PubMed · 4909444
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P J Tomlin, J A Newell. 1970. Cardiac output computation.. https://doi.org/10.1093/bja%2F42.2.124
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OBJECTIVE: To review the literature about the effect of normal pregnancy on cardiac output, with special attention to study design, measurement technique, position of the subject, and parity. DATA SOURCES: For studies from the period 1955-1987, we examined Cumulated Index Medicus (National Library of Medicine Cataloging in Publication. Chicago: American Medical Association). For studies from 1988 to May 1, 1994, we used Medline on Silver Platter (U.S. National Library of Medicine Silver Platter International, 1994). METHODS OF STUDY SELECTION: Thirty-three cross-sectional and 19 longitudinal studies on cardiac output measurement in normal pregnancy were retrieved and reviewed. Thirteen longitudinal studies were excluded from analysis because an unvalidated technique was used or because not all subjects were measured at each study interval. The six remaining studies of genuine longitudinal design with at least two measurements throughout pregnancy were used for the definitive analysis. The results of the cross-sectional studies were included only to demonstrate a trend. DATA EXTRACTION AND SYNTHESIS: By pooling data from cross-sectional studies, a tendency was shown toward a higher cardiac output in the second trimester compared with the first trimester, and a tendency toward lower cardiac output was found in the third trimester compared with the second trimester. After delivery, cardiac output was lower than at any time during pregnancy. Selected longitudinal studies showed that the rise in cardiac output occurred early in the first trimester, and a further rise occurred during the second trimester. During the third trimester, cardiac output rose, fell, or plateaued, irrespective of the method of measurement applied or conditions during measurement. CONCLUSIONS: Cardiac output during the third trimester was widely divergent among the studies and probably dependent on individual factors. The tendency to report cardiac output as averages negated these inter-individual differences.
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Left ventricular (LV) diastolic dysfunction is the first discernible manifestation of heart disease in hypertensive patients. Arterial hypertension with LV hypertrophy leads to reduced preload followed by impaired cardiac output (systolic dysfunction stemming from primary diastolic dysfunction). Diastolic dysfunction leads more often than systolic dysfunction to hypertensive heart failure and is in many cases clearly distinguishable from heart failure with low ejection fraction (EF). Mortality due to heart failure from impaired inotropism is higher than mortality due to diastolic dysfunction, but morbidity is lower. Hypertensive cardiomyopathies can be divided into 4 ascending categories, according to the pathophysiologic and clinical impact of hypertension on the heart: Degree I: LV diastolic dysfunction with no associated LV hypertrophy Degree II: LV diastolic dysfunction with echocardiographic LV hypertrophy Degree IIA: Normal exercise capacity in terms of maximal oxygen consumption Degree IIB: Impaired exercise capacity in terms of maximal oxygen consumption Degree III: Congestive heart failure (severe dyspnea and radiographically determined pulmonary edema with normal (> or = 50%) EF Degree IIIA: LV mass/volume ratio > 1.8 with little or no myocardial ischemia Degree IIIB: LV mass/volume ratio < 1.8 with significant myocardial ischemia Degree IV: Profile of dilated cardiomyopathy; LV hypertrophy and impaired EF (< 50%).