Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function.
A two-dimensional framework can be used for considering the characteristics of left ventricular ejection in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload reserve. An afterload mismatch (reduced velocity and extent of shortening) can be induced acutely in the normal heart under controlled conditions if the preload is not allowed to compensate for an increased afterload, or if the limit of preload (Frank-Starling) reserve has been reached. In the intact circulation the normal heart is sensitive to some degree to acute changes in afterload, perhaps due to impaired venous return; but under basal resting conditions the ejection phase measures (such as the ejection fraction and the mean velocity of circumferential fiber shortening or VCF, corrected for heart size) encompass a relatively narrow range. This finding, and the lack of change in ejection phase measures after the normal heart has adapted to a chronic pressure or volume overload, provides justification for the use of ejection phase indices for detecting depressed inotropic state under basal conditions. When there is mild depression of myocardial inotropic state, with or without accompanying mechanical overload, enhanced preload may allow full compensation, but acute pressure loading may allow early detection of a less than normal preload reserve. When the inotropic state is substantially reduced, however, a mismatch between afterload and contractility (a reduction in mean VCF) will become evident even in the basal state (venous return being presumed to be adequate under these conditions). The concept of afterload mismatch with limited preload reserve provides an explanation for the value of ejection phase indices compared to isovolunic phase measures in assessing the basal level of inotropic state: the former may be more reliable because they are sensitive to afterload. The effects and implications of therapeutic afterload reduction as modulated by the preload also are understood within this framework.
D000818:Animals; D001011:Aorta; D001794:Blood Pressure; D002302:Cardiac Output; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000209:etiology; D006331:Heart Diseases / Q000503:physiopathology / Q000628:therapy; D006334:Heart Function Tests / Q000379:methods*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction; D013997:Time Factors; D016276:Ventricular Function