A patient's SV, the amount of blood pumped from the left ventricle during systole, is usually about 70 ml per heartbeat. Three factors affect SV, preload, afterload, and contractility.
Preload is the force of blood in the ventricle exerted on the ventricular muscle at the end of diastole. The more the muscle fibers are stretched during diastole, the more forcefully they'll contract during systole.
Afterload is the pressure that causes the ventricular muscle to force the aortic valve open and send blood into the aorta. And contractility is the ability of the myocardium to contract normally.
Decreased SV commonly indicates hypovolemia, increased systemic vascular resistance, or heart failure. Increased SV can result from hypervolemia or decreased systemic vascular resistance.
Cardiac Output
A patient's CO, the amount of blood pumped by the ventricles each minute, is usually 5 to 7 liters per minute. You can calculate CO by multiplying a patient's SV by his heart rate for 1 minute.
A decreased CO may indicate that a patient has one of these conditions:
heart failure
decreased blood volume
arterial or venous obstruction
anaphylactic shock
septic shock.
An increased CO may indicate that a patient has one of these conditions:
decreased systemic vascular resistance
sepsis
an intrauterine pregnancy.
Systemic Vascular Resistance
Systemic vascular resistance, the amount of resistance in peripheral blood vessels, also plays a major role in regulating blood pressure. The vasomotor tone of the vessels primarily determines systemic vascular resistance. When vascular resistance is high, a patient's blood pressure rises.
The amount of a patient's circulating blood volume influences his systemic vascular resistance. If blood flow decreases, the body compensates by increasing systemic vascular resistance, making the arteries and arterioles adjust their internal diameter. A small change in the diameter of an artery or arteriole creates a major change in systemic vascular resistance: As the vessel lumen decreases, the resistance increases. This system increases arterial pressure to maintain blood pressure as near normal as possible. In contrast, when systemic vessels dilate and systemic vascular resistance falls, blood pressure decreases
Blood Viscosity and Arterial Elasticity
Two other hemodynamic factors affecting blood pressure are blood viscosity and elasticity of the arterial walls. Increased blood viscosity, which causes increased blood pressure, results from polycythemia, an abnormal increase of RBC mass in relation to blood plasma.
Decreased elasticity of the arterial walls can also cause increased blood pressure. In many cases, decreased elasticity results from arteriosclerosis.
