European Society of Cardiology
Working Group on Myocardial and Pericardial Diseases
Online Only Supplemental material
Triage strategy for urgent management of cardiac tamponade: a position statement
of the European Society of Cardiology Working Group on Myocardial and
Pericardial Diseases
Arsen D. Ristić1* Massimo Imazio,2*# Yehuda Adler,3 Aristides Anastasakis,4 Luigi P Badano,5°
Antonio Brucato6, Alida L.P. Caforio,5 Olivier Dubourg,7° Perry Elliott,8 Juan Gimeno,9 Tiina Helio,10
Karin Klingel,11, Aleš Linhart,12 Bernhard Maisch,13 Bongani Mayosi,14° Jens Mogensen,15 Yigal
Pinto,16 Hubert Seggewiss,17 Petar M. Seferović,1 Luigi Tavazzi,18 Witold Tomkowski,19 Philippe
Department of Cardiology, Clinical Center of Serbia & Belgrade University School of Medicine,
Belgrade, Serbia; 2Department Cardiology, Maria Vittoria Hospital, Turin, Italy; 3Chaim Sheba
Medical Center, Tel Hashomer and Sackler University, Tel Aviv, Israel; 4Unit of Inherited
Cardiovascular Diseases, 1st Department of Cardiology, Athens University Medical School,
Athens, Greece; 5Division of Cardiology, Department of Cardiological, Thoracic and Vascular
Sciences, Centro "V. Gallucci", University of Padova-Policlinico, Padua, Italy, 6Division of Internal
Medicine, Ospedali Riuniti, Bergamo, Italy; 7UFR des Sciences de la Santé Simone Veil, Montigny le
Bretonneux, France, 8The Heart Hospital, University College London Hospitals Trust, London, United
Kingdom; 9Department of Cardiology, University Hospital Virgen de Arrixaca, Murcia, Spain;
Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Meilahti
Hospital, Helsinki, Finland; 11Department of Molecular Pathology, Institute for Pathology, University
Hospital Tübingen, Germany; 12Second Department of Medicine, Department of Cardiovascular
Medicine, General University Hospital and the First Faculty of Medicine, Charles University,
Prague, Czech Republic; 13Department of Internal Medicine-Cardiology, Universitätsklinikum
Gießen & Marburg GmbH, Philipps University, Marburg, Germany; 14Department of Medicine,
Groote Schuur Hospital, Cape Town, South Africa; Department of Cardiology, Odense University
Hospital and Institute of Clinical Research, Faculty of Health Sciences, University of Southern Denmark,
Denmark; 16Department of Cardiology, Academic Medical Centre, Amsterdam, The Netherlands;
Medical Department 1, Leopoldina Hospital, Schweinfurt, Germany; 18Maria Cecilia Hospital—
GVM Care and Research, Ettore Sansavini Health Science Foundation, Cotignola, Italy; 19CardioPulmonary Intensive Care, Division at the National Tuberculosis and Lung Diseases Research
Institute, Warsaw, Poland; 20Referral Center for Inherited Cardiac Diseases, UPMC Université
Paris 6, AP-HP, Hôpital Pitié-Salpêtrière, Paris, France.
* Contributed equally to this statement as the coordinator and the leader of the Study group on
pericardial diseases of the European Society of Cardiology Working group on Myocardial and
Pericardial Diseases.
° Contributed as Internal Reviewers.
# Corresponding author:
Massimo Imazio, MD, FESC
Department of Cardiology, Maria Vittoria Hospital
Via Luigi Cibrario 72, Torino, 10141, Italy
E-mail: [email protected]
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Diagnostic algorithm
Clinical diagnosis
The causes of cardiac tamponade are varied and discussed in the main text (1-13).
Cardiac tamponade includes a haemodynamic spectrum ranging from incipient or
preclinical tamponade (pericardial pressure equals right atrial pressure but it is lower than
left atrial pressure) to initial cardiac tamponade when pericardial pressure equals left atrial
pressure (1-3). Cardiac tamponade is moderate when the pericardial pressure is higher
than 10-12 mmHg and an abnormal jugular pulse can be detected along with signs of
compression of right heart chambers (4). Further elevation of pericardial pressure is
responsible for advanced tamponade characterized by significant reduction of the stroke
volume, blood pressure, and by sinus tachycardia (Table 1s). At this stage pulsus
paradoxus becomes evident (13,20,21).
The rate of pericardial fluid accumulation is critical for the clinical presentation. If
pericardial fluid is quickly accumulating, even less than 250 ml, may cause acute cardiac
tamponade (often called “surgical tamponade”) within few minutes. Conversely, a slowly
accumulating pericardial fluid may allow the collection of 1000-1500 ml or even larger
effusions within days or weeks before a significant elevation of intrapericardial pressure
and the development of cardiac tamponade. Such clinical presentations are less dramatic
and have been also reported as “medical tamponade” to underline that different medical
non-traumatic causes are the underlying cause and different therapeutic approaches may
be considered (13,22).
Classical symptoms of cardiac tamponade include tachycardia, tachypnea, dyspnea
on exertion progressing to orthopnea, chest pain, oliguria and/or a sensation of fullness
(1,20). Additional occasional symptoms due to local compression may include nausea
(diaphragm), dysphagia (oesophagus), hoarseness (recurrent laryngeal nerve), hiccups
(phrenic nerve) (22). Right upper quadrant pain may be present as a symptom related to
hepatic venous congestion. Nonspecific symptoms include also cough, weakness, fatigue,
anorexia, and palpitations reflecting the compressive effect of the pericardial fluid on
contiguous anatomic structures or reduced blood pressure and secondary sinus
The classical findings of cardiac tamponade were described by the thoracic surgeon
Beck in 1935 (23) as a triad including hypotension, increased jugular venous pressure,
and a small and quiet heart. This triad has classically been identified in “surgical
tamponade” with acute haemodynamic collapse due to intrapericardial hemorrhage
caused by trauma, myocardial or aortic rupture. The triad may be lacking in patients with
slowly accumulating pericardial fluid (24). Hypotension may be absolute or relative. Acute
cardiac tamponade is usually associated with low blood pressure (<100 mmHg) but blood
pressure is only slightly reduced in subacute, chronic tamponade. Hypertensive patients
may have normal or even mild elevation of blood pressure concomitant to cardiac
tamponade due to the increased adrenergic tone and circulating catecholamines (25).
Fever is a non-specific sign that may be associated with infectious or immune-mediated
On physical examination classical signs include neck vein distention with elevated
jugular venous pressure, pulsus paradoxus, and diminished heart sounds on cardiac
auscultation. Pulsus paradoxus was described first by Kussmaul in 1873 as a palpable
reduction of radial pulse on inspiration in patients with cardiac tamponade (“waxing and
waning” of the peripheral pulse, in contrast to the unvarying strength of the apical cardiac
impulse) (26). Pulsus paradoxus is defined as an inspiratory reduction of at least 10
mmHg of the systolic blood pressure. It can be easily detected recording the systolic
pressure at which Korotkoff sounds are first audible and the systolic pressure at which
they are audible through the whole respiratory cycle.
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Laboratory findings and imaging-based diagnosis
There are no specific laboratory data in cardiac tamponade.
Sinus tachycardia is the major finding at electrocardiography (ECG). The ECG may show
low QRS voltage and electrical alternans (electrical alternans is an electrocardiographic
phenomenon of alternation of QRS complex amplitude or axis between beats. It is seen in
cardiac tamponade and severe pericardial effusion and is thought to be related to changes
in the ventricular electrical axis due to a swinging heart within the pericardial sac) (Figure
1s). Both findings are usually considered suggestive of a large pericardial effusion, but
have a low reported sensitivity (<50%) (20).
However, a prospective study has demonstrated that low QRS voltages may be a
feature of cardiac tamponade but not of pericardial effusion per se. Low QRS voltage
(defined as maximum QRS amplitude <0.5 mV in the limb leads) was found in 61% of
patients with cardiac tamponade but in none with effusions without cardiac tamponade
(27). Normalization of the QRS amplitude was not recorded immediately after
pericardiocentesis but only after a week (27).
ECG findings seem to have limited sensitivity for cardiac tamponade: low QRS
voltage had a sensitivity of 42%, and electrical alternans of only 16-21%. Atrial
arrhythmias have been rarely reported, whereas widespread ST segment elevation with or
without PR depression in the setting of acute pericarditis was noted frequently (20).
Chest x-ray
In patients with mild to moderate pericardial effusions cardiac silhouette is usually normal,
while the cardiac silhouette has a typical “water bottle” appearance with a large effusion
(Figure 2s). Such a simple sign in the appropriate clinical context (symptomatic patients
with large pericardial effusion) has a high sensitivity for the diagnosis of cardiac
tamponade, but does not determine the urgency of pericardiocentesis. On well-penetrated
chest x-rays in the lateral view (or better in fluoroscopy), pericardial fluid may be
suggested by lucent lines within the cardiac shadow (epicardial halo sign) (28,29).
Echocardiography is the first level diagnostic method for the assessment of the presence,
size and hemodynamic importance of pericardial effusion (3,30) and to guide
pericardiocentesis (Figure 3s). According to a common semiquantitative assessment
pericardial effusions are graded according to the echo-free space in diastole (3, 31,32) as
small (<10 mm), moderate (10-20 mm), and large (>20 mm). Echocardiography is
mandatory for the initial assessment and follow-up of all patients with suspected
pericardial diseases (33). Most cases of cardiac tamponade show moderate to large
pericardial effusion. The swinging of the heart within the pericardial fluid is a common
finding (Supplemental movie 1 and 2) (34). Echocardiographic findings in cardiac
tamponade are determined by transient chambers collapse and increased ventricular
interdependence (34,35). Major signs (Table 2s) include:
1. Diastolic prolonged collapse of the right atrium (RA) is an early sign that can be
detected with moderate to large pericardial effusions without cardiac tamponade,
because the RA is the cardiac chamber with the lowest pressures. A ratio of RA
collapse time to cardiac cycle length >0.34 is a very specific sign of cardiac tamponade.
At the end of diastole the RA volume is minimal while pericardial pressure is maximal
(36), thus diastolic collapse of the RA usually occurs at late diastole while collapse of
RV happens at early diastole.
2. The diastolic collapse of the right ventricle (RV) was first described by Schiller and
Botvinick in 1977 (37). It is less sensitive for the presence of cardiac tamponade than
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the RA collapse but more specific. This sign may be absent in cases of RV hypertrophy
or elevated RV diastolic pressure (38).
3. A left ventricular (LV) collapse is recorded in about 25% of cases with cardiac
tamponade. It is a not usual but specific sign, because LV pressures are higher and the
LV is thicker than RV. This sign can be sometimes seen in regional compression (39).
4. Respiratory variations in volumes and flows of cardiac chambers. Increased
ventricular interdependence observed in cardiac tamponade is responsible for reciprocal
changes of LV and RV volumes and mitral and tricuspid flows during respiratory phases,
as well as for abnormal septal motion during respiratory phases (interventricular septum
moving towards the LV during inspiration and towards the RV during expiration, septal
5. Variations in peak velocities during respiration across the mitral valve, tricuspid
valve, and pulmonary outflow that are greater than 25%, 50%, and 30% respectively
indicate cardiac tamponade, but similar changes are also observed in constrictive
pericarditis (Figure 4s) (17,40,41).
6. Inferior vena cava (IVC) plethora. Less than 50% reduction in the diameter of a dilated
IVC (>20 mm) during inspiration reflects a marked elevation in central venous pressure
and is frequently reported in patients with cardiac tamponade (42). It is a very sensitive,
but not very specific sign, common in other pathologic conditions (e.g. heart failure,
tricuspid regurgitation) (20). In the setting of a large pericardial effusion, IVC plethora is
a sign of cardiac compression by the effusion (Figure 4s).
Points 4 and 5 are consequences of ventricular interdependence. The left (LV) and right
ventricles (RV) are enclosed in a stiff envelope, the pericardium. They have similar enddiastolic volumes, and there is limited space for acute ventricular dilatation within a normal
pericardium, this limit is even more evident in the presence of large effusion with cardiac
tamponade or a rigid pericardium such as in constrictive pericarditis. Thus, when RV enddiastolic volume increases owing to increased RV loading such as during inspiration, it can
only occur at the expense of the space devoted to the left ventricle, thus increased right
ventricle volume and right flows only occur at the expenses of a reduction of the left
ventricle volume and flows.
In a prospective clinical study on the correlation between clinical and echocardiographic
findings in patients with moderate to large pericardial effusions (43), any chamber collapse
had a high sensitivity (90%) but a relatively low specificity (65%). The specificity was
higher for abnormal right-sided venous flows (91%), which were not detectable in one third
of cases. The integration of chamber collapse and abnormal venous flows provided the
highest specificity (98%).
In patients with recent cardiac surgery or trauma the presence of localized cardiac
tamponade should be carefully considered. In these clinical conditions standard
transthoracic echocardiography views can be difficult to obtain due to the inability to put
the patient in an appropriate position, and the surgical wounds. In this setting
transesophageal echocardiography (TEE) may have a higher diagnostic accuracy than
transthoracic echocardiography also for the detection of loculated effusions and localized
compression by hematoma (i.e. especially on the RA) (1,44).
Other imaging techniques
Other imaging techniques, such as computed tomography (CT) and cardiovascular
magnetic resonance (CMR) may detect pericardial effusion and suggest signs of cardiac
tamponade (i.e. large pericardial effusion, distension of venae cavae and hepatic veins,
deformity and compression of cardiac chambers, bowing of the interventricular septum)
(Figure 5s) (45). Moreover CT attenuation values of pericardial effusion can help in the
differentiation of blood, exudative fluid (20–60 Hounsfield units), as found with purulent
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pericarditis, and simple transudative fluid (<10 Hounsfield units).
Coronary sinus compression, an early sign of cardiac tamponade (46), RV wall flattening
and pericardial thickening on CT have been described with hemodynamically significant
pericardial effusion (47). CT and CMR have a large field view and multiplanar capability,
and can image the entire pericardium as well as the complete chest including
abnormalities of the surrounding mediastinum and lungs, which is important if aortic
pathology or neoplastic diseases have to be considered as underlying causes (48). CT
guided catheter insertion with drainage may be useful in the hands of experts, particularly
for loculated effusions or accumulation of fluid in unusual sites.
Cardiac catheterization and invasive haemodynamics
Cardiac catheterization may be considered in case of iatrogenic effusion during
percutaneous interventions, but also when there is a discrepancy between the clinical
picture and non-invasive imaging data, and may particularly useful for the evaluation of
patients with complex hemodynamic disorders (49). Patients in cardiac tamponade usually
demonstrate low arterial pressure and tachycardia, an elevated right atrial pressure, with a
prominent x descent and a diminished or absent y descent (cardiac compression, which
interrupts the venous return is maximal at end-diastole). In cardiac tamponade, the jugular
pressure declines normally with inspiration (Kussmaul's sign absent), reflecting augmented
systemic venous return. On the contrary, in constrictive or effusive-constrictive pericarditis,
right heart failure, or severe tricuspid regurgitation, the mean central venous pressure
does not decline during inspiration, and may even increase (Kussmaul's sign present). The
pulmonary capillary wedge pressure is elevated and nearly equal to the intrapericardial
and right atrial pressure. Except in low-pressure tamponade, diastolic pressures in all
heart chambers are usually 15 to 30 mmHg. In contrast to constrictive pericarditis,
ventricular diastolic pressure does not have the dip and plateau configuration, but is
elevated in early diastole and continues to rise throughout the diastole (49).
pericardiocentesis, if intrapericardial pressure falls to zero or becomes negative, while the
right atrial pressure remains elevated, diagnostic alternatives include effusive-constrictive
pericarditis (especially in patients with tuberculosis or prior irradiation for neoplastic
disease), preexisting left ventricular dysfunction, tricuspid valve disease, and restrictive
cardiomyopathy. The value of cardiac catheterization has been clearly demonstrated for
cases with effusive-constrictive pericarditis, in whom the intrapericardial pressure
decreased after pericardiocentesis, whereas right atrial and end-diastolic right and left
ventricular pressures remained elevated, with a dip-plateau morphology (50). The
presence of effusive-constrictive physiology may be also clinically suspected when jugular
venous pressure remain elevated after pericardiocentesis and echo examination shows
constrictive features.
Differential diagnosis
In a systematic review of the literature (20), five features have been reported in the
majority of patients with cardiac tamponade (>70%): dyspnea (85-90%), cardiomegaly on
chest radiograph (89%), pulsus paradoxus (82%), tachycardia (77%), and elevated jugular
venous pressure (76%). In the setting of a large pericardial effusion, the presence of
pulsus paradoxus (inspiratory decrease of systolic blood pressure >10 mmHg) increased
the likelihood of cardiac tamponade (likelihood ratio 3.3) (16). Surprisingly, hypotension
and soft heart sounds were insensitive (respectively 26% and 28%). Since cardiac
tamponade is primarily a clinical diagnosis, echocardiographic signs are only confirmatory
(20). Differential diagnosis may include acute myocardial infarction (especially with RV
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involvement), pulmonary embolism, and aortic dissection in acute onset cases. In patients
with a subacute onset of symptoms, the differential diagnosis should exclude constrictive
pericarditis, congestive heart failure, advanced liver disease with cirrhosis, rarely Ebstein
Medical management
Medical treatment is only an initial measure until pericardiocentesis or surgical relief can
be performed. Volume infusion may be useful for patients with hypovolemia until correction
of hypovolemia (4), and allows to gain time to perform pericardiocentesis.
On the contrary, it may precipitate or worsen tamponade in normovolemic or hypervolemic
patients (51-53).
The use of inotropes is not supported by clear evidence-based data (51-53).
Although severely hypoxic patients must be intubated and ventilated during the
preparation for pericardiocentesis, positive end-expiratory pressure (PEEP) ventilation
should be avoided since it may decrease the cardiac output further (54,55).
It should be especially pointed out that intravenous administration of diuretics is
strongly contraindicated and could be fatal (3), while volume infusion is useful for patients
with hypovolemia (4).
In patients with cardiac arrest associated with cardiac tamponade (cardiac arrest
with pulseless electrical activity- PEA is the late manifestation of uncorrected cardiac
tamponade), immediate pericardiocentensis is the substantial key of successful
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76. European Society of Cardiology; Committee for Education; Authors/Task Force
Members:, Gillebert TC, Brooks N, Fontes-Carvalho R, Fras Z, Gueret P, LopezSendon J, Salvador MJ, van den Brink RB, Smiseth OA; Observer on behalf of the
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Vahanian A; Contributors and reviewers:, Bauersachs J, Bax J, Burri H, Caforio AL,
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González-Juanatey JR, Hall J, Herpin D, Iaccarino G, Iung B, Kitsiou A, Lancellotti P,
McDonough T, Monsuez JJ, Nuñez IJ, Plein S, Porta-Sánchez A, Priori S, Price S,
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Table 1s. Stages in the hemodynamic spectrum of cardiac tamponade.
Pericardial pressure equals right atrial pressure
but it is lower than left atrial pressure.
INITIAL cardiac tamponade
Pericardial pressure equals left atrial pressure.
MODERATE tamponade
Pericardial pressure is above 10-12 mmHg and
an abnormal jugular pulse can be detected with
signs of compression of right heart chambers.
ADVANCED tamponade
Sinus tachycardia with significant reduction of
stroke volume, blood pressure, and evident
pulsus paradoxus.
Table 2s Main echocardiographic signs for the diagnosis of cardiac tamponade with reported
sensitivity and specificity (35-43).
Diastolic collapse of RA
Diastolic collapse of RV
Inferior IVC plethora
RA= right atrium, RV= right ventricle, IVC= inferior vena cava.
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Figure 1s. Electrocardiogram in a patient with cardiac tamponade. Please note low voltage
and QRS-complex electrical alternans.
Figure 2s. Typical “water bottle” appearance with a large effusion and comcomitant left
pleural effusion on chest x-ray.
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pericardiocentesis. A) Large pericardial effusion from the subxiphoid view: subxiphoid
approach for pericardiocentesis should be applied. B) Large separation of pericardial
layers from the apical view, but very small from the subxiphoid: pericardiocentesis using
intercostal (apical) approach should be performed. C) loculated pericardial effusion with
Figure 4s. Marked variations of mitral peak E velocities (>25%) during respiratory phases
(panel A) and inferior vena cava plethora (panel B) are echocardiographic signs of cardiac
tamponade (see text for explanation).
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Figure 5s. Regional cardiac tamponade by a large hematoma after cardiac surgery.
Supplemental Video 1. Four chamber echocardiography view in a patient with cardiac
taponade revealing swinging-heart and compression on the right-cardiac chambers.
Supplemental Video 2. Subcostal view in the same patient demonstrating large
separation of pericardial layers and compression on the right atrium and the right ventricle.
Pericardiocentesis would be possible both using subxiphoid and apical (intercostal)
Supplemental Video 3. Bedside, echocardiography guided pericardiocentesis.
pericardiocentesis in the cardiac catheterization laboratory, utilizing epicardial halo
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Supplementary Data - European Heart Journal