Respiratory Dysfunction Following Acute and Chronic Pump Failure of the Heart : PANEL DISCUSSION ON PUMP FAILURE OF THE HEART WITH COMPLICATIONS : 49th Annual Scientific Session of the Japanese Circulation Society
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概要
- 論文の詳細を見る
In order to explore pulmonary dysfunction originating in cardiac decompensation, acquired heart diseases were classified into three selected categories; chronic compensated heart, chronic decompensated heart and acute decompensated heart with severe alveolar edema. Pathophysiology in each category was investigated. Hemodynamic variables were measured by cardiac catheterizations and a variety of pulmonary functions based on respiratory physiology were studied. Severe alveolar edema due to acute pump failure of the heart revealed a significant inverse correlation between PaO_2 and PaCO_2 indicating the appearance of decreased PaO_2. A-_aDO_2 remained still high despite a complete resolution of alveolar edema. There are some possibilities that pulmonary dysfunction might be accelerated by repetition of acute cardiac decompensation in chronic heart diseases. Chronic pulmonary involvements caused by chronically decompensated heart must be stressed most important for comprehensive treatments of cardiac pump failure. Lung volumes considerably decreased but ordinarily there was no obvious airflow obstruction in the large central airways. Chronic compromised lung with giant left atrium, however, showed appreciable decrease in FEV_1% (FEV_1/FVC), MMF, V_<50> and V_<25>, indicating an apparent evidence of both central and peripheral airway obstructions. Patients with CTR over 70% were more seriously involved with a significant reduction in lung volumes in addition to total airway obstructions. Under these situations an inverse correlation between PaO_2 and PaCO_2 in chronic decompensated heart was observed showing a contrast difference in chronic compensated heart.
- 社団法人日本循環器学会の論文
- 1986-04-20
著者
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Nakanishi Norifumi
Division Of Cardiology Department Of Medicine National Cardiovascular Center
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Nakanishi Norifumi
National Cardiovascular Center
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Oobayashi Yoshikazu
Department Of Internal Medicine National Cardiovascular Center Hospital
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Okubo Shumpei
Division of Cardiology, Department of Medicine, National Cardiovascular Center
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Nakanishi Norifumi
Cardiac Division, Department of Internal Medicine, National Cardiovascular Center
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Yoshioka Takao
Cardiac Division, Department of Internal Medicine, National Cardiovascular Center
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Okubo Shumpei
Cardiac Division, Department of Internal Medicine, National Cardiovascular Center
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Kunieda Takeyoshi
Cardiac Division, Department of Internal Medicine, National Cardiovascular Center
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NAITO MASAHIRO
Cardiopulmonary Division, Department of Medicine, National Cardiovascular Center
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OOBAYASHI YOSHIKAZU
Cardiopulmonary Division, Department of Medicine, National Cardiovascular Center
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Yoshioka Takao
Division Of Cardiology Department Of Medicine National Cardiovascular Center
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Yoshioka Takao
Cardiac Division National Cardiovascular Center
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Kunieda Takeyoshi
化学療法研究所附属病院 循環器内科
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Kunieda Takeyoshi
Division Of Cardiology Department Of Medicine National Cardiovascular Center
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Kunieda Takeyoshi
国立循環器病センター研究所
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Ookubo Shunpei
Division Of Cardiology Department Of Medicine National Cardiovascular Center
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Okubo Shumpei
国立循環器病センター研究所
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Naito Masahiro
Cardiopulmonary Division Department Of Medicine National Cardiovascular Center
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Naito Masahiro
国立循環器病センター研究所
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Kuriyama Takayuki
Chiba University Graduate Schoolof Medicine
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Nakanishi Norifumi
Cardiac Division Department Of Internal Medicine National Cardiovascular Center
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Yoshioka Takao
国立循環器病センター研究所
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Okubo Shumpei
Division Of Cardiology Department Of Medicine National Cardiovascular Center
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Kunieda Takeyoshi
Cardiac Division Department Of Internal Medicine National Cardiovascular Center
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Yoshioka Takao
Cardiac Division Department Of Internal Medicine National Cardiovascular Center
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