Pericardial Disease: Clinical Features and Treatment

42 Pericardial Disease


Clinical Features and Treatment



The pericardium is a two-layered sac that encircles the heart (Fig. 42-1). The visceral pericardium is a mesothelial monolayer that adheres to the epicardium. It is reflected back on itself at the level of the great vessels, where it joins the parietal pericardium, the tough fibrous outer layer. Under normal conditions, a small amount of fluid (approximately 5–50 mL) separates the two layers and decreases friction between them.



The normal pericardium serves three primary functions: fixing the heart within the mediastinum, limiting cardiac distension during sudden increases in intracardiac volume, and limiting the spread of infection from the adjacent lungs. However, the importance of these functions has been questioned because of the benign prognosis associated with congenital absence of the pericardium.


This chapter discusses the clinical features and treatment of four pathologic conditions involving the pericardium: acute pericarditis, chronic pericarditis, constrictive pericarditis, and pericardial effusions. The hemodynamic effects of pericardial pathology are discussed in Chapter 43.



Acute Pericarditis



Etiology and Pathogenesis


The most common presentation of a pericardial abnormality is acute pericarditis, inflammation of the pericardium (Fig. 42-2). In general, this is a self-limited disease that is responsive to oral anti-inflammatory medication. Acute pericarditis infrequently necessitates hospital admission. It is more common in men than in women and more common in adults than in children. The two most common causes of acute pericarditis in the United States are viral and idiopathic. Other causes include uremia, pericardiectomy associated with cardiac surgery, pulmonary embolism, collagen-vascular diseases, Dressler’s syndrome, malignancy, tuberculosis, fungus (e.g., histoplasmosis), parasites (e.g., ameba), myxedema, radiation, acute rheumatic fever, and trauma (Fig. 42-3).






Differential Diagnosis


The differential diagnosis of acute pericarditis includes other pathologies involving the chest and heart, with two of the most common being myocardial ischemia and pulmonary embolus. Features that distinguish the discomfort of myocardial ischemia from acute pericarditis include previous exertional symptoms, lack of variation with respiration or position, associated symptoms of nausea or diaphoresis, and/or dyspnea. In addition, the discomfort of pericarditis is often described as “sharp” or “stabbing,” whereas the pain of myocardial infarction is pressure-like. ECG changes of ST elevation can be seen in both pericarditis and myocardial ischemia (infarction); however, the ST elevation present with myocardial ischemia or infarction is generally localized to a vascular bed and is accompanied by reciprocal ST depression in myocardial infarction. PR depression is common in acute pericarditis and exceedingly rare in myocardial infarction (it would imply atrial infarction in this setting). Cardiac biomarkers can be elevated in both conditions.


The pain associated with pulmonary embolus can mimic acute pericarditis in that it is pleuritic in nature, but associated symptoms and diagnostic evaluation including arterial blood gas and ECG can help differentiate these conditions. Other conditions that can mimic acute pericarditis include disease states that involve inflammation of structures in close proximity to the pericardium including cholecystitis, pancreatitis, and pneumonia.



Diagnostic Approach


The diagnosis of acute pericarditis is based on clinical criteria, but the ECG can make an important contribution. The lack of ECG changes cannot exclude the diagnosis of pericarditis. That said, most patients progress through one or more of the four stages of ECG changes commonly associated with the evolution of acute pericarditis (see Fig. 42-2 (ECG); Fig. 42-4). Stage I changes accompany the onset of chest pain and include the classic ECG changes associated with acute pericarditis: diffuse concave ST elevation with PR depression (see Chapter 4). Stage II occurs several days later and is represented by the return of ST segments to baseline and T-wave flattening. In stage III, T-wave inversion is seen in most leads. The ECG in stage IV shows the return of T waves to an upright position. The approximate time frame for passage through all four stages of ECG changes in most cases of acute pericarditis is 2 weeks.



Electrocardiographic abnormalities are present in approximately 90% of patients with acute pericarditis, but only about 50% of patients show all four stages. Other ECG presentations include isolated PR depression, absence of one or more stages, and persistence of T-wave inversion. Atrial arrhythmias are seen in 5% to 10% of cases.


Laboratory studies are nondiagnostic in acute pericarditis. Nonspecific markers of inflammation may be present, including an elevated white blood cell count. If concurrent myocarditis is present, serum levels of cardiac biomarkers (creatine kinase and troponin) may be elevated. An echocardiogram may or may not show a pericardial effusion.



Management and Therapy






Constrictive Pericarditis



Etiology and Pathogenesis


Constrictive pericarditis is characterized by a dense, fibrous thickening of the pericardium that adheres to and encases the myocardium, resulting in impaired diastolic ventricular filling (Fig. 42-5). The general paradigm is that constrictive pericarditis occurs over a period of years as a result of an acute injury (e.g., a viral infection) that elicits a chronic fibrosing reaction or as a result of a chronic injury that stimulates a persistent reaction (e.g., renal failure). Clinically, constrictive pericarditis generally is a chronic disease with symptom progression over a period of years. The presentation is that of right-sided heart failure and may resemble restrictive cardiomyopathy, cirrhosis, cor pulmonale, or other conditions. Because pericardial constriction is uncommon, patients occasionally are treated for an incorrect diagnosis (left- or right-sided heart failure, hepatic failure, or others) for years. Patients with pericardial constriction often have even been admitted to a hospital for symptoms attributed to other causes before a definitive diagnosis of constriction is made. Newer diagnostic technologies and a change in the predominant etiologies of constriction have increased the recognition of subacute presentations occurring over a period of months.



The most common causes of constriction in industrialized countries are cardiac surgery, mediastinal radiation, pericarditis, and idiopathic etiologies (Table 42-1). Other causes include infection (e.g., fungal or tuberculosis), malignancies such as breast cancer or lymphoma, connective tissue disease (e.g., systemic lupus erythematosus or rheumatoid arthritis), trauma, and drugs.



Jun 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Pericardial Disease: Clinical Features and Treatment

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