Bacteria can be introduced into the pericardial space by direct injury, pneumonia, extension from head

and neck infections, or hematogenous and lymphatic spread. Patients present with chest pain, fever, and

leukocytosis. The most common organisms in adults are staphylococcus, pneumococcus, and

streptococcus. Purulent pericarditis can evolve rapidly into tamponade and can be confused with septic

shock. Fungal infections are less common, but immunocompromised patients and drug addicts are at

greater risk. Pericardial fluid in purulent pericarditis has low glucose, high protein, and elevated LDH

and neutrophils. An air–fluid level may be seen on chest radiograph with gas-producing organisms.

Treatment includes antibiotics and drainage. Surgical drainage may be needed for thick fluid or

refractory effusions. The prognosis for purulent pericarditis is poor with a survival of 30%.10,17

Uremic Pericarditis

Fifty percent of patients with untreated renal disease develop pericarditis. The incidence is decreased to

approximately 20% in patients on hemodialysis. The exact cause is unknown but is not directly related

to the BUN or creatinine. Other possible etiologies include hypercalcemia, viral infection, and

autoimmune disease. Chest pain is usually less common, and the large effusions accumulate gradually.

Treatment includes more intensive dialysis, NSAIDs, and steroids. The fluid is generally bloody and care

should be taken in heparinizing these patients for dialysis. If patients develop tamponade or the effusion

is unresponsive, pericardiocentesis or surgical drainage is performed.

Vasculitis, Connective Tissue Disease, and Drugs

Pericarditis can result from a variety of vasculitic and connective tissue diseases including rheumatoid

arthritis, Wegener granulomatosis, rheumatic fever, lupus, scleroderma, Reiter syndrome, Behcet

disease, dermatomyositis, polyarteritis nodosa, dermatomyositis, sarcoidosis, and amyloidosis.

Treatment includes management of the underlying disease process and NSAIDs. Pericardiocentesis is

performed if necessary. Several medications can also lead to pericarditis including warfarin,

hydralazine, isoniazid, procainamide, phenytoin, dantroline, cromolyn, and methysergide.

Dressler and Postpericardiotomy Syndrome

Pericarditis can occur following acute myocardial infarction in 3% to 5%.18 Pericarditis can develop

early in the first 1 to 3 days particularly with transmural infarction. Forty percent of large Q-wave

infarctions cause pericardial inflammation although the incidence is decreasing with the use of

thrombolytics and early revascularization. Patients are usually asymptomatic and are found to have a

pericardial rub on examination although they can present with pleuritic chest pain. Treatment is usually

with NSAIDs. Steroids can prevent conversion of infarcted myocardium to scar leading to greater

thinning and risk of rupture.19,20

Patients can also present with pericarditis 1 week to a few months after a myocardial infarction with

a friction rub, typical EKG changes, and chest pain although the incidence has decreased with increased

revascularization. Pericardial inflammation is thought to be from an autoimmune reaction to myocardial

cells.20 Similar symptoms can also occur after cardiac surgery, blunt trauma, and pacemaker placement.

Patients can develop a pericardial effusion and even tamponade. Treatment includes NSAIDs and

colchicine for 2 to 3 weeks and occasionally steroids. The syndrome is usually self-limited.

Radiation-Induced Pericarditis

Pericarditis can result from mediastinal and thoracic radiation for cancer including lymphoma and

breast carcinoma and is related to the dosage delivered. With modern techniques, the incidence is 2%

but can be as high as 20% if the entire pericardium is treated. Patients may develop chest pain and

fever.20 Symptoms are usually self-limited, and tamponade is rare. Delayed symptoms can develop years

later and can result in pericardial constriction. Due to the history of malignancy, the etiology can be

confused with a malignant effusion. If pericardial constriction develops, the treatment is

pericardiectomy although the mortality is higher than for other etiologies.

PERICARDIAL EFFUSION AND TAMPONADE

Any of the etiologies mentioned above for pericarditis can also lead to a pericardial effusion. Other

causes include blunt or penetrating trauma, retrograde bleeding from an aortic dissection, and a

transudative effusion from congestive heart failure. Effusions due to a bacterial or fungal infection, HIV,

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or malignancy have a higher incidence of progressing to tamponade. Twenty percent of large

symptomatic effusions of unknown cause are due to an undiagnosed cancer.21

4 Normally there is only a small reserve volume before pericardial fluid causes significant cardiac

compression and prevents adequate cardiac filling. The hemodynamic significance of a pericardial

effusion depends on the volume and the rate of accumulation. The compensatory adrenergic response to

a pericardial effusion leads to tachycardia and increased contractility, and patients on beta blockers are

less likely to compensate. Tamponade usually occurs when filling pressures reach 15 to 20 mm Hg

although tamponade can occur at lower pressures in conditions where blood volume is reduced

including dialysis, with diuretic therapy, and bleeding. Cardiac pressures become elevated and are most

closely equalized during inspiration. Tamponade generally affects right heart filling first which then

leads to underfilling of the left heart.22

Patients may present with dyspnea, tachycardia, and diaphoresis. The three classic signs of Beck triad

are hypotension, jugular venous distension, and muffled heart sounds although each may be absent in

patients with tamponade.23 Symptoms can be confused with right heart failure and pulmonary embolus.

The jugular waveform changes characteristically with loss of the y descent.24 Since the total heart

volume is fixed in tamponade, blood only enters the heart when blood leaves. The y descent represents

opening of the tricuspid valve and is lost since no blood is ejected from the heart. Pulsus paradoxus is

also noted with a fall in the systolic blood pressure of greater than 10 mm Hg with inspiration. Pulsus

paradoxus is absent in left ventricular dysfunction, atrial septal defect, positive-pressure ventilation,

aortic insufficiency, and regional tamponade. The EKG shows variation in the morphology of every

other QRS complex, or electrical alternans, due to swinging of the heart in the pericardial effusion (Fig.

86-3). Chest radiograph shows an enlarged, rounded cardiac silhouette, and the pericardial fat pad sign

is seen when the pericardial fat is separated from the heart by the effusion.

Echocardiography is the most useful test in diagnosing pericardial effusion and tamponade. Signs of

tamponade include early diastolic right ventricular and right atrial collapse (Fig. 86-4) and distension of

the cava that does not diminish with inspiration. Doppler is useful in evaluating blood flow and shows

exaggerated respiratory variation with an increase with inspiration on the right and decrease on the left

side of the heart. Echocardiography is also useful in identifying localized atrial compression which can

lead to tamponade with the other changes described above.

Figure 86-3. The 12-lead EKG shows electrical alternans with variation in the morphology of every other QRS complex in a

patient with a large pericardial effusion. (From Joffe II, Jacobs LE, Kotler MN. Pericardial tamponade. Circulation 1996;94:2667,

with permission.)

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Figure 86-4. The echocardiogram shows a large pericardial effusion with diastolic right atrial collapse (arrow). (From Joffe II,

Jacobs LE, Kotler MN. Pericardial tamponade. Circulation 1996;94:2667, with permission.)

If there are significant hemodynamic changes, emergent pericardiocentesis should be performed.

Intravenous fluid and inotropes can temporize the hypotension but should not delay pericardiocentesis.

If the effusion is loculated or contains blood clots, open drainage may be necessary. There should be a

higher suspicion for tamponade in situations involving bleeding, bacterial or tuberculous pericarditis, or

an acute or increasing moderate-to-large effusion. The approach to a patient with a large pericardial

effusion is outlined in Algorithm 86-1.

Postoperative Cardiac Tamponade

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

cardiac surgery. Patients may have rising filling pressures, hypotension, and decreased urine and cardiac

output. Mediastinal chest tube output may increase or abruptly stop. Hypovolemia during the

postoperative period can limit the increase in filling pressures. Pulsus paradoxus may also be masked by

positive pressure ventilation. On chest radiograph, the cardiac silhouette is enlarged. In the

postoperative cardiac patient, the epicardial pacing wires may move farther from the pericardium with

increasing tamponade on chest films. Tamponade can result from relatively small amounts of blood with

localized atrial compression from blood clots. There should be a low threshold for reexploration which

also provides a definitive diagnosis. Patients can also present with delayed tamponade after being

started on anticoagulants.

PERICARDIAL CONSTRICTION

Constriction develops when the heart becomes constrained by a fibrotic pericardium. The process can

progress over years, and the most common causes in the developed world are radiation treatment,

postsurgical changes, and idiopathic. Tuberculosis was the most common cause before antitubercular

drug therapy. Other causes include amyloidosis, scleroderma, sarcoidosis, hemochromatosis, and

malignant disease. Patients develop signs and symptoms of right heart failure due to obstruction of the

right ventricular outflow tract including hepatomegaly, ascites, and peripheral edema. Patients can also

have dyspnea, pleural effusions, fatigue, and weight loss. On physical examination, a pericardial knock,

or a loud third heart sound, can be heard which corresponds to the abrupt cessation of diastolic filling.

Kussmaul sign is increased jugular venous distension with inspiration. Atrial fibrillation or flutter is

present in up to 25% of patients, and tricuspid regurgitation is also common.

Pericardial calcification is pathognomonic but is only seen in 40% of cases. Thickened pericardium

can be seen on CT or MRI (Fig. 86-5) although the pericardium was normal in thickness in 18% of

patients in one series.25 The normal pericardial thickness is 2 mm on CT and 4 mm on MRI.

Echocardiography shows thickened pericardium and a septal bounce due to the abrupt displacement of

the septum during early diastole. The ventricles are small with good function. Ventricular filling halts

abruptly in diastole due to the limits of the stiff, fibrotic pericardium. There are signs of systemic

venous congestion with a distended inferior vena cava. In contrast to tamponade, there is no decrease in

early diastolic filling but a sudden decrease in late diastole (Table 86-2).24 When the myocardium is

involved by fibrosis, ventricular dysfunction is present which is associated with a poorer response to

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pericardiectomy.

Algorithm 86-1. This algorithm outlines the initial approach to a patient with a large pericardial effusion.

Figure 86-5. A: Chest CT shows extensive pericardial calcification. (From Cavendish JJ, Linz PE. Constrictive pericarditis from a

severely calcified pericardium. Circulation 2005;112(11):e137–e139, with permission.) B: Chest CT shows thickening of the

pericardium in a patient with constrictive pericarditis. (From Tom CW, Oh JK. A case of transient constrictive pericarditis.

Circulation 2005;111:e364, with permission.).

On right heart catheterization, the y descent is deeper and more rapid than normal. The right atrial

waveform is M- or W-shaped. The right ventricular tracing is described as the square root sign with an

early diastolic decrease with a rapid increase and plateau (Fig. 86-6). Pulmonary artery and right

ventricular pressures can be moderately elevated, but more severe pulmonary hypertension suggests a

different disease process. In addition, hypovolemia can mask these findings, and patients may need to

be volume-challenged to see the diagnostic changes.26

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

important since the treatment is significantly different (Table 86-3). In restrictive cardiomyopathy,

there is no pericardial thickening. Decreased systolic function, mitral regurgitation, and left heart

pressures greater than right are more common in restrictive cardiomyopathy. Early diastolic filling is

slower. In addition, left and right ventricular pressures move in the same direction on inspiration rather

than opposite directions.27

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Constrictive pericarditis is generally progressive although it can be transient after cardiac surgery and

should be observed for several months. Diuretics with fluid and salt restriction help initially, but

pericardiectomy is the only definitive treatment. Tachycardia is a compensatory response, and beta and

calcium channel blockers should be avoided.

NEOPLASTIC PERICARDIAL DISEASE

7 Primary tumors of the pericardium are rare and include benign fibromas, hemangiomas, lipomas,

lymphangiomas, leiomyomas, and neurofibromas. Malignant pleural tumors include mesothelioma,

teratoma, and fibrosarcoma. Surgical resection is therapeutic and diagnostic. Malignancies can also

extend directly from the mediastinum, esophagus, and lung. Metastatic disease is the most common

cause of pericardial effusion. Cardiac involvement is found in 5% to 10% of patients dying of cancer

with 85% of those having pericardial involvement. The most common cancers are lung and breast

carcinoma, lymphoma, melanoma, and leukemia. Patients often present with tamponade. The diagnosis

is made on echocardiography or CT. Cytology of pericardial fluid is negative in 20% to 50% of cases,

and pericardial biopsy may be helpful. Palliation includes sclerosing agents such as tetracycline,

radiotherapy, intrapericardial chemotherapy, and catheter drainage.

DIAGNOSIS

Table 86-2 Distinguishing Cardiac Tamponade and Constrictive Pericarditis

Figure 86-6. A: The right ventricular (RV) pressure tracing shows elevated RV diastolic pressure with the dip-and-plateau

waveform known as the “square root sign.” The EKG tracing shows a large P wave indicative of right atrial enlargement. B: The

postoperative RV tracing shows normalization of the RV waveform. (From Correa SD, Amsterdam EA. Constrictive pericarditis.

Circulation 1998;97:806, with permission.)

PERICARDIOCENTESIS

Pericardiocentesis can be diagnostic and therapeutic. Ideally, it should be performed in the

catheterization laboratory so the hemodynamic response can be monitored. Normal pericardial fluid is

an ultrafiltrate with an LDH 2.4 times serum and protein 0.6 times.28 Uremic fluid is bloody. Rheumatic

effusions are high in protein and leukocytes and low in glucose. Cholesterol crystals are seen with

myxedema, tuberculosis, and rheumatoid arthritis.

DIAGNOSIS

Table 86-3 Distinguishing Constrictive Pericarditis From Restrictive

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Cardiomyopathy

Generally, a 16- to 22-gauge needle is inserted to the left of the xiphoid. The needle is angled at a 45-

degree angle toward the left shoulder (Fig. 86-7). An EKG lead may also be attached to the needle to

monitor for an injury current, although echocardiography is more commonly used for guidance. There is

a 97% success rate with a complication rate of 4.7% (Table 86-4).29 If the effusion is anterior, a

parasternal approach is used 1 to 2 cm to the left of the sternum in the fourth or fifth intercostal space.

The removal of even a small amount of fluid can lead to significant hemodynamic improvement. For

longer-term drainage a catheter can be placed over a guidewire. Pericardiocentesis may not be effective

for purulent or bloody effusions that may require open drainage.

Figure 86-7. Pericardiocentesis is performed by inserting a needle to the left of the xiphoid and toward the left shoulder at a 45-

degree angle. An EKG lead may be attached to the needle to monitor for Q waves indicating contact with the epicardium.

COMPLICATIONS

Table 86-4 Potential Complications From Pericardiocentesis

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PERICARDIAL BIOPSY AND SURGICAL DRAINAGE

Pericardial biopsy is useful when pericardiocentesis is nondiagnostic, which is not uncommon in

neoplastic and tubercular effusions. This can be approached through a subxiphoid incision, anterior

thoracotomy, or thoracoscopically (Fig. 86-8). Open drainage may be useful if the fluid is viscous,

including bloody or purulent effusions, or in patients that have recurrent effusions. Loculated effusions

may also require open drainage. The subxiphoid approach is better for purulent effusions to prevent

contamination of the pleural space. Chronic or malignant effusions can be drained through a pericardial

window into the left pleura. Preinduction pericardiocentesis or intravenous fluids may be necessary for

patients to tolerate general anesthesia.

Figure 86-8. Open pericardial biopsy or drainage is performed through an upper midline incision. The xiphoid is retracted or

removed providing exposure to the pericardium.

RECONSTRUCTION OF THE PERICARDIUM

Generally, the pericardium does not need to be reconstructed after routine opening of the pericardium

during cardiac surgery or when resecting portions of the pericardium for adjacent tumors such as a

thymoma. Primary pericardial closure is often avoided due to concerns for hemodynamic compromise

and perioperative tamponade. Dantas et al. found a temporary, but clinically insignificant, decrease in

hemodynamics in a study of 48 patients with primary closure of the pericardium after open heart

surgery.30

8 Reconstruction of the pericardium should be considered in cases where a future redo sternotomy is

likely such as a bioprosthetic valve that will need to be replaced or a left ventricular assist device that

will be removed at the time of transplant. To prevent hemodynamic compromise, the closure should be

performed without tension. A biologic mesh implant made of porcine extracellular matrix has been used

to prevent adhesions and protect the right ventricle, aorta, and coronary bypass grafts. Reconstruction

of the pericardium was also reported in a retrospective study of 222 patients to decrease the incidence

of atrial fibrillation.31 However, the results of a randomized trial evaluating new-onset postoperative

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