Cardiac Output

Cardiac output is the volume of blood ejected from each ventricle per minute and can vary to meet changing metabolic demands. Cardiac output is calculated by multiplying stroke volume (volume of blood pumped out of one ventricle per beat) by heart rate (the number of heartbeats per minute). Cardiac output is affected by many factors, including hormones and changes in autonomic nervous system activity.

Stroke volume is determined by venous return (the volume of blood returning back to the heart, also known as preload), contractility (the force of contraction), and how much resistance the ventricles are working against in the arteries (afterload). Venous return is increased during activity. As skeletal muscles contract, the compressions on the veins act to pump blood back to the heart. When respiration increases, the changes of pressures in the thoracic and abdominal cavities act to draw blood back to the heart. The total body blood volume directly affects how much blood is available to be returned to the heart. Blood loss will decrease venous return. When changes in blood circulation occur and blood is diverted to different organs, venous return can temporarily be affected. For example, if body temperature increases, a physiological response is to increase blood flow to the skin. Until less blood is sent to other organs, there will be a decrease in the amount of blood available to return to the heart.

The relationship between stroke volume and venous return is the Frank-Starling law of the heart. This law states that when venous return increases, stroke volume increases. As with skeletal muscle, the overlap of the thick and thin filaments in the muscle cells affects the strength of muscle contraction. The myocardium operates at the low end of the curve, so when volume increases in the left ventricle, the muscle cells stretch and the myofilament overlap becomes more optimal for force generation. This increase in the strength of contraction allows the ventricles to fully empty, accommodating for the increased blood volume it is required to move. The strength of muscle contraction when correcting for the muscle length is contractility. Contractility increases with a rise in the exposure to calcium ions, which can occur with an increased activation of the sympathetic nervous system and in the presence of various stimulating agents (epinephrine, thyroxine, glucagon, some drugs). Contractility decreases when concentrations of hydrogen ions and potassium ions increase or when exposed to calcium-blocking drugs. There is a direct correlation between contractility and stroke volume, which in turn affects cardiac output.

Afterload is the amount of resistance the ventricles are working against in the arteries. Afterload only significantly affects cardiac output in individuals suffering from hypertension (high blood pressure). If all other factors stay the same, the stroke volume decreases as afterload increases.

Heart rate is a major contributor to changes in cardiac output. Without neural stimulation, the heartbeat would be around 100 beats/minute. Normal resting levels of healthy adults are lower, so the parasympathetic nervous system, an autonomic division of the nervous system that tends to slow down processes, acts to inhibit the firing rate of the SA node. During periods of exercise or excessive stress, the parasympathetic activity decreases, and sympathetic nervous system activity increases.

Heart rate is also influenced by hormones released by the adrenal glands and thyroid gland and by abnormal ion concentrations in the heart. Adrenal hormones, norepinephrine and epinephrine, are released in response to stress, which results in a higher heart rate. The presences of thyroid hormones increases heart rate. Individuals who do not adequately maintain normal thyroid levels suffer from hypothyroidism (low levels of thyroid hormones) or hyperthyroidism (high levels of thyroid hormones). Hypothyroidism results in a lower than normal resting heart rate, and hyperthyroidism results in an abnormally high resting heart rate. Because normal heart function involves the flow of various electrolytes, changes in these levels can disrupt heart rate. For example, potassium deficiency causes an increased heart rate while high levels result in a decreased heart rate.

Both stroke volume and heart rate are tightly regulated to ensure cardiac output meets the metabolic demands of the body. Deviations in any of the factors controlling these variables will alter the overall cardiac output of an individual.