The pericardium consists of a serous or loose fibrous membrane (visceral pericardium) overlying the epicardium and a dense collagenous sac (parietal pericardium) surrounding the heart. The space between the visceral and parietal pericardium may normally contain up to 50 mL of fluid.28 Because its layers are serosal surfaces and because of its proximity and attachments to other structures, the pericardium may be involved in a number of disease processes (Table 55-6). In this section, the clinical manifestations and evaluation of acute and constrictive pericarditis and nontraumatic cardiac tamponade are discussed.
TABLE 55-6Common Causes of Acute Pericarditis ||Download (.pdf) TABLE 55-6 Common Causes of Acute Pericarditis
Viral (coxsackie virus, echovirus, human immunodeficiency virus)
Bacterial (especially Staphylococcus, Streptococcus pneumoniae, β-hemolytic streptococci [acute rheumatic fever], Mycobacterium tuberculosis)
Fungal (especially Histoplasma capsulatum)
Malignancy (leukemia, lymphoma, metastatic breast and lung carcinoma, melanoma)
Drug induced (procainamide, hydralazine)
Systemic rheumatic diseases (systemic lupus erythematosus, rheumatoid arthritis, scleroderma, polyarteritis nodosa, dermatomyositis)
Postmyocardial infarction (Dressler's syndrome)
The most common symptom of acute pericarditis is sharp or stabbing precordial or retrosternal chest pain. Pain may be of sudden or gradual onset and radiates to the back, neck, left shoulder, or arm, and may be aggravated by inspiration or movement. Referral of pain to the left trapezial ridge (due to inflammation of the joining diaphragmatic pleura) is a particular distinguishing feature. Chest pain due to acute pericarditis may be aggravated by inspiration or movement. Typically, chest pain is most severe when the patient is supine and is relieved when the patient sits up and leans forward.29,30 Associated symptoms include fever, dyspnea due to accentuated pain with inspiration, and dysphagia from irritation of the esophagus by the posterior pericardium.
A pericardial friction rub is the most common and important physical finding in pericarditis but may be difficult to appreciate in a noisy ED. It is best heard with the diaphragm of the stethoscope at the lower left sternal border or apex when the patient is sitting and leaning forward. It may be audible only during a certain phase of respiration and characteristically is intermittent. A pericardial friction rub is most often triphasic, with a systolic component due to ventricular contraction, an early diastolic component during the early phase of ventricular filling, and a presystolic component synchronous with atrial systole. It is less commonly biphasic, with a systolic component with either an early diastolic or presystolic component. A monophasic rub is less common but is most often systolic.
Electrocardiogram Serial electrocardiogram changes during acute pericarditis and its convalescence are characterized by four stages (Table 55-7 and Figure 55-2).
TABLE 55-7Serial Electrocardiogram Changes of Acute Pericarditis ||Download (.pdf) TABLE 55-7 Serial Electrocardiogram Changes of Acute Pericarditis
|Stage ||PR Segment ||ST Segment ||T Wave |
|1 (acute) ||Depression, especially in II, aVF, and V4–V6 ||Elevation, especially in I, V5, and V6; ST amplitude: T-wave amplitude >0.25 ||— |
|2 ||Isoelectric or depressed ||Returns to isoelectric line ||Amplitude decreases, inversion rare |
|3 ||Isoelectric or depressed ||Isoelectric ||T-wave inversion, especially in I, V5, and V6 |
|4 ||Isoelectric ||Isoelectric ||Normal |
This series of three electrocardiograms (ECGs) shows the typical progression of changes associated with acute pericarditis. A. In stage I pericarditis, the ECG shows diffuse ST-segment elevation and PR depression in leads I, II, III, and avF. The ST-segment to T-wave amplitude ratio measured in V6 is 2 mm/4 mm, or 0.50, thus meeting criteria for pericarditis rather than early repolarization (see the text under Diagnosis, Electrocardiogram). B. In stage II pericarditis, ST segments are returning toward the isoelectric point in most leads in which they had been elevated. C. In stage III pericarditis, we see resolution of ST changes and the appearance of diffuse T-wave inversion. These evolutionary changes are typical of and diagnostic for pericarditis and usually occur over several weeks.
If a large pericardial effusion develops during the course of acute pericarditis, low-voltage QRS complexes and electrical alternans may be evident. Pericardial fluid attenuates myocardial electrical signals, and the pendular motion of the heart within the fluid-filled pericardial space results in electrical alternans (see Figure 55-5 in the Nontraumatic Cardiac Tamponade section of this chapter).
Although serial ECG tracings are of diagnostic value in acute pericarditis, sequential ECG assessment is not a diagnostic luxury afforded the emergency physician. Differentiating pericarditis from the normal variant with "early repolarization" is a common problem and can be difficult when only a single 12-lead electrocardiogram is available. The ST-T–wave changes present in the early repolarization or normal variant electrocardiogram mimic those of pericarditis and have been reported in 2% of healthy young adults. However, the ST-segment/T-wave amplitude ratio in leads V5, V6, or I can differentiate pericarditis from early repolarization.31,32 Using the end of the PR segment as a baseline, or 0 mV, the amplitude or height of the ST segment at its onset is measured in V5, V6, or lead I and recorded in millivolts. The height of the T wave in the same lead is measured from the baseline to the T-wave peak. If the ratio of ST amplitude (in millivolts) to T-wave amplitude (in millivolts) is >0.25, acute pericarditis is likely, and if the ratio is <0.25, acute pericarditis is unlikely (Figure 55-2). Sensitivity at an ST/T ratio >0.25 for acute pericarditis is >0.85, and the specificity is >0.8 (positive likelihood ratio of about 4 and negative likelihood ratio of about 0.2). Pericarditis alone does not cause significant cardiac rhythm disturbances.
Radiographic Assessment Chest radiographs are of limited value. The cardiac silhouette may be of normal size and contour in acute pericarditis and, in some instances, the setting of cardiac tamponade. If previous chest radiographs are available for comparison, a recent increase in the size of the cardiac silhouette or an increase in the cardiothoracic ratio without radiographic evidence of pulmonary venous hypertension can distinguish an expanding pericardial effusion from left heart failure. The "epicardial fat-pad sign" is rarely seen on the lateral chest radiograph and has been reported in only 15% of cases of acute pericarditis during fluoroscopy with image intensification. If acute pericarditis is suspected on the basis of history, physical examination, or ECG, a chest radiograph may help establish an underlying cause, such as neoplasm or infection.
Echocardiographic Studies Echocardiography is the procedure of choice for the detection, confirmation, and serial follow-up of patients with acute pericarditis and a pericardial effusion.33 (See http://www.cardiosource.org/Science-And-Quality/Practice-Guidelines-and-Quality-Standards.aspx for more information.)
Normally, the pericardial sac is only a "potential" space, and the myocardium is echocardiographically in direct contact with surrounding thoracic structures. The anterior RV wall is in contact with the chest wall, and the posterior LV wall is in contact with the posterior pericardium and adjacent pleura. When a pericardial effusion is present, the pericardial space fills with echo-free fluid (Figure 55-3).
A. Pericardial effusion on parasternal long-axis view. Ant Eff = anterior effusion; AV = aortic valve; LA = left atrium; LV = left ventricle; Post Eff = posterior effusion; RV = right ventricle. B. Pericardial effusion on (arrows) parasternal short-axis view. [Reprinted with permission from Reardon RF, Joing SA: Cardiac, in Ma OJ, Mateer JR, Blaivas M (eds): Emergency Ultrasound, 2nd ed. Copyright © 2008, The McGraw-Hill Companies, Inc., all rights reserved, Figure 6-24.]
Echocardiographically, a separation is seen between the right ventricle and the chest wall and between the left ventricle and the posterior pericardium. Quantitation of the size of the effusion is arbitrary and is determined by where the echo-free space is seen (anterior or posterior) and when in the cardiac cycle it occurs. For example, when an echo-free space is seen only posteriorly and only during systole, a small effusion is said to be present. The sensitivity of CT for detecting pericardial effusion is similar to that of echocardiography (Figure 55-4).
This CT scan of the chest shows a large pericardial effusion (pe) predominantly posteriorly located in a patient with scleroderma and pericarditis. No pericardial thickening or calcification was detected. Esophageal (e) dilatation is noted. Cardiac function cannot be evaluated. H = heart; L = liver. [Reprinted with permission from Roldan CA: Connective tissue diseases & the heart, in Crawford MH (ed): Current Diagnosis & Treatment in Cardiology, 3rd ed. Copyright © 2009, The McGraw-Hill Companies, Inc., all rights reserved, Figure 33-5.]
Ancillary Laboratory Evaluation Suggested laboratory studies are listed in Table 55-8. Serum creatine kinase–MB fraction and troponins may be elevated in acute pericarditis due to associated myocarditis.11
TABLE 55-8Ancillary Diagnostic Studies in Acute Pericarditis ||Download (.pdf) TABLE 55-8 Ancillary Diagnostic Studies in Acute Pericarditis
|Diagnostic Study ||Considerations |
|Cardiac markers ||Indicate myocardial involvement |
|CBC and differential WBC count ||May suggest infection or leukemia |
|BUN/creatinine ||May suggest a diagnosis of uremic pericarditis |
|Streptococcal serologic testing (antistreptolysin O, anti-DNAse, antihyaluronidase) ||Particularly in patients with a history of rheumatic heart disease or pharyngitis |
|Blood cultures ||If bacterial infection suspected |
|Serologic studies ||Antinuclear antibodies, anti-DNA titers, or rheumatoid factor in patients with systemic symptoms |
|Erythrocyte sedimentation rate ||Will not determine specific diagnosis, but can confirm clinical suspicion of pericarditis and can be followed serially to assess response to therapy |
|Acute and convalescent viral antibody titers ||Measuring viral titers would not be expected to change the course of treatment |
|Thyroid function studies ||Thyrotoxicosis is a rare cause of pericarditis; thyrotoxicosis can cause pericardial effusion without the typical electrocardiogram changes and symptoms of pericarditis |
Treatment and Disposition
Treatment of pericarditis depends on the cause.34 Most patients with idiopathic or presumed viral pericarditis have a benign course lasting 1 to 2 weeks. Symptoms respond well to nonsteroidal anti-inflammatory agents administered for 7 days to 3 weeks. Ibuprofen, 300 to 800 milligrams orally every 6 to 8 hours, may be preferred because of fewer side effects, limited impact on coronary artery blood flow, and large dose range. Colchicine, 0.5 milligram orally twice a day, may be a beneficial adjuvant and may prevent recurrent episodes.35,36 Hospitalization is not necessary in most cases, unless there is associated myocarditis, and follow-up or repeat echocardiography is not needed unless symptoms fail to resolve or reappear or new symptoms are noted.37 Indicators of a poor prognosis include temperature >38°C (100.4°F), subacute onset over weeks, immunosuppression, history of oral anticoagulant use, associated myocarditis (elevated cardiac biomarkers, symptoms of CHF), and a large pericardial effusion (an echo-free space >20 mm).38 In general, patients with these risk factors or with an enlarged cardiac silhouette on chest radiograph should be admitted for echocardiography to assess the extent of the effusion and degree of hemodynamic compromise and cardiac dysfunction.
NONTRAUMATIC CARDIAC TAMPONADE
An increase in the amount of fluid within the pericardial sac results in an increase in intrapericardial pressure. The normal fibrocollagenous parietal pericardium has elastic properties and stretches to accommodate increases in intrapericardial fluid. The initial portion of the pericardial volume-pressure curve is flat: Relatively large increases in volume result in comparatively small changes in intrapericardial pressure. The curve becomes steeper as the parietal pericardium reaches the limits of its distensibility.39 If fluid continues to accumulate, intrapericardial pressure rises to a level greater than that of the normal filling pressures of the right heart chambers. When this occurs, ventricular filling is restricted and results in cardiac tamponade. The point at which this occurs is determined by the rate of fluid accumulation, pericardial compliance (a thickened parietal pericardium is less distensible), and intravascular volume (hypovolemia lowers ventricular filling pressure). Common causes of cardiac tamponade in nontrauma patients are listed in Table 55-9.
TABLE 55-9Common Causes of Cardiac Tamponade in Medical (Nontrauma) Patients ||Download (.pdf) TABLE 55-9 Common Causes of Cardiac Tamponade in Medical (Nontrauma) Patients
|Cause ||Approximate Frequency (%) |
|Metastatic malignancy ||40 |
|Acute idiopathic pericarditis ||15 |
|Uremia ||10 |
|Bacterial or tubercular pericarditis ||10 |
|Chronic idiopathic pericarditis ||10 |
|Hemorrhage (anticoagulant) ||5 |
|Other (systemic lupus erythematosus, postradiation, myxedema, etc.) ||10 |
Symptoms are nonspecific, and patients most commonly complain of dyspnea at rest and with exertion. Additional symptoms may be due to the underlying disease (e.g., uremia or tuberculous pericarditis).
Physical examination may reveal tachycardia and low systolic arterial blood pressure with a narrow pulse pressure. Pulsus paradoxus may also be present. A paradoxical arterial pulse is said to be present when the cardiac rhythm is regular and there are apparent dropped beats in the peripheral pulse during inspiration. There is usually a <10 mm Hg decrease in systolic blood pressure during inspiration in the supine position. A value >10 mm Hg usually separates true tamponade from lesser degrees of restricted cardiac filling.28,40 Pulsus paradoxus is not diagnostic of cardiac tamponade and may be noted in other cardiopulmonary processes. In cardiac tamponade, the neck veins may be distended with an absent "y" descent. The apical impulse is indistinct or tapping in quality. Cardiac auscultation may reveal "distant" or soft heart sounds. Pulmonary rales are usually absent, and there may be right upper quadrant tenderness from hepatic venous congestion.
The chest radiograph may or may not reveal an enlarged cardiac silhouette because this finding depends on the amount of intrapericardial fluid accumulation. The pulmonary vasculature typically appears normal. An epicardial fat-pad sign may occasionally be seen within the cardiac silhouette.
The ECG usually shows low-voltage QRS complexes (<0.7 mV) and ST-segment elevation (due to the inflammation of the epicardium) with PR-segment depression, as in pericarditis. Electrical alternans (beat-to-beat variation in the amplitude of the P and R waves unrelated to the respiratory cycles; Figure 55-5) is a classic but uncommon finding.
This rhythm strip (lead II, top tracing) and plethysmograph (bottom tracing) were recorded in a patient who presented with dyspnea, hypotension, and clinical and echocardiographic evidence of cardiac tamponade. A paradoxical pulse was noted on palpation of the radial artery. The amplitude of the R waves varies from beat to beat (electrical alternans).
The diagnosis should be suspected based on the clinical examination and chest radiograph findings. Echocardiography is the diagnostic test of choice. In addition to a large pericardial fluid volume, typical echocardiographic findings described in cardiac tamponade are right atrial compression, RV diastolic collapse, abnormal respiratory variation in tricuspid and mitral flow velocities, and dilated inferior vena cava with lack of inspiratory collapse.
Treatment and Disposition
Volume expansion with a bolus of normal saline solution (500 to 1000 mL) will increase intravascular volume, facilitate right heart filling, and increase cardiac output and arterial pressure. However, it is a temporary measure. Pericardiocentesis is necessary for definitive therapy and for specific diagnosis.
If there is hemodynamic instability, emergency pericardiocentesis is indicated in the ED. The technique is described in Section 4, Resuscitative Procedures, chapter 34, Pericardiocentesis. However, pericardiocentesis is optimally performed in the cardiac catheterization laboratory using echocardiographic guidance to avoid cardiac perforation and coronary artery laceration. In addition, a pigtail catheter can be inserted to allow continuous fluid drainage and prevention of reaccumulation.
Constrictive pericarditis results from pericardial injury and inflammation, resulting in fibrous thickening of the layers of the pericardium, which prevents passive diastolic filling of the cardiac chambers.16 Some causes include postcardiac trauma with intrapericardial hemorrhage, after pericardiotomy (open-heart surgery, including coronary revascularization), in fungal or tuberculous pericarditis, and in chronic renal failure (uremic pericarditis), but in most cases, a specific cause is not determined.
The symptoms of constrictive pericarditis usually develop gradually and may mimic those of CHF and restrictive cardiomyopathy. However, clinical signs may occur early if fluid also accumulates within the thickened, noncompliant pericardial sac (effusive constrictive pericarditis).
Common signs and symptoms include exertional dyspnea, pedal edema, hepatomegaly, and ascites. Examination of the neck veins with the patient at a 45-degree angle from horizontal will reveal jugular venous distention and a rapid "y" descent of the cervical venous pulse. Elevated venous pressure is also seen in CHF, but a rapid "y" descent is infrequently encountered. The Kussmaul sign (inspiratory neck vein distention) is frequent in constrictive pericarditis but rare in CHF. A paradoxical pulse is uncommon, and its absence does not exclude constrictive pericarditis. On cardiac auscultation, an early diastolic sound, a pericardial "knock," may be heard at the apex 60 to 120 milliseconds after the second heart sound. The pericardial knock sounds like a ventricular gallop but occurs earlier than the S3 of CHF, which it may mimic. The knock is due to accelerated RV inflow in early diastole and early myocardial distention, followed by an abrupt slowing of further ventricular expansion.
Low-voltage QRS complexes and inverted T waves are common, but there are no specific diagnostic electrocardiogram signs.
Chest radiographs most commonly demonstrate a normal or slightly enlarged cardiac silhouette, clear lung fields, and little or no evidence of pulmonary venous congestion. Pericardial calcification may be seen. Thoracic CT and MRI may also demonstrate a thickened pericardium.
On occasion, two-dimensional echocardiography may demonstrate pericardial thickening and abnormal ventricular septal motion in a patient with suspected constrictive pericarditis. However, its diagnostic utility is much less than that in a patient with acute pericarditis. Doppler echocardiography, cardiac CT, and MRI are preferred.
In many instances cardiac catheterization with measurement of intraventricular pressures will be required to confirm the diagnosis. A characteristic dip and plateau (the "square root sign") of the right ventricular pressure trace is characteristic of the disease.41
Treatment and Disposition
In cases of significant constriction and impaired ventricular filling, admission for pericardiectomy is the treatment of choice.