Part of the TeachMe Series

Control of Stroke Volume

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Original Author(s): Abi Badrick
Last updated: 31st December 2020
Revisions: 24

Original Author(s): Abi Badrick
Last updated: 31st December 2020
Revisions: 24

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Cardiac output is defined as stroke volume multiplied by heart rate. This is therefore affected by stroke volume and sympathetic/parasympathetic output to the heart.

Stroke volume is affected by how much the heart fills in diastole and how easy it is for blood to be expelled in systole. This article will look at components of stroke volume, how it is regulated, and Starling’s law.

Stroke Volume

Stroke volume is defined as the difference between the volume of blood in the heart at the end of diastole (filling of the left ventricle) and the volume remaining in the heart at the end of systole- i.e. the volume of blood that is expelled with each heartbeat.

Control of stroke volume is therefore directly related to the amount the heart fills and the heart’s ability to pump blood into the arteries.

There are several factors that can affect stroke volume:

  • Central venous pressure (CVP) is the blood pressure in the vena cava near the right atrium. It reflects the volume of blood returning to the heart and the ability of the heart to pump the blood back into the arteries. Changes to the CVP result in a change to the diastolic filling pressure.
  • Total peripheral resistance/arterial resistance dictates how easy it is for the heart to expel blood.
  • The preload of the heart is the volume of venous blood that stretches the resting cardiac muscle. Preload is increased by an increase in venous return (i.e central venous pressure).

Central venous pressure increases if the volume of blood in the venous system increases. This increases the diastolic filling pressure and therefore increases the volume of blood that is available to be pumped out. This is explained by Starling’s law of the heart.

Fig 1 – Table to show factors affecting stroke volume.

Starling’s Law

Starling’s law states that the more the heart chambers fill, the stronger the ventricular contraction, and the greater the stroke volume. Therefore a rise in central venous pressure will result in an increased stroke volume automatically. This occurs because as the heart muscle fills and stretches, it creates more regions of overlap for actin-myosin cross-bridges to form, allowing for a greater force of contraction. However, as more cross-bridges form, there will be more cross-bridge cycling occurring which requires lots of energy.

This is based on the principle that the force developed in a muscle fibre depends on the degree to which the fibre is stretched. There is an optimal muscle fibre length from which the most forceful contraction occurs. Therefore, when the filling pressure (preload) is too high, the optimal fibre length is surpassed, resulting in a decrease in contractility and stroke volume.

The Starling curve relates stroke volume to venous pressure and the slope defines the contractility of the ventricles.

Fig 2 – Frank-Starling curve showing the relationship between end-diastolic pressure and stroke volume.

Regulation

Contractility is also controlled by the autonomic nervous system. It has both sympathetic and parasympathetic (vagal) innervation that act to increase or decrease heart rate and contractility. The sympathetic nervous system acts via beta-1 adrenoceptors and increases contractility (positive inotropic effect). The parasympathetic nervous system acts via muscarinic (M2) receptors and decreases contractility (negative inotropic effect).

Autonomic control is regulated by the medulla oblongata in the brainstem. It receives sensory input from peripheral and central baroreceptors and chemoreceptors located in the carotid sinus, arch of the aorta and carotid body. This allows for rapid control of the total peripheral resistance (TPR) and blood pressure.

TPR increases with vasoconstriction and increases arterial blood pressure. Consequently, this makes it difficult for the heart to expel blood into the arteries thus reducing stroke volume.

Clinical Relevance – Shock

Shock is defined as an acute condition resulting in inadequate blood flow and reduced tissue perfusion/ oxygenation. This may be due to several causes:

  • Cardiogenic Shock – In this case, the CVP may be normal or raised. This means that the heart is able to fill with blood, but fails to pump effectively, causing a dramatic drop in arterial blood pressure. This reduces tissue perfusion, which in the case of coronary arteries, exacerbates ischemia of the heart muscle.
  • Mechanical Shock – In the case of cardiac tamponade, blood or fluid builds up in the pericardial space which restricts the filling of the heart. This results in high central venous pressure and low arterial blood pressure. However, electrical activity remains normal as the heart still attempts to beat.
  • Hypovolemic Shock – Losing one fifth or more of the body’s circulating blood volume can cause hypovolemic shock. This can be due to direct blood loss eg. via the gastrointestinal tract or fluid loss due to diarrhoea or vomiting. This reduces arterial blood pressure and impairs organ perfusion.

Typical symptoms include tachycardia, rapid and shallow breathing, and reduced blood pressure, although symptoms may vary slightly depending on the cause. Treatment is typically supportive and includes fluid resuscitation and treatment of a specific cause.