Cardiovascular Physiology Concepts
                                    Richard E. Klabunde, Ph.D.


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Arrhythmias

Cardiac Valve Disease

Coronary Artery Disease

Edema

Heart Failure

Hypertension

Peripheral Artery Disease



Click here for information on Cardiovascular Physiology Concepts, published by Lippincott Williams & Wilkins (2005)


 


 

Aortic Stenosis

 

The following describes changes that occur in the left ventricular pressure-volume loop when there is aortic stenosis. In aortic stenosis (red loop in figure), left ventricular emptying is impaired because of high outflow resistance caused by a reduction in the valve orifice area when it opens. This high outflow resistance causes a large pressure gradient to occur across the aortic valve during ejection, such that the peak systolic pressure within the ventricle is greatly increased. This leads to an increase in ventricular afterload, a decrease in stroke volume, and an increase in end-systolic volume. Stroke volume (width of pressure-volume loop) decreases because the velocity of fiber shortening is decreased by the increased afterload (see force-velocity relationship). Because end-systolic volume is elevated, the excess residual volume added to the incoming venous return causes the end-diastolic volume to increase. This increases preload and activates the Frank-Starling mechanism to increase the force of contraction to help the ventricle overcome, in part, the increased outflow resistance.  In mild aortic stenosis, this can be adequate to maintain normal stroke volume, but in moderate stenosis (as shown in the figure) or severe stenosis, the stroke volume may fall considerably because the end-systolic volume increases substantially more than the end-diastolic volume increases. The fall in stroke volume can lead to a reduction in arterial pressure. Stroke volume falls even further if the ventricle begins to exhibit systolic and diastolic dysfunction. Compensatory increases in end-diastolic volume will be limited by ventricular hypertrophy that occurs due to the chronic increase in afterload. This hypertrophy can lead to large increases in end-diastolic pressure.

The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular hypertrophy (remodeling) that decreases ventricular compliance. 

RK Revised 04/05/07

 


DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

© 1999-2008 Richard E. Klabunde, all rights reserved.