Pericardial Disease

   = cavitary pressure – adjacent intrapericardial pressure

Because the intrapericardial pressure is normally negative, this usually adds to the normal transmural pressure gradient (1).

The relationship between intrapericardial and pleural pressures causes a simultaneous fall of pressures in both spaces during inspiration and leads to an increased venous return into the right chambers (increased preload), with a subsequent increase in cardiac output. Inspiration influences filling and cardiac output of the left heart only indirectly and very little. The parietal pericardium is very resistant to acute stretching but adapts and expands to great dimension when subjected to a chronic stretching process. The pericardial pressure–volume curve is generally flat as pericardial volume increases, and when further distention is impossible, a sharp rise in the intrapericardial pressure occurs. This exponential curve accounts for the rapid clinical response when even small amounts of fluid are removed in cardiac tamponade (2).

This chapter deals with the most common clinical pericardial problems encountered in critical care medicine. They include acute pericarditis, pericardial effusion, cardiac tamponade, and pericardial constriction.



Inflammation of the pericardial sac results in acute pericarditis and is either an isolated problem or part of a systemic process. Exudation of inflammatory fluid into the pericardial space can result in pericardial effusion. Depending on the frequency and time course, pericarditis can be acute, recurrent, or chronic. Common causes of acute pericarditis are shown in Table 99.1. Most often, clinically recognizable pericarditis in the adult is idiopathic. In these cases, various viruses are often the suspected causes; an etiologic agent is infrequently demonstrated. The most commonly demonstrated virus is the Coxsackie B group, which causes myopericarditis in children and pleuropericarditis in adults—also called Bornholm disease (3). ECHO, influenza, Epstein–Barr, varicella, hepatitis, mumps, and human immunodeficiency viruses can also cause pericarditis.

Up to one-third of patients with end-stage renal disease will develop uremic pericarditis. Most of them have not started dialysis when they present with pericarditis, and the symptoms usually disappear after beginning or increasing the frequency of dialysis (4). There is no direct association with serum blood urea nitrogen level or serum creatinine and the acute illness. However, it is suspected that increased toxin levels from declining renal function cause the inflammatory process. It is important to remember that the uremic patient is susceptible to infections and that the pericarditis may be infectious. Last but not least, the underlying disease process leading to the renal insufficiency (i.e., lupus erythematosus) may also be the cause for the pericardial inflammation.

Acute pericarditis after myocardial injury is thought to be due to direct irritation of the visceral mesothelium. In the past, pericarditis occurred in up to 20% of patients after transmural myocardial infarction; recently, the frequency has decreased due to the increased use of reperfusion therapy—that is, thrombolytic therapy or angioplasty (5). Typically, symptoms occur 1 to 3 days after the myocardial damage and can mimic recurrent angina pectoris. If the patient is receiving anticoagulants, the inflammation can lead to hemorrhagic intrapericardial effusion and possibly cardiac tamponade. Acute pericardial inflammation is also found after open-heart surgery, implantation of cardiac pacemakers, percutaneous coronary interventions, or external cardiac trauma, and the presentation is similar to that after transmural infarction.

The postpericardiotomy syndrome was originally described as postmyocardial infarction pericarditis. Later, Engle and Ito (6) noted the same clinical syndrome in children and adults who experienced an opening of the pericardium. The syndrome occurs in 10% to 30% of patients who have undergone pericardiotomy and is thought to be an immune complex reaction to the patient’s own pericardium (7). In contrast to pericarditis caused by myocardial injury, these patients usually have symptoms of chest pain and fever beginning several weeks to months after cardiac surgery or other myocardial injury.

Neoplastic pericarditis is most often caused by cancer of the lung, breast, or esophagus as well as lymphoma and melanoma (8). The tumor directly invades the pericardial space or metastasizes through lymphatics or blood vessels; primary pericardial tumors like mesothelioma are rare. The likelihood of finding previously undiagnosed cancer in a patient presenting with pericarditis is about 6% to 7% (9). In patients with known malignancy pericarditis is caused by cancer in only 50% to 60%; idiopathic pericarditis and radiation-induced pericarditis are the most common benign causes (10,11). The prognosis of neoplastic pericarditis and effusion is poor.

TABLE 99.1 Common Causes of Pericarditis

Pericarditis is also seen in patients with systemic lupus erythematosus, rheumatoid arthritis, and scleroderma. Inflammation of the pericardium is often the first manifestation of lupus in female patients; this diagnosis should be ruled out during the workup for a first episode of idiopathic pericarditis. Radiation pericarditis often follows a mediastinal dose of 4,000 rad or more and can lead to pericardial effusion and acute cardiac tamponade. The long-term effects of radiation also can lead to constrictive pericarditis.

Pericarditis caused by infectious organisms other than viruses is less frequent now than it was in the preantibiotic era. Pneumonia is still the most common cause; others include sepsis from peritonitis and urinary tract infection, or direct spread of the infectious process from mediastinitis or necrotizing fasciitis of the head or neck. Immunocompromised and elderly patients are more prone to infectious pericarditis than the general population. In adults, Staphylococcus aureus is still the most common organism, and there is an apparent decline in infections with Streptococcus spp, Pneumococcus spp, and Haemophilus influenzae.

Tuberculous pericarditis was once a common cause of acute and constrictive pericarditis, but with the overall decline of tuberculosis, it has become a rare entity in the United States (12). More recently, states with a high percentage of immigrants have again reported rising numbers of tuberculous pericarditis (13). One to two percent of patients with pulmonary tuberculosis will develop tuberculous pericarditis (14). Mycobacterial infection must be ruled out in any case of suspected purulent pericarditis.

The most common fungal organism to cause pericarditis is Histoplasma capsulatum. Histoplasmosis in the United States is most common in the Mississippi and Ohio River Valleys (15). Diagnosis is usually delayed and made by positive fungal culture of the pericardial fluid and/or a significant rise of serologic antibody titers (>1:32) against H. capsulatum.


The typical patient presenting with pericarditis is young and was previously healthy. Symptoms of acute pericarditis include sharp and, usually, persistent chest pain that is generally increased with respiration and motion. It is worse in the supine position and usually improves sitting up and/or with shallow breathing. The pain can radiate to the neck, and dyspnea may also be present. Other common findings preceding or accompanying pericarditis are fever, myalgia, malaise, and tachycardia. The characteristic and pathognomonic three-component friction rub is best described as coarse, leathery, and superficial—like “pulling Velcro.” The rub is only intermittently heard during the episode of pericarditis, and therefore, it is important to auscultate frequently. The patient is ideally examined in a quiet setting in an upright position leaning forward; the rub is best heard at the left sternal border or the cardiac apex.

An electrocardiogram (ECG) should be obtained in every patient presenting with chest pain. Four ECG stages, evolving over hours to days and weeks, have been described:

  • Stage I includes classic and diffuse ST elevations with a concave ST segment and significant PR-segment depression (Fig. 99.1)
  • Stage II is normalization of the ECG
  • Stage III is the development of diffuse T-wave inversion that may persist or normalize
  • Stage IV is final normalization of the ECG (16)

The ECG may show all, several, or none of the stages during an episode of acute pericarditis. Atrial arrhythmias are rare but do occur in acute pericarditis (17) and can be the first manifestation of acute pericarditis. However, sustained atrial or ventricular arrhythmias are suggestive of concomitant myocarditis.

The key to an ECG diagnosis of pericarditis is the diffuse nature of the ECG changes, the absence of localization to a particular ECG anatomic area, PR-segment depression, and the absence of ST depression except in lead aVR.

Every patient suspected to have pericarditis should have a chest radiograph taken. It will be normal in most cases of pericarditis; a new finding of an enlarged cardiac silhouette is, however, suggestive of a pericardial effusion (>200 mL) and should be further evaluated.

The laboratory may report positive acute-phase reactants (especially the erythrocyte sedimentation rate [ESR]) and an elevated white blood cell count; however, these are nonspecific findings. Cardiac troponin T or I and CK-MB isoenzymes are cardiac—but not pericardium—specific and are often found minimally elevated in acute pericarditis. Viral studies may confirm a viral cause of the pericarditis; however, their yield is low, and the result does not change management. In cases of suspected infectious etiology, cultures from blood and pericardial fluid, if available, should be examined for bacterial and mycobacterial pathogens.

FIGURE 99.1 Electrocardiogram of a patient with acute pericarditis. Note the PR-segment depressions (arrows) and convex ST-segment elevations in the inferolateral leads and PR-segment elevation (arrowhead) and ST-segment depression in lead aVR consistent with stage I of electrocardiogram findings in acute pericarditis.

Echocardiography should be performed in every patient with the suspected diagnosis of pericarditis to evaluate for and follow pericardial effusion (Fig. 99.2) and to help diagnose cardiac tamponade.

FIGURE 99.2 Subcostal echocardiogram showing a giant pericardial effusion (asterisk) in a patient with neoplastic pericarditis.

The triad of typical chest pain, pericardial friction rub, and the aforementioned ECG changes confirms the diagnosis of acute pericarditis. However, this diagnosis should be made only after life-threatening conditions with similar presentation (acute coronary syndrome, pulmonary embolism, aortic dissection, and cardiac tamponade) have been ruled out. Electrocardiographic differential diagnosis also includes variant angina, hypertrophic cardiomyopathy, and the benign finding of early repolarization—all of which can mimic the ECG changes described earlier (Table 99.2).

Aside from history and physical examination, ECG, chest radiographs, blood work, and echocardiogram, it may be necessary to evaluate the patient with computed tomography (CT) of the chest to rule out pulmonary embolism or aortic dissection (Fig. 99.3).


Patients with acute pericarditis have a high likelihood of uncomplicated recovery and can be treated outside the hospital. However, several factors are described as being associated with a complicated course (Table 99.3) and patients with any of these factors should be hospitalized for their initial treatment (18).

TABLE 99.2 Differential Diagnosis of Pericardial Effusion

FIGURE 99.3 Computed tomography (CT) of the chest with large pericardial effusion (asterisk) and small right-sided pleural effusion (plus sign). The dark rim between the pericardial effusion and the right heart represents epicardial fat.

Acute idiopathic or viral pericarditis usually responds to nonsteroidal anti-inflammatory drugs (NSAIDs). The drug regimen consists of high-dose aspirin (325–975 mg three to four times daily for 4 weeks); with the addition of a proton pump inhibitor to lessen gastrointestinal effects. Alternatively, indomethacin (25–50 mg four times daily) or ibuprofen (400–600 mg four times daily) can be given. Recently, Imazio et al. (19) found that routine use of colchicine (0.5 mg twice daily for 3 months) in addition to aspirin or ibuprofen—compared to aspirin or ibuprofen alone—in patients with a first episode of acute pericarditis significantly reduced incessant or recurrent pericarditis. Colchicine added to NSAID treatment (0.5 mg twice daily for 6 months) has also been shown to be effective for patients who have had multiple recurrences of their acute pericarditis (20). Diarrhea is a known side effect of colchicine and may cause discontinuation of drug therapy in about 10% of patients.

Symptoms of acute pericarditis respond rapidly to systemic steroids, but there seems to be an increase in relapse after tapering (21). Therefore, corticosteroid therapy should be reserved only for patients with recurrent pericarditis not responding to NSAIDs and colchicine. The recommended daily regimen is 0.2 to 0.5 mg/kg of prednisone for at least 1 month before slowly tapering the dose by 2.5 to 5 mg/wk until the drug is withdrawn (22). The possible side effects of corticosteroid treatment include peptic ulcer disease, sodium retention, hypokalemia, hyperglycemia, osteoporosis, Cushing syndrome, and suppression of the adrenal axis. Treatment with corticosteroids also requires the exclusion of infection or an appropriate antibiotic regimen before initiation of therapy.

TABLE 99.3 Presenting Factors Predicting Complicated Course

The treatment of choice for uremic pericarditis consists of intensive, initially daily dialysis therapy. Heparin should be used sparingly during dialysis to reduce the risk of intrapericardial hemorrhage and possible tamponade. The presence of acute pericarditis in acute myocardial infarction also requires caution with the use of intravenous anticoagulants. These drugs are not, however, absolutely contraindicated. Thrombolytic agents have been reported to lead to cardiac tamponade and should be used with caution in the patient with acute myocardial infarction and acute pericarditis.

The postpericardiotomy syndrome is usually self-limited if left untreated; however, the disease may increase the risk of early coronary artery bypass graft closure. Therefore, aggressive treatment has been recommended; NSAIDs often decrease symptoms and speed up recovery (23). Colchicine compared to placebo given perioperatively (0.5 mg twice daily 72 hours before and for 1 month after cardiac surgery) significantly reduced the incidence of postpericardiotomy syndrome and showed nonsignificant reduction of postoperative atrial fibrillation (24). Refractory cases may occur but usually respond rapidly to systemic corticosteroids as outlined above. Advocates of corticosteroid therapy claim that this treatment reduces the incidence of late constrictive pericarditis.

Nonviral infectious etiology of pericarditis requires prompt evacuation of purulence from the pericardium, usually by operative intervention, because of the need to establish a definitive diagnosis, eradicate the infection, and prevent constrictive pericarditis.

Recurrence of acute pericarditis is quite common and often requires long-term drug therapy as noted above. In a few selected cases refractory to medical therapy, radical pericardiectomy may need to be considered (21).

In general, acute pericarditis symptoms subside within several days to weeks. The major immediate complication is cardiac tamponade, which occurs in less than 5% of patients. For diagnostic and treatment approach in patients with suspected acute uncomplicated or complicated pericarditis, see Figure 99.4.



Pericardial effusion often develops with acute pericarditis. It is caused by an inflammatory exudation and an occlusion of the normal drainage through epicardial venous and lymphatic systems by the inflammatory process. The most common causes of tamponade include idiopathic pericarditis, cancer of the lung and breast, lymphoma, renal failure, and tuberculosis (25). Pericardial effusion may also occur in the absence of pericardial inflammation—for example, as a hemorrhagic effusion from internal sources such as a pacemaker, angioplasty, coronary artery bypass grafting (CABG) surgery, aortic dissection, ventricular rupture—or external cardiac trauma. Regardless of their size, pericardial effusions can either be clinically silent or cause hemodynamic compromise. The latter situation is called cardiac tamponade. The most important factor contributing to the development of cardiac tamponade is not the total amount of pericardial fluid but the rate at which it accumulates. The pericardium resists sudden stretching but can gradually expand in response to a chronic distending force. A small but rapidly developing effusion—less than 200 mL—in a trauma patient can cause tamponade, because the fibrous pericardial membrane does not have enough time to stretch and accommodate the increased volume. Conversely, a patient with a very large pericardial effusion—1,000 mL—developing over weeks or months may be completely asymptomatic, given that the parietal pericardium has had time to adjust to the increased volume.

FIGURE 99.4 Diagnostic and treatment algorithm for patients presenting with signs and symptoms of acute pericarditis.

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Feb 26, 2020 | Posted by in CRITICAL CARE | Comments Off on Pericardial Disease

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