Question 17

Describe the consequences for the left ventricle of a sudden and sustained increase in afterload.

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College Answer

This question expected a detailed description of the effect of afterload on the left ventricle. This should cover the acute effect of increased afterload on left ventricular end systolic (and diastolic) pressure and volume, contractility, work and oxygen consumption, coronary perfusion pressure and baroreceptor responses. “Sustained” implied more longer term left ventricular exposure which would include the ventricular cellular response, concentric hypertrophy and the subsequent effects on diastolic and elevations of left atrial pressure. Definitions of afterload, cardiac output equations, vascular function curves and LV/PV loops are not required if the above concepts are described in adequate detail. The use of a diagram can assist in explaining concepts however should be linked back to the question in order to demonstrate the candidates understanding of the question being asked.

Discussion

This question is very similar to Question 13 from the first paper of 2016.

Effects of sudden increase in afterload:

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
Preload

Increases, because of:

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

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

Effects of chronically increased afterload:

  • Remodelling of the myocardium:
    • Increased myocyte mass
    • Hypertrophy of the LV wall
  • Results of this
    • Increased contractility
    • Impaired diastolic relaxation
    • Decreased LV compliance
    • Decreased LV end-diastolic volume (if preload is stable)
    • Increased left atrial pressure

References

Tarazi, ROBERT C., and MATTHEW N. Levy. "Cardiac responses to increased afterload. State-of-the-art review." Hypertension 4.3_pt_2 (1982): 8-18.

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.