Chapter 61. Pericardial Disease

The pericardium envelops the heart and portions of the great vessels as a protective capsule. When incised longitudinally and transversely along the diaphragm it can be suspended from a chest retractor to present the heart for surgical procedures. The surgical importance of the pericardium stems from its involvement in alterations of cardiac filling. When the limited space between the noncompliant pericardium and heart acutely fills with blood or fluid, cardiac compression and tamponade may ensue. Constrictive disorders arise when inflammation and scarring cause the pericardium to shrink and densely adhere to the surface of the heart. This chapter discusses pericardial anatomy and function and describes the conditions that commonly give rise to the surgical problems of pericardial constriction and tamponade. The chapter also describes the diagnosis and therapy of these entities, the management of tamponade early and late after cardiac surgery, and the rationale for and against pericardial closure at the time of cardiac surgery.

The pericardium serves two major functions. It maintains the position of the heart within the mediastinum and prevents cardiac distention by sudden volume overload. The pericardium attaches to the ascending aorta just inferior to the innominate vein and the superior vena cava (SVC) several centimeters above the sinoatrial node. The pericardial reflection encompasses the superior and inferior pulmonary veins and encircles the inferior vena cava, thereby making it possible for the surgeon to control the inferior vena cava from within the pericardium. The pericardial reflection attaches to the left atrium near the entrances of the pulmonary veins just below the atrioventricular groove (Fig. 61-1). The pericardiophrenic arteries that travel with the phrenic nerves as well as the branches of the internal mammary arteries and feeder branches directly from the aorta perfuse the pericardium. It is innervated by vagal fibers from the esophageal plexus, and the phrenic nerves course within it.

The pericardium is a conical fibroserous sac made up of two intimately connected layers. The inner layer (serous pericardium) is a transparent monolayer of mesothelial cells. The visceral portion of the serous pericardium, or epicardium, and the parietal portion, which lines the fibrous pericardial sac, are continuous. The oblique sinus lies within the venous confluence and the transverse sinus lies between the arterial (aorta and pulmonary artery) and venous reflections (dome of left atrium and SVC). Such potential spaces allow the pericardium to expand and accommodate a limited amount of fluid. Normal pericardial fluid volume is approximately 10 to 20 mL. The pericardial mesothelial cells contain dense microvilli that are 1 μm wide and 3 μm high, which facilitate fluid and ion exchange.1 Visceral pericardial lymphatic drainage occurs via the tracheal and bronchial mediastinal nodes, whereas the anterior and posterior mediastinal lymph nodes drain the parietal pericardium.

The parietal layer or fibrous pericardium is composed mostly of dense parallel bundles of collagen, which render this layer relatively noncompliant. Because the pericardium is stiffer than cardiac muscle, it tends to equalize the compliance of both ventricles. By doing so, the pericardium contributes to the resting cavitary diastolic pressure of both ventricles, maximizing diastolic ventricular interaction.2 An example of this phenomenon is the diminution of systemic arterial pressure during inspiration. Intrapericardial pressure tends to approximate pleural pressure, and varies with respiration. The negative intrathoracic pressure generated during inspiration augments right ventricular filling. The interventricular septum shifts toward the left to accommodate the increase in right ventricular volume. Because pericardial constraint does not allow equal filling of the left ventricle, the decrease in volume ejected by the systemic chamber results in a slight diminution of systemic arterial pressure during inspiration. This phenomenon is greatly magnified with an increase in intrapericardial pressure (eg, during acute filling of the pericardial space or circulatory volume overload), resulting in pulsus paradoxus.3

Most congenital abnormalities of the pericardium are asymptomatic4 and are often discovered incidentally at the time of surgery or investigation of unrelated problems.5 They are rare and one-third are associated with cardiac, skeletal, and pulmonary abnormalaties.6 Partial absence of the pericardium also occurs and is most commonly seen on the left (70%) due to premature atrophy of the left common cardinal vein. Right-sided and complete defects of the pericardium account for 17 and 13% of these defects, respectively. The right duct of Cuvier goes on to form the superior vena cava and ensures closure of the right pleuropericardial membrane.7 Accordingly, right-sided defects tend to be lethal. MRI provides excellent pericardial imaging without contrast and is the imaging modality of choice. CT and echocardiography are useful for evaluation of pericardial thickening and extent and location of defects.4 Although complete pericardial agenesis is rarely clinically significant, unilateral absence is potentially problematic because it may accentuate cardiac mobility and allow the heart to be displaced into the pleural space with resulting incarceration of the left atrial appendage or left ventricle. Treatment may involve pericardial resection or replacement with a prosthetic patch.6 Both therapies appear to yield good outcomes.

Pericardial cysts are the most common congenital pericardial disorder and are surpassed only by lymphoma as the most prevalent of middle mediastinal masses.8 They occur as asymptomatic incidental findings in 75% of patients; 70% occur in the right costophrenic angle and 22% on the left.5 They do not communicate with the pericardial space and are typically unilocular, smooth, and less than 3 cm in diameter (Fig. 61-2). Symptoms may include chest pain, dyspnea, cough, and arrhythmias, probably owing to compression and inflammatory involvement of adjacent structures. They can also become secondarily infected.9 Contrast CT scan is the modality of choice for diagnosis and follow-up.10,11 Observation by CT in asymptomatic patients is suggested. Percutaneous aspiration is associated with a 30% recurrence rate at 3 years. Sclerosis has been reported to decrease recurrence after aspiration.12 Indications for resection include large size, symptoms, patient concern, and question of malignancy.8 Video-assisted thoracoscopy is the surgical approach most commonly used for excision. Infrasternal mediastinoscopy can be used for anterior cysts. Thoracotomy is also an acceptable technique. Surgery is the only definitive cure.12

Pericardial compression results from disturbance of the normal anatomical and physiologic relationships among the pericardium, pericardial cavity, and the heart. Because the pericardium is relatively noncompliant and pericardial fluid noncompressible, the heart alone must compensate for acute changes in pericardial pressure. Acute volume overload within the confines of a fixed pericardial space results in a rapid, nonlinear increase in intrapericardial pressure (Fig. 61-3), producing cardiac compression.13 The anatomical basis for pericardial compression involves either a space-occupying lesion (ie, cyst or excessive fluid) within the pericardial space or pericardial constriction.

Tamponade

Although blood in the pericardial space is the most common etiology, effusions, clot, pus, gas, or any combination may also produce tamponade. As fluid entering the pericardial space exceeds the ability of the pericardium to accommodate or absorb it, pericardial reserve volume (10 to 20 mL) is rapidly exceeded and intrapericardial pressure rises abruptly. At this point, pericardial fluid volume can only increase by reducing cardiac chamber volumes. Because of its lower filling pressures, the right heart is more susceptible to compression (Fig 61-4). The physiologic consequences are impaired diastolic filling with decreased cardiac output and increased central venous pressure.14 Clinical manifestations include hypotension and jugular venous distention, and, along with decreased heart sounds, comprise Beck's triad.

To preserve cardiac output, higher pressures are required to fill the cardiac chambers, which may be partially achieved by parallel increases in systemic and pulmonary venous pressure by vasoconstriction.15 Other compensatory mechanisms include tachycardia, chronic pericardial stretch, and blood volume expansion.16 The latter two mechanisms have little impact in acute tamponade. As tamponade progresses, right heart filling becomes increasingly volume dependent and limited to inspiration. Increased filling of the right ventricle causes it to encroach on, and impair, filling of the left ventricle. However, during expiration the converse is true, and left ventricular filling and output increase. This exaggeration of physiologic ventricular interdependence is the basis of pulsus paradoxus.13

The clinical spectrum of tamponade varies widely, depending on the severity of hemodynamic impairment and degree of physiologic reserve. Rapid accumulation of as little as 100 mL of fluid in the pericardial space (eg, after a penetrating cardiac wound) may exceed the limited compliance of the parietal pericardium and produce critical tamponade. On the other hand, the pericardium may compensate for large pericardial effusions (>1 L) in chronic inflammatory conditions such as rheumatoid arthritis. The cardiac silhouette may appear normal in acute tamponade, but chronic pericardial distension is often obvious on plain chest radiography (Fig. 61-5), chest tomography (Fig. 61-6), and echocardiography (Fig. 61-7). Furthermore, low-pressure tamponade can also occur in which a pericardial effusion is not hemodynamically significant until the patient becomes hypovolemic, typically from dehydration, blood loss, or diuretic therapy. Venous filling pressures may be normal or mildly elevated in this setting, making this diagnosis difficult.17

Pericardial Constriction

A wide range of conditions promote pericardial scar formation, the pathologic process underlying constrictive pericarditis (CP). As with tamponade, the physiologic basis is compromised cardiac filling leading to systemic venous congestion and low cardiac output. In contrast with tamponade, however, onset is often insidious and symptoms may be present for months or even years.18 Common complaints include fatigue, decreased exercise tolerance with dyspnea/orthopnea, as well as peripheral edema and ascites from hepatic congestion in advanced disease. The principal etiologies behind pericardial scar formation have shifted over the past few decades, with declining incidence of infectious cases (particularly tuberculosis) and increasing incidence of iatrogenic cases (primarily from mediastinal radiation therapy and cardiac surgery).19

Pericardial constriction exerts its pathophysiologic effects by limiting cardiac filling. Unlike tamponade, in which cardiac filling is limited from the onset of diastole, constriction does not restrict filling in early diastole. During diastolic filling the ventricles are prevented from reaching full capacity as they encounter the contracted and noncompliant pericardium. As a result, 70 to 80% of diastolic filling occurs in the first 25 to 30% of diastole.20 Although early diastolic filling pressures are normal (whereas ventricular expansion is not constrained by the surrounding stiff pericardium), later diastolic pressures abruptly increase. The ventricular free walls are then immobilized, leaving the interventricular septum as the last yielding structure; it is rapidly displaced in response to the sudden interventricular pressure differential. This produces the characteristic "septal bounce" seen echocardiographically. Other echocardiographic findings include pericardial thickening, caval plethora, and small chamber volumes. Inspiration exaggerates both leftward septal deviation as well as reciprocal Doppler flows between the right and left sides (the echocardiographic correlate of pulsus paradoxus).

Modern axial imaging with spiral computed tomographic (CT) scanning (Fig. 61-8) or magnetic resonance (MR) imaging (Fig. 61-9) is often able to visualize thickened and/or calcified pericardium, with or without coexisting effusion. Dynamic CT and MR imaging also demonstrate many of the physiologic features seen sonographically.21 Importantly, although pericardial thickening is usually present in constrictive pericarditis, it remains possible to have CP with normal pericardial thickness as well as thickening of the pericardium without CP.22

Prior to the modern era of echocardiography and axial imaging, the diagnosis of CP was dependent on hemodynamic tracings obtained during cardiac catheterization. The sudden increase in diastolic ventricular pressure is reflected in the dip and plateau or "square-root" sign (Fig 61-10). Similarly, right atrial pressure tracings reveal a steep y descent, which correlates with the nadir of the square-root sign. Under normal circumstances, inspiration results in a 3- to 7-mm Hg drop in right atrial pressure. The high pressure of pericardial constriction prevents the right atrium from accepting inspiratory acceleration of blood from the central veins. Instead, neck veins become prominently distended during inspiration in patients with CP, a phenomenon referred to as Kussmaul's sign.

Catheterization remains a valuable illustration of the underlying physiology of CP. In some cases it may help differentiate between CP and restrictive cardiomyopathy (RCM), a nonsurgical condition with a poor prognosis.23,24 RCM is characterized by noncompliant ventricular muscle and diastolic dysfunction, which impede cardiac filling. Restrictive cardiomyopathy is caused by a variety of infiltrative or fibrosing conditions (eg, amyloidosis, sarcoidosis, radiation, carcinoid, anthracycline toxicity). Although RCM may mimic many of the presenting features of CP, it is not a surgical disease and must be distinguished from CP for this reason (Table 61-1). Systolic ventricular function may be normal or near-normal in both conditions, but pulmonary and hepatic congestion are often present in RCM. Evidence of pericardial thickening (>2 mm) favors but does not confirm the diagnosis of CP over RCM. There are instances, particularly in radiation-induced CP, in which the conditions coexist. Distinctive myocardial speckling may be found on echo with amyloidosis or other infiltrative conditions. Endomyocardial biopsy is useful to establish the presence of one of the conditions known to be associated with RCM; unfortunately, a negative biopsy does not rule it out.

In an attempt to provide additional criteria to differentiate patients with CP from RCM, Hurrell and colleagues25 measured respiratory variation of the gradient between left ventricular pressure and pulmonary capillary wedge pressure during the rapid filling phase of diastole. This was done to assess the dissociation of intrathoracic and intracardiac pressures that accompanies constrictive pericarditis. A difference of 5 mm Hg in the gradient between inspiratory and expiratory cycles had 93% sensitivity and 81% specificity for constrictive pericarditis. Furthermore, increased ventricular interdependence was assessed by comparing left ventricular systolic pressure and right ventricular systolic pressure during respiration. Although concordant increases in left ventricular systolic pressure and right ventricular systolic pressure are expected during inspiration, discordant pressures are encountered during inspiration in patients with constrictive pericarditis. This finding has 100% sensitivity and 95% specificity for constrictive pericarditis.

Pericarditis, the most common pericardial disorder, has many etiologies (Table 61-2), including infectious (viral, bacterial, fungal), metabolic (uremic, drug induced), autoimmune (arthritis, thyroid), postradiation, neoplastic, traumatic, postinfarction (Dressler's syndrome, 10 to 15%), post-pericardiotomy (5 to 30%), and idiopathic (Fig. 61-11). The clinical syndrome for all causes is similar. Chest pain (dull, aching, pressure) or chest tightness is usually present and may be associated with constitutional symptoms (eg, weakness and malaise), fever (occasionally with rigors), and other symptoms such as cough or odynophagia. The pain may be pleuritic, and thus exacerbated by inspiration, cough, or recumbency. These patients therefore often sit up and lean forward for relief. Acute disease may become chronic. The cardinal sign of pericarditis is the pericardial rub, which may be positional and muffled because of an effusion.26

Electrocardiography, chest x-ray, and echocardiography are useful in making the diagnosis. The electrocardiogram may range from normal, to nonspecific ST-segment deviations, to diffuse concave elevation of the ST segments without reciprocal depressions or Q waves. PR-segment depression may be present. Troponin may be elevated with a normal CPK. Ventricular arrhythmias and conduction abnormalities are not commonly seen in pericarditis and are suggestive of an underlying cardiac abnormality if present. Echocardiography may reveal fibrinous thickening of the pericardium with or without a small effusion.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment and may be supplemented with colchicine. Chronic pericardial effusion or constrictive pericarditis may follow acute pericarditis as well as tuberculosis, malignancy, radiation, rheumatoid arthritis, or surgery.26

Infectious Pericarditis

Viral Pericarditis

Infectious pericarditis is most often viral and results from immune complex deposits, direct viral attack, or both. The clinical syndrome involves pain, friction rub, and typical changes on the electrocardiogram. It is often difficult to diagnose and thus labeled as idiopathic disease. Treatment is expectant, and symptoms generally resolve within 2 weeks. Surgical intervention is rarely required.

Bacterial Pericarditis

This is currently an uncommon cause of pericarditis because of availability of effective antibiotic therapy. Microorganisms may invade the pericardial space from contiguous infections in the heart (endocarditis), lung (pneumonia, abscess), subdiaphragmatic space (liver or splenic abscess), or wounds (traumatic or surgical). Hematogenous seeding may also occur, most often in the setting of septicemia and immune compromise.

The most common bacteria implicated in bacterial pericarditis are Haemophilusinfluenzae, meningococci, pneumococci, staphylococci, or streptococci.27 Gram-negative rods, Salmonella and opportunistic sources of infection must be excluded. Regardless of the source or organism, acute suppurative pericarditis is life threatening. A toxic presentation with a high fever is typical with an acute, fulminant clinical course. Purulent pericarditis with tamponade or septicemia may require acute surgical intervention via pericardial window or pericardiectomy and treatment of the inciting cause (eg, removal of foreign body or drainage of abscess) (Fig. 61-12). In adults, pneumopyopericardium is often caused by fistula formation between a hollow viscus and the pericardium. However, invasion from contiguous foci, implantation at the time of surgery or trauma, mediastinitis, endocarditis, and subdiaphragmatic abscess can all induce this condition. Scarring, which results in pericardial constriction, may require pericardiectomy. These patients have an excellent outcome when treated appropriately.27

Tuberculous Pericarditis

Although the incidence of tuberculosis (TB) has significantly declined in industrialized countries, it has increased dramatically in Africa, Asia, and Latin America, accounting for 95% of all cases of active TB. This resurgence in TB reflects the increasing incidence of human immunodeficiency virus (HIV) infection.28 The immune response to the acid-fast bacilli penetrating the pericardium induces a delayed hypersensitivity reaction with lymphokine release and granuloma formation. Complement fixing antibodies initiate cytolysis mediated by antimyolemmal antibodies as the cause of the exudative TB pericarditis.28 The definitive diagnosis is established by examining pericardium or pericardial fluid for mycobacteria.

Four pathologic states are recognized:

1. Fibrinous exudation, with robust polymorphonuclear infiltration and abundant mycobacteria

2. Serous or serosanguineous effusions with a mainly lymphocytic exudation and foam cells (Fig. 61-13)

3. Absorption of effusion, with organization of caseating granulomas, and pericardial thickening caused by fibrin and collagen deposition and fibrosis

4. Constrictive scarring, often with extensive calcification occurring over a period of years (Fig. 61-14A,B)

There is a variable clinical course. Effusion usually develops insidiously with fever, night sweats, fatigue, and weight loss to variable degrees. Children and immunocompromised patients may, however, present with a more fulminant course, often demonstrating both constrictive and tamponade physiology. Despite prompt anti-TB antibiotic treatment, constrictive pericarditis, one of the most severe sequelae, occurs in 30 to 60% of patients. Echocardiography is useful for diagnosing effusive and subacute constrictive TB pericarditis. Standard anti-TB therapy is instituted promptly. Steroids remain controversial, especially in HIV-infected patients. Based on physiology and response to therapy, immediate or interval pericardiectomy is performed to avoid chronic constrictive pericarditis. If calcific pericarditis is present, surgery is undertaken earlier.29

Fungal Pericarditis

Fungal infection is an uncommon cause of pericarditis. Nocardia, Aspergillus, Candida, and Coccidioides are implicated, with regional specification, in the setting of immunocompromise, debilitation, HIV, severe burns, infancy, or steroid therapy. Candida and Aspergillus generate an insidious clinical picture, which may develop into tamponade or constriction. Fungi such as Histoplasma that tend to be endemic to certain geographic regions may cause pericarditis in young, healthy, immunocompetent patients. This is usually self-limited and resolves within 2 weeks. Similarly, Coccidioides can also infect young healthy individuals in the setting of pneumonia, osteomyelitis, meningitis, or adenopathy. These conditions often resolve either spontaneously or in response to appropriate antifungal regimens. Surgical intervention is not usually required in the acute setting.

Metabolic Causes of Pericarditis

Pericarditis is known to occur in the setting of renal failure, hypothyroidism, autoimmune diseases (such as rheumatoid arthritis), and pharmacotherapy with certain drugs (eg, procainamide and hydralazine).

Uremic Pericarditis

Uremic pericarditis was first recognized by Bright in 1836.30 Although it is recognized that nitrogen retention (blood urea nitrogen levels are generally >60 mg/dL) is required for uremic pericarditis, the inciting agent is still unknown. The clinical profile typically involves a patient with chronic renal insufficiency who develops pain, fever, and a friction rub.31 There is usually a pericardial fluid collection, which can be exudative or transudative, that is often hemorrhagic. Although the incidence of tamponade is decreasing because of more widespread use of renal replacement therapy,32 it still occurs and remains a primary concern. Initial therapy includes NSAIDs and aggressive dialysis. Pericardial drainage is reserved for hemodynamically significant (tamponade) or refractory effusions (more than 2 weeks despite intensive dialysis), but the latter is the subject of debate.33 Heparin should be administered cautiously, if at all, during dialysis because of the risk of hemorrhagic pericarditis and tamponade.34 Pericardial effusions may also develop in this population because of a variety of conditions such as heart failure, volume overload, and hypoproteinemia. Nonuremic pericarditis is also known to occur in patients on longstanding dialysis.35 Finally, pericardial effusion increases the risk of low-pressure tamponade during dialysis by mechanisms described in the preceding.17

Drug-Induced Pericarditis

Pericarditis may also occur in the setting of a drug-induced hypersensitivity reaction or lupus-like syndrome.36 Procainamide, hydralazine, isoniazid, methysergide, cromolyn, penicillin, and emetine (among others) have been associated with pericardial inflammation. Minoxidil has been associated with pericardial effusion.37 The clinical presentation and guidelines for management in these settings are similar to those for other types of pericarditis. The inciting agent should be discontinued.

Pericarditis Associated with Rheumatoid Arthritis

Pericarditis is common in patients with rheumatoid arthritis (RA). Approximately half of patients with RA have pericardial effusions, and almost half of all patients with RA have significant pericardial adhesions at autopsy.38 The condition is encountered more often in patients with advanced RA, and is thought to be caused by the higher rheumatoid factor titers often seen with more severe underlying disease. Deposition of immune complexes in the pericardium appears to be the inciting event underlying the inflammatory response.39 The diagnosis is often complicated by the many clinical variants and possible intercurrent diseases such as drug-induced and viral pericarditis. Pericardial drainage is often employed early for symptomatic effusions because response to medical therapy of the underlying RA is slow and unpredictable. Pericardiectomy should be considered in patients with longstanding RA who have developed constriction.40

Hypothyroidism

Severe hypothyroidism produces large, clear, high-protein, high-cholesterol, and high-specific-gravity effusions in 25 to 35% of patients.41 The effusion may precede other signs of hypothyroidism. Clinical tamponade is rare because of the slow accumulation of fluid. However, acute exacerbations owing to acute pericarditis, hemorrhage, or cholesterol pericarditis can induce tamponade.42

Radiation Pericarditis

Radiation is now the most common etiology of constrictive pericarditis in the United States. This was first recognized in patients who received high-dose mantle radiation for Hodgkin's lymphoma in the 1960s and 1970s and developed cardiac and pericardial pathology, on average 10 to 15 years after therapy. Radiation induces acute pericarditis, pancarditis, and accelerated coronary artery disease in a dose-dependent relationship.43 Patients may present with a combination of pericardial constriction, restrictive cardiomyopathy, valvular heart disease, and coronary artery disease with a predilection for ostial lesions.44 When symptomatic effusions are drained, fluid should be analyzed to clarify the etiology (ie, malignancy versus radiation effect). Constrictive pericarditis can develop several years later and is best treated by pericardiectomy.45

Neoplastic Pericarditis

Secondary neoplasms of the pericardium (ie, tumors that involve the pericardium by metastasis or infiltration from adjoining structures) account for greater than 95% of pericardial neoplastic diseases. Primary pericardial tumors are rare, and paraneoplastic effusions can also occur in response to remote tumors.46

The most common secondary tumors involving the pericardium in males (including both metastasis and local extension) are carcinoma of the lung (31.7%) and esophagus (28.7%) and lymphoma (11.9%). In females, carcinoma of the lung (35.9%), lymphoma (17.0%), and carcinoma of the breast (7.5%) are most common. Primary pericardial tumors are very uncommon. Benign tumors are generally encountered in infancy or childhood. Malignant tumors such as mesotheliomas, sarcomas, and angiosarcomas most often present in the third or fourth decade of life.47

In both primary and secondary tumor involvement, the clinical presentation is usually silent, and may be associated with large pericardial effusions. Tamponade can result from hemorrhage into a malignant effusion. Occasionally tumors can induce constriction because of neoplastic tissue, adhesions, or both. The role of surgery is limited to diagnosis and palliation in most of these cases. Large refractory effusions associated with tamponade may need surgical drainage. In such cases, a fluid sample should be submitted to confirm the presence of malignant cells or evaluate for other causes of effusion in patients with cancer because this may influence management.48 In terms of therapeutic benefit, pericardiocentesis has a high failure rate, and subxiphoid drainage or percutaneous balloon pericardiotomy are only transiently effective.49 Although extensive resection and debulking may be necessary in persistent or recurrent malignant pericardial constriction, it has only transient benefit without effective adjunctive chemotherapy and/or radiation therapy. Life expectancy of patients with malignant pericardial involvement averages less than 4 months.50 The surgeon should individualize decisions regarding how aggressively to pursue diagnostic or therapeutic interventions.

Traumatic Pericardial Conditions

Penetrating Trauma

Knives, bullets, needles, and intracardiac instrumentation are the most common causes of penetrating trauma to the pericardium and heart. Tamponade is more common in stab wounds than gunshot wounds. The right ventricle is most often involved in anterior chest wounds. Because tamponade provides hemostasis and prevents exsanguination, patients with tamponade have better survival than those with uncontrolled hemorrhage from a penetrating cardiac injury. Diagnosis is often made on clinical grounds supplemented by ultrasonography.51 Stable patients can be explored in the operating theater, but unstable patients should undergo thoracotomy in the emergency department.

Blunt Trauma

Blunt injuries to the heart and pericardium rarely occur in isolation. Trauma owing to compression (including cardiopulmonary resuscitation), blast, and deceleration can produce a spectrum of injuries ranging from cardiac contusion to cardiac rupture and pericardial laceration with herniation or luxation of the heart. Patients with pericardial rupture and cardiac herniation typically have suffered high-energy deceleration trauma and are invariably hypotensive from associated injuries. Hypovolemia may lead to rapid decompensation because cardiac filling becomes increasingly volume dependent in the setting of tamponade. Likewise, patients may initially respond to volume resuscitation. Chest imaging may demonstrate displacement of the heart or presence of free air or intra-abdominal organs within the pericardium. If the heart herniates into the pleura, positioning the patient with the contralateral side down may reduce the herniation. Thoracotomy is required for definitive treatment and repair of associated injuries.52

Acute Postinfarction Pericarditis and Dressler's Syndrome

Postinfarction pericarditis is thought to occur in almost half of patients suffering a transmural myocardial infarction (MI), although it is symptomatic in far fewer. The incidence is decreasing because of more aggressive revascularization in recent decades. Chest pain is almost universally present, and it is important to distinguish the pain of pericarditis from ischemic pain by its positional and pleuritic nature. The pain of early post-MI pericarditis occurs in the first 24 to 72 hours. Dressler's syndrome is a diffuse pleuropericardial inflammation thought to have an autoimmune etiology that occurs weeks to months after infarction. A pericardial rub and effusion may be present but tamponade is rare. In Dressler's syndrome, a pleural rub and effusion may also be present. The electrocardiographic signs of pericarditis may be obscured by those of infarction. Post-MI pericarditis is typically treated with aspirin and/or NSAIDs.53,54 Steroids or colchicine may be used for persistent or recurrent symptoms; however, glucocorticoid use is associated with recurrence of pericarditis.55

Cardiac Surgery and the Pericardium

Postinfarction Pericarditis

Postinfarction pericarditis, as described in the preceding, is an important entity for the surgeon to consider in the evaluation of patients with acute coronary syndromes. To the unwary it may masquerade as postinfarction angina and prompt an unnecessarily early operation after myocardial infarction. Extensive fibrinous adhesions and murky gelatinous fluid may be present in the pericardial space and obscure epicardial vessels. When the pericardium is opened late in such a patient, the surgeon should expect dense pericardial adhesions.

Postpericardiotomy Syndrome

Pericardial friction rubs are almost universal after cardiac surgery; some patients develop Dressler's syndrome with pleural and pericardial effusions, pleuritic pain, and generalized malaise. Such patients almost always respond to NSAIDs or a short course of corticosteroids when the symptoms remain refractory.56 Although this condition is benign, it is important (and sometimes difficult) to distinguish between postoperative pericarditis and myocardial ischemia. This distinction can often be made on clinical grounds based on symptoms, hemodynamics, and pattern of ECG changes.57 Echocardiography or angiography may be used in borderline cases to clarify the etiology.

Postoperative Tamponade

Early postoperative tamponade rarely goes undetected for long because of the high level of vigilance and close hemodynamic monitoring that attend the patient during this time. A vital feature of postoperative tamponade is that a circumferential fluid collection is not required for compromised cardiac function. Hemodynamic deterioration can occur in the setting of localized clot within the pericardium, particularly if it is impinging on the right heart.58 It is also important for surgeons to be aware of the potential for late cardiac tamponade that presents after hospital discharge and often to a clinician other than the cardiac surgeon. This entity is a potentially lethal complication and occurs in 0.5 to 6% of patients after heart surgery, almost exclusively in those on anticoagulation. Late cardiac tamponade (ie, tamponade occurring more than 7 days after cardiac surgery) is more common in younger patients who have undergone isolated valve (as opposed to coronary artery bypass graft) surgery. Patients present on average 3 weeks after surgery, frequently in the setting of an elevated prothrombin time. They are often severely symptomatic, with declining exercise tolerance, dyspnea, an inability to urinate, and sometimes hypotension. Any patient on anticoagulation whose recovery begins an otherwise unexplained decline in this interval should be suspected of having late tamponade and undergo echocardiographic examination. Nearly all patients with late tamponade respond favorably to pericardiocentesis, and are able to safely resume anticoagulation.59

Pericardial Closure

Redo sternotomy may be more hazardous when the heart is adherent to the inner table of the sternum. Closing the pericardium at the time of surgery interposes a protective layer of tissue between the sternum and the heart and may reduce the risks of redo sternotomy. The value of any added protection against cardiac injury on sternal reentry is limited by the relative infrequency of reoperation and the already low incidence of cardiac injury at repeat sternotomy when the pericardium is left open. On the negative side, closing the pericardium can cause kinking of bypass grafts after coronary bypass surgery and may result in hemodynamic compromise caused by cardiac compression.

Several small studies have attempted to answer the question of whether pericardial closure should be performed after cardiac procedures. Rao and associates demonstrated that pericardial closure at the time of cardiac surgery adversely affects postoperative hemodynamics.60 In this ingenious study, the pericardial edges were marked with radiopaque markers and the pericardium was closed with a running suture, the ends of which were exteriorized. After obtaining a postoperative chest film that demonstrated pericardial approximation, a set of baseline hemodynamics was measured. The suture was then removed, another x-ray taken to demonstrate distraction of the pericardial edges, and then the hemodynamic measurements were repeated. Pericardial closure reproducibly resulted in transient, moderate hemodynamic compromise in the first 8 hours after operation (Table 61-3). Although this and other studies have demonstrated adverse short-term hemodynamic consequences of pericardial closure, none have yet reported clinical evidence of worse outcomes.61 Therefore, the risks of pericardial closure must be weighed against its potential benefits and clinical practice should be individualized to the patient.

Mediastinal Reexploration

Postoperative hemorrhage complicates approximately 3 to 5% of cardiac operations, a risk that nearly doubles in the setting of reoperations or valve surgery.62 Common management for the postoperative cardiac surgical patient involves leaving the pericardium open and placing anterior and posterior mediastinal drains. Despite this, postoperative tamponade may still occur. The typical scenario involves declining chest tube output after a period of early postoperative bleeding, development of tachycardia, narrowing of the pulse pressure, increasing right-sided filling pressures, decreasing urine output, acidosis, escalating requirement for inotropes or vasopressors, and decreasing cardiac index. Echocardiography is not routinely helpful because the pericardial space and any associated thrombus may be difficult to visualize in the immediate postoperative period. Subtle echocardiographic findings that have been reported include an inspiratory increase in right ventricular end-diastolic diameter and a reciprocal decrease in left ventricular end-diastolic diameter,63 as well as an increase in early peak tricuspid flow velocity and reduction in flow across the mitral valve.64 Because postoperative hemorrhage and tamponade can precipitate rapid deterioration, expedient mediastinal drainage is imperative. The importance of simultaneous correction of coagulopathy, hypothermia, acidosis, and hypovolemia cannot be overstated.65 Extreme circumstances may dictate that a temporizing decompression be performed in the intensive care unit (ICU) followed by definitive management in the operating room. Reported outcomes among patients explored in the ICU include perioperative survival of 85% and sternal wound infection rate as low as 2%.66

During reexploration the first priority is to achieve prompt relief of tamponade by evacuating retained mediastinal blood and controlling sources of life-threatening hemorrhage. Dramatic hemodynamic improvement is frequently observed upon reopening the chest. Next, mediastinal reexploration is undertaken in a thorough and methodical manner with careful attention to all suture lines. Complete mediastinal evaluation should be performed even if the culprit source is thought to be identified. Inspection usually proceeds from top down while simultaneously obtaining hemostasis; this approach prevents "run-down" from obscuring small sources of bleeding. Copious warm saline irrigation and judicious use of gauze packing are helpful adjuncts.

Pericardiocentesis

Pericardiocentesis is usually performed in a procedure suite under fluoroscopic, sonographic, or computed tomographic guidance.67 Arterial and right heart catheterizations are often performed for hemodynamic monitoring. After administration of 1% lidocaine to the skin and the deeper tissues of the left xiphocostal area, a 25-mL syringe is affixed to a three-way stopcock and then to an 18-gauge spinal needle. This pericardial needle is connected to an electrocardiograph V lead. Under electrocardiographic and imaging guidance, the needle is advanced from the left of the subxiphoid area aiming toward the left shoulder. ST-segment elevation may be seen on the V lead tracing when the needle touches the epicardium. Under these circumstances, the needle is retracted slightly until ST-segment elevation disappears. Once the pericardial space is entered, a guidewire is introduced into the pericardial space through the needle. The needle is removed and a catheter is inserted into the pericardial sac over the guidewire. At our institution, a pigtail-shaped drainage catheter with an end hole and multiple side holes is used. Intrapericardial pressure is measured by attaching a pressure transducer system to the intrapericardial catheter. Pericardial fluid may then be removed. Symptom relief may be immediate and dramatic. In the presence of pericardial tamponade, aspiration of fluid is continued until there is clear clinical and hemodynamic improvement. If blood is withdrawn, 5 mL should be placed on a sponge to see if it clots. Clotting blood suggests that the needle has either inadvertently entered a cardiac chamber or caused epicardial injury. Defibrinated blood that has been present in the pericardial space for even a short time usually does not clot. The pericardial space is drained every 8 hours and the catheter is flushed with heparinized solution and in general is removed within the next 24 to 72 hours. Pneumothorax is a potential complication, and chest radiography is mandatory after the procedure.

Pericardial Window

The purpose of partial pericardial resection (window) is to drain fluid into the pleural or peritoneal compartment to prevent reaccumulation. The procedure can be performed via thoracoscopy, anterior thoracotomy, or subxiphoid incision; although each approach has its unique merits, reported outcomes among the three are relatively similar.68,69 General anesthesia may not be tolerated by some patients in tamponade, in which case the subxiphoid approach under local anesthesia in a semirecumbent position can be employed. When the pericardium is incised, fluid will invariably drain under pressure. The excised portion of pericardium should be as large as is feasible to prevent recurrence.70 The surgeon should remain mindful of the rare possibility of cardiac prolapse. With the transthoracic or thoracoscopic approaches, all accessible pericardium ventral to the phrenic nerve should be excised. Similarly, via the subxiphoid approach, as much diaphragmatic pericardium should be excised as possible.

Pericardiectomy

Chronic pericardial constriction is treated by pericardial excision (Fig. 61-15). Because dense adhesions and calcification can penetrate into the myocardium, pericardial resection can be technically challenging. At most centers, the procedure is done via median sternotomy with the capability to use cardiopulmonary bypass as needed.29 Practice is variable, as some use cardiopulmonary bypass routinely, whereas others prefer to avoid the additional burden of coagulopathy unless absolutely necessary. Also, some surgeons prefer the countertraction provided by the filled heart, which facilitates pericardial stripping. Some surgeons use a left anterior thoracotomy, the approach taken by Edward Churchill, who reported the first pericardiectomy for CP done in the United States.71 The objective of the procedure is to release the ventricles from the densely adherent pericardial shell. The lack of a surgical plane can make this a bloody operation, and attention must be paid to salvage and reinfusion of blood. Epicardial coronary vessels are at risk in this dissection, and particular care must be taken when dissecting in the regions of these vessels. The goal is to excise all anterior pericardium between the phrenic nerves as well as the posterior pericardium around its reflection on the venae cavae and pulmonary veins. Complete resection should restore pressure-volume loops to their normal position. Complete pericardial resection is not feasible in all cases, notably with radiation-induced disease, and leaving densely adherent scar, particularly over the venae cavae and atria, may be safer for the patient.

The results vary with the etiology and severity of the disease. Operative mortality has been reported as high as 10 to 20%,72 but is typically 5 to 6% in most contemporary series,73 and varies based on severity of heart failure, elevation of right atrial pressure, and comorbidities.74 Although surgery alleviates or improves symptoms in the vast majority of patients, long-term survival is diminished in patients who have had prior heart surgery, and particularly in patients with radiation-induced constrictive pericarditis (Fig. 61-16).75

• Tamponade occurs when intrapericardial pressure impedes cardiac filling, causing increased venous pressure, decreased cardiac output and progression to shock, and death if left untreated.
• Pericardial reserve volume is limited; therefore, acute fluid collections can rapidly produce tamponade.
• Constrictive pericarditis, the end result of several inflammatory conditions, is characterized by a prominent y descent, square-root sign, septal bounce, and exaggerated respiratory variation in right- and left-sided flows; it is best treated with pericardiectomy.
• Restrictive cardiomyopathy, a myocardial disorder causing diastolic heart failure, is differentiated from pericardial constriction by the presence of pulmonary hypertension, biatrial enlargement and ventricular thickening; it is not treated surgically.
• Patients with pericardial disease should undergo echocardiography supplemented as needed with catheter-based hemodynamic measurements or drainage for diagnosis.
• Acute pericarditis is often self-limited and responds to NSAIDs.
• The underlying disorder in secondary pericarditis can often be modified to improve the course of the associated pericardial disease.
• Intervention for postoperative hemorrhage and tamponade is required in less than 5% of cardiac surgical cases. It should be undertaken promptly (in the ICU if necessary) with concurrent correction of coagulopathy, hypovolemia, hypothermia, and acidosis.
• Pericardiectomy is associated with decreased short- and long-term survival because of the severity of associated illnesses.

The authors would like to thank Mark S. Adams for the preparation of the figures, echocardiographic images, and photographs for the chapter.