The Pressure—Volume Relationship of the Intact Heart
The relationship of isometric force to sarcomere length transforms, in the intact heart, to the relationship between left ventricular isovolumic pressure and volume. The assumption that this latter relationship is straight and represents an elastance, Emax, implies the visco-elastic model which was disproved for muscle in general by Fenn. If the force-length curve is straight, no resulting pressure-volume curve will be convex to the pressure axis due to geometry. There are also data to show that the pressure-volume relationship is non-linear, thus invalidating Emax. The uniqueness of the pressure-volume diagram as a unique descriptor of left ventricular mechanical function would be invalidated if the slow response of force to length change proved to be present in the intact heart; present data on that point is contradictory between different laboratories. As long as contractility is normal and systole of sufficient duration, the end-systolic pressure-volume curve is identical to the isovolumic one. Then an increase in end-diastolic volume results in an identical increase in stroke volume (at the same ejection pressure) and end-systolic volume is constant. A shift to the left of the end-systolic pressure-volume curve indicates increased myocardial contractility. A shift to the right indicates either a negative inotropic effect or an abbreviation of systole.
KeywordsStroke Volume Aortic Pressure Sarcomere Length Negative Inotropic Effect Positive Inotropic Effect
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