Diastolic dysfunction pathophysiology: Difference between revisions
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Revision as of 11:52, 6 October 2012
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Diastolic dysfunction Microchapters |
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Diastolic dysfunction pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Normally, with reference to the left side of the heart, blood flows from the lungs, into the pulmonary veins, into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled during diastole, blood will back up into the left atrium and, eventually, into the lungs. The result is a higher than normal pressure of blood within the vessels of the lung. As a result of hydrostatic forces, this high pressure leads to leaking of fluid (i.e. transudate) from the lung's blood vessels into the air-spaces (alveoli) of the lungs. The result is pulmonary edema, a condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death.
It is worth re-emphasizing that the pulmonary edema that can develop as a result of diastolic dysfunction is not due to poor pumping function of the left ventricle. Indeed, it has resulted from the left ventricle's inability to readily accept blood trying to enter it from the left atrium.
The primary reason for the left ventricle's inability to properly fill with blood during diastole (i.e. diastolic dysfunction) is that it has become stiff (i.e. non-compliant). In the setting of a stiff left ventricle, it is more difficult for blood to flow into it from the left atrium. In such a situation, filling can be maintained by a combination of coordinated left atrial pumping (i.e. beating) and a relatively slow heart rate. The former actively pumps blood into the stiff left ventricle, and the latter can allow for sufficient time for blood to passively enter the left ventricle from the left atrium.