eMedicine Specialties > Cardiology > Invasive Diagnostic, Interventional, and Surgical Procedures

Pericardiocentesis

Author: Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Coauthor(s): Ravi H Dave, MD, Associate Professor of Medicine, University of California at Los Angeles David Geffen School of Medicine; Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Contributor Information and Disclosures

Updated: Jan 28, 2009

Introduction

Background

Percutaneous pericardiocentesis was introduced during the 19th century.FrankSchuhfirst described this procedure in 1840. By the 20th century, percutaneous pericardiocentesis became a preferred technique for the treatment of patients with pericardial effusion or for diagnostic purposes.

Before the advent of 2-dimensional echocardiography, the procedure used a blind-subxiphoid approach. Serious complications were not uncommon (eg, injury to liver, myocardium, coronary arteries, lungs). Because 2-dimensional echocardiography permits direct visualization of cardiac structures and adjacent vital organs, the procedure now is performed with minimal risk. Since 1979, echo-guided pericardiocentesis has been the preferred initial procedure for the diagnosis and treatment of most pericardial effusions. The technique has been modified and refined in the past 22 years. Percutaneous pericardiocentesis now is the procedure of choice for the safe removal of pericardial fluid. Whenever possible, this procedure should be performed by a surgeon or cardiologist trained in invasive techniques.

Pathophysiology

An increase in production or a decrease in drainage of pericardial fluid can cause pericardial effusion. Increased production can be due to inflammation of the pericardium, usually the visceral pericardium. Typically, the amount of pericardial effusion is larger when caused by lymphatic or venous obstruction. Accumulation of more than 20-30 mL of fluid in the pericardial sac is usually abnormal, and an increase in the pericardiac/cardiac silhouette is detectable when at least 250 mL of fluid accumulates in the pericardial cavity.

The rate of pericardial fluid accumulation is critical. As the pericardium stretches, a large effusion that develops slowly produces no hemodynamic effects until it is massive. A case of subacute cardiac tamponade with 2000 mL of pericardial fluids has been reported with no significant hemodynamic effect because of the gradual accumulation of pericardial fluid.1 Hemodynamic instability can result from rapid collection of fluid.

Hemopericardium can occur as a result of coagulation abnormalities, postsurgical complications, anticoagulation therapy, dissecting aortic aneurysm, or myocardial rupture (eg, in acute myocardial infarction [MI] or traumatic injury). Chylopericardium is a pericardial effusion of chyle, which is often associated with irritation of the pericardium as well (acute or chronic pericarditis). The primary form is rare, and the secondary chylopericardium may be due to radiation, subclavian thrombosis, infections (eg, tuberculosis), mediastinal tumors, following cardiac and aortopulmonary surgeries, or any process that damages the thoracic ducts. Chylopericardium has been reported even following minimally invasive mitral valve repair.2

Pneumopericardium is a rare finding, which has very broad etiologies such as chest trauma, following medical interventions, fistula formation, and a variety of gas-forming infections. Tension pneumopericardium is associated with tamponade and hemodynamic instability and needs immediate attention.

Frequency

United States

The common etiologic factors are acute idiopathic pericardial effusion, iatrogenic (eg, postsurgical, drug-induced), chronic idiopathic pericardial effusion, malignancy, post – myocardial infarction (Dressler syndrome), uremia, infection, and radiation.

International

In some of the developing countries tuberculosis may be the most common cause (generally an extrapulmonary presentation in HIV positive patients) and may account for 70% of all cases.3   

Mortality/Morbidity

Since the advent of 2-dimensional echocardiography, the morbidity and mortality rates have been reduced. A review of 1127 echocardiography-guided pericardiocentesis that were performed during more than 20 years at a major tertiary care center showed a procedural success rate of 97% overall, with a total complication rate of 4.7% (major, 1.2%; minor, 3.5%). This rate may be different from one institute to another, but echocardiographic-guided pericardiocentesis is considered an overall safe procedure with minimal complication and mortality rates.

Clinical

History

The signs and symptoms depend on the amount of pericardial fluid present and the duration of disease. A patient can be asymptomatic when fluid accumulates very slowly or symptomatic when it accumulates very rapidly (eg, trauma, rupture of myocardium after myocardial infarction). An incidental finding of effusion may be found on 2-dimensional echocardiography images, chest CT scans, chest MRIs, or other imaging results. Symptoms of pericardial effusion include the following:

  • Chest pain is a presenting symptom when inflammation is the cause or when effusion is severe. Patients with diseases such as malignancy or chronic renal failure may be pain free.
  • Dyspnea commonly occurs with cardiac tamponade.
  • Cough usually occurs with bronchial encroachment of the pericardium.
  • Fever is associated with infectious or inflammatory causes.
  • Hoarseness of the voice can occur from compression of the recurrent laryngeal nerve by the enlarging pericardial sac.
  • Hiccups generally occur from esophageal compression or irritation of the vagus or phrenic nerves.

Physical

Findings upon physical examination depend on the size of the effusion and the accumulation rate of pericardial fluid. Generally, no physical findings exist if the effusion is very small. Large effusions can cause significant hemodynamic instability by impairing ventricular filling. Patients may have generalized discomfort from a large effusion. Other findings include the following:

  • Tachycardia usually occurs due to increased venous pressure and decreased blood pressure, which indicates hemodynamically significant pericardial effusion.
  • Tachypnea may develop in acute situations (eg, cardiac tamponade).
  • Jugular venous distention is visible in large pericardial effusion and loculated effusion compressing the right atrium or ventricle.
  • Narrow pulse pressure can occur in patients with significant pericardial effusion.
  • Although pulsus paradoxus is a classic finding in patients with pericardial effusion, pulsus paradoxus also can occur in patients with obstructive lung diseases.
  • Pericardial friction rub with a small effusion is most suggestive of pericarditis with secondary effusion.
  • Elevated central venous pressure occurs from increased pressure in the pericardial space and the ventricles. This condition usually is associated with hypotension.
  • The Ewart sign is another potential finding. In the late 1800s,WilliamEwartdescribed a different method of identifying pericardial effusion by physical examination. Pericardial fluid compresses the adjacent lung, producing dullness to percussion, tactile fremitus, and egobronchophony at the angle of the left scapula. This is termed the Ewart sign. Massive cardiomegaly and left pleural effusion can produce a similar finding with dullness in the left axillary area. Most clinicians use chest radiographs and 2-dimensional echocardiography findings for diagnosis of pericardial effusion and to differentiate between pericardial effusion and massive cardiomegaly and left pleural effusion. This sign is only of historic importance.
  • Of note, posterior pericardial effusions can occur following cardiothoracic surgery and can be difficult to detect clinically (see Imaging Studies).
  • In a retrospective literature analysis of patients with pericardial effusion, the presence of cardiac tamponade was associated with 5 features: (1) symptoms of dyspnea, (2) tachycardia, (3) pulsus paradoxus of greater than 10 mm Hg, (4) elevated jugular venous pressure, and (5) cardiomegaly on chest radiograph.4

Causes

A small asymptomatic effusion may be found incidentally in 8-15% of patients and in as many as 43% of healthy pregnant women. In general, most of the causes of pericarditis can also cause the accumulation of fluid in the pericardial sac. In addition to these etiologies, other conditions, such as rupture of a left ventricular (LV) aneurysm, may give a large pericardial effusion with minimal or no inflammation of the pericardium.

In the Mayo Clinic registry with 1127 echocardiography-guided pericardiocenteses, cardiothoracic surgery together with malignancy and perforation from catheter-based procedures accounted for nearly 70% of all therapeutic pericardiocenteses performed.5 Obviously, this pattern can be different at other institutes depending on the number of cardiothoracic surgeries performed at the institute, number and type of cancer patients, and many other factors. The pattern of etiologies of moderate-to-large pericardial effusion is not the same as pericarditis. For example, hypothyroidism is not a common cause of pericarditis, but it is a known etiology of large chronic pericardial effusion.6 The etiology of pericarditis is idiopathic, viral, or autoimmune in most cases.

A 10-year prospective survey from France reported on 114 patients requiring emergency drainage for cardiac tamponade, showed that malignant disease was the primary cause of medical tamponade (74 patients [65%]), followed by viral history (11 patients [10%]) and intrapericardial bleeding due to anticoagulation treatment (4 patients [3%]). One-year mortality was 76.5% in patients with malignant disease and 13.3% in those without malignant disease.7

Most of the causes of pericardial effusion are as follows:

  • Idiopathic
  • Infectious
    • Bacteria (eg, staphylococci, streptococci, pneumococci, Haemophilus influenzae, Mycoplasma species, Neisseria species, Borrelia burgdorferi, Chlamydia species, Legionella species, Salmonella species, Mycobacterium tuberculosis, Mycobacterium avium).
    • Viral (eg, coxsackievirus, adenovirus, Epstein-Barr virus, echovirus, cytomegalovirus, infectious mononucleosis, parvovirus B19, influenza, mumps, varicella, hepatitis B, HIV)
    • Fungal (eg, histoplasmosis, aspergillosis, blastomycosis, coccidioidomycosis, Candida species, Nocardia species)
    • Rickettsial organisms
    • Parasitic (toxoplasmosis, amebiasis)
  • Neoplasm
    • Metastatic (eg, lung or breast carcinoma, lymphoma, leukemia, melanoma)
    • Primary (eg, rhabdomyosarcoma, lipoma, teratoma, fibroma, fibrosarcoma, angioma, angiosarcoma, mesothelioma)
    • Early and late post – myocardial infarction, rupture of ventricular aneurysm, dissecting aortic aneurysm
  • Drugs
    • Procainamide
    • Hydralazine
    • Warfarin
    • Heparin
    • Thrombolytics
    • Methysergide
    • Isoniazid
    • Cyclosporine
  • Autoimmune disorders
  • Trauma
    • Blunt
    • Penetrating
    • Iatrogenic (eg, perforation caused by catheter insertion or pacemaker implantation, status post cardiopulmonary resuscitation)
  • Other
    • Hypothyroidism
    • Amyloidosis and autoimmune diseases
    • Chylopericardium
    • Uremia
    • Radiation
    • Pneumopericardium
    • Post cardiothoracic surgery
    • Idiopathic thrombocytopenic purpura
    • Postpericardiotomy syndrome

More on Pericardiocentesis

Overview: Pericardiocentesis
Differential Diagnoses & Workup: Pericardiocentesis
Treatment & Medication: Pericardiocentesis
Follow-up: Pericardiocentesis
Multimedia: Pericardiocentesis
References

References

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Further Reading

Keywords

pericardiocentesis, percutaneous pericardiocentesis, echo-guided pericardiocentesis, pericardial tap, pericardial disease, heart disease, cardiac disease, cardiac procedure, pericardial effusion, pericardial fluid, hemopericardium, chylopericardium, pneumopericardium, tension pneumopericardium

Contributor Information and Disclosures

Author

Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Ravi H Dave, MD, Associate Professor of Medicine, University of California at Los Angeles David Geffen School of Medicine
Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, Heart Rhythm Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Gary E Sander, MD, PhD, Professor, Department of Internal Medicine, Division of Cardiology, Tulane University Health Sciences Center
Gary E Sander, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Hypertension, Heart Failure Society of America, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Karlheinz Peter, MD, PhD, Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia
Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, Cardiac Society of Australia and New Zealand, and German Cardiac Society
Disclosure: Nothing to disclose.

 
 
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