Skip to main content

Regulation of Stroke Volume


Regulation of Stroke Volume
The stroke volume is regulated by three variables:
  1. the end-diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole;
  2. the total peripheral resistance, which is the frictional resistance, or impedance to blood flow, in the arteries; and
  3. the contractility, or strength, of ventricular contraction.
    The end-diastolic volume is the amount of blood in the ven-
tricles immediately before they begin to contract. This is a work- load imposed on the ventricles prior to contraction, and thus is sometimes called a preload. The stroke volume is directly proportional to the preload; an increase in EDV results in an increase in stroke volume. (This relationship is known as the Frank-Starling law of the heart, discussed shortly.) The stroke volume is also directly proportional to contractility; when the ventricles contract more forcefully, they pump more blood.
In order to eject blood, the pressure generated in a ven- tricle when it contracts must be greater than the pressure in the arteries (because blood flows only from higher pressure to lower pressure). The pressure in the arterial system before the ventricle contracts is, in turn, a function of the total peripheral resistance—the higher the peripheral resistance, the higher the pressure. As blood begins to be ejected from the ventricle, the added volume of blood in the arteries causes a rise in mean arte- rial pressure against the “bottleneck” presented by the peripheral resistance. Ejection of blood stops shortly after the aortic pres- sure becomes equal to the intraventricular pressure. The total peripheral resistance thus presents an impedance to the ejection of blood from the ventricle, or an afterload imposed on the ven- tricle after contraction has begun. This can be medically signifi- cant; a person with a high total peripheral resistance has a high arterial blood pressure, and thus a high afterload imposed on the ventricular muscle.

Comments

Post a Comment

Popular posts from this blog

Frank-Starling Law of the Heart

Frank-Starling Law of the Heart Two physiologists, Otto Frank and Ernest Starling, demonstrated that the strength of ventricular contraction varies directly with the end-diastolic volume (fig. 14.2). Even in experiments where the heart is removed from the body (and is thus not subject to neural or hormonal regulation) and where the still-beating heart is filled with blood flowing from a reservoir, an increase in EDV within the physiological range results in increased contraction strength and, therefore, in increased stroke volume. This rela- tionship between EDV, contraction strength, and stroke volume is thus a built-in, or intrinsic, property of heart muscle, and is known as the Frank-Starling law of the heart.
Post a Comment
Read more

Effect of pH and Temperature

Effect of pH and Temperature on Oxygen Transport In addition to changes in P O 2 , the loading and unloading reac- tions are influenced by changes in the affinity (bond strength) of hemoglobin for oxygen. Such changes ensure that active skeletal muscles will receive more oxygen from the blood than they do at rest. This occurs as a result of the lowered pH and increased temperature in exercising muscles. The affinity is decreased when the pH is lowered and increased when the pH is raised; this is called the Bohr effect. When the affinity of hemoglobin for oxygen is reduced, there is slightly less loading of the blood with oxygen in the lungs but greater unloading of oxygen in the tissues. The net effect is that the tissues receive more oxygen when the blood pH is lowered (table 16.8). Since the pH can be decreased by carbon dioxide (through the formation of carbonic acid), the Bohr effect helps to provide more oxygen to the tissue...
Post a Comment
Read more

Pathophysiology of heart failure

Pathophysiology of heart failure In heart failure, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion. This condition can result from abnormalities of systolic or diastolic function or, commonly, both. Although a primary abnormality can be a change in cardiomyocyte function, there are also changes in collagen turnover of the extracellular matrix. Cardiac structural defects (eg, congenital defects, valvular disorders), rhythm abnormalities (including persistently high heart rate), and high metabolic demands (eg, due to thyrotoxicosis) also can cause HF.
Post a Comment
Read more