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Acute Pericardial Disease
Pericardial disease is encountered less frequently than myocardial disease in the cardiac intensive care unit (CICU). However, its ability to mimic ischemic heart disease and congestive heart failure can make the diagnosis of pericardial disease challenging at times. While many patients with pericardial disease have a subacute or chronic presentation, the astute clinician must always consider pericardial disease in patients who present with hemodynamic embarrassment and shock in the CICU, for the failure to recognize cardiac tamponade can have dire consequences. This chapter will provide clinicians with the tools to recognize, diagnose, and manage patients with pericardial disease in the CICU setting.
Anatomy and Physiology of the Normal Pericardium
The normal pericardium consists of a double-layered membranous sac that envelops the heart and proximal portions of the great vessels. The outer layer, or parietal (fibrous) pericardium, serves to anchor the heart within the thorax, and becomes contiguous with the adventitia of the great vessels. The inner layer, or visceral pericardium, is a serosal monolayer that adheres firmly to the myocardium as the epicardium, reflects over the origin of the great vessels creating the oblique and transverse sinuses and pericardial recesses (major contributors to the pericardial reserve volume), and fuses with the tough, fibrous parietal layer. Under normal physiologic conditions, there is typically less than 50 mL of pericardial fluid (largely an ultrafiltrate of plasma) between the layers of the pericardium.
While not essential for survival, the pericardium and fluid within serves many important yet subtle functions. Briefly, the pericardium limits distention of the cardiac chambers, facilitates ventricular interaction and coupling of the atria and ventricles, equalizes physical forces across the entire myocardial surface, minimizes friction with surrounding structures, and provides an anatomic barrier from the spread of infection.
Clinical Presentation of Pericardial Disease
Although there are relatively few disease processes that primarily affect the pericardium, the pericardium can be affected by many disease states (e.g., trauma, rheumatologic, infectious, metabolic, neoplastic, and congenital disease). As such, the clinical presentation of pericardial disease varies from acute to chronic, and from benign to life threatening, depending on the underlying etiology. This propensity for varying clinical presentation and an ability to mimic life-threatening disease processes (e.g., chest pain and ST segment elevation seen with acute pericarditis mimicking acute myocardial infarction [MI]) make the diagnosis of acute pericardial disease challenging, particularly when time is of the essence. Therefore, the astute intensivist must understand which patients require evaluation for pericardial disease, be able to rapidly and accurately diagnose pericardial disease, and facilitate timely management. The major ways in which pericardial disease may simulate ischemic syndromes are listed in Box 29.1 .
Box 29.1
Major Ways in Which Pericardial Disease May Simulate Ischemic Syndromes
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Pericardial pain simulating ischemic pain
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ST segment deviation suggesting myocardial ischemia
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Dressler syndrome mistaken for reinfarction
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Cardiac tamponade misinterpreted as heart failure
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Severe tamponade mistaken for cardiogenic shock
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Friction rub mistaken for murmur of acute mitral regurgitation
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Friction rub mistaken for murmur of rupture of the ventricular septum
Clinically, diseases of the pericardium present in several ways. Acutely, pericarditis, pericardial effusion (without hemodynamic compromise), and cardiac tamponade remain the primary concern in the CICU setting. Chronic and subacute presentations—including chronic pericardial effusion, constrictive pericarditis, and effusive-constrictive pericarditis—are less commonly observed in the CICU and will not be discussed in any detail.
Acute Pericarditis
Acute pericarditis is the most common disorder involving the pericardium, occurring in up to 0.2% of hospitalized patients and in 5% of patients admitted to the emergency department for nonischemic chest pain. While idiopathic/viral pericarditis remains the most common etiology in the immunocompetent host in developed countries (80% to 90% of cases), radiation therapy, cardiac surgery (postpericardiectomy syndrome), and invasive procedures have become important causes. In contrast, Mycobacterium tuberculosis pericarditis is more common in underdeveloped countries and immunocompromised hosts.
In the CICU setting, pericarditis is most often related to MI and less commonly to cardiac or coronary interventions. Early post-MI pericarditis occurs during the first few days after MI and is caused by transmural necrosis with inflammation affecting the adjacent pericardium. Pericardial involvement is related to infarct transmurality and size and is associated with a poor prognosis. It is often asymptomatic and is identified only by the presence of a friction rub on physical examination. When patients are symptomatic, it is essential to distinguish between recurrent ischemic pain and pericardial pain. Late post-MI pericarditis (Dressler syndrome) is one of the postcardiac injury (autoimmune) syndromes, occurring from a week to a few months after MI; it is less commonly seen in the modern era of early revascularization. Patients may present with pleuritic chest pain, friction rub, fever, leukocytosis, and sometimes pleural effusion or pulmonary infiltrates. The diagnosis is clinical, although objective findings—such as elevated inflammatory markers, electrocardiographic changes, and pericardial effusion on echocardiogram (ECG)—can be helpful.
Clinical Diagnosis
The diagnosis of acute pericarditis can be made in the presence of at least two of the following criteria: (1) typical chest pain, (2) a pericardial friction rub on auscultation, (3) changes on the ECG, and (4) new or worsening pericardial effusion. Elevation of inflammatory markers or evidence of pericardial inflammation on other imaging modalities can help support the diagnosis in atypical cases but are not part of the diagnostic criteria. Modest elevations of troponin reflect concurrent myocardial inflammation. All patients suspected of having acute pericarditis should have the following studies: an ECG, chest radiograph, complete blood count, troponin level, serum C-reactive protein level, renal function panel, blood cultures (if fever >38°C or signs of sepsis), and a transthoracic echocardiogram.
Chest pain is the most common presenting symptom and typically has a sudden onset, variable severity and intensity, and may radiate to the trapezius ridge. The pain is generally pleuritic, becoming worse with inspiration, and is alleviated by sitting up and leaning forward. The pericardial friction rub, auscultated best at the left sternal border with the patient seated and leaning forward, is considered pathognomonic for pericarditis. While highly specific, its absence does not exclude pericarditis, as it may be evanescent, and is heard in only one-third of patients with acute pericarditis. Notably, the pericardial friction rub can be monophasic, biphasic, or triphasic in nature and does not vary with the respiratory cycle, which helps differentiate pericardial from pleural friction rubs. While the friction rub remains an accurate means of diagnosis, all patients presenting to the CICU with chest pain deserve a thorough clinical examination, including assessment of vital signs, jugular venous pressure (JVP) and pulsation, blood pressure determination in each upper extremity, auscultation for cardiac murmurs, and the evaluation for pulsus paradoxus in order to alert the clinician to complications of pericarditis (e.g., tamponade), or suggest alternate pathology (e.g., MI or aortic dissection).
ECG changes are common in pericarditis and typically progress through four stages: stage I, diffuse ST segment elevation and PR segment depression; stage II, normalization of the ST and PR segments; stage III, T-wave inversion that occurs after normalization of the ST segment; and stage IV (which is variably present), normalization of the T waves. These “classic” ECG changes of diffuse ST segment elevation and PR segment depression are seen in the first hours to days of the disease process and have been shown to be present in only approximately 60% of cases of pericarditis ( Fig. 29.1 ). Distinguishing the ECG changes of acute pericarditis from those of acute myocardial ischemia can be challenging. In differentiating the two conditions, it should be remembered that the ST segment elevation seen in pericarditis starts at the J-point, is concave upwards and distributed throughout nearly all leads on the ECG (i.e., in multiple vascular territories), and is associated with PR depression and an absence of Q-waves. In contrast, the ST segment change seen in ST elevation MI (STEMI) originates at the J-point, is convex (dome-shaped), generally occurs in a single coronary vascular territory, does not have associated PR segment changes, and may have reciprocal ST segment changes in other vascular territories of the myocardium. Sustained dysrhythmia is also more common with myocardial ischemia as compared to acute pericarditis (provided that the pericarditis is not the result of a transmural infarction), although atrial arrhythmias complicate 5% to 10% of cases of acute pericarditis. When pericarditis is associated with an acute MI, the degree of ST elevation may be exaggerated, the reciprocal ST segment changes of infarction masked, and atypical T wave evolution or early normalization of inverted T waves may be seen.
While transthoracic echocardiography has little utility in evaluating the pericardium itself, it is invaluable for diagnosing acute pericarditis and its complications (pericardial effusion and tamponade) and for recognizing alternative diagnoses. Because of its noninvasive nature and widespread availability, both the European Society of Cardiology (ESC) and the American Society of Echocardiography recommend that a transthoracic ECG be performed in all patients with suspected acute pericarditis.
Leukocytosis and elevations in the erythrocyte sedimentation rate and C-reactive protein are nonspecific indicators of inflammation and therefore are not useful for the diagnosis of pericarditis; however, they do have prognostic value. For example, in an Italian study of 156 consecutive patients with idiopathic or viral pericarditis, hs-CRP elevation at 1 week was a significant independent risk factor for recurrence of disease (hazard ratio [HR], 2.36). Cardiac troponin has also been evaluated in acute idiopathic or viral pericarditis as a marker for myocardial involvement. In one study, 38 of 118 consecutive patients with pericarditis were found to have troponin elevations. However, after a mean follow-up of 24 months, a similar rate of recurrent pericarditis and constrictive pericarditis was noted among those with positive and negative troponin values and no cases of tamponade were detected in the cohort with positive troponin values.
An exhaustive diagnostic evaluation is not recommended in the immunocompetent patient owing to the diminished value of testing compared to the cost incurred and the low probability of any result having a significant impact on management. However, following a basic evaluation, patients with fever greater than 38°C, subacute onset of symptoms, immunosuppression, trauma, oral anticoagulation therapy, evidence of myopericarditis, moderate or large pericardial effusion, or cardiac tamponade are considered high risk and should be admitted to the hospital (and, if appropriate, to the CICU) for further evaluation of a specific etiology of the pericarditis.
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