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Pericardium and Constrictive Pericarditis
Donald D. Glow
HISTORY
-The earliest descriptions of the pericardium: date back to Hippocrates
-Galen (129–210 a.d.) described the protective function of the pericardium and also reported a pericardial effusion in animals
-The first successful pericardiotomy was performed by Romero in 1819
-the first pericardiocentesis was performed by Franz Schuh in 1840
-Pericardial resection for constrictive pericarditis was proposed by Weill (1895) and Delorme (1898)
ANATOMY
-pericardium: fibrous sac surrounding the heart and mediastinal great vessels
The outer wall of the pericardial sac consists of an outer fibrosa and an inner serosa
-outer pericardial sac folds onto the heart and great vessels, where the epicardium and outer adventitial layer of the heart and great vessels constitute the visceral lining of the pericardial sac
NORMAL PHYSIOLOGY
-The pericardium and pericardial fluid minimize friction and energy loss during cardiac motion
-The normal pericardium and its external attachments maintain cardiac position within the mediastinum in the presence of gravitational or other forces that could impair cardiac filling or function
-The pericardium also serves as a barrier protecting the heart from inflammation or malignancy
-under conditions of acute cardiac dilation, the normal pericardium probably increases diastolic stiffness and limits diastolic filling of both left and right ventricles
-pericardial pressure decreases during inspiration and increases during expiration (inspiration normally decreases left ventricular stroke volume and decreases aortic blood pressure by <10 mm Hg)
PATHOPHYSIOLOGY
Pericardial Effusion
-Pericardial effusion (more than 50–100 ml): the simple result of more fluid transuding into the pericardial space than is resorbed (Pericardial effusions requiring drainage typically contain 500–700 ml of fluid)
-Causes of increased pericardial fluid production: nflammation or infection of the pericardium
-Causes of decreased pericardial fluid resorption: venous hypertension or lymphatic obstruction
-pericardial effusion increases pericardial pressure sufficiently
: cardiac tamponade and pulsus paradoxus
Cardiac Tamponade
-Cardiac tamponade: hemodynamically significant cardiac compression from accumulating pericardial contents that evoke and defeat compensatory mechanisms
-Cardiac tamponade can result from pericardial fluid, pus, blood, air, or tumor
(In a normal pericardium, roughly 200 ml of acute pericardial fluid accumulation can produce tamponade)
-The initial effect of cardiac tamponade
1) Decreased venous return to the right side of the heart
2) Decreased right ventricular filling decreases stroke volume and thus cardiac output
3) Decreased pulmonary venous return to the left side of the heart
Pulsus Paradoxus
-pulsus paradoxus: fall in systolic blood pressure of >10 mm Hg with inspiration
associated with cardiac tamponade (also can be seen in chronic obstructive pulmonary disease, pulmonary embolism, obesity, right-sided heart failure, and ascites as a result of the same mechanism)
-mechanisms of pulsus paradoxus
1) Pooling of blood in the lungs during inspiration[10]
2) Increased right ventricular filling during inspiration caused by lower right ventricular pressure. In turn, right ventricular distension may shift the interventricular septum leftward, thus decreasing septal muscle preload and decreasing left ventricular stroke volume
3) Increased left ventricular afterload (aortic pressure minus pericardial pressure), which decreases left ventricular stroke work
Constrictive Pericarditis
-results when the volume of the pericardial sac itself is sufficiently reduced relative to cardiac volume so that cardiac filling is impaired
-The wall of the pericardial sac is almost always thickened in constrictive pericarditis and may be 3–20 mm thick, versus 1–2-mm thickness for normal pericardium
DIAGNOSIS
History and Symptoms
-symptoms of pericardial disease: fever, malaise, chest discomfort, shortness of breath, pedal edema, and abdominal distension
-Medical history: prior chest trauma, chest irradiation, or exposure to infectious agents such as tuberculosis
Physical Examination
-The peripheral arterial pulse may paradoxically diminish during inspiration (pulsus paradoxus)
-Inspiratory jugular venous distension may be present (Kussmaul’s sign)
-Chest examination may show dullness at the lung bases, muffled cardiac sounds, and a pericardial rub or pericardial knock
-A prominent S3 gallop may be present in constrictive pericarditis
-Abdominal examination may demonstrate hepatomegaly or ascites, and pedal edema may be present. The extremities may be cool and constricted in tamponade
Chest Radiograph
-cardiomegaly in pericardial effusion
-Pericardial calcification can accompany constrictive pericarditis
-Pleural effusion may be present in pericardial effusion, pericardial tamponade
Electrocardiogram
The four stages of ECG changes in acute pericarditis are as follows:
Stage I ST elevation in all leads except AVR and V1
Stage II Normal ST segments but T wave flattening
Stage III T wave inversion without Q waves or loss of R wave voltage
Stage IV Normalization of T wave
Echocardiogram
-easily detects loculated or generalized pericardial effusion, intrapericardial masses, pericardial cysts, pericardial calcification or thickening
Computed Tomography
-demonstrate pericardial effusion, pericardial calcification and thickening, intrapericardial masses, and pericardial cysts
-Relative to magnetic resonance imaging, computed tomography may be more sensitive in detecting calcification but has disadvantages of requiring intravenous contrast injection and more motion artifact
Magnetic Resonance Imaging
-demonstrate pericardial effusion, pericardial thickening, intrapericardial masses, pericardial cysts, and even intracardiac disease
-Compared with computed tomography, magnetic resonance imaging has the advantages of not requiring intravenous contrast injection and having less motion artifact
Cardiac Catheterization
-ardiac fluoroscopy can demonstrate pericardial calcification or abnormally prominent swinging motion of the left ventricle over the cardiac cycle in pericardial effusion -ight-sided heart catheterization can be diagnostic of cardiac tamponade or pericardial constriction
PERICARDIOCENTESIS
-pericardiocentesis: an effective means to rapidly treat cardiac tamponade and obtain pericardial fluid for diagnosis
-performed with the patient in a supine position and using local anesthesia
-Cardiac puncture can be avoided by attaching an ECG to the needle (The needle is withdrawn if the ECG shows sudden negative deflection of the QRS complex)
-Pericardiocentesis is rapid, requires little anesthesia, and is relatively safe Complication rates vary from 5–50% and are increased in smaller effusion
-The rate of recurrent effusion and tamponade after successful pericardiocentesis is high, around 55%
Pericardial Biopsy
-Pericardial biopsy can be performed percutaneously or surgically
-Percutaneous pericardial biopsy is possible by dilating a pericardiocentesis needle tract to accept an introducer sheath. A bioptome can then be paced through the introducer using echocardiographic guidance to obtain pericardial biopsy
PERICARDIAL EFFUSION/NONCONSTRICTIVE PERICARDITIS
Diagnosis
-The diagnosis of pericarditis requires the pathological demonstration of pericardial inflammation, scarring, or thickening (require pericardial biopsy)
-However, the diagnosis of pericarditis can be strongly supported by findings of pericardial effusion or pericardial thickening on echocardiography, computed tomography, or magnetic resonance imaging
-The diagnosis of pericardial effusion requires only an imaging study demonstrating more fluid than normal (>50–100 ml) in the pericardial space
Etiology and Treatment
-A wide variety of etiologies exist for pericardial effusion and pericarditis
-Medical treatment for pericardial effusion varies with the etiology of the effusion
-Pericardial window is indicated in any patient with symptomatic pericardial effusion or in whom the etiology cannot otherwise be defined
-Subxiphoid pericardial window (preferable in patients who are hemodynamically unstable as a result of tamponade but in whom pericardiocentesis is deemed impractical or unsafe)
-Transpleural pericardial window (preferable in patients with good long-term prognosis but with significant likelihood of recurrent pericardial effusion)
Idiopathic Pericarditis
-Idiopathic pericardial effusion is treated symptomaticallySymptoms of low-grade pain and fever can be treated with antiinflammatory agents (indomethacin, ibuprofen, rofecoxib, or celecoxib)
-More severe or refractory symptoms almost always respond to a 2–3-week course of prednisone
Chylopericardium
-Chylopericardium can be idiopathic or follow thoracic surgery
-Chylopericardium can be treated by pericardiocentesis or, if recurrent, by subxiphoid or transthoracic pericardial window with or without low thoracic duct ligation
Hemopericardium
-Hemopericardium can result from trauma, recent mediastinal operation, coagulopathy, cardiac perforation caused by instrumentation, cardiac rupture, or aortic rupture
-the treatment of hemopericardium depends upon the underlying disease process (Hemopericardium caused by percutaneous cardiac puncture in the catheterization laboratory generally can be remedied by placing a pigtail catheter in the pericardial space, reversing anticoagulation, frequently aspirating the pigtail catheter, and watching for cessation of bleeding)
Nonviral Infectious Pericarditis
-The most common bacterial organisms causing pericarditis: Staphylococcus, Streptococcus, and gram-negative organisms in adults/Haemophilus or Staphylococcus in children
-Symptoms of fever and chest pain are common
-Bacterial pericarditis requires both appropriate antibiotic treatment and either acute or chronic pericardial drainage
Viral Pericarditis
-Several viruses, such as coxsackievirus, adenovirus, cytomegalovirus, human immunodeficiency virus (HIV), and herpes simplex virus, have been associated with pericarditis
-Viral pericarditis is usually self-limited, like idiopathic pericarditis
Inflammatory Pericarditis
-Connective tissue or inflammatory diseases such as rheumatoid arthritis and lupus can produce pericarditis in a minority of patients
-The underlying condition should be treated if possible, and the pericardiocentesis or pericardial window is reserved for symptoms refractory to medical treatment or for the need to make a diagnosis
Malignant Pericarditis
-Malignant involvement of the pericardium generally is metastatic and occurs in roughly 10% of patients with noncardiac neoplasm
-The most common tumors to involve the pericardium are lung (38%), breast (29%), lymphoma (7%), and others (26%)
-Primary malignancy of the pericardium is rare and includes mesothelioma (50%), sarcoma, and malignant teratoma
-Malignancy of the pericardium generally presents as cardiac tamponade as a result of malignant pericardial effusion, Pericardial constriction caused by malignancy is infrequent
Radiation-Induced Pericarditis
-Only a small fraction of patients receiving mediastinal irradiation develop clinically significant pericarditis
-Early pericarditis developing within 1 month of initiating mediastinal irradiation generally is self-limited and needs only to be treated symptomatically, like idiopathic pericarditis
-Treatment with pericardiocentesis or pericardial window should be reserved for significant refractory symptoms or concern about other etiologies
Postoperative Pericarditis
-Only 10% of patients undergoing cardiac operation have clinically significant postoperative pericarditis
- Intraoperative use of bioabsorbable films may diminish pericardial scarring without the pericardial capsule formation
Uremic Pericarditis
-Uremic pericarditis occurs in 20% of patients on hemodialysis and in 50% of patients with severe untreated renal disease
-Therapy for uremic pericarditis is focused on treating tamponade
-the incidence of recurrent tamponade in uremic pericardial effusion
:highest with pericardiocentesis alone, better with subxiphoid pericardial window, and best with transthoracic pericardial window