard error for prediction of 0.3 units. Responses to hypoxic pulmonary vasoconstriction in dogs are therefore shown to be predictable and continuous, and the physiological basis for action of each of the variables is discussed.
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The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.
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Recent experimental evidence indicates that the position of a pulmonary arterial catheter within the thorax is important because vertical height gradients from catheter tip to main pulmonary artery and left atrium may alter the validity of the pressure measured. The authors therefore examined the intrathoracic distribution of 314 pulmonary arterial catheters which at insertion were advanced to the most proximal position from which pulmonary wedge pressure could be obtained. Five catheters (1.8 per cent) were 6 cm or more cephalad to the carina, and 16 (5.1 per cent) were 9 cm or more lateral to the midline. With peripheral catheters recordings of pulmonary arterial and wedge pressures may be erroneous because future patient position, initiation of positive end-expiratory pressure, and occurrence of low pulmonary arterial and left atrial pressures may convert the region of lung in which the catheter tip lies to a Zone 1 of the lung.
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