Describe the factors that determine right and left ventricular afterload.
This is a big question and required some structure to cover the material required. A Definition of
afterload, factors specific to left ventricle, right ventricle and both were required. The question
asked to describe and not merely list factors affecting afterload.
Marks were not given for describing pathologies rather than physiological processes that affect
afterload. Candidates seemed to lack depth and understanding on this topic.
As if defining something that defies definition was insufficiently cruel.
| Factor | Right ventricle | Left ventricle |
| Afterload overall | The left ventricle has a much higher afterload than the right, mainly because of the increased arterial vascular resistance in the systemic circulation | |
| Transmural pressure | Increased transmural pressure increases afterload in both ventricles. | |
| Intrathoracic pressure | Negative intrathoracic pressure decreases RV afterload | Negative intrathoracic pressure increases LV afterload |
| Positive intrathoracic pressure increases RV afterload | Positive intrathoracic pressure decreases LV afterload | |
| Radius of the ventricle | Dilation of either ventricle will increase the wall stress | |
| Thickness of the wall | RV wall is thin: this has the effect of increasing afterload | LV wall is thicker: this decreases afterload by sharing it among more sarcomeres |
| Arterial compliance | Pulmonary circulation is highly compliant, which minimises RV afterload | Aortic compliance is usually good, as it is an elastic capacitance vessel - this decreases LV afterload |
| Inertia of the blood | Inertia of the column of blood affects both ventricles by increasing afterload early in systole and decreasing afterload in late systole | |
| Ventricular outflow tract resistance | Both ventricles normally have minimal outflow tract resistance | |
| Pulmonary valve can become stenotic and the RVOT can become obstructed | Aortic valve stenosis and LVOT obstruction due to HOCM can occur | |
| Arterial resistance | Pulmonary arteries have very low resistance | Systemic arterial circulation has a much higher resistance, which makes the afterload of the LV much greater |
| Blood viscosity | Blood viscosity affects the right ventricle more, because the pulmonary system has less shear stress | Blood viscosity affects the left ventricle less, because of the non-Neutonian behaviour of blood (with higher shear stress, its viscosity decreases) |
| Vessel radius | The radius of small vessels affects afterload equally for both ventricles | |
Norton, James M. "Toward consistent definitions for preload and afterload."Advances in physiology education 25.1 (2001): 53-61.
ROTHE, CARL. "Toward consistent definitions for preload and afterload—revisited." Advances in physiology education 27.1 (2003): 44-45.
Vest, Amanda R. "Afterload." Cardiovascular Hemodynamics. Humana, Cham, 2019. 23-40.
Milnor, William R. "Arterial impedance as ventricular afterload." Circulation Research 36.5 (1975): 565-570.
Vlachopoulos, Charalambos, Michael O'Rourke, and Wilmer W. Nichols. McDonald's blood flow in arteries: theoretical, experimental and clinical principles. CRC press, 2011. (Specifically, Chapter 12 is gold)
Baskurt, Oguz K., and Herbert J. Meiselman. "Blood rheology and hemodynamics." Seminars in thrombosis and hemostasis. Vol. 29. No. 05. Copyright© 2003 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.:+ 1 (212) 584-4662, 2003.