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Diastolic heart failure

Diastolic dysfunction
Classification and external resources
ICD-9-CM 428.3
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Diastolic heart failure and diastolic dysfunction refer to the decline in performance of one (usually the left ventricle) or both (left and right) ventricles during diastole. Diastole is the cardiac cycle phase during which the heart is relaxing and filling with incoming blood that is being returned from the body through the inferior (IVC) and superior (SVC) venae cavae to the right atrium and from lungs through pulmonary veins to the left atrium. In diastolic failure, if the patient has symptoms, there is a pathologic cause inducing them. Diastolic dysfunction can be found when doing a Doppler echocardiography in an apparently healthy patient, mainly in an elderly person.

Any condition or process that leads to stiffening of the left ventricle can lead to diastolic dysfunction. Causes of left ventricular stiffening include:

Causes of isolated right ventricular diastolic failure are uncommon. These causes include:

Diastolic failure appears when the ventricle can't be filled properly because it can't relax or because its wall is thick or rigid. This situation presents usually a concentric hypertrophy. In contrast, systolic heart failure has usually an eccentric hypertrophy.

Diastolic failure is characterized by an elevated diastolic pressure in the left ventricle, despite an essentially normal/physiologic end diastolic volume (EDV). Histological evidence supporting diastolic dysfunction demonstrates ventricular hypertrophy, increased interstitial collagen deposition and infiltration of the myocardium. These influences collectively lead to a decrease in distensibility and elasticity (ability to stretch) of the myocardium. As a consequence, cardiac output becomes diminished. When the left ventricular diastolic pressure is elevated, venous pressure in lungs must also become elevated too: left ventricular stiffness makes it more difficult for blood to enter it from the left atrium. As a result, pressure rises in the atrium and is transmitted back to the pulmonary venous system, thereby increasing its hydrostatic pressure and promoting pulmonary edema.


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