eMedicine Specialties > Emergency Medicine > Cardiovascular

Pericarditis and Cardiac Tamponade

Verena T Valley, MD, Associate Professor, Director of Ultrasound, Department of Emergency Medicine, University of Mississippi School of Medicine; Consulting Staff, Department of Emergency Medicine, Singing River Hospital System, Singing River Hospital, and Ocean Springs Hospital
Christopher A Fly, MD, Assistant Professor, Department of Emergency Medicine, Medical College of Georgia

Updated: May 12, 2008

Introduction

Background

Pericarditis and cardiac tamponade are clinical problems that involve the potential space surrounding the heart or pericardium. Pericarditis is one cause of fluid accumulation in this potential space; cardiac tamponade is the hemodynamic result of fluid accumulation.

The use of limited echocardiography by emergency physicians has enhanced the diagnosis of cardiac tamponade from various causes, including trauma and infectious and noninfectious etiologies.

Pathophysiology

The pericardium (pericardial complex) consists of an outer fibrous layer and an inner serous layer. The fibrous pericardium is a flask-shaped, tough outer sac with attachments to the diaphragm, sternum, and costal cartilage. The serous layer is thin and is adjacent to the surface of the heart. The pericardium serves as a protective barrier from the spread of infection or inflammation from adjacent structures.

The potential space produced by these layers contains approximately 20 mL of fluid with electrolyte and protein profiles similar to plasma. Approximately 120 mL of additional fluid can accumulate in the pericardium without an increase in pressure. Further fluid accumulation can result in marked increases in pericardial pressure, eliciting decreased cardiac output and hypotension (cardiac tamponade). The rapidity of fluid accumulation influences the hemodynamic effect.

Frequency

United States

Malignant disease is the most common cause of pericardial effusion with tamponade. The reported incidence of acute pericardial tamponade is approximately 2% of penetrating trauma. The condition is rarely seen in blunt chest trauma.

International

Although malignancy is the most common etiology of pericardial effusions in developed countries, tuberculosis should be considered in endemic areas.

Mortality/Morbidity

The early diagnosis of significant pericardial and cardiac injuries can prevent morbidity and enhance survival.

• Penetrating cardiac injury: Immediate identification of penetrating cardiac injuries via emergency department (ED) echocardiography can improve survival rate and neurologic outcome.
• Nontraumatic pericardial effusion: Prompt identification using ED bedside echocardiography streamlines appropriate therapy and disposition.

Sex

Pericarditis is more common in males than in females.

Age

Pericarditis is more common in adolescents and young adults. In one study, Merce et al found no difference in etiology, clinical course, and prognosis between elderly and younger patients with moderate and large pericardial effusions.¹

Clinical

History

• Pericarditis
  • The most common symptom of acute pericarditis is precordial or retrosternal chest pain, usually described as sharp or stabbing.
  • Pain may be of sudden or gradual onset and may radiate to the back (left trapezial ridge), neck, left shoulder, or arm.
  • Movement or inspiration may aggravate the pain.
  • Pain may be most severe when the patient is supine and can be relieved when the patient leans forward while sitting.
  • Common associated signs and symptoms include low-grade intermittent fever, dyspnea, cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss were commonly noted (80%).
  • Patients can present with acute abdominal pain.
• Cardiac tamponade
  • Patients may present subacutely with symptoms of anxiety, dyspnea, fatigue, or altered mental status.
  • Patients may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal disease (ESRD).
  • Traumatic tamponade may present with acute dyspnea or altered mental status.
  • A waxing and waning clinical picture may be present in intermittently decompressing tamponade.

Physical

• Pericarditis
  • Pericardial friction rub: The most common and important physical finding is a pericardial friction rub, which is best heard at the lower left sternal border or apex when the patient is positioned sitting forward or on hands and knees. Friction rub may be transient from one hour to the next and is present in approximately 50% of cases. A friction rub may be distinguished from a cardiac murmur by its changing character from heartbeat to heartbeat and patient position changes. A friction rub is closer to the ear on auscultation than a murmur.
  • Fever: Fevers are usually low grade but occasionally reach 104°F.
  • Cardiac arrhythmias: Premature atrial and ventricular contractions are occasionally present.
  • Tachypnea and dyspnea: Dyspnea is a frequent complaint and may be severe with myocarditis, pericarditis, and tamponade.
  • Ewart sign (dullness and bronchial breathing between the tip of the left scapula and the vertebral column)
  • Hepatomegaly, ascites
  • Pericardial fluid: As the volume of pericardial fluid increases, the capacity of the atria and ventricles to fill is mechanically compromised, leading to reduced stroke volume and tamponade physiology.
• Cardiac tamponade (influenced by volume and rate of accumulation)
  • Beck triad (jugular venous distention, hypotension, and muffled heart sounds)
  • Hypotension and tachycardia without elevated jugular venous distension, if associated hemorrhage is outside pericardial sac
  • Pulsus paradoxus: Pulsus paradoxus is measured by careful auscultation with a blood pressure cuff. The first sphygmomanometer reading is recorded at the point when beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle. A difference of more than 10 mm Hg defines pulsus paradoxus.
  • Cyanosis
  • Varying degrees of consciousness

Causes

• Acute pericarditis
  • Serous pericarditis: This condition is usually caused by noninfectious inflammation such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The fluid demonstrates few polymorphonuclear neutrophils, lymphocytes, or histiocytes. The usual volume is 50-200 mL and accumulates slowly. Fibrous adhesions rarely occur.
  • Fibrous and serofibrinous pericarditis: These 2 types represent the same basic process and are the most frequent type of pericarditis. Common causes include acute myocardial infarction (AMI), postinfarction (including Dressler syndrome), uremia, radiation, RA, SLE, and trauma. Severe infections may also cause a fibrinous reaction, as does routine cardiac surgery.
  • Purulent or suppurative pericarditis: Organisms may arise from direct extension, hematogenous seeding, or lymphatic extension, or by direct introduction during cardiotomy. Immunosuppression facilitates this condition. The fluid is usually 400-500 mL in volume and shows a thin to creamy pus. Clinical features include fever, chills, and spiking temperatures. Constrictive pericarditis is a serious potential complication.
  • Hemorrhagic pericarditis: Blood mixed with a fibrinous or suppurative effusion most commonly is caused by tuberculosis or direct neoplastic invasion. It can also occur in severe bacterial infections or in patients with a bleeding diathesis. Hemorrhagic pericarditis is common after cardiac surgery and may cause tamponade. The clinical significance is similar to suppurative pericarditis.
  • Caseous pericarditis: Until proven otherwise, caseation within the pericardial sac is tuberculous in origin. Untreated, this is the most common antecedent to chronic constrictive pericarditis of a fibrocalcific nature.
• Chronic pericarditis
  • Adhesive mediastinopericarditis: This reaction usually follows suppurative or caseous pericarditis, cardiac surgery, or irradiation. It is rarely caused by a simple fibrinous exudate. The pericardial potential space is obliterated, and adhesion of the external surface of the parietal layer to surrounding structures occurs. Clinically, systolic contraction of the ribcage and diaphragm and pulsus paradoxus may be observed. The increased workload may cause massive cardiac hypertrophy and dilatation, which can mimic an idiopathic cardiomyopathy.
  • Constrictive pericarditis: This is usually caused by suppurative, caseous, or hemorrhagic pericarditis. The heart may become encased in a 0.5- to 1.0-cm-thick layer of scar or calcification (concretio cordis), resembling a plaster mold. Contrary to clinical findings in adhesive mediastinopericarditis, the heart cannot become hypertrophic or dilate because of insufficient space.
• Cardiac tamponade
  • Tamponade is more common in patients with malignant pericarditis. Effusions caused by tumors often progress to tamponade, eliciting bleeding in the pericardium. Blood accumulates more rapidly than a transudate or exudate and more commonly causes tamponade.
  • Penetrating cardiac injuries: Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires aggressive resuscitation.
    • Hemopericardium is the most common feature of penetrating cardiac injuries.
    • In acute massive hemopericardium, the time is insufficient for defibrination to occur. The hemopericardium organizes and may partially clot, resulting in a pericardial hematoma.
    • The hematoma may appear echogenic instead of echo free.
  • Iatrogenic causes: Potential sources of cardiac perforation include central line placement, pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, and pericardiocentesis.
  • The right atrium is the most common site of perforation from catheter placement. Perforation, as well as direct catheter infusion of fluids, can cause tamponade.
  • A tamponade delay of hours to days has occurred secondary to catheter misplacement.
  • Tamponade was described in one case report as the first manifestation of dermatopolymyositis.²

Differential Diagnoses

Dissection, Aortic

Other Problems to Be Considered

Liver disease has been noted in asymptomatic constrictive pericarditis.

Workup

Laboratory Studies

• CBC count with differential
• Elevated erythrocyte sedimentation rate (ESR)
• Creatine kinase and isoenzymes levels - Troponin I may be elevated in viral or idiopathic acute pericarditis.
• Elevated lactate dehydrogenase and serum glutamic-oxaloacetic transaminase levels
• Human immunodeficiency virus (HIV) testing
• Tuberculosis skin testing
• Thyroid function testing
• Antinuclear antibody, rheumatoid factor testing

Imaging Studies

• Chest radiography
  • This is not helpful in uncomplicated viral pericarditis. A water bottle–shaped heart can be seen with excessive pericardial fluid accumulation.
  • In cardiac tamponade (or large effusions), the chest radiograph may reveal an enlarged cardiac silhouette after 200-250 mL of fluid accumulation. This occurs in patients with slow fluid accumulation, compared with a normal cardiac silhouette seen in patients with rapid accumulation and tamponade. Thus, the chronicity of the effusion may be suggested by the presence of a huge cardiac silhouette.
• Limited echocardiography
  • In pericarditis, the pericardium may have a normal appearance, without evidence of fluid accumulation.
  • Echocardiographers use M-mode to evaluate pericardial fluid and timing during the cardiac cycle.
  • Emergency sonographers essentially note the presence or absence of pericardial fluid, may comment on the amount of fluid, and/or note right ventricular collapse.
  • Very small effusions are located posterior and inferior to the left ventricle.
  • Moderate effusions extend toward the apex of the heart, and large effusions circumscribe the heart. Weitzman criteria define a moderate effusion as an echo-free pericardial space (anterior plus posterior) of 10-20 mm during diastole and a large effusion as an echo-free space more than 20 mm.
  • The emergency sonographer may encounter difficulty using the classic textbook sonographic findings of tamponade, as the trauma patient is often tachycardic and the examination abbreviated.
  • A swinging heart may be present. This is characterized as counterclockwise rotational movement, which occurs in addition to the triangular movement of the heart, producing a dancelike motion.
  • A dilated inferior vena cava (IVC) without inspiratory collapse (plethora) is highly suggestive of tamponade.
• Transthoracic echocardiography: This is limited in its capacity to reveal the entire pericardium and its operator dependence, although it remains the initial test of choice for detecting pericardial effusions and diagnosing tamponade.
• CT scanning
  • CT scanning provides anatomic details of the entire pericardium due to its capacity in providing a wide field of view. CT scanning is less operator dependent. The normal thickness of the pericardium as measured by CT scanning is less than 2 mm.
  • An advantage of CT scanning over other imaging modalities includes its capacity to detect pericardial calcifications. MRI can miss significant calcium deposits. The presence of any calcification is important in patients suspected of having constrictive pericarditis.
  • Limitations of CT scanning include the need for contrast administration, patient exposure to ionizing radiation, and difficulty in differentiating fluid from thickened pericardium.
• MRI
  • MRI can provide anatomic details of the pericardium and heart without ionizing contrast or radiation. The normal pericardium can be up to 4-mm thick.
  • Limitations to use of MRI include the need to gate the image acquisition. A high-quality MRI may need more than 250 regular heartbeats. Thus, the examination may be limited in patients with arrhythmias.

Other Tests

• Electrocardiography
  • Electrical alternans is pathognomonic of cardiac tamponade and is characterized by alternating levels of ECG voltage of the P wave, QRS complex, and T waves. This is a result of the heart swinging in a large effusion.
  • ECG can be diagnostic in acute pericarditis and evolves in 4 stages. Only 50% of patients with pericarditis experience all 4 stages.
    • The first stage is characterized by ST-segment elevation with concave upward ST segments. It can be seen within hours of chest pain and lasts several days. The ST-segment changes usually are noted in all leads except V₁.
    • In the second stage, the ST segments return to baseline with T-wave flattening.
    • The third stage is distinguished by T-wave inversion without Q-wave formation.
    • The fourth stage is characterized by ECG normalization.
  • Another important ECG finding is PR-segment depression, which has been reported in up to 80% of viral pericarditis cases.

Procedures

• Pericardiocentesis
  • The traditional approach is the subxiphoid technique. This technique avoids injury to the coronary arteries.
  • The chest is prepared with Betadine and a 16- to 18-gauge catheter is introduced between the xiphoid and the left subcostal margin.
  • The catheter is directed toward the inferior tip of the left scapula with slow advancement and with negative pressure.
  • If fluid is found, the catheter is advanced and the needle is withdrawn. Fluid is removed via the catheter.
  • The catheter may be sutured in place for subsequent use.
  • Alternatively, a 16- to 18-gauge spinal needle may be used for one-time drainage.
• Echocardiographically guided pericardiocentesis
  • Echocardiographically guided pericardiocentesis has evolved over the past 20 years and is now considered the procedure of choice for removal of pericardial fluid. The technique for echocardiographically guided pericardiocentesis differs from traditional blind pericardiocentesis primarily in the site of needle entry.
  • The left chest wall has become the preferred location for needle entry under echocardiographic guidance. The intended needle trajectory is investigated with echocardiography to confirm the optimal direction and depth for needle advancement. A 16-gauge needle (with poly-Teflon sheath) is advanced in a straight line without side-to-side manipulation. Needle position can be established via echocardiography while agitated sterile saline is injected.
  • The step-by-step approach for echocardiographically-guided pericardiocentesis is as follows:
    • Assess the size, distribution, and ideal needle entry site and trajectory with a 2.5- to 5-MHz ultrasound transducer placed approximately 3-5 cm from the parasternal border. Locate the point where the effusion is closest to the transducer as well as an area of maximal pericardial fluid accumulation.
    • Assess or measure the distance from the skin to the pericardial space. The needle trajectory is established by the angle of the transducer. Keep this trajectory in mind during the procedure.
    • Use a sterile skin preparation such as povidone-iodine and, if readily available, a transparent sterile plastic sheet (one author recommends a 1030 Baxter drape) to allow imaging and a sterile field.
    • Place a sterile 16-gauge catheter on the predetermined location on the chest wall, avoiding the inferior rib margin. Advance in the predetermined direction, angle, and depth. Advance 2 mm further once fluid is obtained. Consider leaving the catheter in place after removing the needle. If needed, a guidewire can be advanced through the catheter.
• Central venous pressure measurement
  • If echocardiography is unavailable, placement of a central venous pressure (CVP) line may reveal increased right-sided pressures. CVP measurements more than 12-14 mm Hg are usually found in cardiac tamponade.
  • Thoracotomy and pericardiotomy may be required in the ED if the patient has rapid deterioration or cardiac arrest.

Treatment

Prehospital Care

Patients with chest pain, regardless of etiology, should routinely be treated with oxygen and cardiac monitor.

• Pericarditis - Routine care as for patients with acute cardiac conditions
• Cardiac tamponade
  • The initial prehospital care is the same as for any major trauma. The diagnosis may be suspected based on the location of penetrating wounds.
  • Consider the possibility of a tension pneumothorax.

Emergency Department Care

The emergency care of the patient centers on prompt diagnosis and treatment of potentially life-threatening entities.

• Pericarditis
  • Ideally, echocardiography should be readily available to determine the presence or absence of a pericardial effusion.
  • If no pericardial effusion is noted, stable patients with presumptive viral pericarditis may be discharged with appropriate instructions and follow-up care.
  • If a small- to medium-sized effusion is present, the patient should be admitted for observation and serial echocardiography. If a large effusion is present, the stable patient may undergo an urgent pericardiocentesis or placement of a pericardial window.
• Cardiac tamponade
  • Treatment depends on stability. Patients who are unstable require immediate treatment of the increase in pericardial pressure with pericardiocentesis. Removing as little as 30-50 mL may produce dramatic hemodynamic improvement.
  • Patients may have subacute tamponade (intermittently decompressing) and may benefit from decompression in the operating room with cardiothoracic care available to treat cardiac injuries.

Consultations

• Nontraumatic pericardial disease - Internal medicine or cardiology specialists
• Traumatic pericardial injury - Trauma or cardiothoracic surgery specialists

Medication

Patients with idiopathic or viral pericarditis should be treated symptomatically. Several small studies have noted successful use of colchicine to prevent recurrence of acute pericarditis after failure of conventional treatment, especially in idiopathic cases.^3,4 One report found marked improvement following corticosteroid therapy in a patient with refractory uremic pleuropericarditis.⁵

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Because pericarditis is primarily due to inflammation, anti-inflammatory medications are considered the drugs of choice.

Ibuprofen (Motrin, Advil, Ibuprin)

Usually DOC for mild to moderate pain, if no contraindications are noted.
Inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclooxygenase, which results in prostaglandin synthesis.

Dosing

Adult

400-800 mg PO q4-8h

Pediatric

<6 months: Not established
6 months to 12 years: 10-70 mg/kg/d PO divided tid/qid; start at the lower end of dosing range and titrate upward to a maximum of 2.4 g/d
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Indomethacin (Indocin)

Often considered the first choice. Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.

Dosing

Adult

25-50 mg PO q6h

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia)

Ketoprofen (Oruvail, Orudis, Actron)

For relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient response.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Naproxen (Anaprox, Naprelan, Naprosyn)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO, followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Meticorten, Meticorten, Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dosing

Adult

5-60 mg/d PO qd or divided bid/qid

Pediatric

4-5 mg/m²/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid

Interactions

Coadministration with estrogens may decrease clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Follow-up

Complications

• Pericarditis may recur in 15-32% of patients.
• Noncompressive effusion may occur.
• Chronic constrictive pericarditis is a potential complication.
• Cardiac perforation may occur at time of pericardiocentesis.
• Bronchopericardial fistula was noted as a complication of multi–drug-resistant tuberculosis in a patient with HIV.⁶
• Liver disease has been reported in asymptomatic constrictive pericarditis.

Prognosis

• The prognosis for patients with pericarditis depends on the etiology of the pericardial infection or inflammation as well as the presence of a pericardial effusion and/or tamponade.
  • Acquired immunodeficiency syndrome: Small asymptomatic pericardial effusions may not require diagnostic evaluation.⁷ Large symptomatic pericardial effusions should be investigated because two thirds of such effusions are potentially infections or neoplasms. Tuberculous pericarditis can occur. Adjunctive prednisolone may reduce mortality in this population.
  • Postmyocardial infarction pericarditis: This may occur in approximately 5% of patients receiving thrombolytic drugs. Dressler syndrome is now considered rare. Most postmyocardial infarction cases have a benign course; however, pericarditis is associated with larger infarcts. Therefore, overall long-term mortality may be increased.
  • Chronic idiopathic pericarditis: This is defined as a pericardial effusion that persists more than 3 months without any apparent etiology. Pericardiocentesis alone results in resolution of large effusions; however, recurrence is common. Pericardiectomy should be considered in recurrent cases because it yields good long-term effects. High-dose prednisone may prevent recurrent pericarditis resistant to NSAIDs.
• Cardiac tamponade
  • For penetrating injuries, the prognosis depends heavily on the rapid identification of tamponade.
  • Favorable factors include minor perforations, isolated right ventricular wounds, systolic blood pressure more than 50 mm Hg, and presence of tamponade.

Miscellaneous

Medicolegal Pitfalls

• Be careful not to confuse this disease entity with esophageal disorders, costochondritis, or other causes of noncardiac chest pain.
• The potential misdiagnosis of pericarditis for AMI has led to unfortunate complications when thrombolytic therapy has been given.
• Tension pneumothorax may mimic cardiac tamponade. Trauma ultrasonography has limited this misdiagnosis.
• Elevated CVP may be absent in patients with preexisting hypovolemia.
• Rarely, air can enter the pericardium and obscure the sonographic evaluation.

Multimedia

Media file 1: This image demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance).

Media file 2: This is a modified subcostal view of the heart. A thick anechoic (dark or black) stripe is seen surrounding the heart. This represents fluid (F) in the pericardium. This is a large amount of fluid and represents tamponade.

Media file 3: A subcostal view of the heart in a patient who sustained a stab wound to the chest. A hemopericardium (Hem) can be seen surrounding the heart (H).

Media file 4: This 12-lead ECG is representative of pericarditis.

Media file 5: The ultrasound image demonstrates a subcostal view of the heart with a large fat pad (black arrows) present anteriorly.

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Keywords

pericardium, pericardial complex, acute pericardial tamponade, pericardial effusion, malignancy, tuberculous pericarditis, precordial chest pain, retrosternal chest pain, end-stage renal disease, ESRD, traumatic tamponade, decompressing tamponade, pericardial friction rub, premature atrial contractions, premature ventricular contractions, cardiac arrhythmias, tachypnea, dyspnea, myocarditis, Ewart sign, hepatomegaly, ascites, Beck triad, jugular venous distention, hypotension, muffled heart sounds, pulsus paradoxus, cyanosis, serous pericarditis, rheumatoid arthritis, RA, systemic lupus erythematosus, SLE, fibrous pericarditis, serofibrinous pericarditis, acute myocardial infarction, AMI, Dressler syndrome, uremia, radiation, suppurative pericarditis, purulent pericarditis, cardiotomy, constrictive pericarditis, hemorrhagic pericarditis, bleeding diathesis, caseous pericarditis, adhesive mediastinopericarditis, concretio cordis, malignant pericarditis, penetrating cardiac injuries, hemopericardium, pericardial hematoma, pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, pericardiocentesis, dermatopolymyositis

Contributor Information and Disclosures

Author

Verena T Valley, MD, Associate Professor, Director of Ultrasound, Department of Emergency Medicine, University of Mississippi School of Medicine; Consulting Staff, Department of Emergency Medicine, Singing River Hospital System, Singing River Hospital, and Ocean Springs Hospital
Verena T Valley, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher A Fly, MD, Assistant Professor, Department of Emergency Medicine, Medical College of Georgia
Christopher A Fly, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

David A Peak, MD, Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eric Legome, MD, Residency Director, Assistant Professor of Emergency Medicine, Department of Emergency Medicine New York University, New York University Hospital, Bellevue Hospital Center, Manhattan VA
Eric Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Charles V Pollack, Jr, MD, MA, FACEP, Professor, Department of Emergency Medicine, University of Pennsylvania College of Medicine; Chairman, Department of Emergency Medicine, Pennsylvania Hospital
Charles V Pollack, Jr, MD, MA, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: sanofi-aventis Honoraria Consulting; sanofi-aventis Honoraria Speaking and teaching; Schering-Polugh Honoraria Consulting; Schering-Plough Honoraria Speaking and teaching; The Medicines Company Honoraria Consulting; GlaxoSmithKline Grant/research funds Other

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