Constrictive pericarditis pathophysiology: Difference between revisions
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{{CMG}}; '''Associate Editor-In-Chief:''' Atif Mohammad, M.D. | {{CMG}}; '''Associate Editor-In-Chief:''' Atif Mohammad, M.D. | ||
== | ==Pathophysiology== | ||
Constrictive pericarditis is due to a thickened, fibrotic pericardium, composed of the tough fibrous parietal pericardium and the smooth visceral pericardium, that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. This results in significant respiratory variation in blood flow in the chambers of the heart. In order to prevent friction between the two pericardial layers there is approximately 50mL of fluid. | Constrictive pericarditis is due to a thickened, fibrotic pericardium, composed of the tough fibrous parietal pericardium and the smooth visceral pericardium, that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. This results in significant respiratory variation in blood flow in the chambers of the heart. In order to prevent friction between the two pericardial layers there is approximately 50mL of fluid. | ||
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Revision as of 13:22, 3 April 2013
Template:Pericardial constriction Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Atif Mohammad, M.D.
Pathophysiology
Constrictive pericarditis is due to a thickened, fibrotic pericardium, composed of the tough fibrous parietal pericardium and the smooth visceral pericardium, that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. This results in significant respiratory variation in blood flow in the chambers of the heart. In order to prevent friction between the two pericardial layers there is approximately 50mL of fluid.
The thickened fibrotic pericardium obstructs the normal late diastolic filling; this distinguishes constrictive from restrictive pericarditis.
During inspiration, the negative pressure in the thoracic cavity will cause increased blood flow into the right ventricle. This increased volume in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. Due to the Frank-Starling law, this will cause decreased pressure generated by the left ventricle during systole.
During expiration, the amount of blood entering the right ventricle will decrease, allowing the interventricular septum to bulge towards the right ventricle, and increased filling of the left ventricle and subsequent increased pressure generated by the left ventricle during systole.
This is known as ventricular interdependence, since the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.
The impairment of diastolic filling uniformly affects both ventricles, especially during the latter third of diastole. The symmetrical constricting effect of the pericardium results in elevation and equilibration of diastolic pressures in all four chambers of the heart. As a result of this constriction and elevated venous filling pressure, most diastolic filling occurs rapidly and early in diastole. This filling abruptly halts when the myocardium encounters the noncompliant pericardium.
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