Abstract
Cardiac afterload is a semiquantitative composite assessment of a determinant of cardiac output. Afterload is the force again which the heart pumps to expel blood into the vasculature and can be understood in the whole heart as the stress encountered by left ventricular myofibers as they contract against the end-diastolic volume. Wall tension can be at least in part described by LaPlace’s equation and aids in the explanation of why a dilated ventricle (with an increased chamber radius) must develop a greater inward force than a smaller heart to generate the same systolic pressure. The dilated ventricle is, therefore, vulnerable to an afterload mismatch whereby a high afterload can significantly decrease cardiac output. Addressing this mismatch with vasodilators is an established therapeutic strategy to augment cardiac output in the setting of both acute and chronic heart failure.
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Suggested Reading
Fuster V, Walsh R, Harrington R. Hurst’s the heart, vol. 1. 1st ed. New York: McGraw Hill; 2011. (Part 2, Chapter 5 and Part 3, Chapter 14).
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Weber T, Chirinos JA. Pulsatile arterial haemodynamics in heart failure. Eur Heart J. 2018;37:2129.
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Vest, A.R. (2019). Afterload. In: Askari, A., Messerli, A. (eds) Cardiovascular Hemodynamics. Contemporary Cardiology. Humana, Cham. https://doi.org/10.1007/978-3-030-19131-3_2
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