Cardiac Tamponade 

  • Author: Chakri Yarlagadda, MD, FACC, FASNC, FSCAI; Chief Editor: Joseph L Fredi, MD   more...
 
Updated: Aug 11, 2011
 

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.

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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 20-50 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. 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 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[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.

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Epidemiology

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.

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Contributor Information and Disclosures
Author

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

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, Heart Rhythm Society, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

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

Amer Suleman, MD  Private Practice

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

Joseph L Fredi, MD  Assistant Professor of Medicine, Director of Acute MI Program, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center

Joseph L Fredi, MD is a member of the following medical societies: American College of Cardiology and American College of Physicians

Disclosure: Nothing to disclose.

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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
 
 
 
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