(1) Heterometric factors affect the preload (the stretch on the heart before it contracts). A greater preload (stretch) on cardiac muscle fibres (myofibrils) just before they contract increases their force of contraction. This is known as the Frank-Starling mechanism. In the body, the preload depends on the volume of blood that fills the ventricles at the end of diastole, the so-called end-diastolic volume (EDV). The greater the EDV, within limits, the more forceful the contraction. The situation is somewhat like stretching a rubber band: the more it is stretched, the harder it snaps back when released. The length of ventricular diastole and venous pressure are the two key factors that determine EDV. When the heart rate increases, the duration of diastole is shorter. Less filling time means a smaller EDV and the ventricles may contract before they are adequately filled. On the other hand, when venous pressure increases, a greater volume of blood is forced into the ventricles, and the EDV is increased. When the heart rate exceeds about 160 beats/min, stroke volume usually declines. At such rapid heart rates, the ventricular filling time is severely shortened. EDV is less, and the preload is thus lower. People who have slow resting heart rates, on the other hand, usually have large stroke volumes because filling time is prolonged and preload thus is larger. The Frank-Starling law of the heart equalises the output of the right and the left ventricles and keeps the same volume of blood flowing to both the systemic and the pulmonary circulations. If the left side of the heart pumps a little more blood than the right side, for example, the volume of blood returning to the right ventricle (venous return) increases. With increased EDV, then, the right ventricle contracts more forcefully on the next beat, and the two sides are again in balance.
(2) Homeometric factors affect the work of the heart without causing any change in the resting muscle fibre length. Instead, they affect the contractility of the heart muscles and the afterload of the heart. Myocardial contractility is the forcefulness of contraction of individual ventricular muscle fibres, i.e., the strength of contraction at any given preload. Substances that increase contractility are called positive inotropic agents while those that decrease contractility are called negative inotropic agents. Thus, for a constant preload, the stroke volume is larger when a positive inotropic substance is present. Positive inotropic effect also gives rise to reduced end-diastolic pressure (EDP), fast-rising left-ventricular pressure (LVP) and brief ejection phase. When the heart is in this state, it is said to be hypereffective.
Go To Page: 1 2
