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Definition, Etiology, PathogenesisTop
Cardiac tamponade represents the most severe and urgent clinical presentation of pericardial effusion. It occurs when pericardial fluid accumulation exceeds the elastic limit of the pericardium, resulting in significantly elevated intrapericardial pressures. Cardiac tamponade is a life-threatening condition resulting from a slow or more rapid compression of cardiac chambers due to the accumulation of pericardial inflammatory/malignant exudates, pus, blood, clots, or gas.
1) Pericarditis (eg, idiopathic; viral; other infectious, including tuberculous pericarditis in developing countries where tuberculosis is endemic).
2) Iatrogenic (eg, invasive procedure–related, as in the case of complications related to percutaneous coronary intervention, atrial fibrillation ablation, pacemaker lead insertion; postpericardiotomy syndrome after cardiac surgery).
3) Neoplasm/malignancy (eg, metastatic breast or lung cancer, lymphoma, melanoma).
5) Systemic autoimmune disease (eg, systemic lupus erythematosus, rheumatoid arthritis, scleroderma).
6) Post–myocardial infarction.
10) Aortic dissection.
Clinical Features and Natural HistoryTop
1. Symptoms: Dyspnea; reduced exercise tolerance; sometimes cough, dysphagia, syncope or presyncope.
2. Signs: Most common signs include tachycardia (in patients with hypothyroidism or uremia it may be absent), pulsus paradoxus with a systolic arterial pressure drop >10 mm Hg with inspiration, an enlarged cardiac silhouette on chest radiography (before pericardiocentesis: Figure 3.5-1; after pericardiocentesis: Figure 3.5-2), and jugular venous distention. Other signs include diminished or muffled heart sounds, hypotension, and tachypnea.
3. Natural history: Slowly accumulating effusions cause gradual distension of the pericardium, which allows the accumulation of large pericardial effusions (often ≥1 L). In the case of rapidly accumulating effusions or reduced pericardial elasticity, the intrapericardial pressures increase promptly and lead to cardiac tamponade with as little as a few hundred mL of fluid. Cardiac tamponade can lead to obstructive shock and cardiac arrest.
1. Electrocardiography (ECG) may occasionally be normal but usually reveals sinus tachycardia. Other potential findings include low QRS voltage (<5 mm in limb leads and <10 mm in precordial leads) and/or electrical alternans of the QRS complex (Figure 3.5-3). The end-stages of tamponade are associated with bradycardia, and death is due to pulseless electrical activity (PEA).
2. Chest radiography: Enlargement of the cardiac silhouette without features of pulmonary congestion. In patients with acute cardiac tamponade, the cardiac silhouette may be normal.
3. Echocardiography is the key diagnostic study for evaluating cardiac tamponade, as recognizing tamponade ultimately remains a clinical diagnosis. In those suspect of having pericardial tamponade, an echocardiogram should be performed without delay. Transthoracic echocardiography can evaluate for the presence of pericardial fluid, and if present, evaluate the size (>20 mm is considered large [Figure 3.5-4]) and hemodynamic consequences. Echocardiographic signs of tamponade physiology include:
1) Late diastolic and early systolic right atrial collapse.
2) Early diastolic right ventricular free wall collapse (this may be absent in patients with a marked right ventricular hypertrophy or elevated right ventricular diastolic pressures).
3) A “swinging heart” within pericardial fluid.
4) Dilation of the inferior vena cava (with loss of the inspiratory collapse).
5) Doppler echocardiography shows exaggerated respiratory variability in mitral and tricuspid inflow velocity.
4. Computed tomography (CT) reveals pericardial effusion. In patients with chylopericardium it may help to locate a connection between the thoracic duct and the pericardium (especially when combined with lymphography).
5. Analysis of the pericardial fluid is used in case of equivocal etiology.
Cardiac tamponade is diagnosed on the basis of clinical features and imaging studies, mainly echocardiography.
Clinical signs of cardiac tamponade should be differentiated from acute right ventricular myocardial infarction and other causes of right ventricular dysfunction.
1. IV fluid bolus may be attempted to temporize (this is not a substitute for definitive treatment); however, only ~50% of patients will have a favorable stroke volume/hemodynamic response to fluid loading.
2. Pericardiocentesis is a life-saving procedure in those with clinical/echocardiographic pericardial tamponade (note that large pericardial effusions do not always cause tamponade, and therefore a clinical and hemodynamic assessment is required). Needle pericardiocentesis with or without pericardial tube insertion using echocardiographic guidance is the preferred method of pericardial fluid drainage if technically feasible.
3. Surgical approaches can be considered if effusion is not amenable to percutaneous needle drainage as well as in case of purulent effusions, recurrent effusions from malignancy requiring pericardial window creation, or hemopericardium with clotted blood.
4. Treatment of chylopericardium depends on the etiology and volume of the lymph in the pericardium. In patients in whom chylopericardium is a postoperative complication, use pericardiocentesis and a diet containing medium-chain triglycerides. If the lymph continues to accumulate, use surgical treatment.
Figure 3.5-1. Chest radiograph of a patient with cardiac tamponade before pericardiocentesis. Figure courtesy of Dr Craig Ainsworth, McMaster University, Hamilton, Canada.
Figure 3.5-2. Chest radiograph of a patient with cardiac tamponade after pericardiocentesis. Figure courtesy of Dr Craig Ainsworth, McMaster University, Hamilton, Canada.
Figure 3.5-3. Electrical alternans of the QRS complex in a patient with cardiac tamponade. Figure courtesy of Dr Craig Ainsworth, McMaster University, Hamilton, Canada.
Figure 3.5-4. Transthoracic echocardiogram showing the apical 4-chamber view and a large pericardial effusion. Figure courtesy of Dr Craig Ainsworth, McMaster University, Hamilton, Canada.