Cardiac afterload

Definitions & Key takeaways

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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Introduction0:00–0:49

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.

Heartbeat Phases0:49–1:22

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).

Cardiac Afterload1:22–2:43

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.

Left ventricular end-diastolic radius2:43–4:02

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.

Systemic Vascular Resistance4:02–5:20

So left ventricular afterload is affected by systemic vascular resistance, as well as aortic pressure, and valve diseases.
Systemic vascular resistance is the resistance of systemic blood vessels to blood flow. In other words, how readily blood vessels allow blood to flow through them.
Now, systemic vascular resistance is mainly affected by changes in the vessel lumen, which is determined by vasodilating and vasoconstricting factors.
Vasodilating factors, such as atrial natriuretic peptide , or ANP, which is secreted by cardiac muscle cells in the walls of the atria in response to an increased blood volume; relax smooth muscle cells within the vessel walls, thereby widening the vessel lumen.
This results in decreased systemic vascular resistance and therefore, decreased afterload. On the other hand, vasoconstricting factors, such as sympathetic stimulation, constrict smooth muscle cells within the vessel walls, thereby narrowing the vessel lumen.
Eventually, this leads to an increase in systemic vascular resistance and therefore, increased afterload. Next one is aortic pressure.

Aortic Pressure5:20–5:42

Increased aortic pressure means that the heart must contract harder and generate more pressure within the left ventricle in order to overcome aortic pressure and open the aortic valve.
Therefore, increased aortic pressure increases afterload, while decreased aortic pressure reduces afterload. And finally, let’s look at valve diseases.

Valve Diseases5:42–6:30

First, let’s start with the aortic valve, which is between the left ventricle and the aorta. If the aortic valve doesn’t open all the way, which is called aortic stenosis, the heart must generate more pressure in order to eject blood during systole.
This increases the stress on the left ventricular wall, therefore increasing afterload. On the flip side, there’s mitral regurgitation, which is when the mitral valve, which is between the left atrium and the left ventricle, doesn’t close all the way.
So during ejection, blood leaks back into the left atrium. This decreases the stress on the left ventricular wall, therefore decreasing afterload.
Alright, as a quick recap. Afterload is defined as the left ventricular wall stress during systole or ejection.

Review6:30–7:31

Through the law of Laplace, we can say that afterload is directly proportional to the left ventricular pressure during ejection and radius during ejection, and indirectly proportional to two times the left ventricular wall thickness.
But, for simplicity's sake, we 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.
Finally, factors that affect left ventricular afterload include systemic vascular resistance, aortic pressure, and valve diseases, such as aortic stenosis and mitral regurgitation.