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2013;6(4):407–416.

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Chapter 86

Pericardium

Jules Lin

Key Points

1 Prompt recognition and treatment of cardiac tamponade can be lifesaving.

2 The echocardiogram is the most useful noninvasive test in evaluating pericardial disease.

3 The electrocardiogram is important in the diagnosis of acute pericarditis and classically shows

diffuse ST elevations.

4 The hemodynamic significance of a pericardial effusion depends on the volume and the rate of

accumulation.

5 Postoperative tamponade should always be in the differential diagnosis with low cardiac output after

cardiac surgery.

6 Distinguishing constrictive pericarditis from restrictive cardiomyopathy can be difficult but is

important since the treatment is significantly different.

7 Metastatic disease is the most common cause of pericardial effusion.

8 Reconstruction of the pericardium should be considered to reduce adhesions in cases where a future

redo sternotomy is likely and is important when there is a risk of cardiac herniation after an

intrapericardial pneumonectomy.

1 The pericardium supports and protects the heart. The smooth pericardial surface and the small amount

of normal pericardial fluid provide a frictionless chamber improving cardiac efficiency as well as

serving as a barrier to infection. The pericardium can be susceptible to a variety of disease processes

including inflammation, infection, malignancy, and trauma. Changes in compliance and the

accumulation of pericardial fluid can impair cardiac function, and the prompt recognition and treatment

of cardiac tamponade can be lifesaving.

HISTORY

Hippocrates first described the pericardium in 460 BC. Three hundred years later, Galen described a

pericardial effusion and the inflammatory changes associated with pericarditis. Lower first reported

pericardial tamponade in humans in 1669. Lancisi and Morgagni described constrictive pericarditis, and

Laennec wrote of the “bread and butter” appearance of acute pericarditis in 1819.1 Kussmaul described

the hemodynamic changes known as pulsus parodoxus, and Beck and Griswald performed experimental

studies in the 1930s leading to a better understanding of the pathophysiology of pericardial effusion.2,3

Karaeneff first described relieving the symptoms of tamponade using pericardiocentesis in 1840.4 Rehn

reported methods to resect the pericardium in 1913.5

EMBRYOLOGY AND ANATOMY

The pleuropericardial membranes fuse during the fifth week of gestation dividing the thoracic cavity

into pleural and pericardial spaces and forming the fibrous pericardium.6 The serous pericardium is a

single layer of mesothelial cells that produce and reabsorb pericardial fluid. The serous and fibrous

pericardium form the parietal pericardium which is normally 2 mm in thickness. The visceral

pericardium covers the heart and the intrapericardial great vessels. The phrenic nerves are contained in

the parietal pericardium, and there is a risk of diaphragmatic paralysis with any operation on the

pericardium. The pericardial folds form the oblique sinus, a blind cul-de-sac behind the left atrium, and

the transverse sinus between the aorta and pulmonary artery superiorly and the left and right atrium

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inferiorly (Fig. 86-1). Lymphatic drainage is to the bronchial and tracheal lymph nodes and the thoracic

duct. The pericardium normally produces 15 to 50 mL of serous fluid with a protein level lower than

plasma.7

NORMAL PHYSIOLOGY

Although there are no significant consequences of the congenital absence or surgical resection of the

pericardium as long as the defect does not lead to cardiac herniation, the pericardium has some function

in the normal patient. The pericardium anchors the heart and prevents torsion and acute distension.8

The pericardium contributes to the diastolic coupling of the ventricles along the Starling curve.

Mechanoreceptors in the pericardium may also regulate blood pressure and heart rate. The pericardium

stretches up to 20% with small changes in pressure but becomes abruptly stiff and resistant with larger

volumes. Compliance depends on the rate of fluid accumulation, and the hemodynamic response is also

partially dependent on intravascular volume status.

The normal pericardial pressure is less than atmospheric pressure and is the same as the intrapleural

pressure. With inspiration, right-sided venous returns and preload increases. Blood pools in the lungs

and decreases left-sided venous return and aortic blood flow. The arterial pressure normally decreases

less than 10 mm Hg with inspiration. The normal jugular waveforms are shown in Figure 86-2. The a

wave is the normal atrial contraction. The c wave reflects the bulging of the atrioventricular valve into

the atrium during isovolumic ventricular systole. The v wave represents passive atrial filling from the

vena cava. The x descent occurs with systolic collapse during ventricular systole and atrial relaxation.

The y descent reflects diastolic collapse with opening of the atrioventricular valve and passive

ventricular filling. Inspiration decreases intrathoracic pressure and leads to a lower x descent compared

to the y descent.

Figure 86-1. This drawing illustrates the pericardial attachments of the great vessels and pulmonary veins. The oblique sinus forms

a blind cul-de-sac behind the left atrium, and the transverse sinus is a space between the aorta and pulmonary artery superiorly

and the left and right atrium inferiorly.

DIAGNOSTIC STUDIES

While the electrocardiogram is nonspecific, it can be helpful in suggesting the diagnosis. In acute

pericarditis the EKG classically shows diffuse ST elevations, and a low-voltage QRS is seen with a large

pericardial effusion. The chest radiograph in a patient with a pericardial effusion shows an enlarged

cardiac silhouette described as a water bottle. Pericardial calcification can be seen in chronic

constrictive pericarditis secondary to tuberculosis.

2 The echocardiogram is the most useful noninvasive test in evaluating pericardial disease. The

echocardiogram can identify an effusion, pericardial thickening, or masses. By using Doppler and

assessing changes in chamber size, echocardiogram is useful in assessing hemodynamics and can help

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differentiate tamponade, constriction, and restriction. It can also be used to help guide procedures like

pericardiocentesis. Computed tomography and magnetic resonance imaging can identify pericardial

masses and pericardial thickening or calcification.9 Cardiac catheterization provides pressure tracings

that help to distinguish cardiac tamponade, constriction, and restriction. Endomyocardial biopsy can

also be useful in diagnosing restrictive cardiomyopathy.

CONGENITAL ABNORMALITIES

Congenital absence of the pericardium is usually partial but can be complete. It is most common on the

left side and is more frequent in males. Associated congenital cardiac defects include atrial septal defect,

a bicuspid aortic valve, and pulmonary malformations. Defects on the right side can lead to cardiac

herniation. Patients can present with chest pain, syncope, or death. The electrocardiogram can show a

right bundle branch block. The pericardial defect can be appreciated on CT or MRI. The treatment of a

partial defect is total pericardiectomy or patch closure with PTFE or bovine pericardium. Total

pericardial absence is usually asymptomatic and is found incidentally.

Figure 86-2. The jugular venous pulse waveform.

Pericardial cysts are rare benign cysts that generally measure 1 to 15 cm in size. They are most

commonly found at the right cardiophrenic angle and are asymptomatic. Patients may present with

mediastinal compression and respiratory symptoms. The differential diagnosis includes a Morgagni

hernia, lipoma, mediastinal tumor, or bronchogenic cyst. CT scans are used to confirm the location and

relationship to surrounding structures. The cyst is excised if the patient is symptomatic, or the diagnosis

is unclear.

ACUTE PERICARDITIS

Acute pericarditis is an inflammatory process that has involved the pericardium for less than 2 weeks

(Table 86-1). Patients often present with a 3- to 7-day prodrome of low-grade fevers, malaise, and

muscle aches. Acute pericarditis occurs in 5% of those who present to the emergency department with

nonischemic chest pain10 and in 1% of those with ST elevation.11 It is important to distinguish

pericarditis from the chest pain of an acute myocardial infarction. Acute pericarditis usually causes

sharp, pleuritic pain that can last several days. The pain most commonly radiates to the trapezius ridge

and is improved by leaning forward. Patients can present with shortness of breath, a nonproductive

cough, and clear lung fields. The differential diagnosis also includes aortic dissection and pneumothorax.

On physical examination, a friction rub may be heard and is sometimes intermittent. The classic friction

rub has three components during systole, early diastolic filling, and atrial contraction.

ETIOLOGY

Table 86-1 Causes of Pericarditis

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3 The electrocardiogram is important in the diagnosis and classically shows diffuse ST elevations

without Q waves or T-wave inversion. PR depression can also be seen. There is a four-stage progression

in the changes seen on EKG with diffuse ST elevations followed by normalization of ST segments with

flattening of T waves. The EKG then evolves with T-wave inversions prior to normalization of the EKG.

Pericarditis and associated myocarditis can cause elevations in creatinine kinase and troponin I.12 The

minimal workup should include an EKG, complete blood count, cultures, chemistry profile, and antibody

titres for collagen diseases.

Idiopathic and Viral Pericarditis

Idiopathic causes of pericarditis are the second most common after neoplastic disease. The majority are

likely viral although routine testing is not usually performed. A virus is only identified in 15% to 20%

of cases with the most common being Coxsackievirus, echovirus, adenovirus, influenza, and

cytomegalovirus. Patients present with chest pain, malaise, and fever and often have an elevated

erythrocyte sedimentation rate. The episode is self-limited in 70% to 90% of cases.10 Initial treatment is

with nonsteroidal anti-inflammatory drugs (NSAIDs). There is a 15% to 30% relapse rate at which point

specific causes such as autoimmune disorders should be investigated.10,13 A repeat course of NSAIDs,

colchicine, or steroids is generally successful. Pericardiectomy is recommended if the patient

unresponsive to medical treatment or constriction develops.

Acquired Immunodeficiency Syndrome

A pericardial effusion develops in up to 20% of patients with HIV and is usually a poor prognostic

sign.14 This may be partly due to a generalized capillary leak syndrome as well as increased cytokine

expression seen in the more advanced stages of HIV. Other contributing factors include tubercular and

mycobacterial infections, lymphoma, Kaposi’s, or congestive heart failure. The majority are idiopathic

and do not require further therapy if asymptomatic. Symptomatic effusions are drained.

Tuberculous Pericarditis

Tuberculous pericarditis occurs in 1% to 8% of patients.15 In immunocompromised patients infection by

Mycobacterium avium or Mycobacterium intracellulare can lead to pericarditis. The incidence of

tuberculous pericarditis has decreased although it continues to be a significant issue in

immunocompromised patients, particularly HIV patients in Africa. Patients present with fever, night

sweats, cough, dyspnea, and weight loss. While infection usually results from hematogenous spread, it

can also extend directly from lymph nodes or through lymphatics. Pericardial changes occur in four

stages including fibrinous, effusive, fibrous, and constrictive fibrous stages. Making the diagnosis from

pericardial fluid alone is rare. Pericardial biopsy with acid fast staining provides the diagnosis 80% to

90% of the time. Treatment includes multidrug antitubercular therapy and pericardiocentesis. Steroids

have not been shown to be beneficial for mortality or progression to constriction but leads to a faster

resolution of symptoms and reaccumulation.16 If patients present with late constriction, pericardiectomy

may be required.

Purulent Pericarditis

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