Cardiac tamponade

I. What every physician needs to know.

Cardiac tamponade occurs when the heart becomes compressed by fluid or gas within the pericardial space, leading to life-threatening cardiogenic shock. The pericardial space can accommodate a wide range of volumes depending on the rate at which fluid accumulates and the stiffness of the pericardium. As the fluid reaches a critical volume, or the limit of pericardial reserve, the intrapericardial pressure begins to compress the heart chambers. This results in decreased cardiac filling, equalization of diastolic pressures between chambers, and ultimately decreased cardiac output and shock.

Urgent treatment requires removal of the fluid in the pericardial space. A high index of suspicion is required to identify patients at risk for cardiac tamponade such that treatment can be initiated.

II. Diagnostic Confirmation: Are you sure your patient has Cardiac Tamponade?

The signs and symptoms of cardiac tamponade are nonspecific, and the diagnosis relies on the use of Doppler echocardiography. Patients who present without findings consistent with acute decompensated heart failure, such as dyspnea, hypotension, and tachycardia, are less likely to have cardiac tamponade. The Beck triad, characterized by decreasing arterial blood pressure, distant heart sounds, and jugular venous distention, was described in surgical patients with acute cardiac tamponade. This triad cannot be used to reliably rule out a tamponade.

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A. History Part I: Pattern Recognition:

Patients with cardiac tamponade present in a similar fashion to patients with heart failure, and may often be indistinguishable. As such, signs and symptoms of tamponade are nonspecific:

Dyspnea – this is the most sensitive finding

Chest pain


Abdominal pain (secondary to hepatic congestion)

Dysphagia (secondary to esophageal compression)




B. History Part 2: Prevalence:

The etiologies of cardiac tamponade are best determined by the time course of fluid accumulation.

Acute cardiac tamponade is usually due to trauma to the pericardium, either blunt or penetrating. Other acute causes include aortic dissection, free wall rupture after myocardial infarction, and iatrogenic causes during cardiac catheterization, cardiopulmonary resuscitation, or pacemaker placement.

Causes of subacute (or chronic) cardiac tamponade include neoplastic, radiation therapy, uremia, viral pericarditis, connective tissue diseases, and idiopathic.

C. History Part 3: Competing diagnoses that can mimic Cardiac Tamponade.

The presentation of cardiac tamponade is nonspecific and can mimic (or result in) many diseases. The focused differential diagnosis includes congestive heart failure, pulmonary hypertension with right-sided heart failure, pulmonary embolus, aortic dissection, myocardial infarction, and pulseless electrical activity during a cardiac arrest.

D. Physical Examination Findings.

There are three exam findings associated with cardiac tamponade:

Pulses paradoxus (>10 mm Hg)

Tachycardia (>100/min)

Elevated jugular venous pressure (>8 cm H2O)

Pulses paradoxus is defined as a >10 mm Hg difference between the expiratory and inspiratory systolic blood pressures. Using a manual sphygmomanometer, listen for the first Korotkoff sound (this will occur during expiration). It should disappear during inspiration. Then deflate the cuff until the first Korotkoff sound can be heard throughout the respiratory cycle. The difference between these two pressures is the pulses paradoxus. The incidence of pulses paradoxus ranges from 12%-75% in cardiac tamponade. Elevated jugular venous pressure is common in other diagnoses such as heart failure and is neither sensitive nor specific for tamponade. Tachycardia is similar in that it is a common finding in hospitalized patients. Additional exam findings that are found less frequently include distant heart sounds, hypotension (hypertensive tamponade is seen in 27%-43% of patients), pericardial rub, and Kussmaul sign (an increase in jugular venous pressure during inspiration). It is important to note that no physical exam finding or constellation of findings can adequately rule-in or rule-out acute cardiac tamponade.

E. What diagnostic tests should be performed?


1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

There are no laboratory studies helpful for the diagnosis of cardiac tamponade.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

An echocardiogram should always be obtained to confirm the diagnosis of cardiac tamponade. Findings on echocardiography include:

Pericardial effusion

Early diastolic collapse of the right ventricular free wall

Late diastolic collapse of the right atrium

Left atrial collapse (less frequent but highly specific)

Increased ventricular ejection fractions

Dilated inferior vena cava without respiratory variation

Doppler flow velocity paradoxus (marked variation in Doppler velocities with respiration)

Electrocardiogram is typically normal but may shows signs of electrical alternans and low voltages. Chest x-ray typically shows cardiomegaly with a sensitivity of approximately 90%. If echocardiography is unobtainable, computed tomography (CT) of the chest with IV contrast may be performed. Typical findings include pericardial effusion, enlargement of the superior and inferior vena cava, enlargement of the hepatic and renal veins, and the refluxing of contrast into the inferior vena cava. None of these findings alone are helpful, but the constellation of these findings increase the probability of tamponade.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

If an echocardiogram can be obtained, there is no need to obtain a CT of the chest.

III. Default Management.

A. Immediate management.

Once the diagnosis of cardiac tamponade is made, the only treatment with proven benefit is pericardial fluid removal. This can be accomplished with percutaneous pericardiocentesis or with surgical drainage. A percutaneous approach is preferred as it is faster, safer, and usually as effective. It is recommended that the procedure be performed under the guidance of echocardiography, fluoroscopy, or CT, as this significantly reduces complications. Surgical drainage is preferred in patients with loculated pericardial effusions, hemopericardium, or in whom pericardiocentesis is unsuccessful.

Medical management is aimed at supporting cardiac output and decreasing systemic vascular resistance while definitive drainage is being obtained. Dobutamine fulfills this criteria by providing inotropic support without increasing resistance. However, there is no evidence that using dobutamine, with or without vasodilators, improves outcomes. In addition, fluid resuscitation, which is a commonly taught supportive measure, may actually worsen tamponade unless the patient is hypovolemic. Mechanical ventilation with positive airway pressure will decrease cardiac output and should be avoided. Large pleural effusions, if present, may contribute to tamponade physiology, and the patient may benefit from a large-volume thoracentesis.

B. Physical Examination Tips to Guide Management.

After pericardiocentesis or surgical drainage, cardiac output should improve rather quickly. Exam findings that would indicate successful alleviation of cardiac tamponade include normal jugular venous pressure, normotension or hypertension, and resolution of pulsus paradoxus. These exam findings should be monitored periodically to screen for reaccumulation of the pericardial effusion.

C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.

If the etiology of the pericardial effusion is unknown, fluid obtained from drainage should be sent for culture, cytology, viral PCR, and adenosine deaminase (if TB is suspected).

D. Long-term management.

Pericardial effusions can reoccur, often when due to malignancy, with rates ranging from 0-77%. Echocardiography should be performed following the drainage procedure and then again in 24 hours (or for any clinical decompensation) to look for reaccumulation of the fluid. Patients who have a recurrence require either balloon pericardiotomy or surgical intervention (pericardiectomy or pericardial window).

E. Common Pitfalls and Side-Effects of Management.

  • Mechanical ventilation with positive airway pressure will reduce cardiac output in patients with tamponade and should be avoided.

  • Volume resuscitation should not be initiated unless the patient is hypovolemic, as this can increase the pericardial effusion worsening the tamponade.

  • As medical management does not improve outcomes, there should be no delay in draining the pericardial space. For patients who are hemodynamically unstable (cardiogenic shock), bedside pericardiocentesis can be performed with echocardiographic guidance (or with landmark guidance alone, if echocardiography is not readily available).

  • In patients with presumed hemopericardium (trauma, iatrogenesis), cardiothoracic surgery should be urgently consulted as surgical drainage may be necessary (and is often preferred).

  • Pulseless electrical activity (PEA) is often the terminal event in cardiac tamponade, and manual compressions are not effective. Drainage of the pericardial space followed by ACLS should be performed emergently.

IV. Management with Co-Morbidities.

A. Renal Insufficiency.

No change in standard management.

B. Liver Insufficiency.

No change in standard management.

C. Systolic and Diastolic Heart Failure.

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease.

No change in standard management.

E. Diabetes or other Endocrine issues.

No change in standard management.

F. Malignancy.

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

No change in standard management.

J. Hematologic or Coagulation Issues.

Coagulopathy should be corrected in all patients with cardiac tamponade.

K. Dementia or Psychiatric Illness/Treatment.

No change in standard management.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

Frequent blood pressure monitoring to look for hypotension.

Need to repeat the echocardiogram if any clinical decompensation to look for reaccumulation of the pericardial effusion.

Who to contact if repeat pericardiocentesis is required.

B. Anticipated Length of Stay.

There is no accepted length of stay for cardiac tamponade.

C. When is the Patient Ready for Discharge?

Discharge is appropriate in patients who do not have a significant recurrence of the effusion visualized on echocardiogram and remain clinically stable. All attempts should be made to determine the etiology of the effusion prior to discharge in order to initiate treatment to reduce the risk of recurrence.

D. Arranging for Clinic Follow-up.

1. When should clinic follow up be arranged and with whom?

Primary care physician within one week of discharge.

Either Cardiology or Cardiothoracic surgery (whoever was consulted during the admission) within one week of discharge.

2. What tests should be conducted prior to discharge to enable best clinic first visit?

Workup of the etiology of the pericardial effusion should be performed (as described above) prior to discharge.

Pericardial biopsy may also be necessary.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit?

A repeat echocardiogram should be performed prior to their visit to either Cardiology or Cardiothoracic surgery.

E. Placement Considerations.

Patients will not have improved functional status from their baseline after cardiac tamponade, such that they will at least require the same level of support prior to admission. Those with prolonged hospital stays will likely require rehabilitation and may benefit from SNF with daily physical therapy or home physical therapy. Those patients with malignant pericardial effusions despite aggressive treatment of the underlying malignancy have poor outcomes, and hospice should be discussed.

F. Prognosis and Patient Counseling.

After successful drainage of the pericardial effusion and resolution of tamponade physiology, prognosis depends on the etiology of the effusion. Recurrences are common with malignant effusions, and overall can occur up to 77% of the time. Patients who require surgical interventions to prevent reaccumulation have a 30-day mortality of up to 60%. Patients should be counseled to return to the emergency department immediately if they experience similar symptoms to their initial presentation of tamponade.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Patients should receive DVT prophylaxis with pneumatic compression devices on admission. Anticoagulation in cardiac tamponade is an absolute contraindication. Stress ulcer prophylaxis is typically not needed unless the patient requires mechanical intubation, or uses a PPI or H2-receptor blocker prior to admission.

VII. What's the evidence?

Ball, JB, Morrison, WL. “Cardiac tamponade”. Postgrad Med J. vol. 73. 1997. pp. 141-5.

Spodick, DH. “Pathophysiology of cardiac tamponade”. Chest. vol. 113. 1998. pp. 1372-8.

Spodick, DH. “Acute cardiac tamponade”. N. Engl. J. Med. vol. 349. 2003. pp. 684-90.

Fiedler, M, Nelson, LA. “Cardiac tamponade”. Int Anesthesiol Clin. vol. 43. 2005. pp. 33-43.

Roy, CL, Minor, MA, Brookhart, MA. “Does this patient with a pericardial effusion have cardiac tamponade”. JAMA . vol. 297. 2007. pp. 1810-8.

Restrepo, CS, Lemos, DF, Lemos, JA. “Imaging findings in cardiac tamponade with emphasis on CT”. Radiographics. vol. 27. 2007. pp. 1595-610.

Argulian, E, Messerli, F. “Misconceptions andfacts about pericardial effusion and tamponade”. Am J Med. vol. 126. 2013. pp. 858-61.

Chandraratna, PAN, Mohar, DS, Sidarous, PF. “Role of echocardiography in the treatment of cardiac tamponade”. echocardiography. vol. 31. 2014. pp. 899-910.

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