Afterload

Last updated June 23, 2024

Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure.^[1] As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system.^[1] Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury (mm Hg).

Hemodynamics

Afterload is a determinant of cardiac output.^[1] Cardiac output is the product of stroke volume and heart rate.^[2] Afterload is a determinant of stroke volume (in addition to preload, and strength of myocardial contraction).^[1]

Following Laplace's law, the tension upon the muscle fibers in the heart wall is the pressure within the ventricle multiplied by the volume within the ventricle divided by the wall thickness (this ratio is the other factor in setting the afterload). Therefore, when comparing a normal heart to a heart with a dilated left ventricle, if the aortic pressure is the same in both hearts, the dilated heart must create a greater tension to overcome the same aortic pressure to eject blood because it has a larger internal radius and volume. Thus, the dilated heart has a greater total load (tension) on the myocytes, i.e., has a higher afterload. This is also true in the eccentric hypertrophy consequent to high-intensity aerobic training. Conversely, a concentrically hypertrophied left ventricle may have a lower afterload for a given aortic pressure. When contractility becomes impaired and the ventricle dilates, the afterload rises and limits output. This may start a vicious circle, in which cardiac output is reduced as oxygen requirements are increased.^[3]

Afterload can also be described as the pressure that the chambers of the heart must generate to eject blood from the heart, and this is a consequence of aortic pressure (for the left ventricle) and pulmonic pressure or pulmonary artery pressure (for the right ventricle). The pressure in the ventricles must be greater than the systemic and pulmonary pressure to open the aortic and pulmonic valves, respectively. As afterload increases, cardiac output decreases. Cardiac imaging is a somewhat limited modality in defining afterload because it depends on the interpretation of volumetric data.^{[ citation needed ]}

Calculating afterload

Quantitatively, afterload can be calculated by determining the wall stress of the left ventricle, using the Young–Laplace equation:^{[ citation needed ]}

${\textstyle \left({\frac {EDP\cdot EDR}{2h}}\right)}$ where

EDP is end-diastolic pressure in the left ventricle, which is typically approximated by taking pulmonary artery wedge pressure,

EDR is end-diastolic radius at the midpoint of the left ventricle, and

h is the mean thickness of the left ventricle wall. Both radius and mean thickness of the left ventricle may be measured by echocardiography.

Factors affecting afterload

Disease processes pathology that include indicators such as an increasing left ventricular afterload include elevated blood pressure and aortic valve disease.^[4]

Systolic hypertension (HTN) (elevated blood pressure) increases the left ventricular (LV) afterload because the LV must work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure in the aorta.^[5]

Pulmonary hypertension (PH) is increased blood pressure within the right heart leading to the lungs. PH indicates a regionally applied increase in afterload dedicated to the right side of the heart, divided and isolated from the left heart by the interventricular septum.^[6]

In the natural aging process, aortic stenosis often increases afterload because the left ventricle must overcome the pressure gradient caused by the calcified and stenotic aortic valve, in addition to the blood pressure required to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 110 mmHg to open the aortic valve and eject blood into the aorta.^[7]

Due to the increased afterload, the ventricle has to work harder to accomplish its goal of ejecting blood into the aorta. Thus, in the long-term, increased afterload (due to the stenosis) results in hypertrophy of the left ventricle to account for the increased work required and also to decrease wall stress since wall thickness and wall stress are inversely proportional.^[8]

Aortic insufficiency (Aortic Regurgitation) increases afterload, because a percentage of the blood that ejects forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure. The diastolic blood pressure in the aorta falls, due to regurgitation. This increases pulse pressure.^[9]

Mitral regurgitation (MR) decreases afterload. In ventricular systole under MR, regurgitant blood flows backwards/retrograde back and forth through a diseased and leaking mitral valve. The remaining blood loaded into the LV is then optimally ejected out through the aortic valve. With an extra pathway for blood flow through the mitral valve, the left ventricle does not have to work as hard to eject its blood, i.e. there is a decreased afterload.^[10] Afterload is largely dependent upon aortic pressure.

Related Research Articles

A heart valve is a biological one-way valve that allows blood to flow in one direction through the chambers of the heart. Four valves are usually present in a mammalian heart and together they determine the pathway of blood flow through the heart. A heart valve opens or closes according to differential blood pressure on each side.

Heart sounds are the noises generated by the beating heart and the resultant flow of blood through it. Specifically, the sounds reflect the turbulence created when the heart valves snap shut. In cardiac auscultation, an examiner may use a stethoscope to listen for these unique and distinct sounds that provide important auditory data regarding the condition of the heart.

The aortic valve is a valve in the heart of humans and most other animals, located between the left ventricle and the aorta. It is one of the four valves of the heart and one of the two semilunar valves, the other being the pulmonary valve. The aortic valve normally has three cusps or leaflets, although in 1–2% of the population it is found to congenitally have two leaflets. The aortic valve is the last structure in the heart the blood travels through before stopping the flow through the systemic circulation.

Heart murmurs are unique heart sounds produced when blood flows across a heart valve or blood vessel. This occurs when turbulent blood flow creates a sound loud enough to hear with a stethoscope. The sound differs from normal heart sounds by their characteristics. For example, heart murmurs may have a distinct pitch, duration and timing. The major way health care providers examine the heart on physical exam is heart auscultation; another clinical technique is palpation, which can detect by touch when such turbulence causes the vibrations called cardiac thrill. A murmur is a sign found during the cardiac exam. Murmurs are of various types and are important in the detection of cardiac and valvular pathologies.

Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.

A ventricle is one of two large chambers located toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the ventricle per beat. Stroke volume is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat from the volume of blood just prior to the beat. The term stroke volume can apply to each of the two ventricles of the heart, although when not explicitly stated it refers to the left ventricle and should therefore be referred to as left stroke volume (LSV). The stroke volumes for each ventricle are generally equal, both being approximately 90 mL in a healthy 70-kg man. Any persistent difference between the two stroke volumes, no matter how small, would inevitably lead to venous congestion of and/or shunt between the systemic and the pulmonary circulation.

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

Mitral stenosis is a valvular heart disease characterized by the narrowing of the opening of the mitral valve of the heart. It is almost always caused by rheumatic valvular heart disease. Normally, the mitral valve is about 5 cm² during diastole. Any decrease in area below 2 cm² causes mitral stenosis. Early diagnosis of mitral stenosis in pregnancy is very important as the heart cannot tolerate increased cardiac output demand as in the case of exercise and pregnancy. Atrial fibrillation is a common complication of resulting left atrial enlargement, which can lead to systemic thromboembolic complications such as stroke.

Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

Mitral regurgitation (MR), also known as mitral insufficiency or mitral incompetence, is a form of valvular heart disease in which the mitral valve is insufficient and does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts. Mitral regurgitation is the most common form of valvular heart disease.

In cardiac physiology, preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole. Preload is directly related to ventricular filling. As the relaxed ventricle fills during diastole, the walls are stretched and the length of sarcomeres increases. Sarcomere length can be approximated by the volume of the ventricle because each shape has a conserved surface-area-to-volume ratio. This is useful clinically because measuring the sarcomere length is destructive to heart tissue. It requires cutting out a piece of cardiac muscle to look at the sarcomeres under a microscope. It is currently not possible to directly measure preload in the beating heart of a living animal. Preload is estimated from end-diastolic ventricular pressure and is measured in millimeters of mercury (mmHg).

A transthoracic echocardiogram (TTE) is the most common type of echocardiogram, which is a still or moving image of the internal parts of the heart using ultrasound. In this case, the probe is placed on the chest or abdomen of the subject to get various views of the heart. It is used as a non-invasive assessment of the overall health of the heart, including a patient's heart valves and degree of heart muscle contraction. The images are displayed on a monitor for real-time viewing and then recorded.

Valvular heart disease is any cardiovascular disease process involving one or more of the four valves of the heart. These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

Volume overload refers to the state of one of the chambers of the heart in which too large a volume of blood exists within it for it to function efficiently. Ventricular volume overload is approximately equivalent to an excessively high preload. It is a cause of cardiac failure.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

<span class="mw-page-title-main">Ventricular outflow tract obstruction</span> Medical condition

A ventricular outflow tract obstruction is a heart condition in which either the right or left ventricular outflow tract is blocked or obstructed. These obstructions represent a spectrum of disorders. Majority of these cases are congenital, but some are acquired throughout life.

The handgrip maneuver is performed by clenching one's fist forcefully for a sustained time until fatigued. Variations include squeezing an item such as a rolled up washcloth.

References

1 2 3 4 Mohrman, David E. (2018). Cardiovascular Physiology, 9e. McGraw-Hill Education LLC. ISBN 9781260026115. OCLC 1055827575.
↑ King, J; Lowery, DR (2019), "article-18897", Physiology, Cardiac Output, Treasure Island (FL): StatPearls Publishing, PMID 29262215 , retrieved 2019-12-20
↑ Kasper, Dennis L; Braunwald, Eugene; Fauci, Anthony; et al. (2005). Harrison's Principles of Internal Medicine (16th ed.). New York: McGraw-Hill. pp. 1346. ISBN 0-07-139140-1.
↑ LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.
↑ Homoud, MK (Spring 2008). "Introduction to Cardiovascular Pathophysiology" (PDF). Tufts Open Courseware. Tufts University. p. 10. Retrieved 2010-05-04.
↑ LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.
↑ LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.
↑ LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.
↑ "Aortic Regurgitation". The Lecturio Medical Concept Library. Retrieved 30 June 2021.
↑ Klabunde RE (2007-04-05). "Mitral Regurgitation". Cardiovascular Physiology Concepts. Richard E. Klabunde. Archived from the original on 3 January 2010. Retrieved 2010-01-01.

External links

Overview at cvphysiology.com

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.

[:0-1] 1 2 3 4 Mohrman, David E. (2018). Cardiovascular Physiology, 9e. McGraw-Hill Education LLC. ISBN 9781260026115. OCLC 1055827575.

[King_Lowery_2019_p.-2] King, J; Lowery, DR (2019), "article-18897", Physiology, Cardiac Output, Treasure Island (FL): StatPearls Publishing, PMID 29262215 , retrieved 2019-12-20

[Harrison's-3] Kasper, Dennis L; Braunwald, Eugene; Fauci, Anthony; et al. (2005). Harrison's Principles of Internal Medicine (16th ed.). New York: McGraw-Hill. pp. 1346. ISBN 0-07-139140-1.

[4] LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.

[Homoud2008-5] Homoud, MK (Spring 2008). "Introduction to Cardiovascular Pathophysiology" (PDF). Tufts Open Courseware. Tufts University. p. 10. Retrieved 2010-05-04.

[6] LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.

[7] LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.

[8] LaCombe, P; Tariq, M; Tariq, S. "Physiology, Afterload Reduction". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 30 June 2021.

[9] "Aortic Regurgitation". The Lecturio Medical Concept Library. Retrieved 30 June 2021.

[KlabundeMR2007-10] Klabunde RE (2007-04-05). "Mitral Regurgitation". Cardiovascular Physiology Concepts. Richard E. Klabunde. Archived from the original on 3 January 2010. Retrieved 2010-01-01.

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]