Question 13

Describe the cardiovascular effects of a sudden increase in afterload.

[Click here to toggle visibility of the answers]

College Answer

It was expected the answer would start with a definition of afterload and then proceeded to 
indicate what effects this increase in afterload would have on ventricular end-systolic pressure, 
ventricular end-diastolic pressure, left atrial pressure, cardiac output, myocardial oxygen 
demand and myocardial work, coronary blood flow and systemic blood pressure. 
Most candidates who failed to pass this question submitted answers that were just too brief, 
only including a small subset of the material required. Very few candidates included any 
mention of myocardial oxygen demand or myocardial work or the impact upon the cardiac 
output. A number of candidates included a detailed description of the Sympathetic Nervous 
System and the Renin-Angiotensin system, material which was not asked for. There were 
quite a number of incorrect perceptions about what effect a sudden increase in afterload would 
have on the systemic blood pressure. Candidates who mentioned the baroreceptor response 
and the stretch receptor response where rewarded with additional credit.


Afterload can be defined as the resistance to ventricular ejection - the "load" that the heart must eject blood against. It consists of two main sets of determinant factors:

  • Myocardial wall stress
  • Input impedance
Physiological Consequences of a Sudden Increase in Afterload
Cardiovascular variable How it changes with increased afterload, and why
Cardiac output

Ideally, remains stable if all the compensatory reflexes work as they are supposed to.

Realistically, will be decreased for a period, and then return to normal

Heart rate

Ideally, remains stable. Or:

  • Decreases, if this increase in afterload is associated with increased carotid pressure
  • Increases, if the increase in afterload is associated with decreased cardiac output and lower blood pressure 
Stroke volume

Decreases; because of:

  • Increase in diastolic pressure (earlier closure of the aortic valve)
  • Increased end-systolic volume

Increases, because of:

  • End-systolic volume and pressure increase
  • This results in an increase in the end-diastolic volume

Increases, because of the acute increase in preload (as above)

  • Thus, Frank-Starling mechanism causes an increase in contractility (this is the basis of the Anrep effect).
  • As a result, stroke volume increases slightly, retuning it closer to normal (unless the ventricle is failing)
Myocardial oxygen consumption
  • Increases because of: increased  intraventricular pressure
Coronary blood flow
  • Should remain stable because of coronary bloodflow autoregulation
  • Capillary perfusion (especially subendocardial) will suffer because of increased LV pressure


Freeman, GREGORY L. "Effects of increased afterload on left ventricular function in closed-chest dogs." American Journal of Physiology-Heart and Circulatory Physiology 259.2 (1990): H619-H625.

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.