Cardiac Tamponade

Ahmed S. Mohamed, M.D.
Aravind Rao Kokkirala, M.D.

Basic Information

Definition

Cardiac tamponade is a life-threatening condition where an accumulation of fluid within the pericardial sac causes equal elevation of atrial, end diastolic pressures in the ventricles, and pericardial pressures, as well as an exaggerated inspiratory decrease in arterial systolic pressure (pulsus paradoxus) along with arterial hypotension.

ICD-10CM CODES
I31.4	Cardiac tamponade

Physical Findings & Clinical Presentation

•

Tachypnea/dyspnea
•

Chest pain may be present
•
Beck’s triad
1. 1.
  
  Absolute or relative hypotension
2. 2.
  
  Elevated jugular venous pressure (with prominent x descent and blunted y descent)
3. 3.
  
  Muffled heart sounds
•

Tachycardia (except in uremia or hypothyroid patients)
•

Pulsus paradoxus (decrease in systolic arterial pressure of 10 mm Hg or more during normal inspiration while in normal sinus rhythm)
•

Pericardial friction rub may be heard in patients with cardiac tamponade due to inflammatory pericarditis.
•

Reduced or absent apical cardiac impulse

Etiology

I.
Acute (rapidly accumulating pericardial effusion leading to cardiac tamponade): does not need a large amount of effusion to cause tamponade; rather, it is the rapidity of fluid accumulation that leads to clinical tamponade. Clinical presentation typically resembles that of cardiogenic shock requiring urgent reduction of pericardial pressure. Causes for acute cardiac tamponade include:
1. 1.
  
  Penetrating trauma
2. 2.
  
  Aortic dissection (more commonly in Type A)
3. 3.
  
  Postinfarction myocardial rupture and/or hemorrhagic pericarditis
4. 4.
  
  Iatrogenic (central line and pacemaker insertions, cardiac ablation, post–coronary bypass surgery or post–percutaneous coronary intervention)
II.
Subacute or chronic: occurs over days to weeks, and the effusion is usually large; causes include the following:
1. 1.
  
  Malignancy (e.g., lung, breast, lymphoma)
2. 2.
  
  Viral pericarditis (e.g., Coxsackie, human immunodeficiency virus, enterovirus, HSV 6, parvovirus, etc.)
3. 3.
  
  Bacterial, fungal, or tuberculous pericarditis
4. 4.
  
  Uremia
5. 5.
  
  Hypothyroidism/myxedema (rare)
6. 6.
  
  Collagen vascular disease (e.g., lupus, rheumatoid arthritis, scleroderma)
7. 7.
  
  Radiation
8. 8.
  
  Post–myocardial infarction or post–cardiac ablation inflammation
9. 9.
  
  Idiopathic
III.

Regional cardiac tamponade occurs when the localized or loculated hematoma compresses only selected cardiac chambers.

Diagnosis

Cardiac tamponade is a clinical diagnosis made at the bedside from history and physical examination. The echocardiogram will help confirm or reject the clinical diagnosis. Tamponade can be confirmed invasively by the measurement of elevated intrapericardial pressures with an intrapericardial catheter and right-sided heart catheterization. Typical findings are diastolic equalization of pressures, usually ranging from 10 to 30 mm Hg (diastolic pulmonary artery pressure = right ventricular diastolic pressure = right atrial pressure = intrapericardial pressure), and lowering of the intrapericardial pressure with fluid drainage. Thereafter, the underlying etiology must be determined with specific laboratory work (see “Laboratory Tests”).

Differential Diagnosis

Other conditions that can also lead to elevated jugular venous pressure, decreased systemic pressure, and pulsus paradoxus include:

•

Chronic obstructive pulmonary disease and asthma exacerbations

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Constrictive pericarditis (Table 1)

TABLE1 Hemodynamics in Cardiac Tamponade and Constrictive PericarditisFrom Fuhrman BP, et al.: Pediatric critical care, ed 4, Philadelphia, 2011, Saunders.

	Tamponade	Constriction
Paradoxical pulse	Usually present	Present in ∼1/3
Equal left- and right-sided filling pressures	Present	Present
Systemic venous wave morphology	Absent y descent	Prominent y descent (M or W shape)
Inspiratory change in systemic venous pressure	Decrease (normal)	Increase or no change (Kussmaul sign)
“Square root” sign in ventricular pressure	Absent	Present

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Restrictive cardiomyopathy
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Right ventricular infarction
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Pulmonary embolism
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Chronic biventricular heart failure

Laboratory Tests

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Electrolytes, blood urea nitrogen, creatinine, erythrocyte sedimentation rate, thyroid function tests, antinuclear antibody, rheumatoid factor, PPD, blood cultures, viral titers, and pericardial fluid analysis including cytology and cultures
•
Possible 12-lead ECG findings:
1. 1.
  
  Sinus tachycardia
2. 2.
  
  PR depression and/or diffuse ST elevations if acute pericarditis is present
3. 3.
  
  Electrical alternans (beat to beat alternations in the QRS complex heights) (Fig. E1)
  
  FIG.E1
  
  Total electrical alternans (P-QRS-T) caused by pericardial effusion with tamponade.
  
  This finding, particularly in concert with sinus tachycardia and relatively low voltage, is a highly specific, although not sensitive, marker of cardiac tamponade.
  
  From Bonow RO: Heart disease, ed 9, Philadelphia, 2012, Saunders.
4. 4.
  
  Low QRS voltage in patients with a pericardial effusion may be a specific manifestation of cardiac tamponade, not of the effusion (QRS complex <0.5 mV in the limb leads and <1.0 mV in precordial leads)

Imaging Studies

•

Chest radiograph (enlarged cardiac silhouette with clear lung fields) (Fig. 2)

FIG.2

Massive pericardial effusion and tamponade.

This 23-year-old male has a history of aortic valve replacement for infective endocarditis. He presented with increased chest pain and dyspnea. His chest x-ray shows a globular cardiac silhouette, suggesting a large pericardial effusion. The lung fields and right costophrenic angle appear clear, although the left costophrenic angle is hidden behind the heart and cannot be assessed. The patient underwent chest computed tomography to evaluate his aorta, as he complained of severe interscapular pain as well (see Fig. 3).

From Broder JS: Diagnostic imaging for the emergency physician, Philadelphia, 2011, Saunders.
•

Chest CT (may overestimate size of the effusion) (Fig. 3)

FIG.3

Massive pericardial effusion.

Same patient as Fig. 2. The patient underwent chest computed tomography (CT) without (A) and then with (B) intravenous contrast to evaluate his aorta, which was normal. However, the CT confirmed a massive pericardial effusion surrounding a normal-appearing heart. Without contrast, note that fluid blood within the chambers of the heart has a slightly lower density than the pericardial effusion, which has a density more similar to that of myocardium. When contrast is administered, the ventricular chambers fill completely, and the myocardium enhances and becomes somewhat brighter than the surrounding pericardial effusion. The heart itself is outlined by a thin stripe of fat, which appears nearly black on soft tissue windows. The patient developed hypotension, suggesting cardiac tamponade, and pericardial window was performed for drainage of the effusion. In the operating room, the effusion was found to be coagulated blood.

From Broder JS: Diagnostic imaging for the emergency physician, Philadelphia, 2011, Saunders.
•
Echocardiogram findings (Fig. 4):
1. 1.
  
  Pericardial effusion
2. 2.
  
  Diastolic collapse of the right atrium in late diastole (during atrial relaxation) is virtually 100% sensitive but has low specificity.
3. 3.
  
  Diastolic collapse of the right ventricle (early diastole) is pathognomonic and very specific.
4. 4.
  
  >30% mitral and >60% tricuspid valve inflow variation on the first beat of inspiration and expiration, respectively
5. 5.
  
  Plethoric inferior vena cava (IVC dilation and <50% decrease in the diameter of the IVC during inspiration)
6. 6.
  
  Left atrial collapse (high specificity)
FIG.4

Two-dimensional echocardiogram of a large, circumferential pericardial effusion (PE).

Ao, Aorta; LV, left ventricle; RV, right ventricle.

From Kabbani SS, LeWinter M: Cardiac constriction and restriction. In Crawford MH, DiMarco JP, [eds]: Cardiology, St Louis, 2001, Mosby.
•

Cardiac catheterization as discussed earlier will see equalization of intracardiac diastolic pressures and increase of right-sided pressures and reduction of left-sided pressures, which subsequently causes pulsus paradoxus (the pathognomonic finding on physical examination)

Treatment

Nonpharmacologic Therapy

•

Cardiac tamponade should be treated emergently with removal of the pericardial fluid.
•

Avoid drugs that reduce preload (e.g., nitrates, diuretics).
•

Large pericardial effusions without hemodynamic compromise (tamponade) can be managed conservatively with careful monitoring, IV fluids, treatment of the underlying cause, clinical follow-up, and frequent serial surveillance echocardiography.

Acute General Rx

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Aggressive intravascular volume expansion (saline or blood).
•

Emergency pericardial fluid removal by pericardiocentesis or surgical pericardiotomy by way of the subxiphoid pericardial window.
•

Pericardiocentesis should be performed under fluoroscopic or echocardiographic guidance when available.
•

Pericardiocentesis is an absolute contraindication if the etiology of the pericardial effusion is aortic dissection, wherein emergent surgical management is indicated.
•

Inotropic or vasopressor support if above measures cannot be performed immediately.

Chronic Rx

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Depends on etiology. Patients with inflammatory causes of pericarditis leading to effusion should be treated with an extended course of colchicine.
•

Pericardiocentesis with draining catheter: the catheter can be left inside the pericardium to allow continued drainage for 24 to 48 hr. If residual fluid still persists with hemodynamic compromise, surgical drainage should be considered. In the absence of hemodynamic compromise or significant residual fluid, discontinuation of the draining catheter can be done with periodic postprocedure echocardiographic monitoring for re-accumulation (e.g., 24 hr, 7 days, 30 days, 3 mo, 6 mo, 12 mo) depending on the etiology and the rate of reaccumulation.
•
Other surgical drainage procedures include:
1. 1.
  
  Subxiphoid pericardiotomy drainage
2. 2.
  
  Pericardial window; draining the pericardial fluid into the left hemithorax
3. 3.
  
  Limited pericardiectomy
4. 4.
  
  Complete pericardiectomy, especially in patients with effusive-constrictive pericarditis, bacterial pericarditis, or tuberculous pericarditis. (see “Pearls & Considerations”)

Disposition

The prognosis of cardiac tamponade depends on the underlying cause.

Referral

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Emergent cardiology consultation along with thorough echocardiographic exam should be made if cardiac tamponade is suspected.
•

Cardiothoracic surgery or interventional cardiology consultation should also be considered if pericardial drainage is indicated.

Pearls & Considerations

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Cardiac tamponade should always be considered during pulseless electrical activity arrest and may require emergent pericardiocentesis at the bedside.
•

Evaluation for pulsus paradoxus should always be performed during normal respiration because deep inspiration may render a false-positive finding.
•

Strong consideration should be given to performing early pericardiocentesis in patients who have pericardial effusion associated with bacterial pneumonia or empyema because the incidence of bacterial pericarditis is especially high in this clinical situation and the subsequent development of cardiac tamponade and severe chronic constrictive pericarditis are ominous complications.
•

Pericardiocentesis is an absolute contraindication if the etiology of the pericardial effusion is due to aortic dissection extending into the pericardial sac.
•

As little as 100 ml of fluid can lead to acute cardiac tamponade if the rate of accumulation is rapid, whereas with gradual accumulation, the pericardial sac can hold up to 5 L of fluid before tamponade occurs.
•

With effusions that are small, organized, and/or loculated, needle aspiration should generally be avoided. An exception is acute cardiac tamponade complicating a cardiac procedure (e.g., percutaneous coronary intervention) with anticoagulation. In this setting, the effusion is often small, but pericardial pressure rises very quickly, resulting in hemodynamic compromise.

Ferri – Cardiac Tamponade