Difference between revisions of "Constrictive pericarditis pathophysiology"

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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 of the heart|Frank-Starling law]], this will cause decreased pressure generated by the [[left ventricle]] during [[systole]].
 
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 of the heart|Frank-Starling law]], this will cause decreased pressure generated by the [[left ventricle]] during [[systole]].
 +
 +
The intrathoracic and intracardiac pressures dissociation leads to the following during inspiration:
 +
 +
* pulmonary venous pressure decreases
 +
* venous return decreases
 +
* Left atrial pressure doesn't change
 +
*pulmonary veins to left atrial (LA) flow decreases
  
 
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]].
 
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]].

Revision as of 21:20, 4 December 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Atif Mohammad, M.D.

Overview

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. The fibrotic shell around the myocardium prevents adequate filling of the ventricles during diastole. This results in significant respiratory variation in blood flow in the ventricles.

The thickened fibrotic pericardium restricts the normal late diastolic filling in Constrictive Pericarditis; where as in restrictive cardiomyopathy the myocardium becomes rigid preventing filling of the ventricles.

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.

The intrathoracic and intracardiac pressures dissociation leads to the following during inspiration:

  • pulmonary venous pressure decreases
  • venous return decreases
  • Left atrial pressure doesn't change
  • pulmonary veins to left atrial (LA) flow decreases

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.

Chronic constrictive pericarditis characterized by obliteration of pericardial cavity by granulation tissue during healing of:[1]

  • An acute episode of fibrinous or serofibrinous pericarditis
  • A resorption of chronic pericardial effusion.

The heart becomes encased by the granulation tissue which gradually contracts may get calcified

The elastic limit of the rigid thickened pericardium is much lesser than that of a normal pericardium and results in limiting the ventricular filling


Pathogenesis:


References

  1. Klein AL, Cremer PC (2018). "Ephemeral Effusive Constrictive Pathophysiology". JACC Cardiovasc Imaging. 11 (4): 542–545. doi:10.1016/j.jcmg.2017.10.028. PMID 29622178.


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