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.
- NONPHARMACOLOQICAL MANAGEMENT OF HEART FAILURE
- PATENT DUCTUS ARTERIOSUS
- SYMPATHOMIMETIC AMINES
- ELECTROPHYSIOLOGY
- ATRIAL SEPTAL DEFECT
- GROSS ANATOMY
- MYOCARDIAL METABOLISM
- SHOCK
- PHYSIOLOGY OF THE CORONARY CIRCULATION
- CARDIAC DEVELOPMENT
- CIRCULATORY PHYSIOLOGY
- CARDIOVASCULAR RESPONSE TO EXERCISE
- VENTRICULAR SEPTAL DEFECT
- HIGH-OUTPUT STATES
- ACYATJOTIC LESIONS
- CONGENITAL HEART DISEASE
- MICROSCOPIC ANATOMY
- PHYSIOLOGY OF THE PULMONARY CIRCULATION
- PHYSIOLOGY OF THE SYSTEMIC CIRCULATION
- EVALUATION OF THE PATIENT WITH CARDIOVASCULAR DISEASE
- MANAGEMENT OF ACUTE PULMONARY EDEMA