Cardiac Tamponade

nature reviews disease primers https://doi.org/10.
1038/s41572-023-00446-1
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Cardiac tamponade
Yehuda Adler 1,2 , Arsen D. Ristić 3,4
, Massimo Imazio5, Antonio Brucato6, Sabine Pankuweit 7
, Ivana Burazor ,
4,8
Petar M. Seferović3,4,9 & Jae K. Oh10

Abstract Sections
Cardiac tamponade is a medical emergency caused by the progressive Introduction
accumulation of pericardial fluid (effusion), blood, pus or air in Epidemiology

the pericardium, compressing the heart chambers and leading to Mechanisms/pathophysiology
haemodynamic compromise, circulatory shock, cardiac arrest and
Diagnosis, screening
death. Pericardial diseases of any aetiology as well as complications of and prevention
interventional and surgical procedures or chest trauma can cause cardiac
Management
tamponade. Tamponade can be precipitated in patients with pericardial
Quality of life
effusion by dehydration or exposure to certain medications, particularly
vasodilators or intravenous diuretics. Key clinical findings in patients Outlook
with cardiac tamponade are hypotension, increased jugular venous

pressure and distant heart sounds (Beck triad). Dyspnoea can progress
to orthopnoea (with no rales on lung auscultation) accompanied
by weakness, fatigue, tachycardia and oliguria. In tamponade caused by
acute pericarditis, the patient can experience fever and typical chest pain
increasing on inspiration and radiating to the trapezius ridge. Generally,
cardiac tamponade is a clinical diagnosis that can be confirmed using
various imaging modalities, principally echocardiography. Cardiac
tamponade is preferably resolved by echocardiography-guided
pericardiocentesis. In patients who have recently undergone cardiac
surgery and in those with neoplastic infiltration, effusive–constrictive
pericarditis, or loculated effusions, fluoroscopic guidance can increase
the feasibility and safety of the procedure. Surgical management is
indicated in patients with aortic dissection, chest trauma, bleeding
or purulent infection that cannot be controlled percutaneously. After
pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be
considered to prevent recurrence and effusive–constrictive pericarditis.
A full list of affiliations appears at the end of the paper. e-mail: yadlercardiol@gmail.com
Nature Reviews Disease Primers | (2023) 9:36 1

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Introduction Epidemiology
The human pericardium is a sac that surrounds the heart and the roots General incidence and prevalence
of the great vessels. The pericardium is comprised of a double-layered To date, few reports have been published on the incidence, prevalence
serosal membrane, with a visceral layer (epicardium) that covers the or exact aetiology of cardiac tamponade in the general population. Only
surface of the heart and a parietal layer that coats the inner surface of indirect data about the epidemiology of conditions that can lead to
the sac. The external surface of the pericardium consists of fibrous cardiac tamponade can be found in the literature. Surprisingly, despite
connective tissue fused to the parietal serosa1. This construction the fairly high frequency of pericardial syndromes in clinical practice
forms the pericardial space, which contains pericardial fluid com- (including acute, incessant, recurrent and chronic pericarditis, pericar-
prised predominantly of plasma filtered through the epicardial capil- dial effusion, cardiac tamponade, and constrictive pericarditis)3, the
laries and probably the parietal layer of the pericardium (Fig. 1a). The incidence or prevalence of these conditions in the general population is
underlying myocardium also contributes a small amount of interstitial unknown and epidemiological data are scarce. However, epidemiologi-
fluid2. Under physiological conditions, the pericardial space contains cal data from national inpatient sample data bases collected between
20–60 ml of fluid drained by the lymphatic capillary bed. The vol- 2008 and 2014 in the USA have been published14. Among 216 million
ume of fluid is determined by the equilibrium between production emergency admissions in patients aged >18 years (mean age ~62 years),
and drainage3. the incidence of cardiac tamponade was 0.05% (115,638 cases); 63.4%
Cardiac tamponade is a potentially life-threatening emergency, of these patients were white, 12.6% were Black and 7.4% were Hispanic.
characterized by progressive intrapericardial accumulation of fluid There was no significant difference in the male-to-female ratio (46.5%
(or pus, blood, clots or air) leading to increased intrapericardial female). The reported causes of cardiac tamponade included chest
pressure and compression of the heart. Diastolic filling and cardiac trauma (2.1%), connective tissue diseases (4.0%), chronic kidney disease
output are subsequently impaired, resulting in haemodynamic (18.4%), cancer (17.0%), sepsis (10.6%) and idiopathic pericarditis (3.7%).
compromise, typical obstructive circulatory shock4 or even cardiac In-hospital mortality was high (14.3%) and remained so throughout the
arrest5,6 (Fig. 1b). study period. Chest trauma, acute kidney injury, metastatic cancer and
Pericardial diseases of any aetiology can cause cardiac tamponade sepsis were significant predictors of mortality14. A post-mortem study
but certain entities have a higher risk of evolution towards circula- focused on haemopericardium found that, among 430,000 postmor-
tory shock (especially tuberculous pericarditis and malignancies)6–9 tems between 1995 and 2004 in a rural English population, mortality
(Table 1). Depending on the aetiology, pericarditis (inflammation of was due to cardiac tamponade in 461 cases15.
the pericardial sac, which can be caused by a bacterial or viral infection,
chest injury, medications or concomitant conditions) is often initially Risk factors
associated with a small pericardial effusion (accumulation of excess Risk factors for cardiac tamponade include pericarditis, malignancies,
fluid in the pericardium) that can increase over time and progress to autoimmune conditions (systemic lupus erythematosus (SLE) and
cardiac tamponade. In patients with massive intrapericardial bleed- rheumatoid arthritis), cardiovascular conditions and iatrogenic (result-
ing (for example, as a consequence of myocardial or coronary artery ing from medical activity such as a treatment or diagnostic procedure)
perforation, extension of aortic dissection, or trauma), acute car- factors such as cardiovascular interventional procedures and surgery.
diac tamponade develops in minutes and is characterized by rapidly
evolving, dramatic clinical haemodynamic deterioration leading to Pericarditis. The most commonly encountered pericardial disease in
cardiac arrest10,11 (Fig. 2a). Pericardial effusion in individuals with the clinic is acute pericarditis, which is the cause of 0.1% of all hospital
severe pulmonary hypertension is a unique, albeit important, subset admissions and 5% of emergency room admissions for chest pain in the
that can be difficult to manage as pericardiocentesis in these individu- USA and Europe3. The reported annual incidence of acute pericarditis
als carries the risk of acute right ventricle failure and can be fatal12. was 27.7 cases per 100,000 of the population in emergency room and
If pericardial effusion occurs slowly, with clinical worsening over hospital admissions from an Italian community16 but was much lower
several days or weeks (Fig. 2b), the compressive effects should be con- in the Finnish national registry for the years 2000–2009 (3.32 cases
sidered as a continuum, with no simple threshold to identify patients per 100,000 of the population)17. These data from Finland only include
in critical condition requiring immediate pericardial drainage9,13, and hospitalized patients and might therefore represent only a minority of
these patients need to be closely monitored to determine if and when cases as many patients with pericarditis are not admitted to hospital.
intervention is needed. Among individuals aged 16–65 years, the risk of pericarditis was higher
In this Primer, we discuss the epidemiology and pathophysiol- in men than in women (relative risk 2.02), and the highest risk difference
ogy of cardiac tamponade as well as the clinical signs and imaging compared with the overall population was among young adults17. In a
features used in diagnosis. This information is based on the 2014 study of 7 million individuals from Danish medical data bases, a much
triage strategy position statement5 and the latest (2015) guidelines higher annual incidence of acute pericarditis was reported (168 cases
on pericardial diseases from the European Society of Cardiology per 100,000 of the population)18. In this investigation, all patients with
(ESC) Working Group on Myocardial and Pericardial Diseases 3 a first-time diagnosis of acute pericarditis during the period 1994–2013
for the diagnosis, scoring and treatment of cardiac tamponade. were identified. Pericarditis was recorded as the primary discharge
We also suggest the best management options for the evacuation diagnosis in 79% of patients. The presence of or progression to cardiac
of pericardial fluid as well as novel strategies for the prevention of tamponade was not evaluated18. This study is more representative that
recurrence. In addition, we discuss patient quality of life in vari- the Italian and Finnish studies as it was not limited to hospital admis-
ous clinical settings. Finally, we highlight gaps in our knowledge sions. A study from the USA revealed that the hospitalization rate
of cardiac tamponade and consider the importance of future stud- in Medicare beneficiaries aged ≥65 years with a principal discharge
ies, clinical trials and registries in addressing important research diagnosis of pericarditis between 1999 and 2012 remained stable dur-
questions. ing the study period (26 per 100,000 person-years)19. The incidence

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a Normal heart Cardiac tamponade
Fibrous pericardium Pericardial sac

filled with fluid
Parietal layer of
serous pericardium
Pericardial cavity
Visceral layer of
serous pericardium
(epicardium)
Myocardium
Endocardium
Pulsus paradoxus
Intrathoracic pressure Expiration

Inspiration Inspiration
Ventricular Left
interdependence ventricle
Right
Septum
ventricle
Pericardial
effusion
Ventricular wall collapse Improvement in cardiac Ventricular wall collapse

during inspiration output during expiration during inspiration
Fig. 1 | Anatomical changes to the heart during cardiac tamponade. arrest. Owing to ventricular interdependence, expansion of the right ventricle
a, Schematic of the heart depicting the layers of the pericardium and excessive during inspiration compresses the left ventricle, resulting in decreased filling
intrapericardial pressure during cardiac tamponade. b, The basic pathogenetic and a drop in stroke volume with a decrease in systolic blood pressure (pulsus
mechanisms of cardiac tamponade. Progressive intrapericardial accumulation paradoxus). During expiration, the left ventricle is filled by the restoration of
of fluid leads to increased intrapericardial pressure and compression of the pulmonary venous return but the right ventricle is compressed and systemic
heart. Diastolic filling and cardiac output are subsequently impaired, resulting venous return is interrupted. Part b adapted with permission from ref. 207,
in haemodynamic compromise, circulatory shock and, eventually, cardiac © The Authors.
of pericarditis in this study is similar to that reported by the Italian between 26 (refs. 16,19) and 168 (ref. 17) cases per 100,000 of the popu-
group15 and was consistently higher in men and in very elderly patients lation, the question remains about what proportion of these patients
(≥85 years of age)19. Adjusted all-cause mortality decreased over the develop pericardial effusion and cardiac tamponade.
study period (from 7.6% in 1999 to 5.7% in 2012 for 30-day mortality, and The incidence of pericardial effusion is estimated to be around
from 19.7% in 1999 to 17.3% in 2011 for 1-year mortality)19. On the basis 20 cases per 100,000 population20. Pericardial effusion in developed
of these studies, assuming an annual incidence of acute pericarditis of countries is most frequently of idiopathic origin (up to 50% of cases),

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Table 1 | Criteria for triage of patients with pericardial effusion at risk for progression to cardiac tamponade
Aetiology Clinical presentation Imaging
Likely to progress to cardiac tamponade

Malignancy (2) Dyspnoea or tachypnoea (1) Cardiomegaly on chest radiography (1)
Tuberculosis (2) Orthopnoea (no rales on lung auscultation) (3) Electrical alternans on ECG (0.5)
Recent radiotherapy (1) Hypotension (SBP <95 mmHg) (1) Microvoltage on ECG (1)
Recent viral infection (1) Distended jugular veins (1) Circumferential pericardial effusion (>2 cm in diastole) (3)
Recurrent pericardial effusion, previous Progressive sinus tachycardia (1) Moderate pericardial effusion (1–2 cm in diastole) (1)
pericardiocentesis (1) Oliguria (1) Right atrial collapse >1/3 of cardiac cycle (1)
Chronic terminal renal failure (1) Pulsus paradoxus >10 mmHg (2) IVC >2.5 cm, <50% inspiratory collapse (1.5)
Immunodeficiency or immunosuppression (1) Rapid worsening of symptoms (2) Right ventricular collapse (1.5)
Iatrogenic haemopericardium (2) Left atrial collapse (2)
Severe trauma with haemopericardium (3) Mitral and/or tricuspid respiratory flow variations (1)
Rupture of the free wall after acute myocardial Swinging heart (1)
infarction (3)
Type A aortic dissection with haemopericardium (6)
Rarely progressing to cardiac tamponade
Early and late pericarditis Dressler syndrome in acute Low-grade fever (0.5) Normal chest radiograph (–1)
myocardial infarction (0) Distant heart sounds (0.5) Normal ECG (–1)
Autoreactive chronic pericardial effusion (0) Pericardial chest pain (0.5) Moderate pericardial effusion (1–2 cm in diastole) (1)
Any other aetiology of chronic pericardial disease (that Pericardial friction rub (0.5) Small pericardial effusion (<1 cm in diastole), no trauma
is, cholesterol pericarditis, chylopericardium) (0) or recent interventional procedure (–1)
Normal blood pressure (–1)
Hypothyroidism or hyperthyroidism (–1)
Slow evolution of the disease (–1)
Systemic autoimmune disease (–1)
Never progressing to cardiac tamponade
Pericardial transudates in heart failure or pulmonary Pulmonary oedema (0) Pericardial effusion only in systole (0)
hypertension (0)
Pericardial transudates in the last trimester of normal
pregnancy (0)
Numbers in parentheses are points in the scoring system for the triage of patients with cardiac tamponade. A total score >6 indicates a need for immediate drainage of pericardial effusion.
ECG, electrocardiography; IVC, inferior vena cava; SBP, systolic blood pressure. Adapted with permission from ref. 5, Oxford University Press.
although cancer (10–25%), infections (15–30%), iatrogenic causes benign, in most cases they reduced in size during follow-up (mean
(15–20%) and connective tissue diseases (5–15%) are also common 50 months) and complete regression occurred in ~40% of cases. The
causes. Tuberculosis is the most frequent cause of pericardial effusion risk of cardiac tamponade was 2.2% per year29. A study conducted in
in developing countries (>60%), where it is endemic21,22. 1999 (study period 1977–1992) reported occasional patients with large,
Pericardial effusion is not uncommon in end-stage renal disease initially asymptomatic effusions30. Patients with suspected idiopathic
(ESRD)3. Two entities unique to patients with kidney disease are uraemic chronic pericardial effusions were prospectively enrolled and fol-
pericarditis (which develops before or within 8 weeks of initiation of lowed up for 18 months to 20 years (median, 7 years). Of 1,108 patients
dialysis) and dialysis-associated pericarditis (which occurs in patients with pericarditis, 461 had a large pericardial effusion and 28 of these
on dialysis for more than 8 weeks). The prevalence of asymptomatic patients were included in the study. Overt tamponade was present in
pericardial effusion, which could be from either pericarditis or volume 8 (29%) patients and 7 of the 8 patients had pericardial effusion for
overload alone, has been reported in 70–100% of these patients23. 1–8 years (median 4 years). During follow up, 10 patients died (due
Initial studies reported the incidence of cardiac tamponade in up 20% to cancer, chronic kidney disease, coronary artery disease, stroke or
of patients with dialysis-associated pericarditis24. dementia) and 1 patient was lost to long-term follow up. Among the
A rising prevalence of ESRD in the modern era of renal replacement remaining 17 patients, pericardial effusion was absent in 14 patients,
therapy has led to an increase in ESRD-related pericardial syndromes, mild in 2 patients and moderate in 1 patient; cardiac tamponade devel-
yet little is known about the prevalence and implications of pericardial oped in 1 patient after 2 years30. The patient population in these two
effusion in this setting25,26. A 2020 retrospective chart review of 2,820 studies differs in some points. The 1999 study included more women
individuals older than 18 years with known ESRD who were undergoing (67% compared with 54% in the 2019 study) and the sum of anterior and
outpatient evaluation for renal transplantation at Mayo Clinic Arizona posterior echo-free spaces at end-diastole ranged from 23 to 54 mm,
(2001–2015) reported a prevalence of moderate-to-large effusions of while the median size of the effusion in the 2019 study was 25 mm.
1.9% and cardiac tamponade in 7 patients26. Furthermore, overt tamponade was present in 29% of cases in the
Cancer or infection account for 15–50% of cases of pericardial 1999 study and the follow-up was longer.
effusion resulting from pericarditis27,28. A study published in 2019 evalu- A prospective, registry-based, case-control study of patients
ated the outcome of idiopathic, chronic (>3 months), large pericardial with the congenital condition pectus excavatum showed that 13.9%
effusions (>20 mm on echocardiography) without initial evidence of of 86 control individuals who underwent chest CT for cardiovascular
pericarditis in 100 patients. These pericardial effusions were usually disease (but did not have pectus excavatum) had a small pericardial

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effusion31. Pericardial effusion was significantly more common among and carboplatin) and 33 (16%) received radiation therapy to the medi-
patients with pectus excavatum than controls (odds ratio 10.91). The astinum within 1 year before the procedure46. Radiation‐induced
authors concluded that the absence of adverse pericardial events at cardiovascular diseases, among which are pericardial syndromes,
follow-up suggested a good prognosis for these effusions31. are well described as a late effect in patients with cancer treated with
Cardiac tamponade has been reported in <15% of patients with radiation therapy. Exposure to ≥250 mg/m2 of anthracyclines increased
idiopathic acute pericarditis and in up to 60% of those with bacterial the relative hazard twofold to fivefold, while cardiac radiation expo-
or neoplastic forms32. In a systematic review of publications on recur- sure of ≥1,500 cGy increased the relative hazard by twofold to sixfold
rent pericarditis published between 1966 and 2006, the rate of cardiac compared with survivors that had not undergone radiation therapy47.
tamponade among patients with idiopathic recurrent pericarditis was Radiation therapy is known to be associated with acute pericarditis and,
3.5%, giving an estimated incidence of ~1–6 cases per 100,000 popu subsequently, with pericardial effusion leading to cardiac tamponade47.
lation. Most of these cases of cardiac tamponade occurred early in the
course of the disease33. Autoimmune diseases. Cardiac involvement is not uncommon in
systemic inflammatory diseases. Several groups have reported on the
Malignancy. In developed nations, cardiac tamponade is most fre- incidence of cardiac tamponade in patients with SLE at their centres.
quently found in patients with cancer34–38, although the exact preva- One group found that 16.4% of 690 patients had SLE-related pericar-
lence is unknown. Cardiac tamponade can occur in the presence of solid dial effusion and 1.5% had cardiac tamponade48. Mortality was higher
tumours (most commonly lung and breast cancers, adenocarcinoma, among patients with than in those without pericardial effusion (30.1%
oesophageal squamous cell carcinoma, melanoma, thymic carcinoma versus 11.3%; P < 0.001)48. A group from India reported that pericarditis
and, rarely, germ cell, renal, or bladder cancer and Ewing sarcoma) or and cardiac tamponade were diagnosed in 25.4% and 5.9%, respectively,
haematological malignancy (usually leukaemia and non-Hodgkin and of 409 patients with SLE49,50.
Hodgkin lymphomas and, rarely, acute and chronic myeloid leukaemia Pericardial effusions are usually clinically silent in rheumatoid
and myelodysplastic syndrome)18,39–43. arthritis51 and are often identified on autopsy52 (11–50% in necropsy
Cardiac tamponade can occur as the result of the malignancy per se44 studies). Asymptomatic pericardial effusions were reported in 20.3%
or the treatment being received (chemotherapy or radiotherapy). of 87 patients with rheumatoid arthritis53, predominantly in men, and
A retrospective analysis of 1,207,580 adult patients (age ≥18 years) coexisted with pleural effusions. Progression of these effusions to
with lung cancer in the 2016–2018 Nationwide Inpatient Sample identi- tamponade is described in case reports54.
fied 7,105 (0.6%) individuals who developed cardiac tamponade. This
outcome was more common in men and among patients who received Cardiovascular conditions. Cardiac tamponade occurs in <1% of
radiation therapy (0.9% versus 0.7%)45. In a study conducted in 2015 of patients with fibrinolytic-treated ST-segment elevation myocar-
1,645 patients with cancer who were referred for pericardial effusions, dial infarction and is associated with increased 30-day mortality55.
212 (13%) underwent percutaneous pericardiocentesis — 186 (88%) According to an analysis of data from over 100,000 patients, increas-
were exposed to chemotherapy (doxorubicin, cyclophosphamide ing age, anterior infarct location, female sex and increased time from
a Rapid pericardial effusion

b Slow pericardial effusion
Cardiac tamponade Cardiac tamponade

Pressure
Pressure
Limit of pericardial stretch
Pericardial reserve volume Pericardial reserve volume
Volume Volume
Fig. 2 | Pressure–volume curves depicting acute and chronic pericardial any further increase in fluid and, consequently, in the rate of expansion will
effusion. a, Rapid fluid accumulation in iatrogenic acute pericardial effusion exceed the limit of pericardial stretch. b, Slow fluid accumulation in chronic
due to, for example, perforation of coronary arteries during percutaneous pericardial effusion10,88. Pericardial stretching over an extended period of time
coronary intervention, myocardial perforation during endomyocardial results in a shift in the pressure–volume curve to the right (stress relaxation).
biopsy or pacemaker lead placement, electrophysiology procedures or Therefore, slowly developing effusions might not necessarily result in cardiac
trauma. When the effusion reaches the maximum pericardial reserve volume, tamponade. Reprinted with permission from ref. 208, Oxford University Press.

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symptom onset to treatment were significant independent predictors associated with an increased risk of pericardial effusion and cardiac
of tamponade55. Importantly, clinicians should consider cardiac tam- tamponade73. Ablation of atrial fibrillation can also be complicated
ponade due to pericardial effusion as a potential cause of hypotension by cardiac tamponade. In a study of 34,943 ablation procedures in
in patients with acute ST-segment elevation myocardial infarction. 25,261 patients at 19 centres, the incidence of tamponade was 0.84%74.
Post-myocardial infarction pericarditis occurs with an incidence of The risk of tamponade was almost twofold higher in women than in
<5% in developed countries and may present as early infarct-associated men, and high-volume centres were associated with a lower risk of this
pericarditis (within 5 days after an acute event) or late post-myocardial outcome74. The reported rate of cardiac tamponade was similar (0.8%)
infarction pericarditis (also known as Dressler syndrome; presents in a single-centre study of 1,500 catheter ablations13.
2–8 weeks after infarction). Delayed angioplasty is a major risk factor Cardiac tamponade can be precipitated by the erroneous use of
for pericarditis. Cardiac tamponade is a rare complication in both56. various medications used to treat other disorders3. Intravenous loop
The incidence of cardiac tamponade has been reported to be diuretics can magnify the effects of a pre-existing effusion (so-called
8–31% in patients with acute aortic dissection57–60. However, many of low-pressure tamponade) and some, such as β-blockers, impair
these patients die before reaching hospital and before a diagnosis can responses that can help compensate for a significant effusion. Others,
be made. In the large cohort of the International Registry of Acute Aor- such as anticoagulants and thrombolytics, can increase the size of an
tic Dissection, 18.7% of 674 patients (mean age 61.8 years) had cardiac effusion or occasionally cause one de novo3.
tamponade as a life-threatening complication of acute type A aortic
dissection60. Tamponade complicating aortic dissection was associated Mechanisms/pathophysiology
with poor in-hospital outcomes and significantly increased mortality60. Anatomical and physiological role of the pericardium
The anatomy of the pericardium supports its most important
Iatrogenic factors. Post-cardiac injury syndrome can manifest in a vari- functions — stabilizing the position of the heart, reducing friction by
ety of circumstances, with one common feature — previous injury to the lubricating the moving surfaces of the heart, and equalizing gravita-
myocardium with blood in the pericardial cavity (haemopericardium). tional and hydrostatic forces mediated by the pericardial fluid75. The
The syndrome can develop after cardiac surgery (post-pericardiotomy pericardium also provides mechanical support, mainly through
syndrome), blunt or penetrating cardiac trauma, or perforation of the the parietal pericardium, by limiting cardiac distension and facilitating
heart with a catheter. ventricular coupling and interaction76. Ventricular coupling (or ven-
Despite advances in cardiac surgery techniques, it remains a tricular interdependence) occurs when the function of one ventricle
common postoperative complication and the cause of surgical rein- is altered by changes in the filling of the other ventricle. By acting as
tervention in 0.1–6% of cases61. Early pericardial effusion appears in a mechanical barrier to infection, the pericardium also has metabolic
the first 48 h after surgery and is related to microvascular bleeding, and immunological functions. Substances produced by the mesothelial
while late-delayed pericardial effusion, which occurs more than 48 h cells of the parietal serosa, such as prostacyclin, eicosanoids and pros-
postoperatively, is attributed to an inflammatory reaction of the taglandin E2, regulate sympathetic neurotransmission and myocardial
pericardium62,63. Late-delayed pericardial effusion does not show spe- contractility and can affect epicardial coronary arterial tone77,78.
cific clinical signs, which makes it more difficult to diagnose than early The movement of fluid through the visceral and parietal layers of
pericardial effusion61. In studies from the early 2010s of the contempo- the pericardium is the result of hydrostatic and/or osmotic pressure
rary features, risk factors and prognosis of post-pericardiotomy syn- equilibrium between the microvasculature and the cavity, with a net
drome, the incidence of cardiac tamponade after cardiac surgery varied pressure difference of 2–10 mmHg, which drives the fluid from the epi-
from 1.9%64 (Italian study, 360 patients) to 4.3%65 (South Korea). In a cardium towards the pericardial cavity3,79. Therefore, total pericardial
2020 retrospective, observational cohort study of 1,460 adult patients volume includes not only the pericardial fluid but also cardiac volume
undergoing heart valve surgery at Odense University in Denmark, the and the volume of the intrapericardial portions of the great vessels.
incidence of cardiac tamponade was 17%66. Under physiological conditions, the pericardium can stretch to accom-
Iatrogenic cardiac tamponade can also be caused by complica- modate changes in cardiac volume but, because of its relatively inelastic
tions of interventional procedures such as electrophysiological tests, and non‐compliant structure, becomes increasingly inflexible when
coronary or valvular interventions, endomyocardial biopsy and pace- the reserve volume is exceeded75,80,81. Normal pericardial pressure is
maker implantation7,11,13. The increasing use of these procedures has best thought of as a contact pressure between the parietal and visceral
led to a rise in the incidence of haemopericardium. In the literature, pericardium, at least regarding its influence on cardiac filling pressure,
the reported prevalence of coronary perforation as the procedural and was quantified in animal models during the 1980s and 1990s82,83.
complication of percutaneous coronary intervention is 0.2–0.6%, with Analysis of samples from 120 consecutive patients who underwent
associated increases in mortality and in rates of pericardial tamponade elective open-heart surgery showed that pericardial fluid is rich in
and cardiogenic shock67. However, the incidence of these complications nucleated cells, protein, albumin and lactate dehydrogenase, at con-
has decreased over the past couple of decades67–70. Among 389 patients centrations consistent with inflammatory exudates in other biological
undergoing transcatheter aortic valve implantation (TAVI) between fluids84. The Light criteria, which were originally developed for pleural
2007 and 2012, cardiac tamponade occurred in 4.3%, and mortality effusions, have traditionally been used to characterize pericardial effu-
among these individuals was 23.5%71. In a more recent analysis (study sions in transudates and exudates85,86. However, we do not recommend
period 2015–2019), cardiac perforation and tamponade occurred the use of the Light criteria to interpret pericardial fluid as they are not
in 0.9% of 2,102 patients undergoing TAVI72. The risk of cardiac tam- validated in this setting. In fact, according to these criteria, normal
ponade was substantially greater and nearly doubled in patients who pericardial fluid would almost always be erroneously interpreted as
required a permanent pacemaker after TAVI versus those who did not an inflammatory exudate. Speculatively, lactate dehydrogenase in
(1.6% versus 0.8%); among 54,317 unweighted hospitalizations for TAVI, particular could be released by mesothelial cells, which are abundant
5,639 (10.4%) required a pacemaker73. Female sex was independently in normal pericardial fluid.

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Pathophysiology of cardiac tamponade The haemodynamic spectrum ranges from preclinical tamponade,
Accumulation of pericardial fluid, pus, blood, clots or air can lead to a when pericardial pressure is equal to right atrial pressure but lower than
rapid (Fig. 2a) or slow (Fig. 2b) increase in intrapericardial pressure and left atrial pressure, to incipient cardiac tamponade, when pericardial
compression of the heart resulting in chronic venous congestion, hypo- pressure is equal to left atrial pressure100. Moderate cardiac tamponade
tension, circulatory shock and, eventually, cardiac arrest75,87,88. When a is when the mean pericardial pressure is >10–12 mmHg, an increased
pericardial effusion reaches the maximum pericardial reserve volume jugular pulse is detectable101–103 and compression of the right ventricles
(the volume at which the pericardium starts to expand), any further can be detected103. Further elevation of pericardial pressure causes
increase in volume will soon pass the limit of pericardial stretch89,90 advanced tamponade (pulsus paradoxus, tachycardia, very low stroke
(Fig. 2). Normally, the pericardium is able to stretch if the effusion volume and blood pressure)89,97,98.
develops slowly over time, but the stretching capacity is determined In pure (non-traumatic, non-haemorrhagic) cardiac tamponade,
by its histological composition (proportion of collagen and elastic early diastolic filling is markedly reduced because of compression
fibres) and the presence of inflammatory or neoplastic infiltrate and is around the heart. Therefore, early diastolic mitral or tricuspid valve
dependent on the effusion accumulation rate. At the limit of pericardial inflow (E velocity) is reduced. Diastolic flow in the hepatic vein is also
stretch, intramyocardial volume is competing with the intrapericar- reduced with prominent diastolic flow reversal. In patients who develop
dial content for the fixed, total pericardial volume. As summarized by effusive–constrictive pericarditis, the mitral inflow filling pattern is
Spodick76,89, the stiffness of the pericardium determines the level of fluid similar to that of constrictive pericarditis with increased early dias-
increase that triggers cardiac tamponade, with an initial slow increase tolic filling104. Utilizing comprehensive echocardiography, a study
followed by an exponential increase. Therefore, cardiac tamponade is found that 16% of patients had effusive–constrictive pericarditis after
a ‘last-drop’ phenomenon, where the last increase in pericardial fluid pericardiocentesis (aspiration of fluid from the pericardial space)105.
leads to critical cardiac compression and the first decrease during These individuals had a higher incidence of hospitalization
drainage produces the greatest relative decompression91. compared with patients who did not have effusive–constrictive
In an acute situation, depending on the aetiology, fairly small pericarditis105. However, contrary to previous studies106, in which a
pericardial effusions (<250 ml) can cause severe cardiac tamponade92. high incidence of pericardiectomy was reported, pericardiectomy
By contrast, large but slowly developing effusions of 1,000–2,000 ml was seldom necessary as constrictive haemodynamics caused by
might not result in overt cardiac tamponade. pericardial inflammation usually resolved spontaneously or with
The most common reasons for an increase in pericardial pres- anti-inflammatory medication105.
sure, which might result in cardiac tamponade, are intrapericardial
fluid accumulation, increased cardiac chamber volume or increased Molecular mechanisms
pericardial stiffness. The most important adverse effects on the heart The inflammasome was first reported in 2002 (ref. 107) and has since
include the aforementioned compressive effect, which limits filling been a major focus of research on innate immunity108–110. The role of
of the heart during diastole, as well as elevated diastolic filling pres- inflammasome activation has been investigated in the pathological
sures and decreased stroke volume and cardiac output, which can progression of various cardiovascular diseases. The NACHT, LRR
rapidly become life threatening if not treated or if no compensatory and PYD domains-containing protein 3 (NLRP3) inflammasome is a
mechanisms are activated76,93. protein complex that acts as a platform for the rapid induction of an
Cardiac tamponade is a haemodynamic event that involves an inflammatory response to infection or sterile injury. NLRP3 induces
equal increase in atrial and pericardial pressures (although inter- not only the production of pro-inflammatory cytokines, by promot-
mediate stages occur where equality is not necessarily present), ing the cleavage and release of IL-1 family cytokines, but also a spe-
a raised expiratory decrease in aortic systolic pressure and arterial cific programmed cell death pathway known as pyroptosis. The NLRP3
hypotension89. Owing to its thinner wall, the right ventricle is more inflammasome is a research area of great promise for idiopathic and
readily affected than the left ventricle by the increased pericardial post-injury pericarditis111 and could also be relevant in patients with
pressure during pericardial effusion. Pressure in the right ventricle overt cardiac tamponade due to idiopathic effusive–constrictive
is overridden by the sudden increase in pericardial pressure caused pericarditis. However, the significance of NLRP3 has not been
by the rise in ventricular volume in early diastole, such that the right demonstrated in tamponade of other aetiologies as suitable animal
ventricle might even collapse94,95, an event that specifically defines models of pericarditis are lacking.
advanced pericardial tamponade89,96. However, whether the volume of In 2021, a study reported on a new experimental model of
the right ventricle actually decreases is unclear owing to the difficulty acute pericarditis in mice through the intrapericardial injection
in quantifying its volume. of zymosan A, an activator of the NLRP3 inflammasome112. Zymosan
As the heart is compressed throughout the cardiac cycle during A causes the classical features of pericardial inflammation, including
tamponade, systemic venous return is impaired. Right atrial and right pericardial effusion, pericardial thickening, upregulation of IL-1α and
ventricular collapse results in left ventricular restriction due to ventricu- IL-1β, and increased expression of apoptosis-associated speck-like
lar interdependence when the total volume of the heart chambers is fixed protein as an unambiguous marker of NLRP3 inflammasome activa-
and any change in the volume of one side of the heart causes the opposite tion. Anti-inflammatory medications, such as ibuprofen (an inhibitor
changes in the other side97–99. In cases of compressive pericardial effu- of prostaglandin G/H synthase 2, also known as cyclooxygenase 2) and
sion, expansion of the right ventricle during inspiration compresses colchicine (an NRLP3 inhibitor), reduced pericardial effusion but not
the left ventricle, resulting in decreased filling and a drop in stroke pericardial thickening. IL-1 blockade via two different IL-1 receptor
volume with a decrease in systolic blood pressure (SBP), termed pulsus antagonists — anakinra and rilonacept — significantly reduced both
paradoxus, of >10 mmHg (ref. 98). During expiration, the left ventricle pericardial effusion and thickening112. However, to date, no promising
is filled again by the restoration of pulmonary venous return, but the data are available that specifically address the inflammasome or any
right ventricle is compressed and systemic venous return is interrupted. other molecular mechanisms in the occurrence of cardiac tamponade.

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Diagnosis, screening and prevention circulatory shock (rapid breathing, sweating, cool extremities, periph-
Clinical presentation eral cyanosis and a decline in consciousness). Jugular venous distension
Cardiac tamponade is a clinical emergency that should be promptly is striking but can be less prominent in patients with hypovolaemia or
recognized (Fig. 3) as a possible cause of dyspnoea (shortness of breath if pericardial effusion accumulates slowly91,117,118. Pulsus paradoxus93,96
or breathlessness) accompanied by elevated systemic venous pres- can be detected during blood pressure measurement as the difference
sure, tachycardia, low blood pressure and paradoxical arterial pulse in between the SBP at which Korotkoff sounds (audible noises used to
the presence of haemodynamically important pericardial effusion on measure blood pressure using a stethoscope) are first audible and the
echocardiography. Ultimately, cardiac tamponade is a clinical diagnosis SBP at which they are audible through the whole respiratory cycle119–121
requiring echocardiographic confirmation113–115. (Fig. 3a). Large pericardial effusions can compress the base of the
Classical symptoms and signs include dyspnoea (progressing to lung, resulting in Bamberger–Pins–Ewart sign (a dullness on percus-
orthopnoea (shortness of breath or breathlessness when lying down, sion in the precordium and under the left scapula), which is present
which necessitates sleeping in a sitting or propped-up position), weak- in a subset of patients with possible cardiac tamponade92. In addition,
ness, fatigue, tachycardia and oliguria (urinary output <400 ml per day fever is a non-specific sign that can be associated with an infectious or
or <20 ml per hour)3,5,10,89. If cardiac tamponade is preceded by acute immune-mediated aetiology of pericarditis. The most widely known
pericarditis, the patient might experience typical chest pain increasing clinical signs of cardiac compression described by Beck in 1935 (ref. 122)
on inspiration and radiating to the trapezius ridge. Local compression (hypotension, increased jugular venous pressure and distant heart
from the pericardial effusion can also occasionally manifest as nausea, sounds) are still frequently quoted as the clinical diagnostic criteria for
dysphagia, hoarseness and hiccups89. Additional clinical manifestations cardiac tamponade; this triad was seen in patients undergoing surgery
depend on the aetiology; some patients with viral aetiology116 present for intrapericardial haemorrhage due to trauma or myocardial or aortic
with right upper quadrant pain due to hepatic venous congestion and rupture102,123. However, many studies and clinical observations have
hepatomegaly. demonstrated that the triad is not sensitive or specific for cardiac tam-
Some but not all traditional physical findings (hypotension, ponade. In a retrospective study of emergency department admissions
increased jugular venous pressure and muffled heart sounds)117 are conducted in 2017, sensitivity of the Beck triad was found to be 0% (range
present in a substantial portion of patients with echocardiographic 0–19.4%) and sensitivity for one finding was 50% (range 28–72%)124.
evidence of cardiac tamponade. In acute cardiac tamponade, SBP is The presence of pericardial effusion or cardiac tamponade is
<90 mmHg but, in subacute cases, blood pressure might be only slightly usually secondary to an underlying pathology, some of which can
reduced, and patients with hypertension have normal to mildly elevated be life threatening such as aortic dissection or free wall rupture. The
blood pressure (relative hypotension)118. Signs of advanced cardiac differential diagnosis of cardiac tamponade includes pulmonary
tamponade reflect varying degrees of reduced cardiac output and embolism, type A aortic dissection without cardiac tamponade and
Fig. 3 | Diagnostic techniques in cardiac

a b tamponade. a, Pulsus paradoxus: inspiratory
150 reduction of >10 mmHg in systolic blood pressure.
b, Chest radiograph showing cardiomegaly
Arterial pressure (mm Hg)
and a ‘water bottle’ shaped cardiac silhouette.

100 c, Electrocardiogram showing tachycardia, low
QRS voltage and electrical alternans (phenomenon
of alternation of QRS complex amplitude; blue and
50 red arrows). Part a reprinted with permission from
ref. 10, Oxford University Press.
0
Expiration Inspiration

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a b c
PE
RV LV
RV
RA LV RA LA
LA
d e f
PE
g h
Fig. 4 | Echocardiography and pericardiocentesis in cardiac tamponade. Large guidance from the apical angle or view (part e) for pericardiocentesis from the
pericardial effusion from the 2D subxiphoid view, M-mode view and apical long- intercostal (apical) approach (part f). Loculated pericardial effusion with massive
axis view with right atrium collapse (arrow) (part a) and subxiphoid approach to adhesions (part g). Surgical drainage: subxiphoid pericardiotomy (also known
pericardiocentesis (part b) guided by echocardiography and fluoroscopy (part c). as sternotomy with pericardiotomy; part h). LA, left atrium; LV, left ventricle;
Large separation of pericardial layers from the apical view (part d, left image) PE, pericardial effusion; RA, right atrium; RV, right ventricle. Reprinted with
but very small from the subxiphoid (part d, right image). Echocardiographic permission from ref. 10, Oxford University Press.
acute myocardial infarction involving the right ventricle. In subacute for the detection of cardiac tamponade3. Two-dimensional echocardio
onset effusive–constrictive pericarditis, congestive heart failure and graphy can detect diastolic right ventricular and atrial wall compres-
advanced liver cirrhosis should be excluded. In contrast to patients with sion, which occurs when intrapericardial pressure increases in cardiac
heart failure, those with cardiac tamponade do not have pulmonary tamponade (Supplementary Video 1). In the 1970s, animal models
crackles or pulmonary oedema — a condition caused by excess fluid established ventricular interdependence as the most characteristic
in the lungs. haemodynamic feature of cardiac compression seen in cardiac tam-
ponade and constrictive pericarditis128,129. Both M-mode and Doppler
Diagnostic tools and modalities echocardiography detect ventricular interdependence by demonstrat-
Echocardiography. Before the introduction of echocardiography, ing respiratory variation in ventricular filling126,130. M-mode echocardio
the detection of pericardial effusion was challenging. Indeed, assess- graphy provides evidence of right ventricle collapse in early diastole
ment of pericardial effusion was one of the first clinical applications and pericardial effusion. Pulsus paradoxus can be easily detected as a
of echocardiography in 1965 (ref. 125). Over the past six decades, echo- characteristic ventricular septal motion by real-time imaging.
cardiography has become the diagnostic modality of choice, not only In most cases of cardiac tamponade, pericardial effusions are mod-
for the detection of pericardial effusion but also for the diagnosis of erate to large (Fig. 4). A swinging, pendular motion of the heart within
cardiac compression and to guide pericardiocentesis126,127. the pericardial fluid is a common finding102,131 (Supplementary Video 2).
In the 2015 ESC guidelines on pericardial diseases, echocardio Other major echocardiographic findings include collapse of the right
graphy is recommended as the single most important diagnostic tool atrium during late diastole (Fig. 4a and Supplementary Video 1),

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collapse of the right ventricle during early diastole, compression of the for cardiac tamponade, a group that is considered to be at high risk of
left atrium and, rarely, the left ventricle (Supplementary Video 3 and requiring pericardiectomy104.
Supplementary Video 4), respiratory variations in flow velocities of
cardiac chambers, expiratory diastolic flow reversal (<50% reduction in Electrocardiography. Electrocardiographic evidence of cardiac tam-
the diameter of the dilated inferior cava vein during inspiration)3,5,10,89,130 ponade includes low QRS voltage and electrical alternans (Fig. 3b).
in the hepatic veins, and congestion of the hepatic veins and inferior After drainage of pericardial effusion, normalization of the QRS
vena cava. However, in patients with pulmonary hypertension or other amplitude can be delayed but this finding is by no means consistent132.
conditions causing right ventricular hypertrophy or elevated right Atrial arrhythmias as well as widespread ST-segment elevation with
ventricular diastolic pressure, collapse of the right ventricle during or without PR depression have been reported in the setting of acute
early diastole can be absent. pericarditis and in patients with pericardial effusions14.
Echocardiography is useful for the differential diagnosis of
effusive–constrictive pericarditis, cardiac tamponade and constric- Chest radiography. In patients with a large effusion, the cardiac
tive pericarditis (Fig. 5). A Mayo Clinic study104 compared echocardio silhouette has a typical ‘water bottle’ shaped appearance (Fig. 3c).
graphy findings obtained between 2002 and 2016 of 22 patients This simple sign in the appropriate clinical context (a symptomatic
(predominantly men, 64%) diagnosed with effusive–constrictive patient with a large pericardial effusion) has a high sensitivity for the
pericarditis who had persistently elevated jugular venous pressure diagnosis of cardiac tamponade but does not determine the urgency
after pericardiocentesis, 30 patients with constrictive pericarditis of pericardiocentesis. Furthermore, cardiomegaly of other aetiologies
and 30 patients with cardiac tamponade with normalized venous pres- cannot be ruled out. In patients with pericardial effusion or cardiac
sure after pericardiocentesis (Fig. 5). Even before pericardiocentesis, tamponade, the lungs can appear dark on the chest radiograph, indi-
effusive–constrictive pericarditis had unique echo-Doppler features cating reduced pulmonary blood volume resulting from an imbalance
(higher medial and lateral e′ velocities; Fig. 5) that distinguished it between right-sided and left-sided cardiac output. If radiographic
from both constrictive pericarditis and cardiac tamponade. Inspir- images have good penetration in the lateral view, pericardial fluid
atory and expiratory mitral E-to-A ratios were higher in effusive– suggested by lucent lines within the cardiac shadow (epicardial fat pad
constrictive pericarditis than in cardiac tamponade but lower than sign) can be used for fluoroscopic guidance of pericardiocentesis in
in constrictive pericarditis. Hepatic vein diastolic reversal velocities the catheterization laboratory133–135.
decreased in cardiac tamponade and remained unchanged in effusive–
constrictive pericarditis. Three patients (all in the effusive–constrictive Cardiac CT and cardiovascular MRI. These modalities are very
pericarditis group) required pericardiectomy for constrictive peri- rarely needed in the clinical diagnosis of cardiac tamponade except
carditis during follow-up (median 481 days). Effusive–constrictive to confirm aetiology in cases of chest trauma or where there is a high
pericarditis occurred in 8% of patients undergoing pericardiocentesis suspicion of aortic dissection129,136–139. CT and MRI provide excellent
Fig. 5 | Echocardiography in the differential

diagnosis of cardiac tamponade. Schematic
of mitral annulus tissue Doppler imaging (TDI),
mitral inflow and hepatic vein Doppler velocities
in cardiac tamponade, effusive–constrictive
Pericardial sac
filled with fluid pericarditis and constrictive pericarditis.
D, diastolic forward flow; DR, diastolic flow
reversal; Exp, expiration; Insp, inspiration;
Cardiac Effusive–constrictive Constrictive S, systolic forward flow. Adapted with permission
tamponade pericarditis pericarditis from ref. 104, Oxford University Press.
Medial TDI
8 cm/s a' a' a'
e'
e' e'
Exp Insp Exp Insp Exp Insp
E E
A A E A E
E A
A
E
A
Mitral inflow
DR DR DR
DR DR DR
Hepatic vein
D
S D S S D
D S D
S S

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Fig. 6 | Cardiac MRI in assessment of pericarditis. Cardiac MRI views of the heart with the inflamed pericardium shown by delayed enhancement (arrows).
delineation of the pericardial anatomy and are sensitive, non-invasive Pericardial fluid and tissue analysis
methods of evaluating loculated or haemorrhagic pericardial effu- Pericardial fluid is rich in various components, including nucleated
sion, constrictive pericarditis, pericardial thickening, pericardial cells, proteins and albumin as well as lactate dehydrogenase, at levels
masses, and congenital anomalies130,140. Right ventricular wall flat- consistent with the inflammatory exudates of other biological fluids
tening and pericardial thickening correlate with haemodynamically such as pleural or peritoneal fluid84. The normal reference values for
significant pericardial effusion, and coronary sinus compression can these components of pericardial fluid were published in 2020 (ref. 84).
be an early sign of cardiac tamponade on CT. Furthermore, CT can be Diagnostic findings from routine analysis of pericardial fluid have
used to determine the feasibility of percutaneous pericardiocentesis been disappointing, limited predominantly to detecting cancer cells
in loculated or complex effusions130 and is particularly sensitive in and bacteria. Pericardioscopy-guided extensive pericardial biopsy
identifying pericardial calcification130. MRI provides information about (of ~20 samples per patient) is a potentially powerful novel diagnostic
the extent of pericardial disease and defects in surrounding structures approach but its usefulness is unclear owing to a lack of validation in a
and enables accurate measurement of pericardial and related struc- sufficient number of patients149,150. In this context, analysis of cytokines,
tures. MRI also provides superior tissue characterization, including inflammatory mediators, and serological and immunological markers
the presence and extent of pericardial inflammation141 (Fig. 6), and could help identify the underlying aetiology of pericardial effusion and
enables the entire chest to be examined and associated abnormalities cardiac tamponade151. In a systematic review of 42 studies (mostly retro-
in the mediastinum and lungs to be detected owing to the greater field spective) performed in various countries (50% of the studies were from
of view than that of echocardiography142–145. the USA) in the period 1972–2020, the diagnostic performance of cytol-
ogy (cell analysis), histology (tissue analysis) or both was assessed152.
Cardiac catheterization and invasive haemodynamics. These pro- Cytology was shown to be superior to histology for detecting cancer
cedures allow the evaluation of heart function146 and can be considered associated with pericardial effusions in most of the studies152. Other
in cardiac tamponade when clinical examination and non-invasive investigators found that the overall sensitivity of combined cytology
imaging are inconclusive and in patients who have complex haemo- and histology for cancer detection in pericardial effusions was 94%153.
dynamic disorders10,32,147. Cardiac catheterization reveals elevated The International System for Reporting Serous Fluid Cytology
right atrial pressure, which is visible on the right atrial pressure curve (ISRSFC)154 was developed to improve diagnosis, standardize report-
as a prominent x descent and the unique finding in the jugular venous ing and facilitate communication among physicians. This system uses
pulse wave, namely an absent y descent, in distinction to the presence five reporting diagnostic categories (non-diagnostic, negative for
of this feature in constrictive pericarditis (because early diastolic malignancy, atypia of undetermined significance, suspicious for malig-
blood flow from the right atrium to the right ventricle is impaired by nancy, and malignant – primary and secondary) linked with variable
the compressive effect of the surrounding pericardial fluid). Diastolic risk of malignancy155. A study tested the performance of this system by
pressures in all ventricles are usually 15–25 mmHg. A ‘dip-and-plateau’ reclassifying 64 pericardial effusion samples using criteria defined
configuration is not observed for ventricular diastolic pressure, by the system and found that the risk of malignancy was 100% for the
which is elevated in early diastole and continues to rise throughout malignant category and 0% for the negative and atypical categories155.
diastole100. Levels of tumour markers (such as adenosine deaminase,
Right-heart catheterization can be conducted at the same alpha-fetoprotein, the cancer antigens CA125, CA72-4, CA15-3 and
time as pericardiocentesis, allowing monitoring as the effusion is CA19-9, carcinoembryonic antigen, and cytokeratin 19 fragment) in
drained. After successful pericardiocentesis, if intrapericardial pres- samples of pericardial fluid can also be assessed following pericar-
sure falls to zero or becomes negative while the right atrial pressure diocentesis. Although the utility of this approach in the diagnosis
remains elevated, the presence of effusive–constrictive pericarditis, of neoplastic pericardial effusion is not well established, low levels of
pre-existing left-sided myocardial, tricuspid valve disease or restrictive adenosine deaminase and high levels of carcinoembryonic antigen and
cardiomyopathy should be considered148. CA72-4 are highly indicative of malignant aetiology156,157.

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Vascular endothelial growth factor is an important mediator of pharmacological therapy, pericardiocentesis and surgery. The only
angiogenesis and vascular permeability produced by cells in healthy tis- effective treatment for cardiac tamponade is prompt percutaneous
sue but also by many tumour cells. Assessment of vascular endothelial or surgical drainage of the pericardial effusion. Open surgery to repair
growth factor levels in pericardial fluid offers potential as a diagnostic the source of the effusion (for example, aortic dissection) might also
tool to discriminate malignant from benign effusions in patients with be required.
breast or lung cancer158–162.
The role of pericardial pro-inflammatory mediators (IL-6 and Pharmacological management
tumour necrosis factor) and immunoregulatory cytokines (trans- Pharmacological treatment of cardiac tamponade is a temporary meas-
forming growth factor-β1 and interferon-γ (IFNγ)) has been studied ure until pericardiocentesis or surgical drainage can be performed.
in neoplastic, autoreactive and viral pericarditis. Levels of IFNγ were Whether inotropic support, with or without vasodilators, is useful in
not correlated with these aetiologies of pericarditis, whereas the hypotensive patients is debated164. However, volume infusion could be
pericardial-to-serum ratio of IL-6 was highest in autoreactive pericar- effective in patients with hypovolaemia and can be used as a ‘bridging’
dial effusion, and the pericardial-to-serum ratios for tumour necrosis therapy until pericardiocentesis can be performed3,167. Intravenous
factor and IFNγ were highest in viral pericardial effusion163. Additional administration of diuretics or vasodilators is strongly contraindicated
studies are needed to establish the diagnostic role of these cytokines. and could be fatal in patients with cardiac tamponade3,5.
Acute pericarditis is a common cause of cardiac tamponade.
Triage of patients In patients with this condition, the evacuation of pericardial fluid
Prompt recognition and management of cardiac tamponade is critical is not sufficient because pericardial fluid rapidly re-accumulates in
but remains challenging in routine clinical practice because of the lack the absence of anti-inflammatory therapy. Corticosteroids, such as
of validated criteria to guide clinicians in the decision-making process. methylprednisolone, are often given intravenously with doses typi-
The triage of patients with cardiac tamponade in the absence of circu- cally ranging from 40 mg to 250 mg. However, if treatment is rapidly
latory shock by a three-step scoring system was proposed by the ESC tapered the condition can recur. In this setting, anti-IL-1 agents can be
Working Group on Myocardial and Pericardial Diseases5. considered, particularly in patients with fever, neutrophil leukocyto-
The first step is to score the aetiology, the second is to score the sis or pleuropulmonary involvement, when C-reactive protein (CRP)
clinical presentation and the third is to score the findings from imag- level is strikingly elevated, and when corticosteroids and NSAIDs are
ing procedures (Table 1). In the absence of contraindications, a total contraindicated (for example, in patients with heart or renal failure,
score ≥6 indicates immediate pericardiocentesis. The ESC scoring ischaemic heart disease, fluid overload, gastrointestinal haemorrhage,
system provides practical support to clinicians for the identification of or recent surgery or those taking anticoagulants)168.
patients needing immediate intervention or who should be transferred Three anti-IL-1 agents are available — anakinra, canakinumab and
to a specialized institution. Although this system is based on available rilonacept. Anakinra is a short-acting IL-1 receptor antagonist that
data and the consensus of experts, systematic, multicentre validation blocks both IL-1α and IL-1β. The drug is administered daily at a dose
is still needed. of 100 mg subcutaneously but this dose can be doubled in cases of
severe, recurrent or colchicine-resistant pericarditis169. In the AIR-
Screening TRIP trial169 of patients with corticosteroid dependency and recur-
Screening for cardiac tamponade includes a thorough evaluation of each rent colchicine-resistant pericarditis, anakinra reduced the risk of
patient with pericardial disease and close follow-up of those presenting recurrence compared with placebo. Some experts consider that
with clinical and haemodynamic worsening. Patients with large pericar- anakinra might be less dangerous than high-dose corticosteroids
dial effusions (>2 cm), high fever, chest trauma and hypotension and in patients with severe infection170 or neoplasm171. In 2022, anakinra
those who do not respond to treatment with anti-inflammatory drugs was used successfully to prevent cardiac tamponade in a patient with
are at high risk for cardiac tamponade. Prompt aetiological diagnosis COVID-19 vaccine-related acute pericarditis172. Anakinra is an estab-
and management directed towards the underlying disease, along with lished drug that is known to be safe. The most common adverse effect
appropriate fluid balance and monitoring, can prevent the development is a short-term, usually mild reaction (redness, swelling and itching)
of haemodynamic instability and overt cardiac tamponade10,164. at the injection site that responds well to topical therapy with ice and
corticosteroids. Patients should be educated about the possibility of
Prevention developing this reaction168,169.
Not all cases of cardiac tamponade can be prevented. However, risk Canakinumab is a human monoclonal antibody directed only
can be reduced by minimizing exposure to bacterial (particularly against IL-1β. Data on its use in recurrent pericarditis are limited to a
tuberculosis) or viral infections and managing underlying medical few case reports and series and the efficacy of this drug, compared with
conditions such as SLE and hypothyroidism. A systematic literature anakinra, is controversial173. The data suggest that both IL-1α and IL-1β
review of 28 cases of cardiac tamponade following influenza infection have a role in the induction of the inflammatory response at the peri-
showed that the onset of tamponade ranged from 1 day to 6 weeks. cardial tissue level, with IL-1α produced locally at the pericardial level168.
Influenza A strain was found in 78.5% of patients and B strain was found Therefore, drugs that target both IL-1α and IL-1β should, theoretically,
in 10.7%165. Vaccination is the most effective way to prevent infection be most effective.
and severe outcomes caused by influenza viruses166. Rilonacept is a dimeric fusion protein consisting of the
ligand-binding domains of IL-1 receptor protein and IL-R, which can
Management block both IL-1α and IL-1β. The efficacy and safety of rilonacept in
Without treatment, cardiac tamponade is invariably fatal. The tim- patients with recurrent pericarditis and elevated CRP levels were demo
ing of interventions is crucial — the longer the delay, the worse the nstrated in the RHAPSODY study174. Rilonacept led to rapid resolution of
outcome. Management of patients with cardiac tamponade includes pericarditis and significantly reduced the risk of recurrence (P < 001)174.

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On the basis of this study, the FDA approved rilonacept for the treat- Marked pericardial inflammation can lead to constrictive haemo-
ment of recurrent pericarditis. The loading dose of rilonacept is 320 mg dynamics after pericardiocentesis. This condition is difficult to man-
administered subcutaneously, followed by 160 mg weekly. Symptom age as constriction induces fluid overload that can be worsened
relief is seen within a few days. However, no data have been published by corticosteroids and NSAIDs. In these patients, moderate doses
describing the effect of rilonacept in cardiac tamponade associated of corticosteroids (for example, 25 mg prednisone) or anakinra could
with acute pericarditis. be considered, particularly when fever, neutrophil leukocytosis and
pleuropulmonary involvement are also present and the CRP level is
Pericardiocentesis elevated168. In a case study of effusive–constrictive pericarditis initially
The best treatment for cardiac tamponade is prompt drainage of the manifesting with cardiac tamponade, treatment with anakinra was
pericardial effusion, which can be lifesaving. Importantly, the clinical effective185. Furthermore, anakinra was shown to have a role in reversal
presentation, aetiology, echocardiographic findings and risk–benefit of incessant or recurrent constrictive pericarditis in 39 patients186.
ratio of the procedure must all be considered when deciding whether Pericardiocentesis in cardiac tamponade resulting from
to drain an effusion. Patients whose condition is unstable and those non-surgical pericardial effusions can be performed from either an
with ongoing haemodynamic compromise have the highest priority apical or subxiphoid approach187. In the case of postsurgical pericardial
for this procedure5,175. effusions localized posterolaterally that spread to the anterolateral part
Aortic dissection and post-infarction rupture of the free wall are of the left ventricle, the apical approach is more frequently used. Thus,
often contraindications for pericardiocentesis3. However, in both situ- the apical approach is a possible important option for the treatment
ations, percutaneous drainage before surgical repair can be considered of postsurgical cardiac tamponade, and it may decrease the need for
when the rate of bleeding is slow. A management algorithm for percu- surgical intervention187.
taneous pericardiocentesis in aortic dissection has been proposed176. Loculated effusions may be removed by echocardiography-guided
Coagulopathy, anticoagulant therapy and thrombocytopenia (<50,000 pericardiocentesis with simultaneous fluoroscopy, which aids the
platelets/mm3) are also contraindications to pericardiocentesis. procedure with safety through the halo phenomenon. This phenom-
If severe coagulation disorders are present, the procedure must be enon allows a precise demarcation of the heart shadow, providing
delayed until adequate blood for transfusion, platelets or coagulation a safer approach while performing an echocardiography-guided
factors are sourced3,177. pericardiocentesis135.
Intubation and ventilation during preparation for pericardiocente- During the 21-year study period from 1979 to 2000, 1,127 thera-
sis are essential in patients with severe hypoxaemia or circulatory shock, peutic echo-guided pericardiocenteses were performed at Mayo Clinic
although positive end-expiratory pressure ventilation might decrease (Rochester, MN, USA), with a procedural success rate of 97% overall.
cardiac output and should therefore be avoided168,178. Pericardiocentesis The total complication rate was 4.7% (major, 1.2%; minor, 3.5%)127.
is best performed under echocardiographic guidance (Fig. 4d–f). Echo- These rates did not change significantly over the study period. The
cardiography is used to identify the chest wall location that is clos- use of a pericardial catheter for extended drainage increased from
est to the greatest accumulation of pericardial effusion in diastole 23% to 75% and rates of effusion recurrence and pericardial surgery
(Fig. 4e), to identify and mark the site of puncture, and to minimize decreased significantly over the study period127. In a Korean study
risk of cardiac perforation and injury to other structures, either in the over the 11-year period from 1993 to 2003 at Yonsei Cardiovascular
subxiphoid or apical region (Fig. 4f). The echocardiographic transducer Center, 291 therapeutic echocardiography-guided pericardiocente-
is used to define needle trajectory before needle insertion. After achiev- sis procedures with pericardial catheter drainage were performed in
ing pericardial access, the plastic cannula should be advanced into 272 patients, with an overall procedural success rate of 99%, a major
the pericardial space and the needle withdrawn. Intrapericardial posi- complication rate of 0.7% (2 cases of right ventricular free wall perfora-
tion is subsequently confirmed by injection of agitated saline contrast tion that required emergency surgery) and only 1 procedure-related
through the plastic cannula. Linear ultrasonography probes should mortality (<30 days)188.
be used when real-time imaging is needed to visualize intraprocedural Pericardiocentesis for cancer and iatrogenic post-surgery compli-
needle position. Curvilinear ultrasonography transducers should cations (as the most common cause of pericardial effusion) had a high
not be used for this purpose, they are unable to accurately identify success rate and relatively low complication rate in a large cohort of
the needle tip179. Echocardiographic guidance can be combined with patients in a Singaporean study189.
fluoroscopy32,135,180,181. During the procedure, measures should be taken In a retrospective observational study of 269 consecutive patients
to prevent secondary bacterial infection of the pericardium. who underwent percutaneous pericardiocentesis between 2006 and
The most serious complications of pericardiocentesis include 2016 at University Hospitals Leuven in Belgium (prospective follow‐up
laceration and puncture of the myocardium and coronary vessels, per- for up to 10 years; ~66% men), most pericardiocentesis procedures were
foration of the peritoneal cavity or abdominal viscera, pneumothorax, performed without complications: the right heart was ‘punctured’ in
and vasovagal bradycardia. Very rare complications include internal 0.7%, pneumothorax occurred in 2.6%, pneumomediastinum occurred
mammary artery fistulas, acute pulmonary oedema and purulent in 0.4%, pneumopericardium occurred in 1.5% and a punctured peri-
pericarditis178. The risk of serious complications was notably dimin- toneal cavity occurred in 0.7%. Among patients undergoing a primary
ished after the introduction of fluoroscopy along with echocardiogra- percutaneous pericardial puncture, 8.6% had a second pericardio-
phy and guidance182,183. Echocardiography-guided pericardiocentesis centesis, 8.2% had a subxiphoid pericardial window and 0.4% had a
was introduced at the Mayo Clinic in 1979 (ref. 184) and is widely used subxiphoid approach followed by video‐assisted thoracoscopy. A small
nowadays. The fluoroscopic approach was the first imaging system effusion was present in 1.9% of patients190.
used for percutaneous pericardiocentesis32 (Fig. 4a–c). Although major In a single centre in Bogotá, Colombia, between 2017 and 2018, sub-
complications are rare, blood for transfusion (400–600 ml) should be xiphoid was the most common pericardiocentesis approach, guided
available and cross-matched before pericardiocentesis32,179. by fluoroscopy (n = 114, 98.2%), The procedure was successful in 98%

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of cases, with perforations of the cardiac chambers in two patients, of treatable. However, in patients with pericardial malignancies or severe
whom one required emergency cardiac surgery62. perimyocarditis, quality of life and long-term prognosis can be poor81.
Patients with malignant effusions also commonly experience cachexia
Surgical management and multiple comorbidities that can detrimentally affect their quality
Urgent surgical treatment for cardiac tamponade is recommended in of life196.
patients with severe recent chest trauma, rupture of the ventricular free Cardiac rehabilitation has been recognized as the most cost-
wall after acute myocardial infarction, type A aortic dissection, purulent effective intervention to ensure favourable outcomes after cardiac
pericarditis or iatrogenic haemopericardium when the bleeding can- surgery by reducing cardiovascular mortality, morbidity, and disability
not be controlled percutaneously and surgical repair of the underlying and improving quality of life197. The Functional Evaluation and Cardiac
source of the effusion (trauma, aortic dissection) is required10. Rehabilitation Working Group of the French Society of Cardiology
Surgical drainage of the effusion, usually through a subcostal inci- reported only 1 patient with cardiac tamponade out of 25,420 patients
sion (Fig. 4g,h), is required in cases when the heart cannot be reached by (78% men) of whom 34.3% after coronary bypass and 18.4% after valvu-
a needle or catheter (loculated effusions situated unilaterally (Fig. 4g) lar surgery in 65 cardiac rehabilitation canters during a 1-year period.
or posteriorly, which is more easily approached thoracoscopically)191, The patient with cardiac tamponade required urgent surgical treatment
in delayed haemopericardium or effusions after cardiac surgery, in after experiencing a cardiovascular event during exercise training after
purulent pericardial effusion, or in tuberculous pericarditis. Open aortic valve replacement198. Patients undergoing cardiac surgery are
surgical drainage procedures usually lead to the creation of a pericar- older and have complex pathologies and several comorbidities197,199.
dial window (Fig. 4h) as an effective long-term solution and involve New components of cardiac rehabilitation have been recom-
excision of a section of the pericardium to allow free drainage of the mended, particularly with regard to the need for appropriate assess-
effusion, either into the mediastinum (subxiphoid) or into the thoracic ment and management of malnutrition and pain200. In patients with
cavity (transpleural)192. depression or anxiety, psychotherapy, medication or collaborative care
Video-assisted thoracic surgery can be considered when a peri- are essential197. Frailty is fairly common in elderly patients (10–50%) and
cardial window is necessary (such as in patients with cancer who is an independent prognostic indicator in this population173. Anecdotal
have recurrent effusions or in loculated effusions, even in effusions evidence suggests that exercise should be avoided in patients with
located posteriorly that cannot normally be reached without open active pericarditis. Complete resolution of the disease can take up to
thoracotomy193). A video-assisted thoracoscopy pericardial window 3 months in severe cases, at which point a return to physical activity
is less traumatic than anterior thoracotomy and provides better should be re-evaluated201–203.
visualization than the subxiphoid approach194.
Open surgery in this setting has several disadvantages. General Outlook
anaesthesia carries a risk of sudden hypotension in patients with large Despite substantial new data and progress towards evidence-based
effusions or cardiac tamponade, and these procedures necessitate a medicine, several issues remain in patients with cardiac tamponade
large (6–8 cm) vertical incision in the upper abdomen and, in some that require further research. First, no worldwide, epidemiological
cases, resection of the xiphoid process. data have been published. Second, most cases of cardiac tamponade
Using a nationally representative sample of 44,637 patients, from single-centre studies are idiopathic in aetiology, and further diag-
of whom 64.7% underwent pericardiocentesis and the rest surgical nostic and therapeutic tools are required to facilitate individualized
drainage for initial management of pericardial effusion or cardiac treatment and to develop guidelines for optimal management of car-
tamponade194, pericardiocentesis was associated with greater odds diac tamponade. Excellent imaging tools are available to help with the
of cardiac complications but lower odds of infection, respiratory diagnosis, management and treatment of pericarditis and tamponade.
failure and blood transfusions compared with surgical drainage194. Furthermore, recent work implicating the inflammasome has contri
Nevertheless, pericardiocentesis was associated with greater odds buted to the use of mechanism-based treatment of common forms
of mortality, reintervention and 30-day readmission but similar of pericarditis. When cardiac tamponade is caused by systemic diseases
30-day cumulative costs compared with surgical drainage. The two that involve the heart, improving the management of these diseases is
strategies yielded similar 30-day cumulative costs194. In a nationwide likely the best approach to improve the treatment and prevention of
survey-based study in the Netherlands195, all interventional cardio cardiac tamponade.
logists and cardiothoracic surgeons were questioned regarding their Several specific open research questions remain unanswered.
preferred diagnostic and treatment modality (pericardiocentesis For example, the appropriate management of patients with large,
versus surgical drainage), revealing substantial variation in the pre- asymptomatic (or oligosymptomatic) idiopathic pericardial effu-
ferred management of pericardial effusions among hospitals and sions is a matter of debate. Some cardiologists favour prompt peri-
clinicians, even within the same centre, possibly due to the lack of cardiocentesis and diagnosis of the underlying aetiology, whereas
specific guidelines195. other centres opt for a more conservative approach (watch and wait).
The conservative approach is adopted because routine analysis of
Quality of life pericardial fluid rarely provides a diagnosis not already presumed by
In the modern era of disease management, patients are living longer and imaging techniques204,205 and because post-cardiac injury syndromes
quality of life has become increasingly important. Cardiac tamponade can occasionally be triggered by invasive procedures such as pericar-
is associated with a spectrum of symptoms affecting patient quality diocentesis and pericardial window27. The superiority of one approach
of life. The underlying aetiology of the pericardial effusion needs to over the other has not yet been demonstrated.
be investigated, diagnosed and treated to minimize the recurrence of To improve the diagnostic utility of pericardial fluid assessment,
cardiac tamponade after treatment. The majority of patients promptly research is needed to determine the levels of protein, albumin and
and completely recover after drainage of pericardial fluid if the cause is lactate dehydrogenase associated with acute pericarditis as compared

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approach better than a surgical approach? Interact. Cardiovasc. Thorac. Surg. 12, 174–178 pathophysiology (Y.A., M.I., S.P. and P.M.S.); Diagnosis, screening and prevention (Y.A. and
(2011). M.I.); Management (Y.A., A.D.R., M.I., A.B. and J.K.O.); Quality of life (Y.A., A.D.R. and P.M.S.);
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outcomes and resource use. PLoS ONE 17, e0267152 (2022).
195. van Dinter, S. et al. Variations in current clinical practice of postoperative pericardial Competing interests
effusion: a questionnaire study. Open Heart 10, e002271 (2023). The institution of A.B. received funding from Kiniksa Pharmaceuticals as an investigative
An important study on variations in clinical practice in the management of post-operative site. A.B. also received an unrestricted research grant from Swedish Orphan Biovitrum AB
pericarditis. (SOBI) and ACARPIA as well as travel and accommodation to attend an advisory committee
196. Zgheib, H., Wakil, C., Shayya, S., Bachir, R. & El Sayed, M. Effectiveness and outcomes organized by SOBI and an advisory board organized by Kiniksa Pharmaceuticals. The other
of 2 therapeutic interventions for cardiac tamponade: a retrospective observational authors declare no competing interests.
study. Medicine 99, e21290 (2020).
197. Ambrosetti, M. et al. Secondary prevention through comprehensive cardiovascular Additional information
rehabilitation: from knowledge to implementation. 2020 update. A position paper from Supplementary information The online version contains supplementary material available at
the Secondary Prevention and Rehabilitation Section of the European Association of https://doi.org/10.1038/s41572-023-00446-1.
Preventive Cardiology. Eur. J. Prev. Cardiol. 28, 460–495 (2020).
198. Pavy, B., Iliou, M. C., Meurin, P., Tabet, J. & Corone, S. Functional Evaluation and Cardiac Peer review information Nature Reviews Disease Primers thanks A. Abbate, M. Chetrit,
Rehabilitation Working Group of the French Society of Cardiology. Safety of exercise C. L. Jellis, M. M. Lewinter and J.-L. Vincent for their contribution to the peer review of this work.
training for cardiac patients: results of the French Registry of complications during
cardiac rehabilitation. Arch. Intern. Med. 166, 2329–2334 (2006). Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in
199. Ghannem, M., Ahmaidi, S., Ghannem, L. & Meimoun, P. Infectious and inflammatory published maps and institutional affiliations.
complications occurring after cardiac surgery in cardiac rehabilitation centres [French].
Ann. Cardiol. Angeiol. 69, 424–429 (2020). Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this
200. Marcassa, C. et al. A retrospective multicenter study on long-term prevalence of chronic article under a publishing agreement with the author(s) or other rightsholder(s); author
pain after cardiac surgery. J. Cardiovasc. Med. 16, 768–774 (2015). self-archiving of the accepted manuscript version of this article is solely governed by the
201. Pelliccia, A. et al. 2020 ESC guidelines on sports cardiology and exercise in patients with terms of such publishing agreement and applicable law.
cardiovascular disease. Eur. Heart J. 42, 17–96 (2021).
Important guidelines about the role of exercise in patients with cardiovascular disease. © Springer Nature Limited 2023
Sackler Faculty of Medicine, Tel Aviv University, Bnei Brak, Israel. 2College of Law and Business, Ramat Gan, Israel. 3Department of Cardiology, University
1
Clinical Centre of Serbia, Belgrade, Serbia. 4Faculty of Medicine, Belgrade University, Belgrade, Serbia. 5Cardiothoracic Department, Cardiology,
University Hospital Santa Maria della Misericordia, Azienda Sanitaria Universitaria Friuli Centrale (ASUFC), Udine, Italy. 6Department of Biomedical
and Clinical Sciences, Fatebenefratelli Hospital, The University of Milan, Milan, Italy. 7Department of Internal Medicine-Cardiology, Philipps University
Marburg, Marburg, Germany. 8Institute for Cardiovascular Diseases “Dedinje“ and Belgrade University, Faculty of Medicine, Belgrade, Serbia. 9Serbian
Academy of Sciences and Arts, Belgrade, Serbia. 10Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.

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nature reviews disease primers https://doi.org/10.

Primer Check for updates

Petar M. Seferović3,4,9 & Jae K. Oh10

Cardiac tamponade is a medical emergency caused by the progressive Introduction

accumulation of pericardial fluid (effusion), blood, pus or air in Epidemiology

with cardiac tamponade are hypotension, increased jugular venous

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a Normal heart Cardiac tamponade

Fibrous pericardium Pericardial sac

Intrathoracic pressure Expiration

Ventricular wall collapse Improvement in cardiac Ventricular wall collapse

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Aetiology Clinical presentation Imaging

Likely to progress to cardiac tamponade

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a Rapid pericardial effusion

Cardiac tamponade Cardiac tamponade

Limit of pericardial stretch

Pericardial reserve volume Pericardial reserve volume

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Fig. 3 | Diagnostic techniques in cardiac

and a ‘water bottle’ shaped cardiac silhouette.

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Fig. 5 | Echocardiography in the differential

Exp Insp Exp Insp Exp Insp

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