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Cor pulmonale. An experimental study utilizing a special cardiac catheter
234
American
Federation
PATHOGENESIS OF PULMONARY EDEMA IN MITRAL STENOSIS. Richard Gorlin, M.D., Florence W. Haynes, M.D. and Lewis Dexter, M.D., Boston, Mass. (From the Medical Clinic, Peter Bent Brigham Hospital, and the Dept. of Medicine, Harvard Medical School.) Seven studies have been made by cardiac catheterization in six patients with mitral stenosis at rest and during exercise. Cardiac outputs were estimated by the direct Fick method; peripheral arterial and mean pulmonary “capillary” pressures (“PC”) were recorded. Assuming “PC” pressure to approximate left atria1 mean pressure, left ventricular diastolic pressure to equal 5 mm. Hg and deriving the diastolic filling period per minute from arterial pressure tracings, the rate of mitral valvular blood flow (MVF) in cc/set. was calculated: Cardiac output (cc./min.) Diastolic filling period per minute (sec./min.) The cross sectional area (MVA) of the mitral valve was calculated according to the equation: MVF 0.7 y’2g(“PC”
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5)
Significant elevations in cardiac output occurred in three of the seven patients on exercise. In six of the seven increases in pulse rate or systolic ejection period occurred with significant decreases in diastolic filling time per minute. Whether due to increase in minute output or to decrease in diastolic filling time per minute, the rate of mitral valvular flow increased and was associated with a marked rise in “PC” pressure. The smaller the valve cross sectional area, the higher the rise in pressure for a given increase in rate of flow. Pulmonary edema on exercise was seen in those with high resting “PC” pressures who developed marked rises in pressure for only small increases in rate of flow. The occurrence of pulmonary edema is closely correlated with the degree and duration of elevation of “PC” pressure, which in turn is directly related to MVA and MVF, the latter being increased by tachycardia, increased systolic ejection period and increased cardiac output. COR PULMONALE. AN EXPERIMENTAL STUDY UTILIZING A SPECIAL CARDIAC CATHETER. Charles 7. Dotter, M.D. and Daniel S.
for Clinical Research Lukas, M.D., New York, N. Y. (From the Depts. of Radiology and Medicine, New York Hospital-Cornell Medical Center. This investigation was supported by a grant from the New York Heart Association.) Although several experimental studies of the problem have been previously reported, the alterations in hemodynamic pattern that occur in acute car pulmonale remain poorly defined. Employing a specially designed double-lumen cardiac catheter with an inflatable balloon near its tip, acute car pulmonale can be induced in the intact experimental animal by sudden closure of the left or right branch of the pulmonary artery. The standard electrocardiographic limb leads and right heart pressures have been recorded simultaneously during such closure in dogs anesthetized with intravenous pentabarbital and striking changes encountered. In fourteen trials in which pulmonary artery obstruction was maintained for an average of three minutes, the right ventricular systolic pressure rose rapidly from an average control level of 23 mm. Hg to 64 mm. Hg with an accompanying elevation of the end-diastolic or ventricular filling pressure of from 2 to 8 mm. Hg. In six experiments the right ventricular hypertension was maintained until obstruction was terminated. In the other eight experiments right ventricular failure characterized by further elevation of the diastolic pressure to abnormal levels and a declining ventricular pulse pressure occurred during the course of the vascular obstruction. In the latter series of experiments the relationship of right ventricular filling pressure to ventricular pulse pressure was found to obey pressure, Starling’s Law. Systemic arterial measured in six experiments, fell following pulmonary arterial obstruction; in three instances marked systemic hypotension persisted for the duration of the obstruction. Despite the development of marked right ventricular hypertension, no appreciable change in electrical axis occurred. Electrocardiographic changes consisted of lowering and inversion of the T waves and depression of the RS-T segments. These were interpreted as representing myocardial ischemia. Abnormal rhythms appeared during advanced right ventricular failure. Possible factors in the genesis of right ventricular hypertension in this study and further uses of the modified catheter in physiologic investigation are discussed. AMERICAN
JOURNAL
OF
MEDICINE
American
Federation
PATHOGENESIS OF PULMONARY EDEMA IN MITRAL STENOSIS. Richard Gorlin, M.D., Florence W. Haynes, M.D. and Lewis Dexter, M.D., Boston, Mass. (From the Medical Clinic, Peter Bent Brigham Hospital, and the Dept. of Medicine, Harvard Medical School.) Seven studies have been made by cardiac catheterization in six patients with mitral stenosis at rest and during exercise. Cardiac outputs were estimated by the direct Fick method; peripheral arterial and mean pulmonary “capillary” pressures (“PC”) were recorded. Assuming “PC” pressure to approximate left atria1 mean pressure, left ventricular diastolic pressure to equal 5 mm. Hg and deriving the diastolic filling period per minute from arterial pressure tracings, the rate of mitral valvular blood flow (MVF) in cc/set. was calculated: Cardiac output (cc./min.) Diastolic filling period per minute (sec./min.) The cross sectional area (MVA) of the mitral valve was calculated according to the equation: MVF 0.7 y’2g(“PC”
-
5)
Significant elevations in cardiac output occurred in three of the seven patients on exercise. In six of the seven increases in pulse rate or systolic ejection period occurred with significant decreases in diastolic filling time per minute. Whether due to increase in minute output or to decrease in diastolic filling time per minute, the rate of mitral valvular flow increased and was associated with a marked rise in “PC” pressure. The smaller the valve cross sectional area, the higher the rise in pressure for a given increase in rate of flow. Pulmonary edema on exercise was seen in those with high resting “PC” pressures who developed marked rises in pressure for only small increases in rate of flow. The occurrence of pulmonary edema is closely correlated with the degree and duration of elevation of “PC” pressure, which in turn is directly related to MVA and MVF, the latter being increased by tachycardia, increased systolic ejection period and increased cardiac output. COR PULMONALE. AN EXPERIMENTAL STUDY UTILIZING A SPECIAL CARDIAC CATHETER. Charles 7. Dotter, M.D. and Daniel S.
for Clinical Research Lukas, M.D., New York, N. Y. (From the Depts. of Radiology and Medicine, New York Hospital-Cornell Medical Center. This investigation was supported by a grant from the New York Heart Association.) Although several experimental studies of the problem have been previously reported, the alterations in hemodynamic pattern that occur in acute car pulmonale remain poorly defined. Employing a specially designed double-lumen cardiac catheter with an inflatable balloon near its tip, acute car pulmonale can be induced in the intact experimental animal by sudden closure of the left or right branch of the pulmonary artery. The standard electrocardiographic limb leads and right heart pressures have been recorded simultaneously during such closure in dogs anesthetized with intravenous pentabarbital and striking changes encountered. In fourteen trials in which pulmonary artery obstruction was maintained for an average of three minutes, the right ventricular systolic pressure rose rapidly from an average control level of 23 mm. Hg to 64 mm. Hg with an accompanying elevation of the end-diastolic or ventricular filling pressure of from 2 to 8 mm. Hg. In six experiments the right ventricular hypertension was maintained until obstruction was terminated. In the other eight experiments right ventricular failure characterized by further elevation of the diastolic pressure to abnormal levels and a declining ventricular pulse pressure occurred during the course of the vascular obstruction. In the latter series of experiments the relationship of right ventricular filling pressure to ventricular pulse pressure was found to obey pressure, Starling’s Law. Systemic arterial measured in six experiments, fell following pulmonary arterial obstruction; in three instances marked systemic hypotension persisted for the duration of the obstruction. Despite the development of marked right ventricular hypertension, no appreciable change in electrical axis occurred. Electrocardiographic changes consisted of lowering and inversion of the T waves and depression of the RS-T segments. These were interpreted as representing myocardial ischemia. Abnormal rhythms appeared during advanced right ventricular failure. Possible factors in the genesis of right ventricular hypertension in this study and further uses of the modified catheter in physiologic investigation are discussed. AMERICAN
JOURNAL
OF
MEDICINE