Myocardial and ventricular function. Part I: Isolated muscle

The force of isometric contraction of cardiac muscle is dependent on the initial muscle length and the contractility. The resting length-tension curve is characterized by a relatively high stiffness of cardiac muscle which can be correlated with the inability to stretch the cardiac sarcomere beyond a length of about 2.2 microns, the length at which the degree of overlap between actin and myosin filaments is optimal for contraction (Lmax). The length-active tension curve shows that an increase in the initial fiber length is associated with an increase in the maximal tension in isometric contractions and an increase in the maximal shortening during unloaded contractions. Increments in resting muscle length are accompanied by proportionate increases in sarcomere length. With active shortening of the sarcomeres tension developed at one muscle length is actually generated at a shorter sarcomere length. Peak isometric force is obtained only with obligatory sarcomere shortening, at the expense of series compliance, during contraction. Developed tension critically depends on sarcomere length at the peak of contractile activity; the final sarcomere length during contraction is primarily determined by the load rather than initial length or mode of shortening. In tetanic contractions, there is no intrinsic difference between isometric and isotonic end-systolic length tension relation. The force velocity relationship helps distinguish two major ways in which cardiac performance may be altered, i.e., changing initial muscle length (the Frank-Starling phenomenon) and changing the contractile state, only the latter of which can affect an increase in the maximal velocity. For a given contractile state, the force-velocity-length relationship is unique; preload is pertinent only insofar as it sets the limit of the length range over which shortening can occur. In cardiac muscle the relationship between muscle length and active tension development is not clearly understood in terms of relating sarcomere length and degree of myofilament overlap to force production. With respect to the mechanics of relaxation, the early filling phase of cardiac diastole is primarily determined by the rate of isovolumetric pressure decline, the latter phase is dominated by the resting or diastolic compliance of the ventricular chamber.