Figure 81.1. Twelve-Lead Electrocardiogram of stage I Pericarditis. Diffuse ST segment elevation is present.

    Individuals with the common EKG variant known as early repolarization display baseline ST elevations that can mimic stage 1 pericarditis. However, in distinction to those with early repolarization, the height of the ST segment in acute pericarditis tends to be >25% of the height of the T wave.

    Blood studies reveal systemic inflammation (leukocytosis, elevated erythrocyte sedimentation rate, and C-reactive protein) and often minor elevation of cardiac-specific troponins. The latter is a reflection of inflammation extending to the neighboring myocardium but does not predict an adverse outcome.

    Most patients with acute pericarditis have no or only a small pericardial effusion, and chest radiography is frequently normal. However, if a large effusion (>250 mL) has accumulated, the cardiac silhouette becomes symmetrically enlarged. Echocardiography is a much more sensitive technique for the detection of pericardial effusion, as it can identify a collection of as little as 15 mL (see Figure 81.2). A small effusion is identified as an echo-free space posterior to the left ventricle (LV). Larger effusions wrap around laterally and, if more than approximately 250 mL have accumulated, anterior to the heart as well.

    Additional testing may be useful when specific etiologies of pericarditis are suspected, such as purified protein derivative (PPD) skin testing for TB, serologic testing (e.g., antinuclear antibodies) for collagen vascular diseases, mammography or chest CT for screening of breast and lung cancers, respectively. Even when a pericardial effusion is present, pericardiocentesis is not recommended in uncomplicated cases as the diagnostic yield is low and rarely affects management. It should be reserved for patients with large effusions or those with evidence of cardiac chamber compression (see below).

MANAGEMENT

There is a scarcity of randomized clinical trials in the management of pericardial diseases, and therefore therapy is generally empirical. Idiopathic or postviral pericarditis is a self-limited condition that tends to improve spontaneously within 1–3 weeks. The immediate goals of therapy are to reduce pericardial inflammation and relieve symptoms. Nonsteroidal antiinflammatory drugs (NSAIDs) are first-line therapy (e.g., ibuprofen 600–800 mg three times daily or aspirin 650 mg/day).

    Useful adjuncts include colchicine (1 mg by mouth twice daily on the first day, then 0.5 mg twice daily), a brief course of narcotic analgesics for severe pain, or as last resort for refractory symptoms, a limited regimen of corticosteroids. Although symptoms do respond promptly to steroids, patients who receive them are more prone to relapses. A recent trial showed that a relatively low dose of prednisone (0.25–0.5 mg/kg/day for 2 weeks followed by a slow taper) is effective and associated with fewer relapses than higher dosages. Hospitalization is appropriate for patients with high fever, large pericardial effusions, or in whom an etiology other than idiopathic/postviral is suspected.

    Aspirin is the preferred antiinflammatory agent for patients with pericarditis early after myocardial infarction, as other NSAIDs may impair healing of infarcted tissue. Patients with delayed post-MI pericarditis (Dressler syndrome) or postpericardiotomy pericarditis characteristically respond promptly to standard NSAID regimens, which can be used with less reservation at that later phase. Tuberculous pericarditis requires prolonged, multidrug, antituberculous therapy. Purulent pericarditis mandates aggressive antibiotic therapy and often catheter drainage of the pericardium. Pericarditis due to uremia is treated with initiation or intensification of dialysis. Forms of pericarditis associated with collagen vascular diseases respond to therapy directed against the underlying disorder, often including NSAID or glucocorticoid therapy. Drug-associated pericarditis responds to cessation of the offending agent. Neoplastic pericarditis is indicative of advanced-stage cancer, and therapy is usually palliative; if tamponade is present, drainage of pericardial fluid can be temporarily lifesaving (see below).

    Recurrent pericarditis develops in up to 30% of patients after an initial episode. Recurrences are less frequent in patients who receive colchicine as part of the original treatment program. Recurrent pericarditis often responds to a renewed course of NSAID and colchicine therapy; refractory cases may require glucocorticoids, usually with a very slow taper (>1 month) to prevent additional occurrences. In addition, reports of small number of patients have suggested benefit of immunosuppressive agents (e.g., azathioprine or methotrexate), intravenous immunoglobulin, and the interleukin-1β receptor antagonist anakinra in suppressing refractory symptoms of pericarditis.

    Two serious complications may follow acute pericarditis: cardiac tamponade and chronic constrictive pericarditis.

CARDIAC TAMPONADE

Cardiac tamponade is characterized by the accumulation of pericardial fluid under sufficient pressure to compress and impair filling of the cardiac chambers. As a result, cardiac output declines substantially, which can lead to hypotensive shock and death.

ETIOLOGY

Any cause of acute pericarditis can lead to tamponade physiology, but the most common etiologies are neoplastic, idiopathic, and uremic pericarditis. Tamponade can also result from acute hemorrhage into the pericardial sac, for example, following chest trauma, as a complication of a proximal aortic dissection, bleeding after cardiac surgery, or myocardial perforation during percutaneous cardiac procedures.

PATHOPHYSIOLOGY

Because the pericardium is a relatively stiff structure, the sudden introduction of even a small volume of fluid into the pericardial space (as with acute hemorrhage) can lead to life-threatening cardiac chamber compression. However, when effusions accumulate more gradually, the parietal pericardium may physically stretch over time and accommodate larger volumes (>1 L) before hemodynamic compromise occurs.

    In tamponade, the surrounding tense effusion limits ventricular filling and causes the diastolic pressure of each cardiac chamber to become elevated and equal to the high pericardial pressure. The right side of the heart is more susceptible to external compression than the left side because of its normally lower pressures. Thus, impaired right-sided chamber filling is one of the earliest signs of tamponade. Because the compressed chambers cannot accommodate normal venous return, systemic venous pressures rise. Limitation of early diastolic ventricular filling across the tricuspid valve is responsible for blunting of the normal y descent in the right atrial and systemic venous pressure tracings. Concurrently, the reduced diastolic ventricular filling decreases stroke volume and forward cardiac output.

    The high pericardial pressure in tamponade exaggerates the relationship of normal ventricular interdependence: the volume of one ventricle can expand only when the size of the other decreases by the same amount. This principle applies to respiratory variations in ventricular filling. In normal individuals inspiration expands the right ventricle, shifts the interventricular septum toward the left, and thus slightly reduces LV filling and output over the next several beats. This results in a normal small inspiratory decline in systolic blood pressure. In cardiac tamponade the situation is amplified because the ventricles share a common, reduced space. Therefore, there is greater inspiratory reduction of LV output and blood pressure, and this is thought to be responsible for pulsus paradoxus (an inspiratory decrease in systolic BP >10 mm Hg) in this condition.

CLINICAL FEATURES

Cardiac tamponade should be suspected when a patient with pericarditis or chest trauma develops signs and symptoms of systemic vascular congestion and decreased cardiac output. The patient may describe shortness of breath and chest discomfort; tachypnea and tachycardia are common. Other key physical findings are (1) hypotension with pulsus paradoxus, (2) jugular venous distension (with absence of the y descent), and (3) muffled heart sounds and inability to palpate the point of maximum cardiac impulse due to the surrounding effusion. Of note, pulsus paradoxus may not appear when coexisting conditions impede respiratory alterations in LV filling, including LV dysfunction, aortic regurgitation, and atrial septal defects. Conversely, pulsus paradoxus may appear in situations other than tamponade that cause large alterations in intrathoracic pressure, including acute and chronic pulmonary disease, and in some patients with constrictive pericarditis (see below).

    The EKG typically demonstrates sinus tachycardia as well as low limb-lead voltage if a large effusion has accumulated. Electrical alternans (alternating height of the QRS complex in sequential beats—see Figure 81.3) is uncommon but highly suggestive of a large effusion, as it results from shifting of the mean electrical axis as the heart swings from side to side within the large pericardial volume.

    Echocardiography is the most useful noninvasive technique to evaluate for tamponade physiology. It can identify the presence, volume, and location of pericardial effusion and assess its hemodynamic significance. Sensitive and specific signs of tamponade include early diastolic collapse of the right ventricle (more specific) and cyclical compression of the right atrium (more sensitive). It is less common to observe cyclical indentation of the left atrium or LV, except in patients with loculated effusions that compress those chambers, as may occur after cardiac surgery. Other echocardiographic findings reflect the abnormal pathophysiology: distension of the inferior vena cava and exaggerated reciprocal respiratory variations in mitral and tricuspid diastolic Doppler velocities. Although these echocardiographic abnormalities are suggestive, it is the clinical characteristics of the patient that determine whether tamponade is present and dictate the aggressiveness of therapeutic interventions.

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