eMedicine Specialties > Cardiology > Pericardial Disease

Cardiac Tamponade

Author: Chakri Yarlagadda, MD, FACC, FASNC, FSCAI, Director, Noninvasive Cardiology, St Joseph Health Center, Warren, OH
Contributor Information and Disclosures

Updated: Dec 22, 2009

Introduction

Background

Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. Cardiac tamponade is a medical emergency. The overall risk of death depends on the speed of diagnosis, the treatment provided, and the underlying cause of the tamponade. (See image below.)

This anteroposterior-view chest radiograph shows ...

This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and conspicuous absence of pulmonary vascular congestion. Reproduced with permission from Chest, 1996: 109:825.

This anteroposterior-view chest radiograph shows ...

This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and conspicuous absence of pulmonary vascular congestion. Reproduced with permission from Chest, 1996: 109:825.


Pathophysiology

The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The parietal pericardium is the outer fibrous layer; the visceral pericardium is the inner serous layer. The pericardial space normally contains 20-50 mL of fluid. Pericardial effusions can be serous, serosanguineous, hemorrhagic, or chylous.

Reddy et al describe 3 phases of hemodynamic changes in tamponade.1

  • Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle, requiring a higher filling pressure. During this phase, the left and right ventricular filling pressures are higher than the intrapericardial pressure.
  • Phase II: With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output.
  • Phase III: A further decrease in cardiac output occurs, which is due to equilibration of pericardial and left ventricular (LV) filling pressures.

The underlying pathophysiologic process for the development of tamponade is markedly diminished diastolic filling because transmural distending pressures are insufficient to overcome the increased intrapericardial pressures.

Systemic venous return is also altered during tamponade. Because the heart is compressed throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous return is impaired and right atrial and right ventricular collapse occurs. Because the pulmonary vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous circulation, at the expense of LV filling. This results in reduced cardiac output and venous return.

The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output, whereas 1000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium over time. A more compliant pericardium can allow considerable fluid accumulation over a longer period without hemodynamic insult.

Frequency

United States

The incidence of cardiac tamponade is 2 cases per 10,000 population in the United States. Approximately 2% of penetrating injuries are reported to result in cardiac tamponade.

Mortality/Morbidity

Cardiac tamponade is a medical emergency. Early diagnosis and treatment are crucial to reduce morbidity and mortality. Untreated, it is rapidly and universally fatal.

Sex

In children, cardiac tamponade is more common in boys than in girls, with a male-to-female ratio of 7:3. In adults, cardiac tamponade appears to be slightly more common in men than in women. The male-to-female ratio of 1.25:1 observed at author's referral center based on the International Classification of Diseases (ICD) code 423.9. However, a male-to-female ratio of 1.7:1 is observed at another level 1 trauma center.

Age

Cardiac tamponade related to trauma or HIV is more common in young adults, whereas tamponade due to malignancy and/or renal failure occurs more frequently in elderly individuals.

Clinical

History

Symptoms vary with the underlying cause and the acuteness of the tamponade. Patients with acute tamponade may present with dyspnea, tachycardia, and tachypnea. Cold and clammy extremities from hypoperfusion are also observed in some patients.

A comprehensive review of the patient's history usually helps identify the probable etiology of a pericardial effusion, which may result in cardiac tamponade.

  • Patients with systemic or malignant disease present with weight loss, fatigue, or anorexia.
  • Chest pain may be the presenting symptom in patients with pericarditis or myocardial infarction.
  • Musculoskeletal pain or fever may be present in patients with an underlying connective tissue disorder.
  • A history of renal failure can lead to a consideration of uremia as a cause of pericardial effusion.
  • Careful review of a patient's medications may indicate drug-related lupus leading to a pericardial effusion.
  • Recent cardiovascular surgery, coronary intervention, or trauma can lead to the rapid accumulation of pericardial fluid and tamponade.2
  • Recent pacemaker lead implantation or central venous catheter insertion can lead to the rapid accumulation of pericardial fluid and tamponade.3
  • Consider HIV-related pericardial effusion and tamponade if the patient has a history of intravenous drug abuse or opportunistic infections.
  • Inquire about chest wall radiation (ie, for lung, mediastinal, or esophageal cancer).
  • Inquire about symptoms of night sweats, fever, and weight loss, which may be indicative of tuberculosis.

Physical

Distended neck veins are a common feature in patients with tamponade. Evidence of chest wall injury may be present in trauma patients. Tachycardia, tachypnea, and hepatomegaly are observed in more than 50% of patients with cardiac tamponade, and diminished heart sounds and a pericardial friction rub are present in approximately one third of patients.

  • The Beck triad or acute compression triad
    • Described in 1935, this complex of physical findings refers to increased jugular venous pressure, hypotension, and diminished heart sounds.
    • These findings result from a rapid accumulation of pericardial fluid. However, this classic triad is usually observed in patients with acute cardiac tamponade.
  • Pulsus paradoxus or paradoxical pulse
    • This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure.
    • To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present.
    • The paradox is that while listening to the heart sounds during inspiration, the pulse weakens or may not be palpated with certain heartbeats, while S1 is heard with all heartbeats.
    • A pulsus paradoxus can be observed in patients with other conditions, such as constrictive pericarditis, severe obstructive pulmonary disease, restrictive cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right ventricular infarction with shock.
    • A pulsus paradoxus may be absent in patients with markedly elevated LV diastolic pressures, atrial septal defect, pulmonary hypertension, and aortic regurgitation.
  • Kussmaul sign
    • This was described by Adolph Kussmaul as a paradoxical increase in venous distention and pressure during inspiration.
    • This sign is usually observed in patients with constrictive pericarditis but occasionally is observed in patients with effusive-constrictive pericarditis and cardiac tamponade.
  • Ewart sign
    • Also known as the Pins sign, this is observed in patients with large pericardial effusions.
    • It is described as an area of dullness, with bronchial breath sounds and bronchophony below the angle of the left scapula.
  • The y descent
    • The y descent is abolished in the jugular venous or right atrial waveform.
    • This is due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles.
  • Dysphoria: Behavioral traits such as restless body movements, unusual facial expressions, restlessness, sense of impending death were reported by Ikematsu in about 26% patients with cardiac tamponade.4   
  • Low-pressure tamponade: In severely hypovolemic patients, classical physical findings such as tachycardia, pulsus paradoxus, and jugular venous distension were infrequent. Sagrista-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac tamponade.5  They also reported low-pressure tamponade in 10% of large pericardial effusions.

Causes

For all patients, malignant diseases are the most common cause of pericardial tamponade. Among etiology of tamponade, Merce et al reported malignant diseases in 30-60% of cases, uremia in 10-15% of cases, idiopathic pericarditis in 5-15%, infectious diseases in 5-10%, anticoagulation in 5-10%, connective tissue diseases in 2-6%, and Dressler or postpericardiotomy syndrome in 1-2%. Tamponade can occur as a result of any type of pericarditis.6

  • HIV infection
  • Infection - Viral, bacterial (tuberculosis), fungal
  • Drugs - Hydralazine, procainamide, isoniazid, minoxidil
  • Postcoronary intervention (ie, coronary dissection and perforation)
  • Trauma
  • Cardiovascular surgery (postoperative pericarditis)2
  • Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome)
  • Connective tissue diseases -Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis
  • Radiation therapy
  • Iatrogenic7 - After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion
  • Uremia
  • Idiopathic pericarditis
  • Complication of surgery at the esophagogastric junction such as antireflux surgery
  • Pneumopericardium (due to mechanical ventilation or gastropericardial fistula)

More on Cardiac Tamponade

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

References

  1. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol. Dec 15 1990;66(20):1487-91. [Medline].

  2. Rylski B, Siepe M, Schoellhorn J, et al. Endoscopic treatment for delayed cardiac tamponade. Eur J Cardiothorac Surg. Sep 17 2009;[Medline].

  3. Lee YM, Kim HJ, Lee JE, et al. Cardiac tamponade following insertion of an internal jugular vein catheter for hemodialysis. Clin Nephrol. Sep 2009;72(3):220-3. [Medline].

  4. Ikematsu Y. Incidence and characteristics of dysphoria in patients with cardiac tamponade. Heart Lung. Nov-Dec 2007;36(6):440-9. [Medline].

  5. Sagristà-Sauleda J, Angel J, Sambola A, Alguersuari J, Permanyer-Miralda G, Soler-Soler J. Low-pressure cardiac tamponade: clinical and hemodynamic profile. Circulation. Aug 29 2006;114(9):945-52. [Medline].

  6. Parvez N, Carpenter JL. Cardiac tamponade in Still disease: a review of the literature. South Med J. Aug 2009;102(8):832-7. [Medline].

  7. Holmes DR Jr, Nishimura R, Fountain R, et al. Iatrogenic pericardial effusion and tamponade in the percutaneous intracardiac intervention era. JACC Cardiovasc Interv. Aug 2009;2(8):705-17. [Medline].

  8. Gold MM, Spindola-Franco H, Jain VR, Spevack DM, Haramati LB. Coronary sinus compression: an early computed tomographic sign of cardiac tamponade. J Comput Assist Tomogr. Jan-Feb 2008;32(1):72-7. [Medline].

  9. Stone MK, Bauch TD, Rubal BJ. Respiratory changes in the pulse-oximetry waveform associated with pericardial tamponade. Clin Cardiol. Sep 2006;29(9):411-4. [Medline].

  10. Boltwood C, Rieders D, Gregory KW. Inspiratory tracking sign in pericardial disease. Circulation. 1984;(suppl II) 70:103.

  11. Monaco F, Barone M, David A, et al. [Cardiac tamponade: a modified video-assisted thoracoscopic approach]. Chir Ital. May-Jun 2009;61(3):321-6. [Medline].

  12. Aikat S, Ghaffari S. A review of pericardial diseases: clinical, ECG and hemodynamic features and management. Cleve Clin J Med. Dec 2000;67(12):903-14. [Medline].

  13. Alam HB, Levitt A, Molyneaux R, et al. Can pleural effusions cause cardiac tamponade?. Chest. Dec 1999;116(6):1820-2. [Medline].

  14. Allen KB, Faber LP, Warren WH, Shaar CJ. Pericardial effusion: subxiphoid pericardiostomy versus percutaneous catheter drainage. Ann Thorac Surg. Feb 1999;67(2):437-40. [Medline].

  15. Beauchamp KA. Pericardial tamponade: an oncologic emergency. Clin J Oncol Nurs. Jul 1998;2(3):85-95. [Medline].

  16. Chen Y, Brennessel D, Walters J, et al. Human immunodeficiency virus-associated pericardial effusion: report of 40 cases and review of the literature. Am Heart J. Mar 1999;137(3):516-21. [Medline].

  17. Eisenberg MJ, de Romeral LM, Heidenreich PA, et al. The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG. A technology assessment. Chest. Aug 1996;110(2):318-24. [Medline].

  18. Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Curr Probl Cardiol. Sep 2004;29(9):503-67. [Medline].

  19. Griffin S, Fountain W. Pericardio-peritoneal shunt for malignant pericardial effusion. J Thorac Cardiovasc Surg. Dec 1989;98(6):1153-4. [Medline].

  20. Guberman BA, Fowler NO, Engel PJ, et al. Cardiac tamponade in medical patients. Circulation. Sep 1981;64(3):633-40. [Medline].

  21. Kaplan LM, Epstein SK, Schwartz SL, et al. Clinical, echocardiographic, and hemodynamic evidence of cardiac tamponade caused by large pleural effusions. Am J Respir Crit Care Med. Mar 1995;151(3 Pt 1):904-8. [Medline].

  22. Medary I, Steinherz LJ, Aronson DC, La Quaglia MP. Cardiac tamponade in the pediatric oncology population: treatment by percutaneous catheter drainage. J Pediatr Surg. Jan 1996;31(1):197-9; discussion 199-200. [Medline].

  23. Müller-Stich BP, Linke G, Leemann B, Lange J, Zerz A. Cardiac tamponade as a life-threatening complication in antireflux surgery. Am J Surg. Jan 2006;191(1):139-41. [Medline].

  24. Patel MR, Meine TJ, Lindblad L, Griffin J, Granger CB, Becker RC. Cardiac tamponade in the fibrinolytic era: analysis of >100,000 patients with ST-segment elevation myocardial infarction. Am Heart J. Feb 2006;151(2):316-22. [Medline].

  25. Paunovic B, Sharma S, Miller A. Swan-Ganz Catheterization. eMedicine Journal [serial online]. 2005. [Full Text].

  26. Reddy PS, Curtiss EI. Cardiac tamponade. Cardiol Clin. Nov 1990;8(4):627-37. [Medline].

  27. Spodick DH. Diseases of the pericardium. In: Chatterjee K, ed. Cardiology: An Illustrated Text/Reference. Vol 2. New York, NY: Gower Medical; 1991:10.38-10.64.

  28. Spodick DH. Pericarditis, pericardial effusion, cardiac tamponade, and constriction. Crit Care Clin. Jul 1989;5(3):455-76. [Medline].

  29. Spodick DH. The normal and diseased pericardium: current concepts of pericardial physiology, diagnosis and treatment. J Am Coll Cardiol. Jan 1983;1(1):240-51. [Medline].

  30. Tsang TS, Freeman WK, Sinak LJ, Seward JB. Echocardiographically guided pericardiocentesis: evolution and state-of-the-art technique. Mayo Clin Proc. Jul 1998;73(7):647-52. [Medline].

  31. Tsang TS, Oh JK, Seward JB. Diagnosis and management of cardiac tamponade in the era of echocardiography. Clin Cardiol. Jul 1999;22(7):446-52. [Medline].

  32. Walensky P. Pericardial diseases. In: Linhart JW, Joyner CR, eds. Diagnostic Echocardiography. St. Louis, Mo: Mosby-Year Book; 1982:109.

Further Reading

Keywords

cardiac tamponade, tamponade, pericardial effusion, pericardial tamponade, ventricular filling, effusive-constrictive pericarditis, constrictive pericarditis, restrictive cardiomyopathy, hemodynamic compromise, pericarditis, Dressler syndrome

Contributor Information and Disclosures

Author

Chakri Yarlagadda, MD, FACC, FASNC, FSCAI, Director, Noninvasive Cardiology, St Joseph Health Center, Warren, OH
Chakri Yarlagadda, MD, FACC, FASNC, FSCAI is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography, American Society of Nuclear Cardiology, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

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 Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
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

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.