Page 8, Cardiac Performance, Dr. D. Penney


Afterload - Increased tension on a muscle fiber after contraction begins; usually due to increased aortic/arterial blood pressure and/or decreased compliance; imposed during systole.

Afterload, that load applied after a muscle begins to contract, alters stroke volume (Figure 2.03). It is a function of arterial blood pressure, aortic compliance and resistance (impedance), and ventricular dimensions. Systemic hypertension, aortic stenosis, and atherosclerosis all increase afterload, mean ejection pressure, and end-systolic volume. As afterload rises, stroke volume decreases. At a great enough afterload the aortic valve fails to open and ejection is prevented, bringing external cardiac work to zero. Tension is still generated and ATP consumed, actually at an elevated rate, while work efficiency becomes zero.



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