Diastolic dysfunction pathophysiology: Difference between revisions
Jump to navigation
Jump to search
| Line 31: | Line 31: | ||
*Left ventricular end diastolic pressure will become high. | *Left ventricular end diastolic pressure will become high. | ||
*Pulmonary capillary pressure increases.<ref name="Mann">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.</ref> | *Pulmonary capillary pressure increases.<ref name="Mann">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.</ref> | ||
**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 | **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<ref name="pmid18794390">{{cite journal| author=Zile MR, Bennett TD, St John Sutton M, Cho YK, Adamson PB, Aaron MF et al.| title=Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures. | journal=Circulation | year= 2008 | volume= 118 | issue= 14 | pages= 1433-41 | pmid=18794390 | doi=10.1161/CIRCULATIONAHA.108.783910 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18794390 }} </ref><ref name="pmid21440865">{{cite journal| author=Zile MR, Adamson PB, Cho YK, Bennett TD, Bourge RC, Aaron MF et al.| title=Hemodynamic factors associated with acute decompensated heart failure: part 1--insights into pathophysiology. | journal=J Card Fail | year= 2011 | volume= 17 | issue= 4 | pages= 282-91 | pmid=21440865 | doi=10.1016/j.cardfail.2011.01.010 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21440865 }} </ref><ref name="pmid21549292">{{cite journal| author=Adamson PB, Zile MR, Cho YK, Bennett TD, Bourge RC, Aaron MF et al.| title=Hemodynamic factors associated with acute decompensated heart failure: part 2--use in automated detection. | journal=J Card Fail | year= 2011 | volume= 17 | issue= 5 | pages= 366-73 | pmid=21549292 | doi=10.1016/j.cardfail.2011.01.011 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21549292 }} </ref>. | ||
*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]]. | *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. | *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. | ||
Revision as of 15:45, 29 January 2013
|
Diastolic dysfunction Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Diastolic dysfunction pathophysiology On the Web |
|
American Roentgen Ray Society Images of Diastolic dysfunction pathophysiology |
|
Risk calculators and risk factors for Diastolic dysfunction pathophysiology |
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.
Underlying Pathophysiological Mechanisms of Diastolic dysfunction
Impaired Extent and/or Speed of Myocardial Relaxation
- Myocardial relaxation is an ATP dependent process regulated by the rate of re-uptake of cytoplasmic calcium into the sarcoplasmic reticulum.
- Low concentration of calcium, as seen in ischemia, is associated with a slowed down myocardial relaxation.
Increased Myocardial Stiffness
- Myocardial stiffness can be secondary to cardiac muscle hypertrophy (for example as seen in hypertension). Concentric hypertrophy (increased mass and relative wall thickness) and remodelling (normal mass but increased wall thickness) are associated with diastolic dysfunction due to impaired filling.
- Myocardial stiffness can be the result of infiltrative diseases like amyloidosis.
- Scarred heart muscle, occurring after a heart attack, are relatively stiff.
- Diabetes can be a cause of cardiac stiffness as a result of glycosylation of the heart muscle.
Extrinsic Constraints
- Extrinsic constraints can be seen in pericardial compression.
Chamber Dilatation
- Severe systolic dysfunction that has led to ventricular dilation can be associated with diastolic dysfunction. When the ventricle has been stretched to a certain point, any further attempt to stretch it more, as by blood trying to enter it from the left atrium, meets with increased resistance and thus decreased compliance.
Miscelleneous
- In mitral stenosis, blood cannot readily flow out from the left atrium into the left ventricle since the valve between those two heart chambers is blocked which causes the blood to back up into the left atrium and, eventually, the lungs. Pulmonary edema may result.
- Diastolic dysunction secondary to mitral stenosis is especially seen when the heart rate is elevated, as occurs in exercise and pregnancy. Thus, there will be insufficient time for the blood to traverse the narrowed passageway (i.e. mitral valve) between the left atrium and left ventricle.[1]
Sequence of Events in Diastolic dysfunction
- Impaired cardiac muscle relaxation or/and decreased left ventricular compliance leads 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
- ↑ 1.0 1.1 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.