Preload, afterload, and the role of afterload mismatch in the descending limb of cardiac function.
Ventricular function can be analyzed from measures of the ejecting phase of contraction (e.g. velocity and extent of wall shortening) in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload. In the normal heart, under controlled conditions an afterload mismatch can be readily induced if the preload is not allowed to compensate for an increased afterload, or if the limit of the Frank--Starling reserve has been reached. In the conscious animal and in man, measures such as the mean velocity of fiber shortening (VCF, corrected for heart size) are relatively constant in the basal state, and when the normal left ventricle adapts successfully over several weeks to sustained experimental volume or pressure overload, the ejection phase measures remain normal per unit of muscle. However, if the inotropic state is considerably reduced, a mismatch between afterload and contractility (reduced VCF) will be evident in the basal state even when the afterload is normal. Failure to maintain normal ejection indices under conditions of acute or chronic mechanical overload can be explained in terms of an excessive afterload relative to the degree of hypertrophy, the level of inotropic state, and the Frank--Starling rereserve. The concept of afterload mismatch is illustrated by experimental data and used as a basis for characterizing responses to afterload changes in the clinical setting.
D000818:Animals; D001017:Aortic Coarctation / Q000503:physiopathology; D002302:Cardiac Output; D002306:Cardiac Volume; D002908:Chronic Disease; D004285:Dogs; D004548:Elasticity; D006331:Heart Diseases / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D008433:Mathematics; D009200:Myocardial Contraction; D010210:Papillary Muscles / Q000502:physiology* / Q000503:physiopathology; D016276:Ventricular Function