Diastolic dysfunction pathophysiology: Difference between revisions
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*The underlying pathophysiology of the [[diastolic dysfunction]] resides mainly in the impairment of myocardial relaxation or/and in the increase of cardiac muscle stiffness (and thus decreased compliance). | *The underlying pathophysiology of the [[diastolic dysfunction]] resides mainly in the impairment of myocardial relaxation or/and in the increase of cardiac muscle stiffness (and thus decreased compliance). | ||
**Given the fact that muscle relaxation is an ATP dependent process, the impairment of myocardial relaxation occurs in the setting of cardiac [[ischemia]] due to the depletion of ATP. | **Given the fact that muscle relaxation is an ATP dependent process, the impairment of myocardial relaxation occurs in the setting of cardiac [[ischemia]] due to the depletion of ATP. | ||
**An increase in muscle stiffness and hence a decrease in cardiac muscle compliance is observed secondary to cardiac [[hypertrophy]] (for example, due to [[hypertension]]) or [[infiltrative diseases]] (for example, due to [[amyloidosis]]). | **An increase in muscle stiffness ,and hence a decrease in cardiac muscle compliance, is observed secondary to cardiac [[hypertrophy]] (for example, due to [[hypertension]]) or [[infiltrative diseases]] (for example, due to [[amyloidosis]]). | ||
*The sequence of events that occur in [[diastolic dysfunction]] is the following: | *The sequence of events that occur in [[diastolic dysfunction]] is the following: | ||
** Impaired cardiac muscle relaxation or/and decreased left ventricular compliance lead to delay in left ventricular filling. | ** Impaired cardiac muscle relaxation or/and decreased left ventricular compliance lead to delay in left ventricular filling. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Rim Halaby
Overview
Diastolic dysfunction is the impairment of the heart muscle in its ability to properly relax and fill with blood during diastole. Diastolic dysfunction is mainly the result of either impaired myocardial relaxation or increased cardiac muscle stiffness. As a result, the pressure in the left ventricle increases at the end of diastole and causes a build up of pressure in the left atrium and consequently in the pulmonary circulation. The result is pulmonary edema and dyspnea.
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.
- Diastolic dysfunction is the inability of the heart to properly relax and fill with blood during diastole.
- The underlying pathophysiology of the diastolic dysfunction resides mainly in the impairment of myocardial relaxation or/and in the increase of cardiac muscle stiffness (and thus decreased compliance).
- Given the fact that muscle relaxation is an ATP dependent process, the impairment of myocardial relaxation occurs in the setting of cardiac ischemia due to the depletion of ATP.
- An increase in muscle stiffness ,and hence a decrease in cardiac muscle compliance, is observed secondary to cardiac hypertrophy (for example, due to hypertension) or infiltrative diseases (for example, due to amyloidosis).
- The sequence of events that occur in diastolic dysfunction is the following:
- Impaired cardiac muscle relaxation or/and decreased left ventricular compliance lead to delay in left ventricular filling.
- Left ventricular end diastolic pressure will become high.
- Pulmonary capillary pressure increases.[1]
- 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. Life threatening episodes of pulmonary edema can occur due to sudden decompensation. This is called flash pulmonary edema. The left ventricle diastolic pressure rises progressively prior to the acute onset failure[2][3][4].
- 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.
- 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.
- Conditions that increase the heart rate, for example exercise and pregnancy, decrease the diastolic filling time and hence worsens the diastolic dysfunction in the setting of a non-compliant heart.
References
- ↑ Mann D.L., Chakinala M. (2012). Chapter 234. Heart Failure and Cor Pulmonale. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison's Principles of Internal Medicine, 18e.
- ↑ Zile MR, Bennett TD, St John Sutton M, Cho YK, Adamson PB, Aaron MF; et al. (2008). "Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures". Circulation. 118 (14): 1433–41. doi:10.1161/CIRCULATIONAHA.108.783910. PMID 18794390.
- ↑ Zile MR, Adamson PB, Cho YK, Bennett TD, Bourge RC, Aaron MF; et al. (2011). "Hemodynamic factors associated with acute decompensated heart failure: part 1--insights into pathophysiology". J Card Fail. 17 (4): 282–91. doi:10.1016/j.cardfail.2011.01.010. PMID 21440865.
- ↑ Adamson PB, Zile MR, Cho YK, Bennett TD, Bourge RC, Aaron MF; et al. (2011). "Hemodynamic factors associated with acute decompensated heart failure: part 2--use in automated detection". J Card Fail. 17 (5): 366–73. doi:10.1016/j.cardfail.2011.01.011. PMID 21549292.