The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the heart, which states that the more the heart fills with blood during diastole (the relaxation phase), the greater the force of contraction during systole (the contraction phase). Preload is proportional to end-diastolic volume (EDV), the volume of blood in the ventricles at the end of diastole. Two factors determine EDV: the duration of ventricular diastole and venous return and the volume of blood returning to the right ventricle.
Contractility, the second factor, pertains to the strength of ventricular muscle fiber contraction at any given preload. Substances that increase contractility are called positive inotropic agents, and those that decrease it are negative inotropic agents. Positive inotropic agents often promote calcium inflow, strengthening the force of contraction. Factors like stimulation of the sympathetic division of the autonomic nervous system, hormones like epinephrine and norepinephrine, increased intracellular calcium levels, and certain drugs can have positive inotropic effects.
Afterload is the third factor and refers to the pressure that must be exceeded before the ejection of blood from the ventricles can occur. Increased afterload can cause stroke volume to decrease, leaving more blood in the ventricles after systole. Conditions like hypertension and atherosclerosis can increase afterload.
