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Effects of altitude stress on the human circulatory system
Research American ABWRACT~
Society
Abstracts
Federation
for Clinical
OF PAPERS PRESENTED AT THE MIDWESTERN
SECTIONAL MEETING
Research IN CHICAGO, ILLINOIS,
NOVEMBER 1, 1951 EFFECTS OF ALTITUDE STRESS ON THE HUMAN CIRCULATORY SYSTEM. Sanford A. Franpblau, M.D., Gordon F. Vawter, M.D. (by invitation); Clarence V. Pestel, M.D. (by invitation) and John P. Marbarger, M.D., Ph.D. (by invitation). (From the University of Illinois, Chicago, Ill.) Observations are reported on ten normal young adult males taken to simulated altitudes of 10,000 and 18,000 feet in an air-conditioned, low-pressure chamber while resting on a horizontal, low-frequency, critically damped ballistocardiograph: arterial blood oxygen, carbon dioxide and cellular components, simultaneous electrocardiogram, ballistocardiogram, direct arterial and venous .blood pressure readings, respiratory rate, depth and the composition of alveolar air were determined. Analysis of the records appears to justify these conclusions: Total effective peripheral resistance to blood flow decreases markedly upon exposure to ambient atmosphere at simulated altitudes up to 18,000 feet. “Useful work of the left ventricle” is not significantly altered after ten minutes exposure to ambient atmosphere at a simulated altitude of 10,000 feet but is increased by approximately 50 per cent after as short an exposure as five minutes to an altitude of 18,000 feet. The administration of “100 per cent oxygen” at a simulated altitude of 18,000 feet causes an almost immediate return of these measurements to ground-level values. Sudden exposure to the inhalation of ambient air at 18,000 feet increases both the pulse rate and stroke volume. The pulse rate reaches its maximum value within ten minutes. The stroke volume continues to increase as the time of exposure continues (up to twenty minutes). Increased stroke volume plays an important role in increasing cardiac output at high altitudes, especially noteworthy when cardiac output is increased to more than 50 per cent above the ground-level value. OBSERVATIONS ON THE ERYTHROCYTE SEDIMENTATION RATE IN CONGESTIVE HEART FAILURE. Albert E. McGinnis, A.B. (by invitation), W. MAY, 1952
603
Edward
Lansche, A.B. (by invitation) and Robert M.D. (From the Department of Internal Medicine and the Oscar Johnson Institute for Medical Research, Washington University School of Medicine, St. Louis City Hospital and the Barnes Hospital, St. Louis, MO.) Evidence supporting the rather widely held dictum that the erythrocyte sedimentation rate (ESR) is normal in congestive heart failure is limited. In order to elucidate this particular point, the ESR was determined serially for fortyeight patients during fifty-one separate bouts of congestive heart failure. Of these, thirty-eight were acute episodes from which the patients recovered, six were classified chronic because the patients failed to regain compensation and seven terminated fatally. None of the patients exhibited demonstrable evidence of other complications such as myocardial or pulmonary infarction, thrombophlebitis, infection, pregnancy or other conditions known to lead to elevation of the ESR. In acute congestive heart failure (thirty-eight instances), the ESR was normal in twelve (31.5 per cent) and elevated in twenty-six (68.5 per cent); after recovery the respective values were four (10.5 per cent) and thirty-four (89.5 per cent). The ESR in chronic intractable failure (six instances) was normal in one patient and elevated in five, not only on admission but throughout the hospital stay. In the seven cases in which congestive failure was fatal, four of the patients had a normal ESR on entry; terminally, the ESR was normal in five and elevated in two. These results suggest that the ESR is usually not normal in either acute or chronic congestive heart failure. The ESR is therefore of little value in confirming the presence or absence of any of the several complications which occur commonly in patients suffering from cardiac decompensation. ANALYSIS OF THE IMPORTANCE OF ANTITHROMBIN IN THROMBOEMBOLISM. 7. D. Pemrick, M.D. and M. M. Musselman, M.D. (From the
3.
Glaser,
Society
Abstracts
Federation
for Clinical
OF PAPERS PRESENTED AT THE MIDWESTERN
SECTIONAL MEETING
Research IN CHICAGO, ILLINOIS,
NOVEMBER 1, 1951 EFFECTS OF ALTITUDE STRESS ON THE HUMAN CIRCULATORY SYSTEM. Sanford A. Franpblau, M.D., Gordon F. Vawter, M.D. (by invitation); Clarence V. Pestel, M.D. (by invitation) and John P. Marbarger, M.D., Ph.D. (by invitation). (From the University of Illinois, Chicago, Ill.) Observations are reported on ten normal young adult males taken to simulated altitudes of 10,000 and 18,000 feet in an air-conditioned, low-pressure chamber while resting on a horizontal, low-frequency, critically damped ballistocardiograph: arterial blood oxygen, carbon dioxide and cellular components, simultaneous electrocardiogram, ballistocardiogram, direct arterial and venous .blood pressure readings, respiratory rate, depth and the composition of alveolar air were determined. Analysis of the records appears to justify these conclusions: Total effective peripheral resistance to blood flow decreases markedly upon exposure to ambient atmosphere at simulated altitudes up to 18,000 feet. “Useful work of the left ventricle” is not significantly altered after ten minutes exposure to ambient atmosphere at a simulated altitude of 10,000 feet but is increased by approximately 50 per cent after as short an exposure as five minutes to an altitude of 18,000 feet. The administration of “100 per cent oxygen” at a simulated altitude of 18,000 feet causes an almost immediate return of these measurements to ground-level values. Sudden exposure to the inhalation of ambient air at 18,000 feet increases both the pulse rate and stroke volume. The pulse rate reaches its maximum value within ten minutes. The stroke volume continues to increase as the time of exposure continues (up to twenty minutes). Increased stroke volume plays an important role in increasing cardiac output at high altitudes, especially noteworthy when cardiac output is increased to more than 50 per cent above the ground-level value. OBSERVATIONS ON THE ERYTHROCYTE SEDIMENTATION RATE IN CONGESTIVE HEART FAILURE. Albert E. McGinnis, A.B. (by invitation), W. MAY, 1952
603
Edward
Lansche, A.B. (by invitation) and Robert M.D. (From the Department of Internal Medicine and the Oscar Johnson Institute for Medical Research, Washington University School of Medicine, St. Louis City Hospital and the Barnes Hospital, St. Louis, MO.) Evidence supporting the rather widely held dictum that the erythrocyte sedimentation rate (ESR) is normal in congestive heart failure is limited. In order to elucidate this particular point, the ESR was determined serially for fortyeight patients during fifty-one separate bouts of congestive heart failure. Of these, thirty-eight were acute episodes from which the patients recovered, six were classified chronic because the patients failed to regain compensation and seven terminated fatally. None of the patients exhibited demonstrable evidence of other complications such as myocardial or pulmonary infarction, thrombophlebitis, infection, pregnancy or other conditions known to lead to elevation of the ESR. In acute congestive heart failure (thirty-eight instances), the ESR was normal in twelve (31.5 per cent) and elevated in twenty-six (68.5 per cent); after recovery the respective values were four (10.5 per cent) and thirty-four (89.5 per cent). The ESR in chronic intractable failure (six instances) was normal in one patient and elevated in five, not only on admission but throughout the hospital stay. In the seven cases in which congestive failure was fatal, four of the patients had a normal ESR on entry; terminally, the ESR was normal in five and elevated in two. These results suggest that the ESR is usually not normal in either acute or chronic congestive heart failure. The ESR is therefore of little value in confirming the presence or absence of any of the several complications which occur commonly in patients suffering from cardiac decompensation. ANALYSIS OF THE IMPORTANCE OF ANTITHROMBIN IN THROMBOEMBOLISM. 7. D. Pemrick, M.D. and M. M. Musselman, M.D. (From the
3.
Glaser,