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Cardiac afterload




Cardiovascular system

Cardiac afterload


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High Yield Notes
10 pages

Cardiac afterload

10 flashcards

USMLE® Step 1 style questions USMLE

1 questions

A researcher is studying the effect that different pathologies have on cardiac physiology. Which of the following conditions will most likely result in a decreased cardiac afterload?  

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Content Reviewers:

Viviana Popa, MD

Cardiac afterload is one of the main factors that influence how much blood the heart pumps out with each heartbeat, or stroke.

Now, remember that the heart has two upper chambers: the left atrium, which receives oxygenated blood from the lungs via the pulmonary veins; and the right atrium, which receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava.

From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries.

Alright, now, each heartbeat consists of two phases: systole, which is when the heart contracts and pumps the blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood.

And as the left ventricle fills with blood during diastole, the pressure within it rises.

Then the left ventricle contracts, increasing the pressure within the left ventricle even more and forcing blood through the aortic valve into the aorta and whole arterial system.

So, cardiac afterload can be defined as the ventricular wall stress during systole or ejection.

And it can be calculated using the law of Laplace, which states that wall stress = pressure (P) x radius (R) / 2 x wall thickness (W).

Another way to say this is that cardiac afterload is directly proportional to the pressure inside the left ventricle during ejection as well as the radius of the left ventricle, and indirectly proportional to two times the ventricular wall thickness.

To visualize this, let’s look at a cross-section of the left ventricle, which looks a bit like a doughnut, with little dough.

A diet doughnut, if you will. Now, the little dough circle represents the wall of the left ventricle, and its thickness is the ventricular wall thickness, or W. Pressure, or P, on the other hand, refers to the pressure exerted by the ventricular wall on the ventricular cavity during systole.

And finally, the radius is the distance from the center of the ventricle to the outer edge. So...actually, the radius, or R, comprises of an inner radius, or Rin, which is the radius of the ventricular cavity, and the full radius is Rin plus the ventricular wall thickness.

And if you thought we were done with math, hold your horses. There’s one more formula we need to calculate the inner radius, which is: Rin=3 square root 3V / 4π, where V is the volume of the left ventricle, or Rin = (3V/4π)⅓.

And then we can add wall thickness to the inner radius to determine the left ventricular end-diastolic radius, or R.

Now, it’s important to note that this formula isn’t used in clinical practice.

Instead, clinicians simplified the equation by eliminating two variables: radius and wall thickness.

So for simplicity’s sake, we can say that left ventricular wall stress during ejection is proportional to left ventricular pressure during ejection.

And if we assume that left ventricular pressure during ejection is equal to aortic pressure during ejection, then we can say that left ventricular pressure during ejection is equal to what we commonly know as systolic blood pressure.

This leads us to a most commonly used definition of afterload, which says that afterload is the amount of resistance that the ventricles must overcome during systole.


Afterload is the amount of work the heart has to do to pump blood to the rest of the body. It's determined by the resistance to flow in the arteries. Blood vessels can become narrower (vasoconstriction) or wider (vasodilation), and this affects afterload.

The heart muscle contracts and relaxes to pump blood. During systole, contraction occurs, which ejects blood from the ventricles into the aorta and other arteries. Then, during diastole, relaxation occurs and blood flows back into the ventricles from the atria.

Afterload directly affects how much force is needed to eject blood from the ventricles during systole. If afterload is high, the ventricles have to work harder to pump blood out, and this can lead to heart failure. There are many factors that can influence the afterload, such as valvular heart diseases, hypertension, and narrowing of arteries by conditions such as atherosclerosis.

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  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Afterload mismatch and preload reserve: A conceptual framework for the analysis of ventricular function" Progress in Cardiovascular Diseases (1976)
  6. "Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies" The Lancet (2002)