CIRCULATORY PHYSIOLOGY
The interaction between myosin and actin, coupled with ATP produced by oxidative phosphorylation, is thought to be the basis for the contraction of each myofibril and therefore the contraction of the whole muscle. Each myofibril exhibits a property called contractility (or inotropic state) that represents the ability of the fiber to develop contractile force. The force exhibited by the fiber is influenced not only by its contractile state but also by its initial length, or preload, according to the Starling curve (Fig. 1-7). This concept can be expanded from the single fiber to describe the function of the entire ventricle. Thus, the abscissa, formerly preload or fiber length, becomes left ventricular filling pressure or volume (i.e., the amount of stretch on the myocardial fibers in diastole); and the ordinate, formerly tension, becomes stroke volume or stroke work (i.e., the ability of the heart to generate tension). Note that as diastolic pressure increases, the normal heart is able to increase its stroke volume, up to a point. This relationship is referred to as a ventricular function curve and, given identical states of contractility and afterload (see below), defines the amount of work that a heart is able to perform. Several factors determine left ventricular filling pressure.
- CIRCULATORY PHYSIOLOGY
- PATENT DUCTUS ARTERIOSUS
- PHYSIOLOGY OF THE SYSTEMIC CIRCULATION
- ELECTROPHYSIOLOGY
- ATRIAL SEPTAL DEFECT
- CARDIAC DEVELOPMENT
- MICROSCOPIC ANATOMY
- HIGH-OUTPUT STATES
- GROSS ANATOMY
- NONPHARMACOLOQICAL MANAGEMENT OF HEART FAILURE
- MYOCARDIAL METABOLISM
- MANAGEMENT OF ACUTE PULMONARY EDEMA
- PHYSIOLOGY OF THE PULMONARY CIRCULATION
- ACYATJOTIC LESIONS
- SYMPATHOMIMETIC AMINES
- CARDIOVASCULAR RESPONSE TO EXERCISE
- EVALUATION OF THE PATIENT WITH CARDIOVASCULAR DISEASE
- PHYSIOLOGY OF THE CORONARY CIRCULATION
- CONGENITAL HEART DISEASE
- VENTRICULAR SEPTAL DEFECT
- SHOCK