Editing Afterload (section)

== Factors affecting afterload ==

Disease processes [[pathology]] that include indicators such as an increasing [[left ventricle|left ventricular]] afterload include elevated [[blood pressure]] and [[aortic valve]] disease.<ref>{{cite web |last1= LaCombe | first1= P |last2= Tariq |first2= M |last3= Tariq |first3= S |date= | url= https://www.ncbi.nlm.nih.gov/books/NBK493174/ | title= Physiology, Afterload Reduction
| website= National Center for Biotechnology Information, U.S. National Library of Medicine |access-date= 30 June 2021}}</ref>

[[Systolic hypertension]] (HTN) (elevated blood pressure) increases the left ventricular (LV) afterload because the LV must [[Work (physics)|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.<ref name='Homoud2008'>{{cite web|url=http://ocw.tufts.edu/data/50/636804.pdf |title=Introduction to Cardiovascular Pathophysiology |access-date=2010-05-04 |last=Homoud |first=MK |date=Spring 2008 |work=Tufts Open Courseware |publisher=Tufts University|page=10 }}</ref>

[[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]].<ref>{{cite web |last1= LaCombe | first1= P |last2= Tariq |first2= M |last3= Tariq |first3= S |date= | url= https://www.ncbi.nlm.nih.gov/books/NBK493174/ | title= Physiology, Afterload Reduction
| website= National Center for Biotechnology Information, U.S. National Library of Medicine |access-date= 30 June 2021}}</ref>

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.<ref>{{cite web |last1= LaCombe | first1= P |last2= Tariq |first2= M |last3= Tariq |first3= S |date= | url= https://www.ncbi.nlm.nih.gov/books/NBK493174/ | title= Physiology, Afterload Reduction
| website= National Center for Biotechnology Information, U.S. National Library of Medicine |access-date= 30 June 2021}}</ref>

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.<ref>{{cite web |last1= LaCombe | first1= P |last2= Tariq |first2= M |last3= Tariq |first3= S |date= | url= https://www.ncbi.nlm.nih.gov/books/NBK493174/ | title= Physiology, Afterload Reduction
| website= National Center for Biotechnology Information, U.S. National Library of Medicine |access-date= 30 June 2021}}</ref>

[[Aortic insufficiency|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 [[Systole (medicine)|systolic]] blood pressure. The diastolic blood pressure in the aorta falls, due to regurgitation. This increases pulse pressure.<ref>{{cite web |url= https://www.lecturio.com/concepts/aortic-regurgitation/ | title= Aortic Regurgitation | website= The Lecturio Medical Concept Library |access-date= 30 June 2021}}</ref>

[[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.<ref name='KlabundeMR2007'>{{cite web|url=http://www.cvphysiology.com/Heart%20Disease/HD009c.htm |title=Mitral Regurgitation |access-date=2010-01-01 |author=Klabunde RE |date=2007-04-05 |work=Cardiovascular Physiology Concepts |publisher=Richard E. Klabunde | archive-url= https://web.archive.org/web/20100103195916/http://cvphysiology.com/Heart%20Disease/HD009c.htm| archive-date= 3 January 2010 | url-status= live}}</ref>  Afterload is largely dependent upon aortic pressure.