Constrictive pericarditis pathophysiology

Jump to: navigation, search

Constrictive Pericarditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Constrictive Pericarditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Constrictive pericarditis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Google Images

American Roentgen Ray Society Images of Constrictive pericarditis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Constrictive pericarditis pathophysiology

CDC on Constrictive pericarditis pathophysiology

Constrictive pericarditis pathophysiology in the news

Blogs on Constrictive pericarditis pathophysiology

Directions to Hospitals Treating Type page name here

Risk calculators and risk factors for Constrictive pericarditis pathophysiology

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

Overview

The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles. This is known as ventricular interdependence, where the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion. pericarditis causes that can trigger the development of constrictive pericarditis are tuberculosis, viral infection, radiation therapy, trauma, post-cardiac surgery.

Pathophysiology

The pathophysiology of constrictive pericarditis is [1] [2] [3]. The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion.

Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles[4]

Chronic constrictive pericarditis characterized by obliteration of pericardial cavity by granulation tissue during healing of:[5]

  • 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 rigid thickened pericardium limits the normal elasticity of the pericardium and hence limits the ventricular filling. Ventricular filling in early diastole is not affected as it is impeded only when the pericardium elastic limit is reached.

During inspiration, the negative pressure in the thoracic cavity will cause increased blood flow into the right ventricle (increased intrathoracic pressure). 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. Because constrictive pericarditis limits the ability of the ventricles to expand, the intracardiac pressure variation during respiratory cycle occurs only between right and left ventricles.

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.

Triggers:

The following are pericarditis causes that can trigger the development of constrictive pericarditis:

  • Tuberculosis
  • Viral infection
  • Radiation therapy
  • Trauma
  • Post-cardiac surgery



References

  1. Mehta A, Mehta M, Jain AC. Constrictive pericarditis. Clin Cardiol 1999; 22:334-44.
  2. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of constrictive pericarditis. Am Heart J 1987; 113:354-60.
  3. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation 1999; 100:1380-6.
  4. Lee MC, LeWinter MM, Freeman G, Shabetai R, Fung YC (1985). "Biaxial mechanical properties of the pericardium in normal and volume overload dogs". Am J Physiol. 249 (2 Pt 2): H222–30. doi:10.1152/ajpheart.1985.249.2.H222. PMID 3161344.
  5. 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.


nl:Pericarditis constrictiva



Linked-in.jpg