Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Cardiac Tamponade

  • Author: Chakri Yarlagadda, MD, FACC, FSCAI, FASNC, CCDS; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Jan 27, 2015
 

Practice Essentials

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. The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death.

Signs and symptoms

Symptoms vary with the acuteness and underlying cause 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. Other symptoms may include the following:

  • Elevated jugular venous pressure
  • Pulsus paradoxus
  • Musculoskeletal pain
  • Fever
  • Dysphoria

See Clinical Presentation for more detail.

Diagnosis

Prompt diagnosis is key to reducing the mortality risk for patients with cardiac tamponade. Although echocardiography provides useful information, cardiac tamponade is a clinical diagnosis. Echocardiography can be used to visualize ventricular and atrial compression abnormalities as blood cycles through the heart. The following may be observed with 2-dimensional (2-D) echocardiography:

  • An echo-free space posterior and anterior to the left ventricle and behind the left atrium
  • Early diastolic collapse of the right ventricular free wall
  • Late diastolic compression/collapse of the right atrium
  • Swinging of the heart in its sac
  • LV pseudohypertrophy
  • Inferior vena cava plethora with minimal or no collapse with inspiration
  • A greater than 40% relative inspiratory augmentation of right-side flow
  • A greater than 25% relative decrease in inspiratory flow across the mitral valve

See Workup for more detail.

Management

Removal of pericardial fluid is the definitive therapy for tamponade and can be done using the following three methods:

  • Emergency subxiphoid percutaneous drainage
  • Echocardiographically guided pericardiocentesis
  • Percutaneous balloon pericardiotomy

The role of medication therapy in cardiac tamponade is limited.

See Treatment and Medication for more detail.

Next

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. The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death. (See Pathophysiology, Etiology, and Prognosis.)

The overall mortality risk depends on the speed of diagnosis, the treatment provided, and the underlying cause of the tamponade. Untreated, the condition is rapidly and universally fatal (see the image below). (See Presentation, Workup, Treatment, and Medication.)

This anteroposterior-view chest radiograph shows a 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.
Previous
Next

Pathophysiology

The pericardium, which is the membrane surrounding the heart, is composed of 2 layers. The thicker parietal pericardium is the outer fibrous layer; the thinner visceral pericardium is the inner serous layer. The pericardial space normally contains 20-50mL of fluid.

Reddy et al describe 3 phases of hemodynamic changes in tamponade, as follows[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 (see the Cardiac Output calculator)
  • Phase III - A further decrease in cardiac output occurs, which is due to the equilibration of pericardial and left ventricular (LV) filling pressures

Pericardial effusions, which cause cardiac tamponade, can be serous, serosanguineous, hemorrhagic, or chylous.

The underlying process for the development of tamponade is a marked reduction in diastolic filling, which results when transmural distending pressures become insufficient to overcome increased intrapericardial pressures. Tachycardia is the initial cardiac response to these changes to maintain the cardiac output.

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 diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output,[2] 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.

Previous
Next

Etiology

For all patients, malignant diseases are the most common cause of pericardial tamponade. Among etiologies for tamponade, Merce et al reported the following incidence rates:

  • Malignant diseases - 30-60% of cases
  • Uremia - 10-15% of cases
  • Idiopathic pericarditis - 5-15%
  • Infectious diseases - 5-10%
  • Anticoagulation - 5-10%
  • Connective tissue diseases - 2-6%
  • Dressler or postpericardiotomy syndrome - 1-2%

Tamponade can occur as a result of any type of pericarditis. Pericarditis can result from the following[3] :

  • Human immunodeficiency virus (HIV) infection
  • Infection - Viral, bacterial (tuberculosis), fungal
  • Drugs - Hydralazine, procainamide, isoniazid, minoxidil
  • Postcoronary intervention - Ie, coronary dissection and perforation
  • Acupuncture [4]
  • Postcardiac percutaneous procedures - Including mitral valvuloplasty, atrial septal defect (ASD) closure, left atrial appendage occlusion
  • Trauma to the chest
  • Cardiovascular surgery - Postoperative pericarditis [5]
  • Postmyocardial infarction - Free wall ventricular rupture, Dressler syndrome
  • Connective tissue diseases - Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis
  • Radiation therapy to the chest
  • Iatrogenic [6] - After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion
  • Uremia
  • Anticoagulation treatment
  • Idiopathic pericarditis
  • Complication of surgery at the esophagogastric junction - Eg, antireflux surgery
  • Pneumopericardium - Due to mechanical ventilation or gastropericardial fistula
  • Hypothyroidism
  • Still disease
  • Duchenne muscular dystrophy
  • Type A aortic dissection
Previous
Next

Epidemiology

Occurrence in the 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.

Sex- and age-related demographics

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. A male-to-female ratio of 1.25:1 was observed at the 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 was observed at another level 1 trauma center.

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.

Previous
Next

Prognosis

Cardiac tamponade is a medical emergency. The prognosis depends on prompt recognition and management of the condition and the underlying cause of the tamponade. Untreated, cardiac tamponade is rapidly and universally fatal.

Haneya et al retrospectively (2005-2011) evaluated the impact of timing and indication of reexploration for bleeding or tamponade following cardiac surgery in 209 patients and found that reexploration was associated with higher rates of mortality and morbidity.[7] Multivariate analysis indicated it was the adverse effects of reexploration (eg, blood loss, transfusion requirements) rather than the procedure itself that were independent risk factors for death. Adverse outcomes were more likely in those whose reexploration was delayed and who suffered from cardiac tamponade.[7]

In a separate study, Le et al indicated that following cardiac surgery, there is no advantage for the use of multiple mediastinal chest tubes over a single chest tube in preventing return to the operating room for bleeding or tamponade.[8]

In addition to treatment for the tamponade, all patients should also receive treatment for the condition’s underlying cause in order to prevent recurrence.

In a study of patients with cardiac tamponade, Cornily et al reported a 1-year mortality rate of 76.5% in patients whose tamponade was caused by malignant disease, compared with 13.3% in patients with no malignant disease. The investigators also noted a median survival of 150 days in patients with malignant disease.[9]

Previous
 
 
Contributor Information and Disclosures
Author

Chakri Yarlagadda, MD, FACC, FSCAI, FASNC, CCDS Director of Non-Invasive Cardiology, St Joseph Health Center; Invasive Cardiologist, Ohio Heart Institute

Chakri Yarlagadda, MD, FACC, FSCAI, FASNC, CCDS is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography, Society for Cardiovascular Angiography and Interventions, Heart Rhythm Society, American Society of Nuclear Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Russell F Kelly, MD Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP 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; Bayer Grant/research funds Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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

  2. Saito Y, Donohue A, Attai S, Vahdat A, Brar R, Handapangoda I, et al. The syndrome of cardiac tamponade with "small" pericardial effusion. Echocardiography. 2008 Mar. 25(3):321-7. [Medline].

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

  4. Ernst E, Zhang J. Cardiac tamponade caused by acupuncture: a review of the literature. Int J Cardiol. 2011 Jun 16. 149(3):287-9. [Medline].

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

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

  7. Haneya A, Diez C, Kolat P, et al. Re-exploration for bleeding or tamponade after cardiac surgery: impact of timing and indication on outcome. Thorac Cardiovasc Surg. 2015 Feb. 63(1):51-7. [Medline].

  8. Le J, Buth KJ, Hirsch GM, Légaré JF. Does more than a single chest tube for mediastinal drainage affect outcomes after cardiac surgery?. Can J Surg. 2015 Feb 1. 58(1):006814-6814. [Medline].

  9. Cornily JC, Pennec PY, Castellant P, Bezon E, Le Gal G, Gilard M, et al. Cardiac tamponade in medical patients: a 10-year follow-up survey. Cardiology. 2008. 111(3):197-201. [Medline].

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

  11. Roy CL, Minor MA, Brookhart MA, Choudhry NK. Does this patient with a pericardial effusion have cardiac tamponade?. JAMA. April 2007. 297(16):9. [Medline].

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

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

  14. Busko, M. ESC Group Issues Triage Strategy to Manage Cardiac Tamponade. Medscape Medical News. Accessed July 21, 2014.

  15. Ristic AD, Imazio M, Adler Y, et al. Triage strategy for urgent management of cardiac tamponade: A position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2014; DOI:10.1093/eurheartj/ehu217.

  16. Towbin R. The bowed catheter sign: a risk for pericardial tamponade. Pediatr Radiol. 2008 Mar. 38(3):331-5. [Medline].

  17. 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. 2008 Jan-Feb. 32(1):72-7. [Medline].

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

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

  20. Petcu DP, Petcu C, Popescu CF, Bataiosu C, Alexandru D. Clinical and cytological correlations in pericardial effusions with cardiac tamponade. Rom J Morphol Embryol. 2009. 50(2):251-6. [Medline].

  21. Sagristà-Sauleda J, Angel J, Sambola A, Permanyer-Miralda G. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation. 2008 Mar 25. 117(12):1545-9. [Medline].

  22. Motas C, Motas N, Rus O, Horvat T. Left paraxiphoidian approach for drainage of pericardial effusions. Interact Cardiovasc Thorac Surg. 2010 Jan. 10(1):4-5. [Medline].

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

 
Previous
Next
 
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.
A 12-lead electrocardiogram showing sinus tachycardia with electrical alternans. Reproduced with permission from Chest, 1996; 109:825.
Early diastolic collapse of right ventricular free wall (subcostal view).
Early diastolic collapse of right ventricular free wall (parasternal short-axis view at aortic valve).
Late diastolic collapse of right atrium (subcostal view).
Dilated inferior vena cava.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.