Afterload
|
WikiDoc Resources for Afterload |
|
Articles |
|---|
|
Most recent articles on Afterload |
|
Media |
|
Evidence Based Medicine |
|
Clinical Trials |
|
Ongoing Trials on Afterload at Clinical Trials.gov Clinical Trials on Afterload at Google
|
|
Guidelines / Policies / Govt |
|
US National Guidelines Clearinghouse on Afterload
|
|
Books |
|
News |
|
Commentary |
|
Definitions |
|
Patient Resources / Community |
|
Patient resources on Afterload Discussion groups on Afterload Directions to Hospitals Treating Afterload Risk calculators and risk factors for Afterload
|
|
Healthcare Provider Resources |
|
Causes & Risk Factors for Afterload |
|
Continuing Medical Education (CME) |
|
International |
|
|
|
Business |
|
Experimental / Informatics |
| Cardiology Network |
 Discuss Afterload further in the WikiDoc Cardiology Network |
| Adult Congenital |
|---|
| Biomarkers |
| Cardiac Rehabilitation |
| Congestive Heart Failure |
| CT Angiography |
| Echocardiography |
| Electrophysiology |
| Cardiology General |
| Genetics |
| Health Economics |
| Hypertension |
| Interventional Cardiology |
| MRI |
| Nuclear Cardiology |
| Peripheral Arterial Disease |
| Prevention |
| Public Policy |
| Pulmonary Embolism |
| Stable Angina |
| Valvular Heart Disease |
| Vascular Medicine |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]
Description
In cardiac physiology, afterload is used to mean the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle. However, the strict definition of the term relates to the properties of a single cardiac myocyte. It is therefore only of direct relevance in the laboratory; in the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent.
Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber. Everything else held equal, as afterload increases, cardiac output decreases.
In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the peripheral blood pressure in order to open the aortic valve.
Pathology
Disease processes that increase the left ventricular afterload include increased blood pressure and aortic valve disease.
Hypertension (Increased blood pressure) increases the left ventricular afterload because the left ventricle has to 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.
Aortic stenosis increases the afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order 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 150 mmHg in order to open the aortic valve and eject blood into the aorta.
Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure as well as dialostic blood pressure.
Mitral regurgitation decreases the afterload. During ventricular systole, the blood can regurgitate through the diseased mitral valve as well as be ejected through the aortic valve. This means that the left ventricle has to work less to eject blood, causing a decreased afterload. Afterload is largely dependent upon aortic pressure.