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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Cardiovascular Physiology Concepts textbook cover

Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2012)


Cardiovascular Physiology Concepts textbook cover

Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)


 


Aortic Stenosis

effects of aortic stenosis on ventricular pressure-volume loops
The following describes changes that occur in the left ventricular pressure-volume (PV) 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 wall stress (afterload), a decrease in stroke volume, and an increase in end-systolic volume. Stroke volume (width of PV 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 a large increase in end-diastolic pressure that is associated with reduced end-diastolic volumes because the increased stiffness of the ventricle prevents normal ventricular filling.

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. Therefore, the red loop depicted in the figure only represents what may occur under a given set of conditions.

Revised 07/02/2015



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