eMedicine Specialties > Emergency Medicine > Cardiovascular

Pericarditis and Cardiac Tamponade

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
Coauthor(s): Christopher A Fly, MD, Assistant Professor, Department of Emergency Medicine, Medical College of Georgia
Contributor Information and Disclosures

Updated: Dec 1, 2009

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 departments 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.²
  • 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-cm–thick to 1-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.³

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