Editing Afterload (section)

== Hemodynamics ==
Afterload is a determinant of [[cardiac output]].<ref name=":0" />  Cardiac output is the product of [[stroke volume]] and [[heart rate]].<ref name="King Lowery 2019 p. ">{{citation | last=King | first=J | last2=Lowery | first2=DR | title=Physiology, Cardiac Output | chapter=article-18897 | publisher=StatPearls Publishing | location=Treasure Island (FL) | year=2019 | pmid=29262215 | url=http://www.ncbi.nlm.nih.gov/books/NBK470455/ | access-date=2019-12-20 }}</ref>  Afterload is a determinant of stroke volume (in addition to [[Preload (cardiology)|preload]], and [[Contractility|strength of myocardial contraction]]).<ref name=":0" /> 

Following [[Young–Laplace equation|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.<ref name="Harrison's">{{cite book|author1=Kasper, Dennis L |author2=Braunwald, Eugene |author3=Fauci, Anthony |title=Harrison's Principles of Internal Medicine |url=https://archive.org/details/harrisonsprincip00kasp |url-access=limited |edition=16th |publisher=McGraw-Hill|location=New York|year=2005|pages= [https://archive.org/details/harrisonsprincip00kasp/page/n1374 1346]|isbn=0-07-139140-1|display-authors=etal}}</ref>

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 valve|aortic]] and [[pulmonic valve]]s, 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|date=August 2011}}