Physician's personal in-flight medical kit.
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Biomedical subjects
Publications and source records attributed to K Rehder.
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Tidal volume (VT) and inspiratory (TI) and expiratory (TE) times were measured during enflurane and halothane anesthesia in 12 prone dogs before and after bilateral vagotomy. "Elastic" loading or airway occlusion was used to obtain a VT-to-TI relationship in each state and to examine the rate of change in airway pressure. VT, TI, and TE were significantly (P less than 0.05) larger during enflurane than during halothane anesthesia, both before and after bilateral vagotomy. Before vagotomy, the rate of change in airway pressure during airway occlusion was similar for the two agents, as was an index of impedance of the respiratory system (Z'rs). Thus the difference in maximal pressure generated and in VT was most likely due to the difference in TI. Before vagotomy, TI increased as VT decreased with loading during enflurane but not halothane anesthesia, demonstrating a different effect of the two agents on the phasic vagal inspiratory inhibitory mechanism. After bilateral vagotomy, TI was unaltered during elastic loading with both agents but was still significantly longer during enflurane than halothane anesthesia. Thus it was concluded that TI was longer in the enfluraneanesthetized dogs than in the halothane-anesthetized dogs because of a different effect of these two agents on the bulbopontine "pacemaker" mechanism and not because of different effects on the phasic vagal inspiratory inhibitory mechanism.
Lung volumes, static pressure-volume curves, maximal expiratory flow-volume curves, right-to-left intrapulmonary shunts (Qs/Qt), and distributions of ventilation and perfusion relative to the alveolar ventilation and perfusion ration (VA/Q) were determined in seated normal men before chest strapping while breathing air (Cair) and during chest strapping while breathing air (Sair) or 100% oxygen (So2). With Sair and So2, mean vital capacity was reduced by 44% from control. Elastic recoil pressure [Pst(L)] of the lung at 50% control total lung capacity (TLC) increased significantly (P less than 0.05) from 4.64 +/- 0.39 cmH2O (mean +/- SE) to 7.00 +/- 0.47 cmH2O with Sair and to 7.24 +/- 0.70 cmH2O with So2. Maximal expiratory flow at 50% of control TLC increased significantly (P less than 0.05) from 3.22 to 0.25 l/s (mean +/- SE) to 5.84 +/- 0.69 l/s with Sair and to 5.50 +/- 0.68 l/s with So2. With Sair, no significant increase in Qs/Qt from control was observed. With So2, mean Qs/Qt increased significantly (P less than 0.05) from 0 to 2.2 +/- 0.9% of the cardiac output. It is therefore unlikely that the development of atelectasis, as indicated by an increase in Qs/Qt, accounts for the increase in Pst (L) with Sair and So2. Current evidence suggests that either change in alveolar surface compliance or distortion of the lung or both are responsible for the increased recoil pressure but that neither mechanism alone appears to explain it totally.
The effects on lung mechanics of equal (37%) reduction in total lung capacity (TLC) by rib cage or abdominal restriction were studied in 10 healthy males. Lung recoil pressure (Pst) was simultaneously measured from three sites in the esophagus. This also provided an estimate of the vertical pleural pressure gradient (PPG). Deformation of the right hemithorax was quantified by roentgenograms in three subjects. At the same lung volume, abdominal restriction decreased lung height and increased anteroposterior diameter compared with the control case, whereas rib cage restriction had opposite effects. Maximum expiratory flow increased equally with both types of restriction, and average Pst increased equally with both types of restriction. There was a significant correlation between degree of TLC reduction and increase in Pst that was similar for both types of restriction. This study indicates that changes in lung mechanics depend primarily on the amount of volume reduction and not on the type of deformation producing the volume decrease.
The effects of high-frequency oscillation (HFO) on 1) regional pulmonary 133Xe clearance after equilibration, 2) regional distribution and subsequent clearance of 133Xe after right atrial bolus injection, and 3) pulmonary gas exchange were examined in anesthetized supine dogs. After equilibration 133Xe cleared similarly from all lung regions with HFO at 16 and 30 Hz and a stroke volume of 2.6 ml/kg. Pulmonary gas exchange was adequate. 133Xe, injected as a bolus into the right atrium, was preferentially distributed to dependent lung regions during both HFO and apnea, indicating vertical gradients in pulmonary perfusion. During the subsequent pulmonary clearance of 133Xe, regional 133Xe concentrations (CrXe) increased initially in nondependent regions. By contrast, CrXe decreased immediately in the dependent lung region; after CrXe's became similar in dependent and nondependent regions, all lung regions started to clear at similar rates. The initial increases of CrXe in nondependent regions were attributed to interregional mixing, which may contribute to the uniformity in regional pulmonary 133Xe clearance after equilibration.
The effect of flow of inspired gas on intrapulmonary gas distribution was examined by analysis of regional pulmonary 133Xe clearances and of total pulmonary 133Xe clearance measured at the mouth after equilibration of the lungs with 133Xe. Five awake healthy volunteers (24 to 40 yr of age) and another 5 healthy, anesthetized-paralyzed volunteers (26 to 28 yr of age) were studied while they were in the right lateral decubitus position. The awake subjects were studied at 3 inspiratory flows (0.4, 0.7, and 1.0 L/s) and the anesthetized-paralyzed subjects at 4 inspiratory flows (0.2, 0.5, 1.1, and 1.6 L/s). Interregional differences in 133Xe clearances along the vertical axis were significantly less during anesthesia-paralysis and mechanical ventilation than during spontaneous breathing in the awake state. No differences in the regional or total pulmonary 133Xe clearances were detected at these different flows in either of the two states, i.e., the difference between the awake and anesthetized-paralyzed states persisted.
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To assess the effects of chronic exposure to low levels of nitrous oxide on neural function of man, the authors evaluated the neurologic condition, motor and sensory nerve conduction, and computerized tests of sensation of approximately half of the dentists in Rochester, Minnesota. Results of scored tests of neural function were not significantly different for dentists who used nitrous oxide extensively in their practices and dentists who did not. To assess the effects of chronic exposure to high levels of nitrous oxide on neural function and structure of experimental animals, groups of rats were exposed to 70 per cent N2O in 30 per cent oxygen for four hours, five days a week, for six months. Rats exposed to N2O and control rats showed no difference in well-being, in caudal nerve conduction, in axonal content and transport of acetylcholinesterase and dopamine-beta-hydroxylase, or in number and size distribution and pathologic abnormality of teased myelinated fibers. Although these results indicate a lack of peripheral nerve neurotoxicity of N2O in the rat, one cannot assume a similar lack of neurotoxicity in man with heavy exposures.
Changes in the anterior-posterior (AP) and lateral diameters of the rib cage and abdomen were assessed by magnetometry in seven anesthetized supine dogs during spontaneous respiration (SR) and mechanical ventilation after muscle paralysis (MV). Regional distribution of inspired gas was measured for both modes of ventilation by determining regional 133Xe clearances. Marked differences in chest wall motion were observed between SR and MV: during MV, the changes in lateral rib cage diameter from FRC to end inspiration were larger, and the changes in both abdominal diameters smaller than during SR. AP rib cage diameter changes were similar for both modes of ventilation. Inward motion of the lateral rib cage during initial inspiration was observed in four dogs during SR; it disappeared consistently with MV. Regional 133Xe clearances were not significantly different: there was no cephalocaudal gradient, and the vertical gradient in regional ventilation was similar with MV and SR. We conclude that significant changes in chest wall motion and shape are not necessarily associated with detectable differences in the distribution of regional ventilation.
Functional residual capacity (FRC) and quasi-static deflation pressure-volume (PV) curves of the total respiratory system, lung, and chest wall were measured in eight trained dogs lying supine, first awake and then anesthetized with halothane. Two of the eight dogs were repetitively examined 10 times during a 15-mo period. FRC decreased with anesthesia in six of the eight dogs and incresed with anesthesia in the remaining two dogs. There was a significant mean anesthesia-induced reduction in FRC of 16.9% (P < 0.05). FRC change with anesthesia varied between studies in one of the two dogs repetitively examined. Mean PV curves of the total system, lung, and chest wall of the six dogs whose FRC decreased with anesthesia were shifted to the right by anesthesia. PV curves from the two dogs whose FRC increased with anesthesia were shifted to the left. Anesthesia produced a significant reduction (P < 0.05) in mean lung compliance and significant increases (P < 0.05) in mean chest wall and total system compliances.
Pulmonary gas exchange is disturbed during general anaesthesia; both oxygenation and elimination of carbon dioxide are impaired. The shape of the chest wall alters after induction of anaesthesia-paralysis in recumbent subjects, and its motion during inspiration is also altered. The mechanical properties of lung and chest wall are also affected and FRC may be reduced. Inspired gas distribution changes after induction of anaesthesia-paralysis with mechanical ventilation of the lungs. Distribution of pulmonary blood flow is altered in subjects in the sitting and right lateral decubitus positions, but the distribution is not adjusted to the altered distribution of inspired gas. This results in an increased mismatching of ventilation to perfusion, with development of lung regions that have low and high ventilation-to-perfusion ratios. Some lung regions with low ventilation-to-perfusion ratios develop into right-to-left shunt on breathing 100 per cent oxygen. The following sequence of events probably occurs after induction of anaesthesia-paralysis. The initial effect of anaesthesia seems to be on the shape and motion of the chest wall. This may alter the mechanical properties of both the chest wall and the lung. Intrapulmonary gas distribution is altered secondarily. Pulmonary bloodflow distribution, which is primarily determined by gravity, does not seem to adjust to the altered distribution of inspired gas. Hence, an increased mismatching of ventilation to perfusion develops. This includes the development of lung regions with low ventilation-to-perfusion ratios. These regions may progress into right-to-left shung during 100 per cent oxygen breathing. The low ventilation-to-perfusion regions and the shunt may both impair oxygenation. The development of lung regions with high ventilation-to-perfusion ratios after induction of anaesthesia-paralysis contributes to the inefficient elimination of carbon dioxide.
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Distributions of ventilation and perfusion relative to Va/Q were determined in seven young healthy volunteers (24-33 yr) while they were either in the supine or right lateral decubitus position. The subjects were studied first awake and then while anesthetized-paralyzed and breathing 30% oxygen and again while breathing 100% oxygen. In the awake state, no statistically significant differences were observed in the distribution of ventilation and perfusion relative to Va/Q between the supine and right lateral decubitus positions or on changing the inspired oxygen concentrations. After induction of anesthesia-paralysis, Va/Q mismatching increased significantly but only small right-to-left intrapulmonary shunts developed. Ventilating the lungs with 100% oxygen further increased the dispersion of blood flow distribution during anesthesia-paralysis; lung units with low Va/Q or right-to-left intrapulmonary shunts (or both) developed. With induction of anesthesia-paralysis and intubation of the trachea, the anatomic dead space was decreased and the alveolar dead space increased.