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Cardiac Output II: Effect of Stroke Volume on Cardiac Output

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Cardiac output is the amount of blood pushed by one ventricle per minute.

A key component of cardiac output is stroke volume, the blood volume pushed from one ventricle per heartbeat.

Stroke volume is influenced by three main factors: preload, afterload, and contractility.

Firstly, preload is the degree of stretch of the ventricular cardiac myocytes at the end of diastole, influenced by blood returning to the heart.

Factors like elevated blood volume and increased venous return raise preload, while dehydration and blood loss decrease it.

Next, afterload is the pressure the left ventricle must overcome to eject blood during systole. Higher afterload from arterial vasoconstriction decreases stroke volume, whereas lower afterload from arterial vasodilation increases it.

Finally, contractility, the heart muscle's ability to contract, impacts stroke volume. Increased contractility, influenced by the sympathetic nervous system and certain medications, boosts stroke volume and cardiac output.

Factors like hypoxia and acidosis reduce contractility and stroke volume.

Overview

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Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.

Preload

Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The preload is proportional to the left ventricular end-diastolic pressure. According to the Frank-Starling law, an increase in preload leads to a greater force of contraction up to a physiological limit, thereby increasing stroke volume. Factors that increase preload include elevated blood volume and increased venous return, while factors such as dehydration, blood loss, and the use of vasodilators decrease preload.

Afterload

Afterload, the resistance the left ventricle must overcome to circulate blood is influenced by systemic vascular resistance and arterial blood pressure. An increase in afterload, such as arterial vasoconstriction, decreases stroke volume as the heart works harder to pump the blood. Conversely, arterial vasodilation reduces afterload, enhancing stroke volume by decreasing the resistance against which the heart pumps. Conditions that raise afterload include hypertension and aortic stenosis, whereas factors like vasodilating agents can reduce it.

Contractility

Contractility denotes the intrinsic ability of cardiac muscle fibers to contract at any given muscle fiber length, independent of preload and afterload. Enhanced contractility increases stroke volume and cardiac output and is influenced by sympathetic nervous system activity, circulating catecholamines, and certain medications such as inotropic agents. Factors that negatively impact contractility include hypoxia, acidosis, and beta-blockers. The relationship between muscle fiber length and contraction strength, as explained by the Frank-Starling law, is crucial here: the greater the stretch during filling (within limits), the more forceful the following contraction.

Certain pathological conditions, such as heart failure, can significantly impact stroke volume and, accordingly, cardiac output, underscoring the importance of understanding these physiological mechanisms.

Transcript

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