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
Hemodynamics
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
Electrocardiography
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
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
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First Aid
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ACE inhibitors p. 634
preload/afterload effects p. 292
Afterload
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
Vasodilators
afterload effects p. 292
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Transcript
Content Reviewers
Viviana Popa, MDCardiac 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.
Summary
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.
Sources
- "Medical Physiology" Elsevier (2016)
- "Physiology" Elsevier (2017)
- "Human Anatomy & Physiology" Pearson (2017)
- "Principles of Anatomy and Physiology" Wiley (2014)
- "Afterload mismatch and preload reserve: A conceptual framework for the analysis of ventricular function" Progress in Cardiovascular Diseases (1976)
- "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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