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[Changes in passive left ventricular pressure-volume relations in acute volume expansion].

Authors
Type
Published Article
Journal
Archives des maladies du coeur et des vaisseaux
Publication Date
Volume
76
Issue
7
Pages
759–770
Identifiers
PMID: 6412645
Source
Medline
License
Unknown

Abstract

The passive left ventricular pressure-volume relationship characterises left ventricular distensibility. However, it has recently been shown that acute pharmacological intervention can significantly change the position of the diastolic pressure-volume curve. We studied the effects of acute volumic expansion on the passive left ventricular pressure-volume relationship. In fact, the interpretation of left ventricular function curves during acute volumic expansion assumes that the left ventricular pressure-volume relationship remains unchanged. We measured the heart rate, cardiac output, left and right ventricular pressures with micromanometers, ventricular volumes by cineangiography 50 frames/sec (n = 6) or ventricular diameters by M mode echocardiography (n = 6) in 12 patients without valvular or coronary heart disease during rapid volumic expansion, and calculated stroke volumes and indices of left ventricular performance; the passive left ventricular pressure-volume or pressure-diameter relationship was adjusted to an exponential function P = a.ekp.V or P = a'.ek'p.De. After volumic expansion the cardiac output rose due to an increase in heart rate and stroke volume. The increase in stroke volume was related to that of end diastolic volume, the end systolic volume remaining unchanged: there was little difference in the indices of left ventricular performance. The pressure-volume and pressure-diameter curves were considerably shifted upwards and to the left during acute volumic expansion: this seemed to be due mainly to an increased intrapericardial pressure secondary to the increase in intrapericardial content. The relationship obtained by subtracting the simultaneous right ventricular from the instantaneous left ventricular pressure after volumic expansion was identical to the basal left ventricular pressure-volume curve. These observations demonstrate the importance of external factors of left ventricular compression in the changes in the passive left ventricular diastolic relationship during acute volumic expansion and invalidate the use of function curves obtained under these conditions for the assessment of left ventricular systolic function. The end diastolic pressure cannot be considered to reflect end diastolic volume and the function curves, in fact, illustrate changes in diastolic distensibility.

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