Acute hemodynamic interventions with angiotensin and nitroprusside produced substantial shifts in the diastolic pressure-volume curve in 16 patients, likely due to external mechanical constraints.
Observational (n=16)
Do acute hemodynamic interventions shift the diastolic pressure-volume curve in patients?
Acute hemodynamic interventions shift the diastolic pressure-volume curve, demonstrating that end-diastolic pressure cannot be used interchangeably with end-diastolic volume when interpreting the Frank-Starling mechanism.
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 pressure-volume 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-diastolic fiber length when interpreting systolic events in terms of the Frank-Starling mechanism.
Alderman et al. (1976) reported an observational. Hemodynamic interventions (angiotensin, nitroprusside) was evaluated on Diastolic pressure-volume curve shifts. Acute hemodynamic interventions with angiotensin and nitroprusside produced substantial shifts in the diastolic pressure-volume curve in 16 patients, likely due to external mechanical constraints.