Afterload

Afterload is the tension or stress developed in the wall of the left ventricle during ejection. In other words, it is the end Load against which the heart contracts to eject blood. Afterload is readily broken into components; aortic pressure and/or the pressure the ventricle must over come to eject blood. The greater the aortic/pulmonary pressure, the greater the after load on the left/right ventricle, respectively. Following Laplace's law, the tension upon the muscle fibers in the heart wall is the product of the pressure within the ventricle, multiplied by the volume within the ventricle, divided by the wall thickness. 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. Conversely, a hypertrophied left ventricle has a lower afterload. 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.

Afterload can also be described as the pressure that the chambers of the heart must generate in order to eject blood out of the heart and thus is a consequence of the 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.

Preload best describes the maximum viscous blood volume at the end of diastole while afterload better describes the maximum tension of the myocardial muscle mass at the end of systole. Precise mathematical labeling of afterload and preload is a challenge since both maximum measurements (volume/tension) occur simultaneously in late systole.

Read more about Afterload:  Pathology

Other articles related to "afterload":

Afterload - Pathology
... pathology that include indicators such as an increasing left ventricular afterload include elevated blood pressure and aortic valve disease ... blood pressure) increases the left ventricular (LV) afterload because the LV must work harder to eject blood into the aorta ... 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 intraventricular cardiac septum ...
Stroke Volume - Determinants - Afterload
... Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume ... affecting stroke volume in healthy individuals, increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume ... Increased afterload may be found in aortic stenosis and arterial hypertension ...
Contractility - Model As A Contributing Factor
... to be Heart rate Conduction velocity Preload Afterload Contractility By this model, if myocardial performance changes while preload, afterload, heart rate, and conduction velocity are all held ... An increase in afterload will increase contractility (through the Anrep effect) ...