cardiovascular disorders
Pericarditis
Diagnosis of Pericarditis
Electrocardiography (ECG) and chest x-ray Echocardiography Tests to identify cause (eg, pericardial fluid aspiration, pericardial biopsy) Electrocardiography and chest x-ray are done. The diagnosis is based on the presence of the following clinical findings and ECG abnormalities, which are not always present in all cases. Characteristic chest pain Pericardial rub ECG abnormalities Pericardial effusion Serial ECGs may be needed to show abnormalities. The ECG in acute pericarditis may show abnormalities confined to ST and PR segments and T waves, usually in most leads. (ECG changes in lead aVR are generally in the opposite direction of other leads.) Unlike MI, acute pericarditis does not cause reciprocal depression in ST segments (except in leads aVR and V1), and there are no pathologic Q waves. ECG changes in pericarditis can occur in 4 stages although not all stages are present in all cases. Stage 1: ST segments show upward concave elevation; the PR segments may be depressed (see figure Acute pericarditis: Stage 1 ECG ). Stage 2: ST segments return to baseline; T waves flatten. Stage 3: T waves are inverted throughout the ECG; T wave–inversion occurs after the ST segment has returned to baseline and thus differs from the pattern of acute ischemia or MI. Stage 4: T wave changes resolve. Echocardiography in acute pericarditis typically shows an effusion, which helps confirm the diagnosis, except in patients with purely fibrinous acute pericarditis in whom echocardiography is often normal. Findings indicating myocardial involvement include new focal or diffuse left ventricular dysfunction. MRI can detect the presence, severity, and acuity of pericardial inflammation but is generally not required to diagnose acute pericarditis. J points, except aVR and V1, are elevated. T waves are essentially normal. ST segments show upward concave elevation. PR segments, except aVR and V1, are depressed. PR deviations are commonly absent in one limb lead (here, aVL). Because the pain of pericarditis may resemble that of acute MI or pulmonary infarction, additional tests (eg, serum cardiac marker measurement, lung scan) may be required if the history and ECG findings are atypical for pericarditis. Troponin is often elevated in acute pericarditis due to epicardial inflammation, so it cannot discriminate between pericarditis, acute infarction, and pulmonary embolism. Very high levels of troponin may indicate myopericarditis. The CK-MB (creatine kinase muscle band isoenzyme) level, which is less sensitive than the troponin level, is usually normal in acute pericarditis unless myocarditis is also present. Postpericardiotomy and post-MI syndromes may be difficult to identify and must be distinguished from recent MI, pulmonary embolism, and pericardial infection after surgery. Pain, friction rub, and fever appearing 2 weeks to several months after surgery and a rapid response toaspirin, nonsteroidal anti-inflammatory drugs (NSAIDs),colchicine, or corticosteroids aids diagnosis. Diagnosis is suggested by clinical findings but often is suspected only after finding an enlarged cardiac silhouette on chest x-ray. On ECG, QRS voltage is often decreased, and sinus rhythm remains in about 90% of patients. With large, chronic effusions, the ECG may show electrical alternans (ie, P, QRS, or T wave amplitude increases and decreases on alternate beats). Electrical alternans is associated with variation in cardiac position (swinging heart). Echocardiography estimates the volume of pericardial fluid; identifies cardiac tamponade, sometimes acute myocarditis, and/or heart failure; and may suggest the cause of pericarditis. Although CT can detect a pericardial effusion (often incidentally on a scan done for other conditions), it may overestimate its size and is not a first-line test to evaluate possible pericardial effusion. Patients with a normal ECG, small (<50 mL) effusion, and no suspicious findings from the history and examination may be observed with serial examination and echocardiography. Other patients must be evaluated further to determine etiology. Diagnosis may be suspected based on clinical, ECG, chest x-ray, and Doppler echocardiography findings, but cardiac catheterization and CT (or MRI) are usually required. Rarely, right heart biopsy is needed to exclude Restrictive Cardiomyopathy . changes are nonspecific. QRS voltage is usually low. T waves are usually nonspecifically abnormal. Atrial Fibrillation occurs in about one third of patients; Lateral chest x-rayoften shows pericardial calcification best, but the finding is nonspecific. also is nonspecific. When the right and left ventricular filling pressures are equally elevated, Doppler echocardiography helps distinguish constrictive pericarditis from Restrictive Cardiomyopathy . During inspiration, mitral diastolic flow velocity usually falls > 25% in constrictive pericarditis but < 15% in restrictive cardiomyopathy. In constrictive pericarditis, inspiratory tricuspid flow velocity increases more than it normally does, but it does not do so in restrictive cardiomyopathy. Determining tissue velocities at the mitral annulus may be helpful when excessively high left atrial pressure blunts respiratory variation in transvalvular velocities. Mitral annular velocities (especially at the septal location) increase in constrictive pericarditis; they decrease in restrictive cardiomyopathy. Presence of a septal bounce (shift of the interventricular septum towards the left ventricle during inspiration and away from the left ventricle during expiration) and hepatic vein expiratory diastolic flow reversal (which occurs due to reduced filling of the right ventricle) can also be visible in constrictive pericarditis. Respiration-related ventricular septal shift, preserved or increased medial annular velocity, and hepatic vein expiratory diastolic flow reversal collectively are referred to as the Mayo criteria, but each factor is independently associated with constrictive pericarditis ( Diagnosis reference ). Cardiac Catheterization , Mean pulmonary artery occlusion pressure (pulmonary capillary wedge pressure), pulmonary artery diastolic pressure, right ventricular end-diastolic pressure, and mean right atrial pressure are roughly equal, all at about 10 to 30 mm Hg. The pulmonary artery and right ventricular systolic pressures are normal or modestly elevated, so that pulse pressures are small. In the atrial pressure curve,xandydescents are typically accentuated. In the ventricular pressure curve, a diastolic dip occurs at the time of rapid ventricular filling. During peak inspiration, right ventricular pressure increases when left ventricular pressure is lowest (sometimes called mirror-image discordance, suggesting increased ventricular interdependence). Because ventricular filling is restricted, ventricular pressure tracings show a sudden dip followed by a plateau (resembling a square root sign) in early diastole. Measuring these changes requires simultaneous right and left heart cardiac catheterization, using separate transducers. These hemodynamic changes almost always occur with significant constrictive pericarditis but may be masked during hypovolemia. Right ventricular systolic pressure of>50 mm Hg often occurs in restrictive cardiomyopathy but less often in constrictive pericarditis. When the pulmonary artery occlusion pressure equals the right atrial mean pressure and an early diastolic dip in the ventricular pressure curve occurs with largexandywaves in the right atrial curve, either disorder may be present. CT or MRIcan identify pericardial thickening > 5 mm. Pericardial thickening > 5-mm, with typical hemodynamic changes (assessed by echocardiography and catheterization), can confirm constrictive pericarditis. When no pericardial thickening or fluid is seen, the diagnosis of restrictive cardiomyopathy is favored but not proved. A normal pericardial thickness does not exclude constrictive pericarditis. Increased T2-weighted short TI inversion recovery (STIR) signal and late gadolinium enhancement on cardiac MRI can document active inflammation and resolution of constriction in response to anti-inflammatory therapy, whereas their absence suggests chronic constrictive pericarditis that is unlikely to be responsive to medical therapy. The degree of late gadolinium enhancement of the pericardium may be especially helpful in identifying patients in whom constriction will reverse or resolve. Low voltage and electrical alternans on the ECG suggest cardiac tamponade, but these findings lack sensitivity and specificity. When tamponade is suspected, echocardiography is done unless even a brief delay might be life threatening. Then pericardiocentesis is done immediately for diagnosis and treatment. Echocardiographic findings that support tamponade include the following: Respiratory variation of transvalvular and venous flows Compression or collapse of right cardiac chambers in the presence of a pericardial effusion Inferior vena caval plethora (decrease in the proximal venal caval diameter by<50% during deep inspiration) However, cardiac tamponade is primarily a clinical diagnosis. Significant cardiac tamponade is a clinical diagnosis; echocardiographic findings alone are not an indication for pericardiocentesis. If tamponade is suspected but not yet confirmed (eg, by clinical findings and echocardiography), right heart (Swan-Ganz) catheterization may be done. In cardiac tamponade: There is no early diastolic dip in the ventricular pressure record. Diastolic pressures are elevated (about 10 to 30 mm Hg) and equal in all cardiac chambers and in the pulmonary artery. In the atrial pressure curve,xdescent is preserved andydescent is lost. In contrast, in severe congestive states due to dilated cardiomyopathy, pulmonary artery occlusion or left ventricular diastolic pressure usually exceeds right atrial mean pressure and right ventricular diastolic pressure by ≥ 4 mm Hg. Right heart catheterization should be considered particularly when draining an effusion, not only to confirm tamponade, but also to uncover possible constrictive pericarditis with effusion. After pericarditis is diagnosed, tests to determine etiology and the effect on cardiac function are done. In a young, previously healthy adult who presents with a viral infection and acute pericarditis, an extensive evaluation is usually unnecessary. Differentiating viral from idiopathic pericarditis is difficult, expensive, and generally of little practical importance. In other cases, a biopsy of pericardial tissue or aspiration of pericardial fluid may be needed to establish a diagnosis. Acid-fast stains and cultures of pericardial fluid are essential if tuberculosis (TB) is considered possible (TB pericarditis can be aggressive and can worsen rapidly with corticosteroid therapy). Samples are examined for malignant cells. However, complete drainage of a newly identified pericardial effusion is usually unnecessary for diagnosis. Persistent (usually>3 months) or progressive effusion, particularly when the etiology is uncertain, also warrants pericardiocentesis. The choice between needle pericardiocentesis and surgical drainage depends on institutional resources and physician experience, the etiology of the effusion, the need for diagnostic tissue samples, and the prognosis of the patient. Needle pericardiocentesis is often best when the etiology is known or the presence of tamponade is in question. Surgical drainage is best when the presence of tamponade is certain but (because pericardial biopsy can be done surgically) the etiology is unclear. Laboratory tests of pericardial fluid other than culture and cytology are usually nonspecific. But specific diagnoses are sometimes possible using newer visual, cytologic, and immunologic analysis of fluid obtained via pericardioscopic-guided biopsy. Cardiac catheterization may be useful for evaluating pericarditis and identifying the cause of reduced cardiac function. CT or MRI can help identify metastases, although echocardiography is usually sufficient. Other tests include complete blood count, acute-phase reactants, routine chemistry tests, cultures, autoimmune tests, and, when appropriate, tests for HIV, histoplasmosis complement fixation (in endemic areas), and antibody tests for coxsackievirus, influenza virus, echovirus, and streptococcus. Anti-DNA and anti-RNA antibody tests may be useful. A tuberculin skin test (usually PPD) or Interferon gamma Release Assay is done, but they can give false negative results; TB pericarditis can be ruled out only by culture of pericardial fluid for acid-fast bacilli. 1.Welch TD, Ling LH, Espinosa RE, et al: Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria.Circ Cardiovasc Imaging7:526, 2014. 