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LEFT VENTRICULAR VOLUME IN MAN: THE RELATION TO HEART RATE AND TO END‐DIASTOLIC PRESSURE
Author(s) -
WILCKEN D. E. L.
Publication year - 1968
Publication title -
australasian annals of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0571-9283
DOI - 10.1111/imj.1968.17.3.195
Subject(s) - cardiology , medicine , ventricle , diastole , heart rate , stroke volume , end diastolic volume , cardiomyopathy , stenosis , blood pressure , heart failure
Summary Resting left ventricular end‐diastolic and end‐systolic volumes were measured by means of a dye‐dilution method in 37 patients, nine with normal cardio‐vascular systems, nine with mitral stenosis, nine with aortic valve disease, and 10 with other conditions. Ventricular volumes were related to heart rate and to the simultaneously measured end‐diastolic pressure. Evidence is presented to indicate that the method is capable of detecting changes in ventricular size, and is not affected by changes in heart rate over the range studied. In the normal subjects there was a significant inverse relationship between heart rate and end‐diastolic volume. There was a direct relationship between the ratio of end‐systolic volume to end‐diastolic volume and heart rate, and an inverse relationship between stroke volume and heart rate. The mean systolic size of the ventricle was smaller at faster heart rates. Such a relationship would tend to minimize increases in myocardial energy expenditure with increases in heart rate. The patients with mitral stenosis had smaller left ventricular volumes than the normal subjects, but the end‐diastolic pressures were also smaller, which finding was consistent with similarity of ventricular distensibility in the two groups. Evidence for an abnormally stiff left ventricle was found in one of the four patients with severe aortic stenosis, in one patient with cardiomyopathy, and in two of the three patients with extreme obesity. The third patient had clinically unsuspected high output left ventricular failure. Evidence for a flabby ventricle was found in two patients with cardiomyopathy and in one patient with predominantly ischæmic heart disease. It seems likely that variations in ventricular stiffness occur during the progression of left ventricular disease and contribute importantly to the production of symptoms, because of effects on left atrial and pulmonary capillary pressures.