Cardiac tamponade is defined as a decompensated form of cardiac compression caused by the accumulation of pericardial effusion and rising intrapericardial pressure.1 Cardiac tamponade may complicate any medical condition associated with pericardial effusion, although it is not synonomous with a large pericardial effusion and has its own specific diagnostic criteria based on hemodynamic and echocardiographic signs. Cardiac tamponade causes obstructive shock and should be regarded as a medical emergency. Medical professionals in the disciplines of surgery, internal and emergency medicine should be familiar with the pathophysiology, clinical presentation, and natural progression of cardiac tamponade to avoid delays in the evaluation and management of this life-threatening condition. Echocardiography is an essential tool for the diagnosis of cardiac tamponade and the evacuation of pericardial fluid. Bedside echocardiography is often performed by intensivists as a part of point of care ultrasonography of critically ill patients; therefore, the recognition of the echocardiographic features of cardiac tamponade is essential for the critical care provider.



In a healthy individual, pericardial pressure is lower than atmospheric pressure and essentially equates to negative intrathoracic pressure. While the pericardium expands to accommodate fluid accumulation over a long period of time, the pericardial space remains constant and fixed at any particular moment. Thus, during systole, pericardial pressure becomes more negative due to the rapid reduction in ventricular size. The lower pericardial pressure combined with the forward flow of blood generated by systolic ventricular contraction contribute to increased venous return to the atria. During diastole pericardial pressure increases due to ventricular expansion, which creates a pressure gradient between the atria and ventricles propelling blood forward and defines a rapid filling diastolic phase. Atrial contraction completes ventricular filling during diastole. Cardiac tamponade occurs when pericardial pressure reaches the point at which diastolic pressures in the cardiac chambers equilibrate, atrioventricular and interventricular “competition” for filling volumes occurs and hemodynamic compromise results.24

First, in late diastole, pericardial pressure exceeds central venous and atrial pressures causing right atrium and caval veins to collapse, thus decreasing right ventricular filling volume. Left atrial collapse is observed in approximately 25% of patients and is a very specific sign of cardiac tamponade.5 When right ventricular contraction occurs, pericardial pressure decreases and relieves right atrial compression. As pericardial fluid accumulates and the intrapericardial pressure continues to rise, even slight additional pressure increases during early diastole cause the right atrium and ventricle to collapse.4 The duration of right atrial collapse at >30% of the cardiac cycle and early diastolic RV collapse both have high specificity (>80%) for cardiac tamponade.6

Interventricular competition appears more prominent as a function of the respiratory cycle. During inspiration, intrathoracic pressure decreases (becomes more negative), accelerating blood flow to the right-sided cardiac chambers. Because pericardial pressure is substantially elevated in the setting of cardiac tamponade, the right ventricle accommodates additional blood volume by invaginating the interventricular septum (IVS) into the left ventricle (LV) (Figure 12-1). This results in a lower LV stroke volume and a reduction in systemic blood pressure during inspiration. During expiration, when intrathoracic pressure increases (becomes less negative) systemic venous return decreases. The right ventricle expands less because it needs to accommodate less volume, which in turn, allows for the restoration of pulmonary venous return to the left-sided cardiac chambers, now causing the IVS to bulge into the right ventricle. This impedes systemic venous return and causes a “vicious cycle” that leads to hemodynamic compromise.7

Figure 12-1

(A) Parasternal long-axis view. Spatial relationship between pleural, pericardial effusions, and descending aorta. Pericardial effusion lies anterior to and pleural fluid is posterior to the descending aorta in supine position. (B) White lines indicate approximate borders of pleural, pericardial effusion, and descending aorta. LV, left ventricle; RV, right ventricle; PCF, pericardial effusion; PLF, pleural effusion; DA, descending aorta; AA, ascending aorta; LA, left atrium.

Epidemiology and Etiology


In a recent retrospective review of 50 patients treated for a large pericardial effusion, Kabukcu et al. identified causative factors in 80% of patients.8 The most common etiology of a large pericardial effusion was cancer (30%) followed up by idiopathic disorders (20%). Other causes included uremia (22%), viral infection (10%), and autoimmune disorders (8%). A small number of cases were attributed to Dressler’s syndrome, tuberculosis, purulent pericarditis, and trauma. In another Europian series, which included 322 patients, the most common causes of a large pericardial effusion were the iatrogenic complications of cardiac surgery or endovascular procedures (14%), cancer and myocardial infarction (each 9%), and chronic renal failure (7%). In this series, however, the most common cause of cardiac tamponade, as opposed to just a large pericardial effusion, was acute idiopathic pericarditis (23%) and not an iatrogenic effusion (only 18%).9 In a retrospective analysis of 4561 patients undergoing open-heart surgery, Joseph et al. found that only 1% of them had moderate to large pleural effusion, with approximately 1/3 of those having features of cardiac tamponade on ultrasound examination.10 The use of anticoagulants in the preoperative period, female gender and valve surgery were associated with a higher risk for the development of pericardial effusion in this patient population. The prevalence of cardiac tamponade in the general ICU population has not been systematically studied. Most of the studies have focused on the presence of pericardial effusion.

Clinical and Laboratory Investigation


Cardiac tamponade is a medical emergency and establishing the diagnosis in a timely manner is of great importance. In many cases, clinicians may identify the underlying disease that led to pericardial fluid accumulation and eventually cardiac tamponade. Soliciting a history of malignancy, recent open-heart surgery or endovascular procedure, uncontrolled hypothyroidism or connective tissue disorder in patients presenting with shock, can help identify important risk factors that contribute to cardiac tamponade. The hemodynamic pattern of cardiac tamponade is obstructive shock. The patient is usually hypotensive and tachycardic with signs of global hypoperfusion, such as an elevated lactate level and end-organ dysfunction. Tachycardia represents a mechanism that allows for the maintenance of cardiac output in the setting of reduced stroke volume. Patients may complain of shortness of breath, chest pain, abdominal discomfort, and dysphagia, likely reflecting visceral congestion.11 Palpitations may also be present. These features, however, are nonspecific; hence, a broad differential diagnosis should be considered.

Beck’s triad was first described in surgical patients who developed acute cardiac tamponade after cardiothoracic procedure by the American surgeon Claude S. Beck in 1935.12 The classic signs of this triad include arterial hypotension, jugular venous distention, and muffled (or distant) heart sounds. Medical patients who accumulate a pericardial effusion over long periods of time may accommodate large fluid volumes in the pericardial space and exhibit tamponade physiology on ultrasound examination with minimal or no symptoms.13 Another valuable finding on physical examination, which may direct clinicians to further investigate for cardiac tamponade is pulsus paradoxus (PP).14 The PP is a reduction of systolic blood pressure (SBP) of >10 mmHg during inspiration. The underlying mechanism for this excessive reduction in SBP represents impaired LV filling during inspiration due to the bowing of the IVS into the LV space, which results in decreased LV stroke volume. As described above, this process relates to increased systemic venous return to the right cardiac chambers during spontaneous inspiration and an inability of the pericardial space to simultaneously accommodate an expanding RV. The term PP is a misnomer since it is not a “paradox” at all and merely represents an accentuation of the process that takes place in healthy individuals. The measurement of PP is documented by deflating the cuff of the sphygmomanometer until the first Korotkoff tone is auscultated, at which point the examiner should notice the tone’s disappearance during inspiration and reappearance during expiration. Then, the cuff is allowed to deflate further until the Korotkoff tone is clearly auscultated during both phases of the respiratory cycle. The difference in SBP between these two points is called the “pulsus paradoxus.” Sometimes substantial reductions in pulse intensity on inspiration can be noticed by simply palpating the pulse of the patient, a sign that was first described by Kussmaul in 1873. While PP is most often described in connection with cardiac tamponade, the differential diagnosis of PP includes other potential causes of obstructive shock, such as a massive pulmonary embolism and tension pneumothorax.

Patients with cardiac tamponade may have an audible pericardial rub contrary to the common belief that a pericardial rub is only present in acute pericarditis.13,15 When larger amounts of fluid accumulate in the pericardial space, the experienced examiner may recognize Ewart’s sign, which is bronchial breathing in the base of the left lung due to the left lower lobe bronchus’s compression by the large pericardial effusion.

Chest x-rays (CXR) lack the necessary sensitivity needed to establish a diagnosis of cardiac tamponade; however, it is sensitive enough to diagnose a large pericardial effusion. In acute “surgical” tamponade, the rapid accumulation of a small amount of fluid may cause tamponade without any changes on CXR. The cardiac silhouette on CXR usually remains unchanged until at least 200 cc of fluid build up in pericardial space. As the pericardial effusion becomes larger, the cardiac shadow on CXR appears more globular in shape. One of the late and specific signs of a large pericardial effusion on CXR is the “fat pad” sign, best visualized on a lateral view of the CXR. This sign signifies a separation of epicardial and retrosternal adipose tissue by the large pericardial effusion.16 One meta-analysis found cardiomegaly on CXR to be associated with a sensitivity of >89% for the diagnosis of cardiac tamponade.17 Pulmonary edema is not a characteristic CXR feature of “medical” cardiac tamponade and should prompt the practitioner to look for alternative explanations.

The electrocardiogram (EKG) should be a part of the critically ill patient’s work up. “Electrical alternans” is the term describing the alternating amplitude of one or more complexes on the EKG. It is a very specific sign of a large pericardial effusion and when >2 waves are involved (QRS, P or T waves), it is a pathognomonic feature of pericardial tamponade.18 Electrical alternans results from alterations of the heart’s electrical axis that occur with every beat due to the large cardiac swings in fluid-filled pericardium (Video 12-4). Other commonly cited EKG signs include low QRS voltage and arrhythmias.

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