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

Pericardiocentesis: Differential Diagnoses & Workup

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

Differential Diagnoses

Other Problems to Be Considered

Postpericardiotomy syndrome

Workup

Laboratory Studies

  • Routine laboratory studies indicated includeCBCcount with differential, prothrombin time/international normalized ratio, activated partial thromboplastin time, and basal metabolic panel.
  • Specific tests such as cardiac enzymes, thyroid-stimulating hormone, autoantibodies, and viral or rickettsial serologic tests are indicated depending on the clinical information and differential diagnosis.
  • Routine tests on pericardial fluid are often indicated including cell count with differential, lactate dehydrogenase (LDH), protein, glucose, Gram stain, and routine bacterial cultures. Smear for acid-fast bacilli staining, adenosine deaminase, tuberculosis culture, viral cultures, and cytology are indicated depending on the degree of suspicion of tuberculosis, specific viral, or cancer etiology. By Light's established criteria, most pericardial effusions would be classified as exudative, with the biochemical and cell count composition yielding minimal diagnostic assistance.8 Further specific tests on pericardial fluid usually depend on the results of the initial test.

Imaging Studies

  • Chest radiographs usually show a large bilaterally distended cardiopericardial silhouette. Lungs are usually clear, unless the patient is in heart failure or has significant lung disease. Absence of vascular congestion in the lungs in patients with pericardial effusion and tamponade is an important radiographic clue to differentiate these conditions from congestive heart failure when in both conditions the heart size in the chest radiograph is higher than the normal range.
  • Two-dimensional echocardiography is the best method of obtaining the diagnosis of pericardial effusion. The 2003 Task Force of the AmericanCollege of Cardiology (ACC), the American Heart Association (AHA), and the American Society of Echocardiography (ASE) have given a class 1 recommendation to use echocardiography for the evaluation of all patients with suspected pericardial disease.
    • This imaging study is highly sensitive and specific. It can detect a pericardial effusion as small as 30 mL and show characteristic findings of a pericardial effusion larger than 100 mL.
    • Small nonloculated pericardial effusions usually present in the posterior part of the pericardial space while the patient is in the supine position. As the amount of fluid increases, it starts to accumulate anteriorly and laterally. A significant large effusion usually is circumferential. It allows free motion of the heart within the fluid (swinging of the heart). A small loculated effusion can produce a hemodynamically significant problem depending on the location of the effusion and the structure that is compressed by that.
    • Echocardiographic findings may include swinging of the heart within the effusion, right atrial collapse, early right ventricular collapse, reciprocal changes in right and left ventricular volume, and motion of the chamber wall with breathing (see Media files 1-2).
  • CT scan and MRI are reliable methods for helping detect pericardial fluid or pericardial thickening. They are not the diagnostic modality of choice to evaluate the pericardial effusion. However, they give useful information about the other structures in the chest, and they are helpful when echocardiography is inconclusive.

Other Tests

Electrocardiography may show some evidence of the pericardial diseases, but often the ECG findings are nonspecific. However, because ECG is a noninvasive and widely available test, it is usually indicated in evaluation of suspected pericardial diseases.

  • The electrocardiographic hallmark of pericardial effusion is low-voltage QRS complexes, which occur as the fluid surrounds the heart. Definition of low voltage is the QRS amplitude less than 0.5 mV in limb leads and less than 1 mV in precordial leads. Low QRS voltage is neither a sensitive nor a very specific sign for pericardial effusion, and therefore it should not be used to confirm the suspected diagnosis of pericardial effusion or to rule it out.
  • A variety of other cardiac conditions (eg, constrictive pericarditis, amyloidosis, scleroderma, cardiac neoplasm, myocardial fibrosis in chronic ischemic heart disease) and a variety of noncardiac conditions (eg, COPD, pneumothorax, pleural effusion, obesity) may present with low QRS voltage on the ECG. No strong correlation exists between the degree of decrease in QRS voltage and the amount of fluid in the pericardial sac. Although an increase in QRS voltage is expected following the pericardiocentesis, it may not happen immediately if some degree of fibrin has deposited.
  • Electrical alternans, which is beat-to-beat variation of the amplitude of QRS voltage, is another ECG finding suggestive of large pericardial effusion or cardiac tamponade. With large pericardial effusion and no clinical tamponade, the heart has some freedom of movement and therefore small variation in QRS amplitude can be seen in many of these cases. However, significant alternans in the  p wave, QRS complex, and T wave, which is called total electrical alternans, is a specific finding for cardiac tamponade.
  • The pressure produced by fibrin or fluid may induce a current of injury, which may appear as ST-segment changes on 12-lead surface ECG. Acute pericarditis typically appears with diffuse ST-segment elevation and PR depression on ECG.

Procedures

As the fluid increases in the pericardial space, the right atrial and central venous pressure increase correspondingly. Ideally, right heart catheterization shows high pressure during ventricular diastole and equal pressure in the right atrium and ventricular diastolic pressure.

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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