The left and right ventricles pump blood into the systemic and pulmonary arterial trees, respectively. Cardiac output, the volume of blood ejected from each ventricle during 1 minute, is the product of heart rate and stroke volume. Stroke volume (the volume of blood ejected with each heartbeat) depends in turn on preload, myocardial contractility, and afterload.
Preload refers to the load that stretches the cardiac muscle prior to contraction. The volume of blood in the right ventricle at the end of diastole, then, constitutes its preload for the next beat. Right ventricular preload is increased by increasing venous return to the right heart. Physiologic causes include inspiration and the increased volume of blood that flows from exercising muscles. The increased volume of blood in a dilated ventricle of congestive heart failure also increases preload. Causes of decreased right ventricular preload include exhalation, decreased left ventricular output, and pooling of blood in the capillary bed or the venous system.
Myocardial contractility refers to the ability of the cardiac muscle, when given a load, to shorten. Contractility increases when stimulated by action Jofthe sympathetic nervous system, and decreases when blood flow or oxygen delivery to the myocardium is impaired.
^Afterload refers to the vascular resistance against which the ventricle must ntract. Sources of resistance to left ventricular contraction include the tone in the walls of the aorta, the large arteries, and the peripheral vascular tree (primarily the small arteries and arterioles), as well as the volume of blood already in the aorta.
athologic increases in preload and afterload, called volume overload and ressure overload respectively, produce changes in ventricular function that iay be clinically detectable. These changes include alterations in ventricu-r impulses, detectable by palpation, and in normal heart sounds. Patho-3gic heart sounds and murmurs may also develop.
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