Cardiac tamponade

INTRODUCTION — The pericardium is a fibroelastic sac surrounding the heart that contains a thin layer of fluid. A pericardial effusion is considered to be present when accumulated fluid within the sac exceeds the small physiologic amount (15 to 50 mL). Cardiac tamponade results from pericardial fluid accumulating under pressure, impairing cardiac filling and reducing stroke volume.

The pathophysiology, clinical presentation, diagnosis, and treatment of cardiac tamponade will be reviewed here. A general approach to pericardial effusion is discussed separately. (See "Pericardial effusion: Approach to diagnosis".)

PATHOPHYSIOLOGY — In cardiac tamponade, the primary abnormality is compression of cardiac chambers due to increased pericardial pressure exceeding cardiac filling (diastolic) pressures [1,2]. When there is free-flowing pericardial fluid, this compression may affect all cardiac chambers. Pericardial adhesions or organization of the pericardial fluid can result in localized and, thus, atypical cardiac tamponade.

The pericardium has some degree of elasticity, but once the elastic limit is reached, the heart must compete with intrapericardial fluid for the fixed intrapericardial volume. As cardiac tamponade progresses, chamber diastolic compliance is reduced with the following consequences:

●Progressive decline in systemic venous return – Venous return is normally bimodal, with peaks during ventricular systole and early diastole. The effusion produces compression throughout the cardiac cycle, and cardiac volume is smallest during ejection. Thus, as cardiac tamponade becomes more severe, venous return is progressively shifted to systole as the peak associated with early diastolic filling diminishes. When cardiac tamponade is very severe, total venous return falls, the cardiac chambers shrink, stroke volume declines, and blood pressure falls.

●Enhanced ventricular interdependence – Inspiratory decline in thoracic pressure is transmitted through the pericardium to the right side of the heart and the pulmonary vasculature. As a result, systemic venous return to the right heart increases with inspiration, and pulmonary venous return to the left heart decreases with inspiration. Under normal conditions, the right ventricle (RV) expands with little impact on left heart volume.

In cardiac tamponade, the effective compliance of cardiac chambers is limited to that of the tightly stretched pericardium. The ensuing distension of the RV is limited to the interventricular septum, which along with relative underfilling of the left ventricle causes the septum to bulge to the left, reducing left ventricular compliance and contributing to further decreased filling of the left ventricle during inspiration. This concept is referred to as "ventricular interaction" or "ventricular interdependence." (See "Pulsus paradoxus in pericardial disease".)

The pericardial effusion volume at which cardiac tamponade occurs depends on the rate of pericardial fluid accumulation and pericardial compliance (which is impacted by pericardial scarring and inflammation), which are related to the underlying cause of pericardial effusion [1,3]. As examples:

●Rapid accumulation – Acute bleeding (eg, due to traumatic cardiac rupture or perforation) into the pericardial sac can rapidly lead to cardiac tamponade with a small pericardial effusion. As intrapericardial volume increases, there is an initial small increase in intrapericardial pressure followed by an almost vertical ascent (figure 1).

●Gradual accumulation – By comparison, subacute or chronic accumulation of a pericardial effusion (eg, due to renal failure or malignancy) allows the pericardial compliance to increase gradually. As a result, intrapericardial pressure increases more slowly until a critical point is reached when an almost vertical ascent is again seen (figure 1). In this setting, cardiac tamponade may not occur until 2 liters or more have accumulated.

Once the pericardium can no longer stretch, very little fluid needs to accumulate to produce cardiac tamponade (figure 1) [1]. At this point, the initial removal of fluid during pericardiocentesis produces the largest reduction in intrapericardial pressure.

ETIOLOGY — The causes of cardiac tamponade include all of the causes of pericardial effusion or hemorrhage into the pericardium, including iatrogenic causes (table 1 and table 2). Cardiac tamponade occurs more frequently in patients with identifiable causes of pericardial effusion than in patients with idiopathic pericardial disease. As an example, in one series, cardiac tamponade occurred in 61 percent of those with neoplastic, tuberculous, or purulent pericarditis and in 14 percent of patients with idiopathic pericarditis [4]. (See "Etiology of pericardial disease" and "Pericardial disease associated with cancer: Clinical presentation and diagnosis" and "Tuberculous pericarditis".)

In a series of 340 patients with cardiac tamponade, the most common etiologies were complications of invasive percutaneous cardiac procedures (33 percent), postpericardiotomy syndrome (>7 days after cardiac surgery; 23 percent), neoplasm (15 percent). inflammatory processes (pericarditis associated with connective tissue disease, infectious, or noninfectious conditions; 12.5 percent), complications of cardiac surgery (9 percent), uremia (2 percent), and acute myocardial infarction (1.5 percent) [5]. Other causes included aortic dissection, post-myocardial infarction syndrome, radiation, chest trauma, and coagulopathy. Only three cases were deemed to have no known cause. The largest volumes of pericardial fluid drainage were in patients with post-myocardial infarction syndrome, uremic, and neoplastic etiologies. (See "Post-cardiac injury syndromes" and "Overview of the management of chronic kidney disease in adults", section on 'Pericarditis' and "Pericardial disease associated with cancer: Clinical presentation and diagnosis".)

In a Swedish nationwide registry study, among 44,497 patients undergoing 58,770 invasive electrophysiology procedures, 200 patients experienced a procedure-related cardiac tamponade (procedural risk of 0.34 percent) [6]. During five-year follow-up, iatrogenic cardiac tamponade was associated with an increased risk of hospitalization for pericarditis but no association with mortality rate or other adverse cardiovascular outcomes.

In a 15-year, single-center experience of 5222 catheter ablations of atrial fibrillation (3483 patients), cardiac tamponade complicated 51 procedures (1 percent) [7]. No clinical factors were associated with cardiac tamponade, but it occurred less often after cryoablation than radiofrequency ablation.

Cardiac tamponade has been described in less than 1 percent of patients with an acute myocardial infarction treated with fibrinolytic therapy; the risk may be lower in patients treated with percutaneous coronary intervention. The two major mechanisms are left ventricular free wall rupture and hemorrhagic pericarditis [8]. Cardiac tamponade is a frequent complication of type A aortic dissection, occurring in 19 percent of patients in an international registry [9]. (See "Pericardial complications of myocardial infarction", section on 'Clinical presentation and diagnosis' and "Clinical features and diagnosis of acute aortic dissection".)

A systematic review of pericarditis associated with coronavirus disease 2019 (COVID-19) included 34 patients and reported pericardial effusions in 76 percent and cardiac tamponade in 35 percent [10].

CLINICAL PRESENTATION

History — Patients with cardiac tamponade commonly have an apparent cause such as a complication of invasive procedures (eg, invasive electrophysiologic or catheter-based procedures or cardiac surgery), traumatic injury, or conditions such as cancer, myocardial infarction, aortic dissection, or infection. However, some patients require additional evaluation to identify the cause. (See "Pericardial effusion: Approach to diagnosis", section on 'Identifying the etiology'.)

Symptoms in patients with cardiac tamponade include chest pain, dyspnea, fatigue, syncope, and presyncope.

Physical findings — Patients with cardiac tamponade commonly have one or more characteristic signs (particularly tachycardia and elevated jugular venous pressure). Physical signs vary depending upon the type and severity of cardiac tamponade, although none of the findings alone are highly sensitive or specific for the diagnosis [11]. (See 'Types of cardiac tamponade' below.)

The combination of signs known as Beck triad, namely low arterial blood pressure, dilated neck veins, and muffled heart sounds, are all present in only a minority of cases of acute cardiac tamponade [12].

Tachycardia and hypotension — Sinus tachycardia is seen in nearly all patients with cardiac tamponade, while hypotension (an ominous sign suggesting failure of tachycardia to compensate for decreased stroke volume) is more variably present. In the setting of cardiac tamponade, sinus tachycardia is a compensation for hemodynamic compromise and should prompt urgent pericardial fluid drainage, even if hypotension has not yet developed.

However, tachycardia may not be present when the underlying disease is associated with bradycardia, as with a pericardial effusion and subacute cardiac tamponade associated with hypothyroidism. Tachycardia also may not be seen in some patients with early cardiac tamponade even though they have other signs of a hemodynamically significant effusion, such as an elevated jugular venous pressure.

Elevated jugular venous pressure — The jugular venous pressure is almost always elevated in cardiac tamponade and may be associated with venous distension in the forehead and scalp. The x descent is preserved, while the y descent is attenuated or absent because of the limited or absent late diastolic filling of the ventricle. (See "Examination of the jugular venous pulse", section on 'Estimating right atrial pressure' and "Examination of jugular venous waveforms", section on 'Abnormalities of the y-descent'.)

However, absence of jugular venous pressure does not exclude cardiac tamponade. Some patients with severe hypovolemia have low-pressure cardiac tamponade and do not have elevated jugular venous pressure, as described above (See 'Low-pressure cardiac tamponade' below.)

Kussmaul sign (the absence of a decline or increase in jugular venous pressure with inspiration) is seen in a variety of cardiovascular disorders with elevated jugular venous pressure but is rarely identified in patients with cardiac tamponade. (See "Examination of the jugular venous pulse", section on 'Respirophasic changes (Kussmaul sign)'.)

Pulsus paradoxus — Pulsus paradoxus, defined as an abnormally large decrease in systolic blood pressure (>10 mmHg) on inspiration, is a common finding in moderate to severe cardiac tamponade and is the direct consequence of ventricular interdependence. The limitation on outward expansion of the RV as blood flows in during inspiration, along with relative underfilling of the left ventricle during inspiration, results in bulging of the interventricular septum into the left ventricle. Both the bulging of the interventricular septum and the reduction in left ventricular filling contribute to a large decrease in stroke volume (waveform 1 and waveform 2 and waveform 3) [13,14].

However, not all patients with cardiac tamponade have pulsus paradoxus (eg, those with chronic hypertension leading to elevated ventricular diastolic pressures, those with a coexistent atrial septal defect, or those with aortic insufficiency), and the finding of pulsus paradoxus is not specific for cardiac tamponade. (See "Pulsus paradoxus in pericardial disease".)

Other signs — Patients with cardiac tamponade may have other physical signs related to the cause of pericardial effusion. As an example, a fever may be present in patients with an infectious etiology.

A pericardial rub is a sign of acute pericarditis that is heard in some patients with pericardial effusion caused by inflammatory pericarditis (movie 1) (see "Acute pericarditis: Clinical presentation and diagnosis"). Although some have postulated that a pericardial rub may be generated by friction between the visceral and parietal layers of the pericardium, the presence of a rub does not correlate with the size of pericardial effusion and a rub is present in some patients with cardiac tamponade [15,16].

Types of cardiac tamponade — The clinical manifestations of cardiac tamponade depend largely upon the length of time over which pericardial fluid accumulates and the clinical setting. The following types of cardiac tamponade differ in acuity, intravascular volume status, and distribution of tamponade.

Acute cardiac tamponade — Acute cardiac tamponade occurs within minutes and causes cardiogenic shock requiring urgent intervention with pericardial fluid drainage [17]. Causes include traumatic rupture of the heart or aorta, aortic dissection, or a cardiac or coronary artery perforation caused by an invasive procedure. Symptoms may include chest pain, dyspnea, and tachypnea. The jugular venous pressure is markedly elevated and may be associated with venous distension in the forehead and scalp. The heart sounds are often muted. (See 'Management' below and "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Cardiac injury'.)

Hypotension, narrow pulse pressure, and tachycardia are common due to the decline in cardiac output. Patients in cardiogenic shock typically have cool extremities, peripheral cyanosis, and decreased urine output. As noted above, the pericardial effusion in such patients is usually small because the pericardium is inelastic in the setting of acute pericardial fluid accumulation (figure 1). (See 'Pathophysiology' above.)

Subacute cardiac tamponade — Subacute cardiac tamponade occurs over days to weeks with causes including neoplastic, uremic, and idiopathic pericarditis. Patients may be asymptomatic early in the course, but once intrapericardial pressure reaches a critical value, they complain of dyspnea, chest discomfort or fullness, peripheral edema, fatigability, or other symptoms referable to increased filling pressures and limited cardiac output.

The physical examination in subacute severe cardiac tamponade may reveal hypotension with a narrow pulse pressure, reflecting the limited stroke volume. However, patients with preexisting hypertension may remain hypertensive due to increased sympathetic activity in the setting of cardiac tamponade.

Low-pressure cardiac tamponade — Low-pressure (occult) cardiac tamponade is a subset of subacute cardiac tamponade that occurs in patients who are severely hypovolemic. Patients who are severely hypovolemic (due to causes such as traumatic hemorrhage, hemodialysis or ultrafiltration, or overdiuresis) may have low-pressure cardiac tamponade in which symptoms of tamponade such as fatigue may be present but the intracardiac and pericardial diastolic pressures are only 6 to 12 mmHg, so jugular venous distension may be absent [1]. The hemodynamic significance of these effusions can be demonstrated on echocardiography by right heart chamber collapse and respiratory variations in transvalvular flows. A fluid challenge with a rapid infusion of 1 liter of isotonic saline in the catheterization laboratory will usually elicit typical cardiac tamponade hemodynamics.

The clinical characteristics of low-pressure cardiac tamponade were illustrated in a series of 279 patients who underwent combined pericardiocentesis and cardiac catheterization [18]. Patients were considered to have cardiac tamponade if intrapericardial pressures were equal to right atrial (RA) pressure prior to pericardiocentesis. Among 143 patients with cardiac tamponade, low-pressure cardiac tamponade was diagnosed in 29 patients who had an initial intrapericardial pressure <7 mmHg and an RA pressure after pericardiocentesis <4 mmHg. The following findings were noted:

●Clinical findings commonly associated with cardiac tamponade (eg, elevated heart rate, jugular venous distention, and pulsus paradoxus) were significantly less common in low-pressure cardiac tamponade than in classic cardiac tamponade. (See 'Physical findings' above.)

●Echocardiographic abnormalities (eg, size of the pericardial effusion, right sided chamber collapse, and exaggerated respiratory changes in mitral and tricuspid valve flow) were similar in frequency and magnitude to patients with classic cardiac tamponade. (See 'Echocardiography' below.)

●The spectrum of etiologies was similar to patients with classic cardiac tamponade. (See 'Etiology' above.)

Regional cardiac tamponade — Regional cardiac tamponade occurs when a loculated, eccentric pericardial effusion or hematoma produces tamponade in which at least one but not all cardiac chambers are compressed. As a result, the typical physical, hemodynamic, and echocardiographic signs of cardiac tamponade, including pulsus paradoxus, diastolic pressure equalization, and chamber compression in standard apical and parasternal views, may be absent or attenuated in some cases.

Regional cardiac tamponade is most often seen after pericardiotomy (eg, after cardiac surgery), aortic dissection, iatrogenic myocardial or coronary perforation, or myocardial infarction with rupture. Clinical suspicion should be heightened in these settings. Establishing the diagnosis by echocardiography is challenging and may require additional echocardiographic views (eg, subcostal or transesophageal), other advanced imaging techniques (eg, computed tomography [CT]), and, in some cases, surgical exploration. (See 'Limitations' below.)

Initial tests — Patients suspected of having cardiac tamponade should be evaluated with an electrocardiogram (ECG), echocardiogram, and chest radiograph; urgent echocardiography may be the initial test in unstable patients with a high suspicion for cardiac tamponade.

Electrocardiogram — The ECG in patients with cardiac tamponade typically shows sinus tachycardia and may also show low voltage. If pericarditis is present, the ECG findings typical of that disorder are also seen (waveform 4). (See "Pericardial effusion: Approach to diagnosis", section on 'ECG findings'.)

While the frequency of low voltage is higher among patients with cardiac tamponade than among patients with pericardial effusion without tamponade, the presence of low voltage is not specific for tamponade. In a study of ECG findings in 224 patients with moderate or large pericardial effusion, low voltage in limb and/or precordial leads was present in 66 percent of patients with cardiac tamponade and in 34 percent of patients without cardiac tamponade [19]. Low voltage is more common with moderate or large pericardial effusions than with small effusions (eg, 83 versus 13 percent in one series [20]).

Electrical alternans is characterized by beat-to-beat alterations in the QRS complex and, in some cases, other electrocardiographic waves that reflect the swinging of the heart in the pericardial fluid (waveform 5 and movie 2). Electrical alternans with sinus tachycardia is a highly specific sign of pericardial effusion, usually with cardiac tamponade, but is only modestly sensitive. As a result, its absence does not exclude cardiac tamponade. In the above-cited study of ECG findings in 224 patients with moderate or large pericardial effusion, electrical alternans was observed in 35 percent of patients with cardiac tamponade and in only 7 percent of patients without tamponade [19]. (See "ECG tutorial: Miscellaneous diagnoses", section on 'Electrical alternans'.)

Chest radiograph — In general, the findings on a chest radiograph are neither sensitive nor specific for the diagnosis of cardiac tamponade. A chest radiograph showing an enlarged cardiac silhouette with clear lung fields may be seen in slowly developing cardiac tamponade (image 1) [11]. Cardiomegaly is not usually seen in acute cardiac tamponade since at least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges [1]. A chest radiograph may identify concomitant conditions (eg, pleural effusion, mediastinal mass) that may or may not be related to the cause of tamponade.

Rare case reports suggest that a large pleural effusion (without pericardial effusion) can compress cardiac chambers and cause cardiac tamponade [21].

Echocardiogram — Echocardiographic findings of cardiac tamponade are discussed below. (See 'Echocardiography' below.)

DIAGNOSIS

When to suspect tamponade — Cardiac tamponade is associated with a variety of abnormalities that lead to changes on the ECG, chest radiograph, and echocardiogram. The diagnosis is suspected in patients with characteristic symptoms (such as fatigue, dyspnea, syncope, presyncope) and signs (sinus tachycardia, elevated jugular venous pressure, pulsus paradoxus, hypotension). (See 'History' above and 'Physical findings' above.)

Diagnostic criteria — The following clinical triad highly suggests a diagnosis of cardiac tamponade:

●Symptoms, signs, and/or ECG findings suggestive of cardiac tamponade (See 'History' above and 'Physical findings' above and 'Electrocardiogram' above.)

●Identification of a pericardial effusion by cardiac imaging (usually echocardiography); rarely, a pleural effusion may be identified causing cardiac chamber compression. (See 'Cardiac testing' below.)

●Echocardiographic signs of tamponade (cardiac chamber collapse, respiratory variation in ventricular volumes and transvalvular flow, inferior vena cava plethora, and alterations in hepatic vein flow). (See 'Echocardiography' below.)

However, the diagnosis of cardiac tamponade is definitively confirmed only by the hemodynamic and clinical response to pericardial fluid drainage. (See 'Cardiac catheterization' below.)

Cardiac testing — Other imaging techniques, such as CT and cardiovascular magnetic resonance (CMR) imaging, are usually not necessary for diagnosis of pericardial effusion and cardiac tamponade; these tests are generally reserved for patients who have undergone echocardiography and require additional imaging to identify and characterize the pericardial effusion (eg, for loculated collections) or other pericardial disease (such as constrictive pericarditis).

Echocardiography — Although cardiac tamponade is a clinical diagnosis, echocardiography plays a key role in identification of a pericardial effusion and assessing its hemodynamic significance [2,11,22].

●Pericardial effusion – Echocardiography enables assessment of the size, distribution, and features of pericardial effusion (such as loculation and density suggestive of transudate, exudate, or hematoma). In most cases of cardiac tamponade, a moderate to large effusion is present, and swinging of the heart within the effusion may be seen (movie 2). However, the pericardial effusion may be small in the setting of acute accumulation of pericardial fluid. (See 'Pathophysiology' above and 'Acute cardiac tamponade' above.)

●Signs of cardiac tamponade – The following are the major echocardiographic signs of hemodynamic changes associated with cardiac tamponade:

•Chamber collapse – Any cardiac chamber may collapse when intrapericardial pressure exceeds intracardiac pressure within the chamber (ie, transmural pressure gradient is transiently reversed), but right-sided chamber collapse is most common [11,23]. Both the right atrium (RA) and RV are compliant structures, so increased intrapericardial pressure causes their collapse when intracavitary pressures are only slightly exceeded by those in the pericardium [24]. (See "Echocardiographic evaluation of the pericardium".)

When timely echocardiography is performed in patients with cardiac tamponade, cardiac chamber collapse is typically present prior to hemodynamic collapse. However, chamber collapse may not be identified in standard echocardiographic views in patients with regional cardiac tamponade or pulmonary hypertension.

-Diastolic collapse of the right atrium – At end-diastole (during atrial relaxation), the RA volume is minimal, but pericardial pressure is maximal, causing the RA to buckle (movie 3) [25]. RA collapse, especially when it persists for more than one-third of the cardiac cycle, is highly sensitive and specific for cardiac tamponade. In contrast, brief RA collapse can occur in the absence of cardiac tamponade [25].

-Diastolic collapse of the right ventricle – RV diastolic collapse occurs in early diastole when the RV volume is still low (movie 4 and movie 5 and movie 6) [23]. RV diastolic collapse is less sensitive for the presence of cardiac tamponade than RA diastolic collapse, but is highly specific for cardiac tamponade [26]. RV collapse may not occur when the RV is hypertrophied or its diastolic pressure is greatly elevated [24].

-Left-sided chamber collapse – Left atrial collapse is seen in approximately 25 percent of patients with hemodynamic compromise and is very specific for cardiac tamponade [1,11,23,27,28]. Left ventricular collapse is less common since the wall of the left ventricle is more muscular, but it can be seen in cases of regional cardiac tamponade [11,23,28].

•Respiratory variation in volumes and flows – Reciprocal changes in left and right ventricular volumes occur with respiration; during inspiration, the interventricular and interatrial septa move leftward, and, during expiration, these septa shift rightward (image 2 and waveform 6). As noted above, these changes play a central role in the pathogenesis of pulsus paradoxus. (See 'Pulsus paradoxus' above.)

Also, the respiratory variation of mitral and tricuspid flow velocities is greatly increased and out of phase, reflecting increased ventricular interdependence in which the hemodynamics of the left and right heart chambers are directly influenced by each other to a much greater degree than normal. Normally, there is no more than 20 to 25 percent variation in the amplitude of inflow and outflow signals across the valves during respiration. However, in cardiac tamponade, mitral flow variation usually exceeds 30 percent, and tricuspid valve flow variation usually exceeds 60 percent, when referenced to expiration. The changes in velocity are greatest on the first beat of inspiration and expiration [29]. This pattern is seen at all sampling sites and is best appreciated at slow sweep speeds (waveform 2). Increased respiratory variation of carotid arterial and aortic blood flow may also be seen [30].

Respiratory variation of flows alone should not be used to diagnose tamponade in the absence of accompanying chamber collapse or abnormal hepatic vein flow.

•IVC plethora and hepatic vein flow – In patients with tamponade, marked elevation in central venous pressure is reflected as dilation of the inferior vena cava (IVC) and less than a 50 percent reduction in the diameter during inspiration (image 3 and image 4). In one report, IVC plethora was associated with pulsus paradoxus and was present in 92 percent of those with pericardial effusion requiring pericardial drainage [31]. IVC plethora is sensitive but not at all specific for cardiac tamponade.

Hepatic venous flow abnormalities (blunting or frank reversal of diastolic flow with expiration and systolic venous flow predominance) have high positive and negative predictive values for cardiac tamponade (82 and 88 percent respectively) but cannot be adequately assessed in approximately one-third of patients [32].

Limitations — While the above clinical findings are typical for cardiac tamponade, they are not present in all patients with tamponade depending upon the severity of tamponade, the location of the pericardial effusion or hematoma, and concurrent conditions. For example, in patients with pulmonary hypertension, echocardiographic signs of tamponade are less sensitive and specific [33,34].

In a prospective study of 110 patients with a moderate to large pericardial effusion [32], the reference standard was clinical cardiac tamponade (venous hypertension, pulsus paradoxus, or otherwise unexplained arterial hypotension, and resolution of the syndrome after removal of the pericardial effusion), which was present in 38 patients. The following findings were noted:

●Any chamber collapse had a sensitivity and specificity of 90 and 65 percent, respectively.

●The sensitivity was lower and specificity higher (75 and 91 percent) for abnormal right-sided venous flows (systolic predominance and expiratory diastolic reversal), but the latter could not be evaluated in more than one-third of patients.

●The specificity was highest (98 percent) for the combination of RA and RV collapse plus abnormal venous flow.

Echocardiography (transthoracic or transesophageal) is less sensitive for cardiac tamponade (often regional) developing early after cardiac surgery. In a study of 414 patients who underwent echocardiography for suspected tamponade during the first four weeks after cardiac surgery, cardiac tamponade was confirmed in 105 intraoperatively by identification of pericardial fluid or blood under pressure or hemodynamic improvement upon pericardial evacuation [35]. The sensitivity of echocardiography for tamponade was 36.8 percent within 24 hours postoperatively, 50 percent within 24 to 72 hours, and 73.8 percent after 72 hours, while its specificity ranged from 91.5 to 95 percent.

CT and CMR — Other imaging modalities such as CT and CMR are generally not necessary for the diagnosis and evaluation of a pericardial effusion. However, pericardial effusion may be first detected by CT, especially when CT is used to detect pulmonary embolus, a more common cause of shortness of breath and hypotension.

CT and CMR may help determine the feasibility of percutaneous versus surgical drainage due to a loculated or complex effusion, with CT generally preferred in patients with a subacute presentation [29]. CT and CMR findings associated with cardiac tamponade include identification of pericardial effusion, distention of the venae cavae and hepatic veins, deformity and compression of the cardiac chambers, bowing of the interventricular septum, and reflux of contrast into the azygos vein and inferior vena cava (image 5 and image 6) [36]. Cardiac tamponade may also be associated with coronary sinus (CS) compression [37] or low CS/IVC ratio on CT [38].

Cardiac catheterization — When feasible, hemodynamic assessment via cardiac catheterization is performed in patients with suspected cardiac tamponade during the pericardial fluid drainage procedure. The diagnosis of cardiac tamponade is confirmed by identifying typical hemodynamic findings prior to pericardial fluid removal and resolution of hemodynamic abnormalities after drainage.

The following hemodynamic findings are typical of cardiac tamponade:

●Jugular venous pressure is generally elevated and the y descent is attenuated. In some patients with cardiac tamponade, the x’ descent is prominent. (See "Examination of jugular venous waveforms", section on 'Abnormalities of the y-descent'.)

However, patients who are hypovolemic at presentation may have low-pressure cardiac tamponade with intracardiac diastolic pressures of 6 to 12 mmHg [22]. (See 'Low-pressure cardiac tamponade' above.)

●Equilibration of average intracardiac diastolic pressures (usually between 10 and 30 mmHg).

●A combination of inspiratory increase in right-sided pressures and reduction in left-sided pressures (which causes pulsus paradoxus) (waveform 2 and waveform 3).

If intracardiac diastolic pressures remain elevated after pericardiocentesis, an effusive-constrictive process with persistent pericardial constriction is suspected, as discussed separately. (See "Constrictive pericarditis: Management and prognosis", section on 'Management of effusive-constrictive pericarditis'.)

Evaluation of the etiology — The etiology of cardiac tamponade may be apparent in many cases (eg, post-cardiac injury syndrome, iatrogenic cardiac or coronary artery perforation, hematoma following cardiac surgery, neoplasm, uremia). In cases in which the diagnosis has not been established, clinical evaluation including pericardial fluid analysis may aid diagnosis. Evaluation of the cause of pericardial effusion is discussed separately. (See "Pericardial effusion: Approach to diagnosis", section on 'Identifying the etiology'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of cardiac tamponade depends upon the clinical presentation:

●Acute cardiac tamponade – Acute tamponade with elevated jugular venous pressure and hypotension should be distinguished from other clinical conditions with a similar acute presentation, such as an acute myocardial infarction (especially with RV involvement), aortic dissection, and hemodynamically significant pulmonary embolism.

Myocardial infarction is generally associated with characteristic ECG changes of infarction, and aortic dissection without cardiac tamponade does not generally cause an increase in jugular venous pressure. Neither myocardial infarction nor aortic dissection is associated with pulsus paradoxus. Pulmonary embolus can cause shortness of breath, hypotension, elevated jugular venous pressures, and is occasionally associated with pulsus paradoxus.

●Subacute cardiac tamponade – Patients with subacute cardiac tamponade typically present with dyspnea, fatigue, elevated jugular venous pressure, and edema. Conditions which may present similarly include constrictive pericarditis, heart failure, and advanced liver disease with cirrhosis. Echocardiography is critically important in making this distinction, as it may identify other cardiac pathology consistent with heart failure or constrictive pericarditis. In addition, patients with cirrhosis typically have jaundice and abnormalities of hepatic synthetic function (eg, elevated prothrombin time).

A subset of patients presenting with cardiac tamponade have effusive-constrictive pericarditis. In patients with this condition, hemodynamics do not normalize after pericardial fluid drainage due to the presence of constrictive pericarditis, as described separately. (See "Constrictive pericarditis: Clinical features and causes", section on 'Effusive-constrictive pericarditis' and "Constrictive pericarditis: Diagnostic evaluation", section on 'Effusive-constrictive pericarditis'.)

MANAGEMENT

Urgent drainage — Patients with cardiac tamponade require urgent pericardial fluid drainage to alleviate symptoms and prevent hemodynamic collapse. This approach generally results in rapid and dramatic improvement in symptoms and hemodynamics. If the cause of the pericardial effusion is unknown, pericardial fluid analysis may aid in identifying the cause.

An occasional patient with borderline signs of cardiac tamponade (eg, right atrial [RA] collapse during ≤1/3 of the cardiac cycle) may be observed with close clinical follow-up including serial physical examinations and echocardiograms (eg, every two to three days or sooner if clinically indicated) to enable prompt identification and treatment of cardiac tamponade.

Pericardial fluid is most commonly drained via percutaneous pericardiocentesis (algorithm 1). If percutaneous drainage is not appropriate or feasible, the pericardial fluid is drained via a surgical approach. Indications for surgical pericardial fluid drainage include a pericardial effusion which is inaccessible to percutaneous drainage or a critical cardiac or aortic bleeding site (eg, type A aortic dissection, ventricular free wall rupture after acute myocardial infarction, traumatic cardiac rupture, or iatrogenic hemopericardium which cannot be controlled percutaneously). (See "Pericardial effusion: Approach to management", section on 'Choice of pericardial drainage procedure'.)

Pericardial fluid removal is generally well tolerated. Rare complications of pericardiocentesis for cardiac tamponade include bleeding and heart failure (caused by posttap fluid shift into the central circulation). (See "Pericardial effusion: Approach to management", section on 'Complications of pericardial fluid removal'.)

Catheter drainage is continued following pericardial fluid removal until the volume of flow is <25 mL/day.

Supportive care — While preparing for pericardial fluid drainage, patients with cardiac tamponade are treated with volume repletion with agents such as blood, plasma, dextran, or saline, but only as a temporizing measure. The effects of volume replacement were shown to be variable in a study of 49 patients with a large pericardial effusion and hemodynamic criteria for cardiac tamponade who were given 500 mL of intravenous normal saline over 10 minutes; cardiac index increased by >10 percent in 47 percent of patients, remained unchanged in 22 percent, and decreased in 31 percent [39]. Volume expansion significantly increased intrapericardial pressure, RA pressure, and left ventricular end-diastolic pressure. Systolic blood pressure <100 mmHg was predictive of a favorable response to volume expansion.

Inotropic support is rarely indicated, and vasodilator therapy should be avoided.

Positive pressure mechanical ventilation should be avoided, if possible, because the positive thoracic pressures can further impair cardiac filling [40]. Among patients with cardiac arrest and pericardial effusion, the benefit of external cardiac compression is markedly reduced since additional cardiac filling is difficult to achieve [22].

Monitoring — Monitoring is required for patients with pericardial effusion at risk for developing cardiac tamponade (prior to or following pericardial drainage).

A patient with a pericardial effusion without cardiac tamponade, and in whom fluid sampling is not needed for diagnostic purposes, does not require pericardiocentesis and can be observed with serial clinical and echocardiographic follow-up [22].

Following either percutaneous or surgical drainage of a pericardial effusion in a patient with cardiac tamponade, the patient should generally be monitored with continuous telemetry and frequent vital signs for at least 24 to 48 hours. Subsequent monitoring with two-dimensional and Doppler echocardiography (eg, prior to and following discharge from the hospital) is warranted to confirm adequate fluid removal, detect possible recurrent fluid accumulation, and identify signs of early constrictive pericarditis [22]. In general, an early follow-up echocardiogram should be performed within one to two weeks following discharge, with an additional follow-up study in 6 to 12 months; however, the frequency of follow-up should be individualized according to the patient's clinical status, etiology of the effusion, and recurrence of effusion.

Treatment of the underlying condition — Management of the etiology of pericardial effusion is discussed separately. (See "Pericardial effusion: Approach to management", section on 'Treatment of cause'.)

In some instances, inflammatory effusions associated with "early" cardiac tamponade (eg, idiopathic pericardial effusion/pericarditis, connective tissue disease, etc) may resolve with antiinflammatory therapy (eg, nonsteroidal antiinflammatory drugs [NSAIDS] and colchicine), with resolution of cardiac tamponade. Effusions which progressively enlarge and lead to worsening symptoms suggestive of cardiac tamponade require pericardial fluid drainage.

PREVENTION OF RECURRENCE — As noted above, catheter drainage is continued following pericardial fluid removal until the volume of flow is <25 mL/day. After completion of this postprocedural drainage period, most patients who have been treated with pericardial fluid removal for cardiac tamponade require no additional drainage procedure. However, a minority of patients (particularly patients with malignant pericardial effusion) require intervention (eg, surgical pericardial window) to treat or prevent recurrent pericardial effusion. In the above-cited series of 340 patients treated for cardiac tamponade, 3 of 50 patients with a neoplastic pericardial effusion and three patients with an inflammatory pericardial effusion subsequently required a pericardial window [5]. (See "Pericardial disease associated with cancer: Management", section on 'Prevention and treatment of recurrent malignant pericardial effusion' and "Pericardial effusion: Approach to management", section on 'Management of recurrent pericardial effusion'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pericardial disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Basics topics (see "Patient education: Cardiac tamponade (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Pathophysiology – Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to impaired cardiac filling and hemodynamic compromise. Progressive decline in systemic venous return and enhanced ventricular interdependence are largely responsible for the physical and imaging signs of cardiac tamponade. (See 'Pathophysiology' above.)

●Clinical presentation – The clinical manifestations of cardiac tamponade vary according to the rate of pericardial fluid accumulation.

•Acute – Acute cardiac tamponade occurs within minutes and causes cardiogenic shock requiring urgent intervention with pericardial fluid drainage. Symptoms may include chest pain, dyspnea, and tachypnea. Signs include markedly elevated jugular venous pressure, tachycardia, hypotension, and narrow pulse pressure. Causes include traumatic rupture of the heart or aorta, aortic dissection, or a cardiac or coronary artery perforation caused by an invasive procedure. The pericardial effusion is often small. (See 'Acute cardiac tamponade' above.)

•Subacute – Subacute cardiac tamponade occurs over days to weeks with causes including neoplastic, uremic, and idiopathic pericarditis. Symptoms may include fatigue, dyspnea, chest discomfort or fullness, and peripheral edema. Hypotension may be present, although some patients may be hypertensive. The pericardial effusion is often moderate or large. (See 'Subacute cardiac tamponade' above.)

•Low-pressure – Low-pressure (occult) cardiac tamponade occurs in patients who are severely hypovolemic, so jugular venous distension may be absent. (See 'Low-pressure cardiac tamponade' above.)

•Regional – Regional cardiac tamponade is caused by a localized pericardial effusion or hematoma compressing at least one but not all cardiac chambers. Typical findings of cardiac tamponade may be absent or attenuated. (See 'Regional cardiac tamponade' above.)

●Diagnosis – A diagnosis of cardiac tamponade is highly suggested when the following three elements are all present:

•Symptoms, signs, and/or ECG findings suggestive of cardiac tamponade (See 'History' above and 'Physical findings' above and 'Electrocardiogram' above.)

•Pericardial effusion identified by cardiac imaging (usually echocardiography); rarely, a pleural effusion may be identified causing cardiac chamber compression. (See 'Cardiac testing' above.)

•Echocardiographic signs of tamponade (cardiac chamber collapse, respiratory variation in ventricular volumes and transvalvular flow, inferior vena cava plethora, and alterations in hepatic vein flow). (See 'Echocardiography' above.)

However, the diagnosis of cardiac tamponade is definitively confirmed by the hemodynamic and clinical response to pericardial fluid drainage. (See 'Diagnosis' above.)

●Management of tamponade – Patients with cardiac tamponade require urgent pericardial fluid drainage to alleviate symptoms and prevent hemodynamic collapse. Pericardial fluid is most commonly drained via percutaneous pericardiocentesis (algorithm 1). If percutaneous drainage is not appropriate or feasible, the pericardial fluid is drained via a surgical approach. (See 'Management' above.)

Intravenous volume repletion may provide temporary benefit in patients with cardiac tamponade, but is only a temporizing measure. (See 'Supportive care' above.)

●Monitoring – Monitoring is required for patients with pericardial effusion at risk for developing cardiac tamponade (prior to or following pericardial drainage). A patient with a pericardial effusion without cardiac tamponade, and in whom fluid sampling is not needed for diagnostic purposes, does not require pericardiocentesis and can be observed with serial clinical and echocardiographic follow-up. Patients who have undergone percutaneous or surgical drainage should generally be monitored with telemetry and frequent vital signs for 24 to 48 hours and subsequent clinical and echocardiographic follow-up to detect possibly recurrent fluid accumulation and identify signs of early constriction. (See 'Monitoring' above.)