Skip to main content
UploadLanguage (EN)Support
BusinessMobileSocial MediaMarketingTechnologyArt & PhotosCareerDesignEducationPresentations & Public SpeakingGovernment & NonprofitHealthcareInternetLawLeadership & ManagementAutomotiveEngineeringSoftwareRecruiting & HRRetailSalesServicesScienceSmall Business & EntrepreneurshipFoodEnvironmentEconomy & FinanceData & AnalyticsInvestor RelationsSportsSpiritualNews & PoliticsTravelSelf ImprovementReal EstateEntertainment & HumorHealth & MedicineDevices & HardwareLifestyle
DR.NABAJYOTI HAZARIKA, profile picture
Uploaded byDR.NABAJYOTI HAZARIKA
PPTX, PDF11,060 views

Chronic constrictive pericarditis

Chronic constrictive pericarditis is a condition where the pericardium thickens and scar tissue forms, restricting the heart's ability to fill with blood. It results from various causes like infections, radiation, surgery, or idiopathic. On examination, elevated jugular venous pressure and hepatomegaly are seen. Imaging shows thickened pericardium. Catheterization demonstrates equal pressures in the heart chambers. Definitive treatment is surgical removal of the pericardium (pericardiectomy), which improves symptoms in most patients.

Health & Medicine◦
Dr. NABAJYOTI HAZARIKA CTVS DEPTT. (GMCH)
DEFINITION Chronic constrictive pericarditis is a chronic inflammatory process that involves both fibrous and serous layers of the pericardium, and that leads to pericardial thickening and compression (constriction) of the ventricles. The resultant impairment in diastolic filling reduces cardiac function.
This disorder results when the healing of an acute fibrinous or serofibrinous pericarditis or the resorption of a chronic pericardial effusion is followed by obliteration of the pericardial cavity with the formation of granulation tissue, which latter gradually contracts and forms a firm scar, which may be calcified, encasing the heart and interfering with filling of the ventricles. Pericardial fluid is generally absent or of normal volume. Thickened wall of pericardial sac, may be 3-20mm thick, versus 1-2 mm thickness for normal pericardium.
CAUSES Idiopathic (most common in developed nations) Irradiation Postsurgical Infectious (most common in developing nations) Neoplastic Autoimmune (connective tissue) disorders Uremia Post-trauma Sarcoid Methysergide therapy Implantable defibrillator patches
 The end result is dense fibrosis, often calcification, and adhesions of the parietal and visceral pericardium. Scarring is usually more or less symmetric and impedes filling of all heart chambers. In a subset of patients, the process develops relatively rapidly and is reversible. This variant is seen most commonly after cardiac surgery.
PATHOPHYSIOLOGY The pathophysiologic consequence of pericardial scarring is markedly restricted filling of the heart.[This results in elevation and equilibration of filling pressures in all chambers and the systemic and pulmonary veins. Impairs cardiac filling only in late diastole. Early diastolic filling of RV occurs breifly in constrictive pericarditis untill the ventricle suddenly reaches the rigid constraint of the pericardium, producing the “square root” sign in the LV and RV diastolic filling pressure waveforms. CVP tracing has a prominent y descent that corresponds to the initial dip of the “square root” sign. This y descent results from exaggerated diastolic collapse of the normal venous pressure as rapid atrial filling occurs.
Systemic venous congestion results in hepatic congestion, peripheral edema, ascites and sometimes anasarca, and cardiac cirrhosis.  Reduced cardiac output is a consequence of impaired ventricular filling and causes fatigue, muscle wasting, and weight loss.  In “absolute” constriction, contractile function is preserved, although ejection fraction can be reduced because of reduced preload. The myocardium is occasionally involved in the chronic inflammation and fibrosis, leading to true contractile dysfunction that can at times be quite severe and predicts a poor response to pericardiectomy.
Representation of transvalvular and central venous flow velocities in constrictive pericarditis. During inspiration, the decrease in left ventricular filling results in a leftward septal shift, allowing augmented flow into the right ventricle. The opposite occurs during expiration
CLINICAL PRESENTATION  The usual presentation consists of signs and symptoms of right-sided heart failure. At a relatively early stage, these include lower extremity edema, vague abdominal complaints, and passive hepatic congestion.  Later on hepatic congestion worsens and can progress to ascites, anasarca, and jaundice due to cardiac cirrhosis.  Elevated pulmonary venous pressures, leading to exertional dyspnea, cough, and orthopnea, may also appear with progressive disease.
 Atrial fibrillation and tricuspid regurgitation  In end-stage constrictive pericarditis, the effects of a chronically low cardiac output are prominent, including severe fatigue, muscle wasting, and cachexia.  Other findings include recurrent pleural effusions and syncope.  Can be mistaken for any cause of right-sided heart failure as well as end-stage primary hepatic disease.
PHYSICAL EXAMINATION  Markedly elevated jugular venous pressure with a prominent, rapidly collapsing y descent.  Kussmaul sign.  In cases with extensive calcification and adhesion of the heart to adjacent structures, the position of the cardiac point of maximal impulse may fail to change with changes in body position.  Pericardial knock in around 50% cases.  Widening of second heart sound splitting.  Prominent S3 gallop may be present.  Secondary tricuspid regurgitation with its characteristic murmur.  Abdominal examination reveals hepatomegaly, often with palpable venous pulsations, with or without ascites. Other signs of hepatic congestion or cardiac cirrhosis include jaundice, spider angiomas, and palmar erythema.  Lower extremity edema.
 Inspiratory increase in right atrial pressure (Kussmaul’s sign)
"A" wave: atrial contraction (ABSENT in atrial fibrillation) "C" wave: ventricular contraction (tricuspid bulges). "X" descent: atrial relaxation "V" wave: atrial venous filling (occurs at same of time of ventricular contraction) "Y" descent: ventricular filling (tricuspid opens)
CHEST X-RAY  Shows. pericardial calcification
ECG with low voltage
ECHOCARDIOGRAPHY  Pericardial thickening,  Abrupt displacement of the interventricular septum during early diastole (septal “bounce”).  Premature pulmonic valve opening as a result of elevated right ventricular early diastolic pressure may also be observed.  Exaggerated septal shifting during respiration is often present.  Transesophageal echocardiography is superior to transthoracic echocardiography for measuring pericardial thickness and has an excellent correlation with CT.
CT SCAN CT showing dialated SVC relative to AA and DA
 CT with thickened pericardium
CARDIAC CATHETERIZATION  CVP greater than 14 mm hg  Near equalization of CVP, PA diastolic pressure, and capillary wedge pressures.  Decreased cardiac output.  “square root” sign in RV and LV pressure tracings  Prominent y descent  Accentuated by 500ml volume change
Right sided pressure tracings showing near equalization of pressures
 Simultaneous RV and LV tracings with early diastolic pressure dip (characteristic “square root” sign)
CONSTRICTION RESTRICTION Prominent y descent in venous pressure Present Variable Paradoxical pulse 1/3rd of cases Absent Pericardial knock Present Absent Equal right- and left-sided filling pressures Present Left at least 3-5 mm Hg > right Filling pressures >25 mm Hg Rare Common Pulmonary artery systolic pressure >60 mm Hg No Common “Square root” sign Present Variable Respiratory variation in left- and right-sided pressures or flows Exaggerated Normal Ventricular wall thickness Normal Usually increased Atrial size Possible left atrial enlargement Biatrial enlargement Septal bounce Present Absent Tissue Doppler E′ velocity Increased Reduced Pericardial thickness Increased Normal
MANAGEMENT  With the exception of patients with transient constriction, surgical pericardiectomy is the definitive treatment.  Patients with major comorbidities or severe debilitation and radiation-induced disease are relatively contraindicated for pericardiectomy.  Medical management with diuretics and salt restriction. Because sinus tachycardia is a compensatory mechanism, beta-adrenergic blockers and calcium antagonists that slow the heart rate should be avoided. In patients with atrial fibrillation and a rapid ventricular response, digoxin is recommended as initial treatment to slow the ventricular rate before resorting to beta blockers or calcium antagonists.
PERICARDIECTOMY  Usually done through a median sternotomy.  Possible through bilateral thoracotomies, and left anterolateral thoracotomy has been used to achieve effective pericardiectomy.  For sternotomy a midline incision is made from just inferior to the suprasternal notch to the inferior extent of the xiphoid process.  Sternum is divided with a sternal saw and opened with a sternal retractor.  Relatively thin area of anterior pericardium is incised and a plane between the epicardium and the pericardium is established using sharp dissection.  Pericardium is opened in the midline from the level of the diaphragm to the base of the great vessels.
 LV should be freed first, to avoid RV distension.  Ant. Pericardium is freed 1-2 cm anterior to both phrenic nerves.  Dense epicardial scar can be removed with grid pattern of crossing lines 1-2 cm apart.  Once the pericardium is freed from the epicardium, it is excised using low electrocautery to achieve hemostasis.  Anterior pericardiectomy described above provides maximal hemodynamic benefit in relieving right ventricular constriction and usually can be performed without cardiopulmonary bypass.  Resection of the diaphragmatic pericardium, atrial pericardium and posterior pericardiectomy remains unclear benefit.
 Intraoperative findings of pericardial thickening.
OUTCOME  Pericardiectomy provides excellent symptomatic improvement, with 85% of late survivors being NYHA class I and the remainder being class II.  Operative mortality 14%, primarily as a result of low cardiac output in 70% of deaths.  The operative mortality rate varies with NYHA class- 1% for class I-II 10% for class III 46% for class IV
TUBERCULOUS CONSTRICTIVE PERICARDITIS  Pericardiectomy should be performed early and as radically as possible.  A combination of chemotherapy and surgery yields gratifying results.  Tuberculous pericarditis affects 1% to 2% of all patients with TBC by direct extension from the mediastinal lymph nodes and, occasionally, by hematogenous spread or by contiguous spread from the myocardium.  Triple-drug antituberculous therapy is to be administered for a minimum of 9 months.  In patients in whom pericardial effusion persists or recurs despite the use of anti-TBC drugs, 3 months of corticosteroid therapy may be a useful adjunct.
APPENDIX  Kussmaul's Sign  Kussmaul’s Sign In Effusive Constrictive Pericarditis
Chronic constrictive pericarditis