Cardiac afterload


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Cardiac afterload

Cardiovascular system

Anatomy and physiology

Cardiovascular system anatomy and physiology

Lymphatic system anatomy and physiology

Coronary circulation


Blood pressure, blood flow, and resistance

Pressures in the cardiovascular system

Laminar flow and Reynolds number

Resistance to blood flow

Compliance of blood vessels

Control of blood flow circulation

Microcirculation and Starling forces

Cardiac output

Measuring cardiac output (Fick principle)

Stroke volume, ejection fraction, and cardiac output

Cardiac contractility

Frank-Starling relationship

Cardiac preload

Cardiac afterload

Law of Laplace

Cardiac and vascular function curves

Altering cardiac and vascular function curves

Cardiac cycle and pressure-volume loops

Cardiac cycle

Cardiac work

Pressure-volume loops

Changes in pressure-volume loops

Cardiovascular physiological responses

Physiological changes during exercise

Cardiovascular changes during hemorrhage

Cardiovascular changes during postural change

Auscultation of the heart

Normal heart sounds

Abnormal heart sounds

Myocyte electrophysiology

Action potentials in myocytes

Action potentials in pacemaker cells

Excitability and refractory periods

Cardiac excitation-contraction coupling


Electrical conduction in the heart

Cardiac conduction velocity

ECG basics

ECG normal sinus rhythm

ECG intervals

ECG QRS transition

ECG axis

ECG rate and rhythm

ECG cardiac infarction and ischemia

ECG cardiac hypertrophy and enlargement

Blood pressure regulation



Renin-angiotensin-aldosterone system


Cardiac afterload


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USMLE® Step 1 questions

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High Yield Notes

10 pages


Cardiac afterload

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USMLE® Step 1 style questions USMLE

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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?  

External References

First Aid








ACE inhibitors p. 634

preload/afterload effects p. 292


auscultation and p. 297

cardiac output p. 291

hydralazine p. 325

in shock p. 319

Angiotensin II receptor blockers p. 634

preload/afterload effects p. 292


afterload effects p. 292

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Content Reviewers

Viviana Popa, MD


Filip Vasiljević, MD

Evan Debevec-McKenney

Salma Ladhani, MD

Pauline Rowsome, BSc (Hons)

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.


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.


  1. "Medical Physiology" Elsevier (2016)
  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)

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