Cardiac output is defined as stroke volume multiplied by heart rate. Cardiac output is therefore affected by stroke volume.
It 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 is defined as the difference between the end diastolic volume (EDV), the volume of blood in the heart at the end of diastole, and the end systolic volume (ESV) the volume remaining in the heart at the end of systole. Simply put, stroke volume is the amount 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.
Factors affecting stroke volume
There are several factors that can affect stroke volume: central venous pressure (CVP) and Total Peripheral Resistance (TPR).
Central Venous Pressure (CVP)
CVP is the blood pressure in the vena cava as it enters the right atrium. It reflects the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries. Changes to the CVP result in a change to stroke volume. The larger the CVP, the larger the stroke volume, up to a certain point. This is due to two main reasons:
- More blood enters the heart during diastole, leading to an increase in end diastolic volume (EDV)
- The increased filling of the heart leads to increased ventricular contraction and thus a decrease in end systolic volume (ESV), due to Starling’s Law
Increases in central venous pressure leads to an increase in the diastolic filling pressure and stretching of the myocytes. This is also known as preload, so it can be said that increasing central venous pressure increases preload.
Total Peripheral Resistance (TPR)
TPR is the pressure in the arteries that blood must overcome as it passes through them, and thus dictates how easy it is for the heart to expel blood. This is also known as afterload.
Starling’s law states that: the more the heart chambers fill, the stronger the ventricular contraction, and therefore the greater the stroke volume. Therefore, a rise in central venous pressure will result in an increased stroke volume automatically. This is because, as the heart chamber 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 contractile force a muscle fibre can exert depends upon how much it is stretched. There is an optimal muscle fibre length at which the most forceful contraction occurs. At muscle fibres lengths above this however, the fibres cannot overlap more and may end becoming overstretched. 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.
Autonomic regulation of stroke volume
Stroke volume 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 (inotropy). The sympathetic nervous system acts via B1 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 and subsequent ischaemia. This may be due to several causes:
- Cardiogenic shock – In this case, the CVP may be normal or raised. This means the heart is able to fill with blood, but it cannot pump blood effectively. This causes 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/obstructive shock – In cardiac tamponade or constrictive pericarditis, blood or fluid builds up in the pericardial space. This 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 20% or more of the body’s circulating blood volume can cause hypovolemic shock. This can be due to direct blood loss e.g. via the gastrointestinal tract or fluid loss due to diarrhoea or vomiting. The reduced volume of blood reduces arterial blood pressure and impairs organ perfusion.
- Distributive shock – In cases of sepsis, anaphylaxis and spinal cord injury, blood flow (and thus blood pressure) drops due to widespread vasodilation. This vasodilation occurs as a result of cytokine release as part of the inflammatory response or due to loss of sympathetic innervation.
Typical symptoms include tachycardia, rapid and shallow breathing, and hypotension, although symptoms may vary slightly depending on the cause. Treatment is typically supportive and includes fluid resuscitation, vasopressors and treatment of the underlying cause.