A view from the center.
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Biomedical subjects
Publications and source records attributed to C A Guenter.
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A 4-week, province-wide nurses' strike in Alberta in 1982 caused the closure of 57% of the acute care beds, including 47% of the intensive care beds, in Calgary. The effects of the strike on patient care at Foothills Provincial General Hospital, where nurses did not strike, were assessed. The number of emergency admissions, severity of illness and rate of death in the intensive care unit increased. On the other hand, the rate of death, length of stay and number of unexpected deaths on the medical wards were similar to those in the control periods before and after the strike. A subjective perception by hospital personnel of deteriorating patient care caused much anxiety; however, the results of analysis of measurable aspects of care suggested that the patients admitted to hospital received care during the strike that was comparable to care given before or after the strike. The inconvenience and potential harm to the patients not admitted because they had less severe illness were not measured.
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Patients undergoing upper abdominal surgery characteristically develop changes in lung function and are liable to develop atelectasis in the lower lobes. We studied 15 patients to assess lung function and, in particular, diaphragm function in patients undergoing cholecystectomy. Postoperatively, forced expiratory volume in one second and vital capacity decreased in all patients. The alveolar-arterial oxygen difference widened in the 10 patients in whom it was measured. Chest roentgenograms demonstrated patchy atelectasis in 9 of the 10 patients in whom films were obtained. There was a significant reduction in tidal volume with no change in minute ventilation immediately postoperatively. Diaphragm function was assessed by: changes in transdiaphragmatic pressure swings during quiet tidal breathing, the ratio of changes in gastric to esophogeal pressure swings, and the ratio of changes in abdominal to rib cage diameters. The results showed a significant decrease in changes in transdiaphragmatic pressure and the ratio of changes in gastric to esophogeal pressure swings in the postoperative period. In the 4 patients studied with magnetometers, there was a reduction in the ratio of changes in abdominal to rib cage diameters in all patients. These data indicate reduced diaphragm activity in the postoperative period, with a shift from predominantly abdominal to rib cage breathing. There was a reversal toward normal function by 24 h. This reduction in diaphragm function may be responsible for the atelectasis, reduced vital capacity, and hypoxemia in postoperative patients.
Respiratory failure is a common sequel to and a major cause of death in patients with multiple organ system injury. Detailed patient care requires monitoring of lung mechanical properties, gas-exchange, and oxygen transport in the blood. Furthermore, early recognition of lung edema, lung infection, or impaired respiratory muscle function may permit therapeutic maneuvers to prevent progressive deterioration of lung function. Unfortunately, each intervention carries with it a significant risk. Consequently, monitoring must include assessment of the adverse effects of oxygen, mechanical ventilation, artificial airways, and intravascular catheters. Shrewd analysis of limited data may commonly be more effective than sophisticated invasive monitoring with its attendant risks.
The pulmonary effects of endotoxin-induced, repetitive, intravascular leukocyte sequestration were studied in dogs and were compared to the effects of intratracheal papain. Lung specimens from 7 animals receiving 20 to 23 weekly injections were histologically and physiologically similar to those from 10 control animals. Dogs receiving 50 injections of endotoxin during 17 wk developed histologic evidence of emphysema as seen on whole lung sections, a significant increase in mean linear intercept, and loss of elasticity at high lung volumes. The group of animals given intratracheal papain also developed histologic evidence of emphysema, with increased mean linear intercepts and loss of lung elasticity. However, the effects on lung elasticity were much greater in the papain group. Endotoxin-induced, repetitive leukocyte sequestration in the lungs results in mild emphysema; however, similar changes in alveolar size appear to cause less effect on the pressure-volume loop than does papain-induced emphysema.
Patients with the fat embolism syndrome are reported to have a severe course, with mortality as high as 15 percent. Recent studies have attributed improved prognosis to one or another treatment modality. We reviewed the 54 patients with clinical evidence of the posttraumatic fat embolism syndrome documented at the Foothills Hospital from 1968 to 1977. The criteria for diagnosis were fever (54/54), hypoxemia (52/52), diffuse pulmonary infiltrates (49/54), changes in sensorium (41/54), and petechiae (39/54). Therapy included supplemental oxygen (54), assisted ventilation with positive end-expiratory pressure (5), and corticosteroids (7). There were no deaths. Patients who have the fat embolism syndrome without associated life-threatening disease have a relatively good prognosis with modern therapy, in contrast to reports in most of the published literature.
In experimental models pulmonary emphysema may be produced in hours to days; however, in human subjects emphysema commonly develops over a period of many years. In this report we document a case of severe emphysema which developed in less than six months in association with an unexplained illness characterized by dyspnea, hypoxemia and bilateral lung parenchymal disease. There was no hereditary predisposition. The diffuse alveolar injury syndrome must be considered as a potential cause of alveolar disruption.
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This report documents the first known case of bilateral diaphragmatic paralysis following blunt trauma to the chest. The important role of diaphragmatic function in maintaining ventilation, particularly with the patient in the supine position, is illustrated by the reduced total lung capacity, functional residual capacity, and vital capacity. Severe hypoxemia with the patient in the supine position, was markedly improved by elevation of the patient to 30 degree and was further improved by sitting the patient upright. Following an initial period of acute respiratory failure, the patient was managed acceptably by maintaining an elevated position for sleeping until diaphragmatic function returned, about nine months after the injury.
This is a case report of a patient who had one of the first Hufnagel ball-valve prostheses inserted in 1954 for severe aortic incompetence. He obtained relief of symptoms for 14 years before recurrence necessitated the insertion of a Starr-Edwards valve. The patients was symptom-free for another seven years before the original valve, which had been left in place, caused his death by eroding through the aorta.
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A 12-bed medical-surgical intensive care unit in a provincial, university-affiliated teaching hospital had 810 admissions during an 18-month period. Most patients were admitted under the care of a family physician. Quality care in the ICU was maintained by the efforts of dedicated unit managers, specialists and house staff. The overall mortality in the ICU of 8.1%, when added to the post-ICU mortality of 2.7% (giving a total hospital mortality of 10.8%), compares favourably with the best reported figures. Strong emphasis on selection of patients with potentially reversible disease, prompted in part by the limited facilities, may have played a role in yielding such favourable statistics. It is possible to retain participation of all members of the health care team during the brief phase of severe illness requiring intensive care.
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Sixteen healthy, active men were studied to determine the effects of severe arterial hypoxemia on the electrocardiograms during exercise. The electrocardiograms were all normal at maximum heart rate while the subject breathed ambient air. During maximal exercise breathing ten percent oxygen (mean arterial oxygen pressure [Po2] of 31 mm Hg), only one of the 16 had ST segment changes suggestive of ischemia. These were not present on a repeated study. The widely held view that systemic hypoxemia causes ischemic changes on the electrocardiogram was not confirmed in this study.
The grave clinical aspects of septic shock have stimulated the search for an experimental animal model which more closely relates to human pathophysiology. This study of the cardiovascular-pulmonary-morphologic responses of the baboon to slow infusions of live Escherichia coli organisms was designed to approximate more closely the human clinical entity. Anesthetized young adult baboons received 3-hour intravenous infusions of organisms at an average dosage of 8 times 10-9 organisms per kg. body weight. Responses of animals were followed during a period of 6 hours in the anesthetized state. There was progressive systemic hypotension and steadily decreasing cardiac output. Total peripheral resistance was uniformly depressed during the infusion, but was variable during the post-infusion survival period. Increases in heart rate, alveolar-arterial oxygen tension gradient, and oxygen uptake were uniformly present. These alterations bear close resemblance to those seen in other subhuman primates administered short term doses of live organisms. There were extensive morphologic changes in pulmonary, cardiac, and renal beds. Glomeruli contained multiple fibrin thrombi and disrupted platelets, and the glomerular capillary endothelium was focally edematous and disrupted. The myocardium exhibited capillary endothelial edema and fluid accumulation in interfiber and intrafiber spaces. There were sequestration, degranulation, and fragmentation of polymorphonuclear leukocytes and platelets, and characteristic endothelial lesions within the pulmonary vascular bed. Findings demonstrate both cardiovascular-pulmonary dysfunction and renal, cardiac, and pulmonary morphologic lesions. The baboon shock model appears to be well suited for studies of experimental septic shock and bears close resemblance to the human clinical entity.