Diastolic Heart Failure - Physiology of Diastolic Dysfunction

Physiology of Diastolic Dysfunction

Diastolic dysfunction may be divided mathematically in several directions such as pathology of the left/systemic/body vs. pathology of the right/pulmonary/lungs under (immediate vs. insidious) failure. In optimal left sided performance of the heart, blood mass loads forward 60-80 times per minute in an unobstructed cascade from the lungs, into the pulmonary veins, then into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled due to deterioration of preload, compliance and/or E/A ratio during diastole, the pressurized cascade begins to fail and incrementally reverses. Eventually blood then regurgitates back into the left atrium in a backward pathologic spiral gradient towards the lungs.

Diastolic dysfunction may contribute to an opposed or secondary type of high blood pressure known as pulmonary hypertension or PH. Unchecked PH can lead to a multitude of lung difficulties, the worst being pulmonary edema. Physiologically this process results in a higher than normal mismatch pressure gradient of blood within both the large and alveolar vessels of the lungs. Diastolic dysfunction paired with pulmonary hypertension is a significant negative prognostic indicator of heart failure with normal (or preserved)ejection fraction, commonly referred to as HFpEF.

As a result of hydrostatic forces, this pressure mismatch leads to leaking of fluid (i.e. transudate) from the pulmonary blood vessels into the air-spaces (alveoli) of the lungs. The result of this hydrostatic mismatch is sometimes pulmonary edema, a dreaded condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death. Pulmonary edema developed as a result of diastolic dysfunction is not fully imparted by failing pump systolic function of the left ventricle and may be insidious in nature or sudden depending upon the pathophysiology involved. The pressure gradient reversal inherent to diastolic dysfunction may further result from the left and/or right ventricle's pathologic inability to readily accept blood entering the ventricles from the atria. Pressure mismatches then may cause or impart pathologic geometric deformational changes of individual heart chambers leading to a gradual loss of optimal valvular coaptation and subsequent regurgitant (sagging/leaking) valvular heart disease.