EFFECT OF AFTERLOAD AND PRELOAD
Independent Effects of Afterload
If afterload is increased by increasing aortic pressure, the isovolumetric contraction phase is prolonged because the ventricle will need to generate a higher pressure to overcome the elevated aortic diastolic pressure. Therefore, ejection begins at a higher aortic diastolic pressure. If preload (end-diastolic volume) and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume (red loop in figure). Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected (see force-velocity relationship). A reduced stroke volume at the same end-diastolic volume results in reduced ejection fraction. If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases (green loop in figure).
Independent Effects of Preload
To examine the independent effects of preload, assume that aortic systolic and diastolic pressure (afterload), and inotropy are held constant. The left ventricle is filled with blood from the pulmonary veins. If pulmonary venous flow is increased, the ventricle will fill to a greater extent (end-diastolic volume is increased; red loop in figure). As the ventricle contracts, it will eject blood more rapidly because the Frank-Starling mechanism will be activated by the increased preload. With no change in afterload or inotropy, the ventricle will eject blood to the same end-systolic volume despite the increase in preload. The net effect will be an increase in stroke volume, shown by an increase in the width of the PV loop (100 compared to 75 ml in figure). Ejection fraction (EF) will increase slightly from 60 to 67%. This ability to contract to the same end-systolic volume is a property of cardiac muscle that can be demonstrated using isolated cardiac muscle and studying isotonic (shortening) contractions under the condition of constant afterload. When muscle preload length is increased, the contracting muscle shortens to the same minimal length as found before the preload was increased (see Effects of Preload on Cardiac Fiber Shortening). If pulmonary venous flow decreases, then the ventricle will fill to a smaller end-diastolic volume (decreased preload; green loop in figure). This will cause stroke volume to decrease (from 75 to 50 ml in figure) and EF to decrease from 60 to 50%, but the end-systolic volume will be unchanged. To summarize, changes in preload alter the stroke volume; however, end-systolic volume is unchanged if afterload and inotropy are held constant.
CONTENT DEVELOPER: Vinayak chalia
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