Acute hemodynamic interventions shift the diastolic pressure-volume curve in man.

Abstract

SUMMARY Frame-by-frame analysis of angiograms in 16 patients revealed that hemodynamic interventions are capable of producing substantial shifts in the diastolic pressure-volume curve. Angiotensin raises blood pressure and shifts the entire pressurevolume curve up, and nitroprusside lowers blood pressure and shifts the curve down. Indirect measurements of pleural pressure in seven patients (via esophageal pressure) showed that pleural pressure changes were too small to account for these shifts. Analyzing our results in terms of a theoretical pressure-volume equation previously validated in dog studies did not show the observed shifts to be the product of acute changes in the elasticity of the myocardium itself. This same analysis suggested that indirect changes in the external mechanical constraints acting on the left ventricle such as the right ventricular pressure, the pericardium, and perhaps viscoelastic effects related to changes in filling rate account for the pressure-volume curve shifts with intervention. The fact that one cannot in general relate a specific volume to a given pressure in the face of hemodynamic interventions calls into question the use of end-diastolic pressure interchangeably with end-iastolic fiber length when interpreting systolic events in terms of the Frank-Starling mechanism.DURING DIASTOLE the left ventricle fills passively, with its pressure and volume related by a curve which reflects both ventricular geometry and the elasticity or stiffness of cardiac muscle. One generally describes the passive elasticity of cardiac muscle by means of an exponential curve relating stress (force/area) to strain (percentage distension), with the muscle becoming stiffer as it is stretched.' The pressure-volume relationship has been assumed to be sufficiently constant over the short term to use left ventricular end-diastolic pressure interchangeably with enddiastolic circumferential fiber length in analyses of ventricular function based on the Frank-Starling mechanism. Chronic cardiac disease may cause the ventricle to dilate or hypertrophy, and these geometric changes distort its diastolic pressure-volume relationship.2 In addition, disease might change the passive elasticity of the myocardium itself, altering the pressure-volume relationship.3-6 In an acute situation, however, it is assumed that hemodynamic interventions simply move the ventricle up and down the same pressure-volume curve. This assumption is based on the fact that no agents are known to affect passive elasticity of normally oxygenated papillary muscle,' and the fact that the ventricle cannot acutely become hypertrophied.We explored this assumption of constancy of the pressure-volume relationship by measuring diastolic pressurevolume curves based on frame-by-frame analysis of angiograms in 16 patients. Acute interventions with nitroprusside and angiotensin usually noticeably shifted the diastolic pressure-volume curve. This result brings into question the assumption that the diastolic pressure-volume relationship remains constant ...

Changes of left ventricular diastolic function in exercising dogs without and with ischemia.

“…16,42,43 The individual LV diastolic P-V curves in our study exhibited a rightward and upward shift in early diastole but no consistent displacement of the entire curve during ischemic exercise although, in one dog, there was a clear upward shift (Figure 5B) and in another a mild upward displacement was apparent, whereas the averaged P-V curves demonstrated no upward shift ( Figure 6B). A shift upward of the diastolic P-V curve after pacing-induced ischemia in humans has been described.…”

Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man.

“…Based on analysis of esophageal pressures, which correlate closely with pleural pressures, 33 Alderman et al 3 have demonstrated that although pleural pressure varied markedly between patients, it remained relatively constant during a state of held inspiration in individual patients. Thus, acute changes in pleural pressures would not be expected to account for the displacement of ventricular pressure-volume curves in specific individuals under the standardized respiratory conditions used in our study.…”

Factors which affect the diastolic pressure-volume curve.

“…7 -'"• l4 -IB-2.1. 41 j n j s f act> c o m 5i n e c i with the technical difficulties of measuring pressure-volume curves in people, a variable baseline due to pleural pressure differences from one individual to the next, 10 and the interaction between the two ventricles, probably explains the large within-groups variance that all investigators report in their parameters' values. This scatter makes it difficult, if not impossible, to resolve a patient population into subgroups; often different investigators' data break into different subgroups despite uniformly good measurement technique.…”