Afterload

Uses your system voice; voice and rate in settings.

Snapshot

≈ 3 min read

Names in other languages

No names in other languages are held for this entry yet.

Article bodies are English and are not machine-translated. A name in another language is not a translation of the article.

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. 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. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury (mm Hg). The clinical concept of afterload was given its modern operational definitions through the work of American cardiologist Edmund Sonnenblick and colleagues at the National Institutes of Health in the early 1960s. Sonnenblick's force-velocity studies of isolated cardiac muscle demonstrated that afterload directly determines the velocity of myocardial fiber shortening, providing the theoretical basis for afterload reduction as a therapeutic strategy in heart failure.

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. 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. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury (mm Hg). The clinical concept of afterload was given its modern operational definitions through the work of American cardiologist Edmund Sonnenblick and colleagues at the National Institutes of Health in the early 1960s. Sonnenblick's force-velocity studies of isolated cardiac muscle demonstrated that afterload directly determines the velocity of myocardial fiber shortening, providing the theoretical basis for afterload reduction as a therapeutic strategy in heart failure. \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. ==References== ==Further reading== ==External links== Overview at cvphysiology.com

Text derived from https://en.wikipedia.org/w/index.php?oldid=1348285660 under CC BY-SA 4.0; modifications have been made.