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Diagnosis and Treatment of Pericardial Effusion - UpToDate
Diagnosis and Treatment of Pericardial Effusion - UpToDate
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Literature review current through: Nov 2021. | This topic last updated: Apr 23, 2020.
INTRODUCTION
The normal pericardium is a fibroelastic sac surrounding the heart that contains a thin layer
of fluid. A pericardial effusion is considered to be present when accumulated fluid within the
sac exceeds the small amount that is normally present. Pericardial effusion can develop in
patients with virtually any condition that affects the pericardium, including acute pericarditis
and a variety of systemic disorders. The development of a pericardial effusion may have
important implications for prognosis (as in patients with intrathoracic neoplasm), diagnosis
(as in myopericarditis or acute pericarditis), or both (as in dissection of the ascending aorta).
Pericardial effusions may develop rapidly (acute) or more gradually (subacute or chronic).
The normal pericardium can stretch to accommodate increases in pericardial volume, with
the amount of stretch related to how quickly the effusion develops. The ability to stretch is
greater with slowly developing effusions. However, regardless of how quickly an effusion
develops, with ongoing accumulation of pericardial fluid into a closed space, eventually the
intrapericardial pressure begins to increase. When the intrapericardial pressure becomes
high enough to impede cardiac filling, cardiac function becomes impaired, and cardiac
tamponade can be considered to be present. (See "Cardiac tamponade".)
A general overview of the diagnosis and treatment of pericardial effusion will be presented
here. The full spectrum of causes of pericardial disease, management of specific causes of
pericardial disease, and the details of pericardial fluid drainage are discussed separately. (See
"Etiology of pericardial disease" and "Acute pericarditis: Clinical presentation, diagnostic
evaluation, and diagnosis" and "Emergency pericardiocentesis".)
ETIOLOGY
Pericardial effusions can occur as a component of almost any pericardial disorder ( table 1
), but the majority result from one of the following conditions (see "Etiology of pericardial
disease"):
The frequency of the different causes of pericardial effusion varies in published reports,
depending primarily upon geography and the patient population ( table 2). Patients with
hemorrhagic pericardial effusions have a somewhat different distribution of causes,
although the overlap with serous effusions is significant. (See "Etiology of pericardial
disease", section on 'Spectrum of clinical presentation' and 'Establishing the cause of the
effusion' below.)
CLINICAL PRESENTATION
The presence of pericardial effusion may be suspected from the history, physical
examination, electrocardiogram (ECG), and chest radiograph.
tamponade usually present with signs and symptoms related to impaired cardiac function
(ie, fatigue, dyspnea, elevated jugular venous pressure, edema). (See "Cardiac tamponade".)
● Low voltage – Low voltage of the QRS complexes ( waveform 1) is present when the
total amplitude of the QRS complexes in each of the six limb leads is 5 mm (0.5 mV) or
less. Low voltage in the limb leads may or may not be accompanied by low voltage in
the chest leads (defined as a total QRS amplitude of 10 mm or less in V1 to V6).
The combination of low voltage and sinus tachycardia should raise concern about
pericardial effusion with cardiac tamponade. In one prospective cohort study of 43
patients with a pericardial effusion, cardiac tamponade was present in 23 patients, with
low QRS voltage in 14 of those 23 (61 percent) but in none with an effusion without
cardiac tamponade [2]. After treatment with either pericardiocentesis or anti-
inflammatory medication, low voltage resolved within one week. However, the
combination of low voltage and sinus tachycardia is not specific to patients with
pericardial effusion, as this may also be seen in patients with chronic obstructive
pulmonary disease, pleural effusion, cardiomyopathy, and prior cardiac surgery (
table 3). (See "Cardiac tamponade".)
● Electrical alternans – Another ECG pattern that can occur with pericardial effusion and
cardiac tamponade is electrical alternans, which is also usually present with sinus
tachycardia ( waveform 2). This abnormality is characterized by a cyclic beat-to-beat
shift in the QRS axis (and more subtly in other waveforms) in the limb and precordial
leads in association with mechanical swinging of the heart to-and-fro, usually in a large
pericardial effusion. The pattern is usually most apparent in one or more of the
precordial leads.
lung fields ( image 1). However, an enlarged cardiac silhouette on chest radiograph is not
specific and cannot be considered diagnostic for the presence of a pericardial effusion.
DIAGNOSTIC APPROACH
● Unexplained persistent fever with or without an obvious source of infection, which also
raises the possibility of purulent pericarditis. (See "Purulent pericarditis".)
● Presence of isolated left (or left larger than right) pleural effusion [3].
● Fever or hemodynamic deterioration in a patient with another disease process that can
involve the pericardium.
Once a pericardial effusion is suspected, the diagnostic approach consists of three steps:
confirming the presence of a pericardial effusion; assessing its hemodynamic impact, if any;
and, whenever possible, establishing the cause of the pericardial effusion.
image 3). However, in the case of a free flowing effusion, the site of accumulation
may be positional as there is gravity dependence. As the effusion increases in size, it is
typically seen anterior to the right ventricle. (See 'Quantification of the pericardial
effusion' below.)
● Cross-sectional imaging – In cases with a high suspicion for pericardial effusion but
non-diagnostic echocardiography, additional thoracic imaging with computed
tomography (CT) or magnetic resonance imaging (MRI) is helpful in establishing the
presence of an effusion. We do not routinely perform CT or MRI unless both TTE and
TEE are non-diagnostic, or unless there is concern for other pericardial pathology (eg,
pericardial thickening and constrictive pericarditis). CT and MRI may be useful when
quantification and localization of pericardial fluid is important, when the effusion is
complex, and when epicardial fat and pleural effusions need to be excluded. These
imaging modalities (especially MRI) also are capable of characterizing the nature of the
effusion [5]. (See "Constrictive pericarditis", section on 'Evaluation'.)
● Cardiac biomarkers – Among patients with pericardial effusion, cardiac biomarkers (CK-
MB, troponin) may be elevated in those in whom the effusion occurs in association with
acute myopericarditis or myocardial infarction. Troponin elevations, typically modest,
may occur in association with a variety of other acute illnesses. (See "Elevated cardiac
troponin concentration in the absence of an acute coronary syndrome" and "Acute
pericarditis: Clinical presentation, diagnostic evaluation, and diagnosis", section on
'Cardiac biomarkers' and "Myopericarditis".)
● Small effusions (50 to 100 mL) are only seen posteriorly, typically less than 10 mm in
thickness, and only cause minimal separation between the epicardial (visceral)
pericardium and the thicker parietal pericardial sac.
● Moderate effusions (100 to 500 mL) tend to be seen along the length of the posterior
wall but not anteriorly; the echo-free space is 10 to 20 mm at its greatest width.
● Large effusions (>500 mL) tend to be seen circumferentially ( image 5 and image 6
); the echo-free space is greater than 20 mm at its greatest width.
Factors that determine the degree of hemodynamic compromise include the volume of
pericardial fluid, the rate at which the effusion accumulates, and whether or not the
pericardium is scarred or adherent. Localized pericardial adhesions or organization of the
pericardial fluid can result in localized, and thus atypical, cardiac tamponade. Diffuse
pericardial inflammation and/or scarring with effusion can result in effusive constrictive
pericarditis [6].
Acute versus subacute cardiac tamponade — Cardiac tamponade can occur acutely (eg,
due to rupture of the heart or aorta, trauma, or as a complication of catheter or pacemaker
procedures) or subacutely (eg, due to neoplasm, uremia, or idiopathic pericarditis). (See
"Cardiac tamponade".)
● Acute cardiac tamponade is by definition rapid in onset, may be associated with chest
pain and dyspnea, and is life-threatening if not promptly treated. The jugular venous
pressure is markedly elevated, while hypotension is common due to the decline in
cardiac output. The heart sounds are often muted. In most acute cases, the effusion is
relatively small because the pericardium cannot stretch rapidly.
subacute cardiac tamponade may reveal hypotension with a narrow pulse pressure,
reflecting the limited stroke volume. However, patients with preexisting hypertension
may remain hypertensive due to the increased sympathetic activity that is usually
present in cardiac tamponade [7].
● Sinus tachycardia
● Elevated jugular venous pressure
● Pulsus paradoxus
● Collapse of the right atrium at end-diastole and the right ventricle in early diastole (
movie 2 and movie 3).
● Reciprocal changes in left and right ventricular volumes with respiration, which are
important in the pathogenesis of pulsus paradoxus ( figure 1). (See "Pulsus
paradoxus in pericardial disease".)
● Increased respiratory variation of mitral and tricuspid valve inflow velocities (drop in
mitral flow by 30 percent, and tricuspid valve flow by 60 percent on the first beat of
inspiration and expiration, respectively).
● Dilation (plethora) of the inferior vena cava and less than a 50 percent reduction in its
diameter during inspiration, reflecting systemic congestion ( image 7 and image 8
).
Establishing the cause of the effusion — Clinical data and examination of the pericardial
fluid and pericardium can be used to establish the cause of the effusion. Frequently, the
cause of a pericardial effusion is suspected by the clinical setting in which it occurs. Examples
include patients with breast or lung cancer, a recent myocardial infarction, severe
hypothyroidism, or end-stage kidney disease. In other cases, the diagnosis may be less
apparent. In cases where the cause is not apparent, confirming the precise etiology of a
pericardial effusion generally requires sampling of the effusion and/or the pericardium for
laboratory analysis. The frequency of different causes of pericardial effusion varies in
published reports, depending in part upon geography and patient demographics, as well as
the aggressiveness with which an underlying diagnosis is sought ( table 2) [8-11]. (See
'Etiology' above and "Etiology of pericardial disease".)
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In many cases, the specific etiology of a pericardial effusion cannot be established even
when fluid and/or pericardial tissue is available for analysis. The likelihood of establishing a
specific cause appears to increase with larger effusions. In series of patients with acute
pericarditis (including those with small or undetectable effusions), the underlying diagnosis
was established in only about 15 to 20 percent [12,13]. In contrast, studies evaluating
moderate to large pericardial effusions have revealed diagnoses in up to 90 percent of cases
when very aggressive diagnostic approaches are taken [9]. Such aggressive approaches are
often not warranted in clinical practice, however, given the benign natural history of many of
these effusions. (See "Acute pericarditis: Clinical presentation, diagnostic evaluation, and
diagnosis", section on 'Establishing a definite etiology'.)
The presence or absence of these features suggested, but did not confirm, a specific
diagnosis [8]:
● The presence of inflammatory signs was associated with acute idiopathic pericarditis
(likelihood ratio 5.4).
● A large effusion without inflammatory signs or cardiac tamponade was associated with
chronic idiopathic pericardial effusion (likelihood ratio 20).
Laboratory tests — If the initial history and physical examination do not suggest a specific
diagnosis, extensive laboratory testing seeking an etiology is unlikely to be helpful. In such
cases, we limit routine testing to:
A serum antinuclear antibody (ANA) test should be considered in a young woman with an
effusion and associated acute pericarditis since, rarely, this can be the initial presentation of
systemic lupus erythematosus. A careful history directed toward the presence of a coexisting
rheumatologic disorder should also be obtained. It is important to keep in mind that a
positive ANA is a non-specific finding. In cases where a rheumatologic diagnosis is being
considered in a patient with pericarditis and an effusion, a rheumatology consultation should
be sought.
The invasive nature of pericardiocentesis and pericardial biopsy must be weighed against
two factors: a relatively low diagnostic yield from the procedure, and the clinical relevance of
a specific diagnosis, as many low-risk patients can be managed empirically without making a
specific diagnosis. The yield of diagnostic pericardiocentesis has varied in different series,
but in most, a definitive diagnosis has been made following pericardiocentesis in less than 40
percent of cases [9,10,12]. When an etiology for the pericardial effusion was confirmed,
malignancy, purulent infection, and tuberculosis were the most frequently identified causes.
We consider pericardial fluid analysis and pericardial biopsy separately since they are
frequently helpful, but many patients are successfully managed without either procedure.
Our approach is in general agreement with the 2015 European Society of Cardiology
guidelines for the diagnosis and management of pericardial disease [4].
● Cytology
● AFB stain and mycobacterial culture along with adenosine deaminase, interferon-
gamma, or lysozyme (for tuberculous pericarditis) [16]
Parameters such as protein, LDH, glucose, red cell count, and white cell count are rarely
helpful in establishing an etiology; specifically, Light's criteria, used for differentiating
transudative versus exudative pleural effusions, do not reliably distinguish exudative from
transudative pericardial effusions and should not be applied to pericardial fluid analysis
[17,18]. However, a polymerase chain reaction for specific viruses can be ordered when
management may be affected by the results, such as identifying CMV in a transplant patient,
although the yield of PCR remains fairly low in many instances [19]. (See "Etiology of
pericardial disease" and "Tuberculous pericarditis" and "Approach to the diagnosis of
cytomegalovirus infection".)
If patient characteristics and local expertise favor pericardial drainage via percutaneous
pericardiocentesis, analysis is limited to the pericardial fluid. However, whenever surgical
drainage is performed, we also recommend pericardial biopsy. In addition, pericardial biopsy
should be performed in any patient in whom there is ongoing diagnostic uncertainty as to
the etiology, if a specific diagnosis would significantly change the management.
Pericardioscopy enables endoscopic inspection and targeted biopsy of the parietal and
visceral pericardium [1]. This approach has been used in patients with unexplained
pericardial effusions or to diagnose recurrent idiopathic effusion [20-23]. When performed in
one of the few centers with a special interest and expertise in using this approach, a specific
diagnosis was established in 49 to 65 percent of patients, a value higher than generally
obtained by pericardial biopsy performed under fluoroscopic guidance [20-22].
TREATMENT
Several issues must be considered in the management of patients with a pericardial effusion,
including [24]:
● Diagnosis and treatment of the underlying disease (See 'Underlying disease' below.)
The choice between pericardiocentesis and open surgical drainage is based upon local
preference and experience, and upon individual patient considerations. Pericardial fluid
drainage should achieve several objectives, including:
● Procurement of fluid for appropriate analysis (which may include biochemical, cytologic,
bacteriologic, and/or immunologic testing)
● In patients on heparin, the procedure can be postponed until the partial prothrombin
time is normal, or protamine can be given to reverse the heparin effect.
● In patients on chronic warfarin in whom the INR exceeds 1.4, the options are:
important to have a skilled nurse, a monitor technician, and a sonographer present to assist
with the procedure.
● Monitoring the position of the needle during the initial puncture is easier and more
convenient than with fluoroscopy.
● Agitated saline with microbubbles, rather than radiopaque contrast, is used to verify
that the needle is in the pericardial effusion.
Echocardiographic guidance allows the operator to select the shortest route to the effusion,
generally near the cardiac apex or along an edge of the sternum, as well as the utilization of
a puncture site with the largest collection of fluid and shortest distance from the skin. In the
largest published series (1127 therapeutic echocardiographically-guided pericardiocentesis
cases), the para-apical location was the most frequently utilized location (68 percent), while
the subcostal or subxiphoid was utilized as the ideal location in only 15 percent of cases [27].
When the apical route is chosen, the needle is directed parallel with the long axis of the left
ventricle towards the aortic valve. For parasternal insertion, the puncture is made 1 cm
lateral to the sternal edge in an effort to avoid both inadvertent puncture of the internal
mammary artery when too medial as well as pneumothorax when too lateral.
Once the pericardial space has been accessed, a thin-walled pigtail catheter should be
inserted for ongoing drainage. This catheter, with a three-way stopcock attached, may also
be used for pericardial pressure measurement. Following catheter insertion and initial
pericardial pressure measurement, fluid is then aspirated, and pressures are often
remeasured every several minutes to ascertain the hemodynamic result. We also agree with
the 2015 European Society of Cardiology guidelines, which recommend drainage of fluid in
<1000 mL sequential steps to avoid acute right ventricular dilatation, although this is a rare
complication [4,33]. The procedure is continued until pericardial pressure is <5 mmHg, at
least during inspiration.
Bleeding during pericardiocentesis may be silent, induce typical pericardial pain, or be the
cause of acute cardiac tamponade. When pressure measurement, fluid analysis, or contrast
injection (using saline bubbles or radiopaque media) demonstrate that a cardiac chamber
has been entered and this event is followed by pain or hemodynamic deterioration, the
central venous pressure should be reassessed. A value higher than that measured before the
puncture indicates cardiac tamponade until proven otherwise.
The management of specific underlying disease states associated with pericardial effusion,
including acute pericarditis, uremia, and malignancy, is discussed separately. (See "Acute
pericarditis: Treatment and prognosis" and "Recurrent pericarditis", section on 'Treatment'
and "Tuberculous pericarditis", section on 'Treatment' and "Purulent pericarditis", section on
'Treatment' and "Pericardial disease associated with malignancy", section on 'Treatment'.)
fluid sampling for diagnostic purposes may be indicated ( algorithm 1). Such patients may
be treated conservatively, with careful hemodynamic monitoring, serial echocardiographic
studies (every five to seven days or sooner if clinically indicated), avoidance of volume
depletion (including avoidance or judicious use of diuretics), and therapy aimed at the
underlying cause of the pericardial effusion. Effusions that progressively enlarge, lead to
worsening symptoms suggesting definite cardiac tamponade, or that are otherwise
refractory to a conservative approach should be treated with pericardial fluid drainage.
Chronic and recurrent effusions — In patients with large chronic effusions, we perform
pericardiocentesis initially because the effusion may not reaccumulate ( algorithm 1). If
pericardiocentesis is undertaken, careful follow-up over days to weeks is essential because of
the significant and unpredictable incidence of future cardiac tamponade. If the effusion
reaccumulates, we perform repeated pericardiocentesis or pericardiectomy. The major
indication for pericardiectomy is the reaccumulation of pericardial fluid despite repeated
pericardiocenteses. For both chronic and recurrent effusions, the 2015 European Society of
Cardiology (ESC) guidelines for the management of pericardial disease suggested surgical
pericardiectomy only in patients with symptomatic effusions in whom medical therapy and
repeated pericardiocentesis were not successful [4]. (See 'Pericardial fluid drainage' above
and "Recurrent pericarditis", section on 'Role of pericardiectomy'.)
Pericardial effusions may persist for extended periods and can also recur with repeated
episodes of pericarditis. As in other cases of pericardial effusion, management in these
settings is based upon the treatment of the underlying disorder, with percutaneous drainage
of the effusion reserved for hemodynamically significant or persistently symptomatic
effusions [37].
Pericardial effusions that are present for weeks to months, or longer, are referred to as
chronic effusions or chronic effusive pericarditis. In such cases, the diagnostic work-up often
fails to reveal the cause, although an etiology may emerge over time.
The incidence and significance of chronic effusions has varied somewhat in different
reported case series:
● In a report of 100 consecutive patients with idiopathic chronic large pericardial effusion
who presented to one of three Italian referral centers between 2000 and 2015, only
eight patients developed cardiac tamponade during follow-up (mean 50 months) [38].
While 45 patients underwent a drainage procedure at some point, there was significant
regression of the effusion over follow-up in the remaining patients without a drainage
procedure.
● In a series of 1108 patients who initially presented with pericarditis between 1977 and
1992, only a very small fraction (28 patients, 2.5 percent) had a large idiopathic effusion
that persisted for a median duration of three years [39]. In this study, 58 percent
developed cardiac tamponade at some point during follow-up (median three years).
Thus, although chronic effusions are often asymptomatic and hemodynamically tolerated,
cardiac tamponade can unexpectedly occur at any time.
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Pericardial disease".)
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles on
a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Beyond the Basics topics (see "Patient education: Pericarditis (Beyond the Basics)")
● Pericardial effusion can develop in patients with virtually any condition that affects the
pericardium ( table 1), including acute pericarditis and a variety of systemic disorders.
The frequency of different causes of pericardial effusion varies in published reports,
depending in part upon geography and patient demographics, as well as the
aggressiveness with which an underlying diagnosis is sought ( table 2). (See
'Introduction' above and 'Etiology' above.)
● The presence of pericardial effusion may be suspected from the history, physical
examination, electrocardiogram (ECG), and chest radiograph. However, in the absence
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of cardiac tamponade, physical signs are not sensitive or specific for pericardial
effusion. Therefore, the diagnosis in most patients is confirmed using
echocardiography. (See 'Diagnostic approach' above.)
● The diagnostic approach to the patient with a suspected pericardial effusion consists of
the following steps:
• Establish the cause of the effusion – In some cases, the most likely cause of the
pericardial effusion will be clear due to the presence of another illness or systemic
disorder known to involve the pericardium. If the cause is not apparent, the routine
use of a broad panel of screening laboratory tests is not usually helpful. In such
cases, evaluation of the pericardial fluid and pericardium itself may suggest an
etiology, particularly if the effusion is large. (See 'Establishing the cause of the
effusion' above.)
aimed at the underlying cause (if known) of the pericardial effusion. (See 'Initial
management of asymptomatic patients with large effusions' above.)
● Although the greatest experience has previously been with fluoroscopic guidance and a
subcostal approach, pericardiocentesis with echocardiographic guidance is now the
preferred method in many institutions. Echocardiographic guidance allows the operator
to select the shortest route to the effusion, generally near the cardiac apex or along an
edge of the sternum, as well as utilizing a puncture site with the largest collection of
fluid and shortest distance from the skin. We recommend using an
echocardiographically-guided approach for pericardiocentesis whenever possible. (See
'Pericardiocentesis technique' above.)
● Pericardiocentesis does not completely evacuate the effusion in most cases, and active
secretion of fluid or bleeding may result in reaccumulation of an effusion. For these
reasons, we recommend that the pericardial catheter be left in place for 24 to 48 hours
or until the volume of drainage is less than 25 mL/day. (See 'Management following
pericardiocentesis' above.)
● Pericardial effusions that are present for three months or more are referred to as
chronic effusions or chronic effusive pericarditis. In patients with large chronic
effusions, we perform pericardiocentesis initially because the effusion may not
reaccumulate. If pericardiocentesis is undertaken, careful follow-up over days to weeks
is essential because of the significant and unpredictable incidence of future cardiac
tamponade. If the effusion reaccumulates, we perform repeated pericardiocentesis or
pericardiectomy. (See 'Chronic and recurrent effusions' above.)
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effusion. Heart 2019; 105:477.
39. Sagristà-Sauleda J, Angel J, Permanyer-Miralda G, Soler-Soler J. Long-term follow-up of
idiopathic chronic pericardial effusion. N Engl J Med 1999; 341:2054.
Topic 4941 Version 34.0
GRAPHICS
Infectious
Viral – Coxsackievirus, echovirus, adenovirus, Epstein-Barr virus, cytomegalovirus, influenza,
varicella, rubella, HIV, hepatitis B, mumps, parvovirus B19, vaccina (smallpox vaccine), severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2)
Noninfectious
Autoinflammatory diseases (especially familial Mediterranean fever and tumor necrosis factor
associated periodic syndrome [TRAPS], IgG4-related disease)
Neoplasm
Paraneoplastic
Cardiac
Late postcardiac injury syndrome (Dressler syndrome), also seen in other settings (eg, post-
myocardial infarction and post-cardiac surgery)
Myocarditis
Trauma
Blunt
Penetrating
Metabolic
Uremia
Radiation
Drugs (rare)
References:
1. LeWinter M. Clinical practice. Acute pericarditis. N Engl J Med 2014; 371:2410.
2. Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart 2015; 101:1159.
3. Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012; 27:308.
2000
(n = 269)
(n = 322)
Size of effusion, >10 >10 NR >10 >10 (98%)
mm
Tamponade, 37 NR NR 100 88
percent
Etiologies, percent
Idiopathic* 29 (9% 7 48 0 26
chronic)
Malignancy 13 23 15 38 25
Uremia 6 12 2 6 3
Iatrogenic 16 0 0 9 21
Post-acute 8 0 0 5 1
myocardial
infarction
Infection 6 27 16 28 7
Collagen 5 12 10 6 3
vascular
disease
Hypothyroidism 2 0 10 5 0
Other 15 23 0 3 14
Adapted from:
1. Sagrista-Sauleda J, Merce J, Permanyer-Maralda G, et al. Clinical clues to the causes of large pericardial effusions. Am J
Med 2000; 109:95.
2. Corey GR, Campbell PT, VanTrigt P, et al. Etiology of large pericardial effusion. Am J Med 1993; 95:209.
3. Levy PY, Corey R, Berger P, et al. Etiologic diagnosis of 204 pericardial effusion. Medicine (Baltimore) 2003; 82:385.
4. Ma W, Liu J, Zeng Y, et al. Causes of moderate to large pericardial effusion requiring pericardiocentesis in 140 Han
Chinese patients. Herz 2012; 37: 183.
5. Strobbe A, Adriaenssens T, Bennett J, et al. Etiology and long-term outcome of patients undergoing pericardiocentesis. J
Am Heart Assoc 2017; 6: e007598.
Low voltage of the limb leads is present when the amplitude of the QRS
complex in each of the three standard limb leads (1, 2, and 3) is <5 mm.
Each large box represents 5 mm (calibration: 1 mV = 10 mm).
Adrenal insufficiency
Anasarca
Artifactual or spurious, eg, unrecognized standardization of ECG at one-half the usual gain (ie, 5
mm/mV)
Constrictive pericarditis
Normal variant
Obesity
Pericardial effusion
Pleural effusions
* Dilated cardiomyopathy may be associated with the combination of relatively low limb lead voltages
and prominent precordial voltages.
Electrical alternans
ECG: electrocardiogram.
Normal ECG
The long (panel A) and short axis (panel B) two- dimensional images
show a small pericardial effusion (arrows). The M-mode
echocardiogram (panel C) shows the posterior wall to be separated
from the pericardium (arrow).
Pericardial effusion
In panel A, a diagrammatic representation of the long axis of the heart is seen on top; the transducer (T) sit
anterior chest wall in the precordial parasternal window and the beam is swept from apex to base. The app
echocardiogram at three beam positions on the diagram is designated by the arrows connecting the diagra
echocardiogram which displays the cardiac structures that are imaged by the beam (bottom panel). A peric
(PE) is seen as an echo-free space posterior to the left ventricle. This space diminishes and finally disappear
the heart is approached because the pericardium reflects at mid atrium. Panel B shows a still frame two-dim
M-mode Doppler from the parasternal long axis view at the level of the mitral valve (corresponding to arrow
Ao: aorta; Inf-Lat LVW: inferolateral LV wall; LA: left atrium; LV: left ventricle; MV: mitral valve; P: pericardium
effusion; RV: right ventricle; Ant RVW: anterior RV wall.
RV: right ventricle; LV: left ventricle; LA: left atrium; dAo: descending
aorta.
The apical four chamber view shows a moderate to large anterior and
posterior pericardial effusion (PE), but the curvature of the right atrium
(RA) is normal. In panel B there is diastolic expiratory invagination,
compression, or collapse of the RA. Collapse of the RA is a highly sensitive,
but relatively nonspecific, sign of hemodynamically important tamponade.
More importantly, the left atrium (LA) also appears compressed. This latter
sign is felt to be more specific for tamponade.
The subcostal view in a normal subject shows the inferior vena cava (IVC).
Left panel: Prior to inspiration, the normal diastolic IVC diameter (arrows)
is less than 20 mm. Right panel: During inspiration, the IVC collapses to
less than 50 percent of its original diameter.
L: liver.
(A) The subcostal view of the inferior vena cava (IVC) in a patient with tamponade.
The IVC is plethoric measuring over 20 mm in diameter.
(B) During inspiration, the IVC diameter fails to decrease. There is a large
pericardial effusion (PE) surrounding the right atrium (RA).
* Clinical features that support cardiac tamponade:
Symptoms: Chest pain, presyncope or syncope, dyspnea or tachypnea, orthopnea
Physical exam: Hypotension, tachycardia, elevated JVP, absent lung crackles, diminished
heart sounds, pericardial rub (rare), peripheral edema
Pulsus paradoxus (decrease in systolic BP >10 mmHg on inspiration)
ECG: Not sensitive or specific: Tachycardia, low voltage (maximum QRS amplitude <0.5
mV in the limb leads), electrical alternans, no features of acute myocardial ischemia
Chest radiograph: Not sensitive or specific, may show enlarged cardiac silhouette,
pleural effusions, clear lung parenchyma
¶ Echocardiogram findings that support cardiac tamponade:
Pericardial effusion
Swinging of heart in fluid
Increased respiratory variation in mitral (>30%) or tricuspid (>60%) flow velocity
Early diastolic collapse of RV, late diastolic collapse of RA (collapse of any chamber:
sensitivity 90%; specificity 65%)
IVC dilated less than a 50% reduction in the diameter during inspiration
Δ Non-cardiac tamponade indications for prompt fluid removal include:
Suspected bacterial, tuberculous, or neoplastic pericarditis
Large chronic (>3 months) idiopathic pericardial effusion
Symptomatic moderate to large effusions not responsive to medical therapy
◊ Caution is required, as drainage of too much fluid may lead to loss of support of right
ventricle and increased tricuspid regurgitation. However, in most cases the potential benefit of
relieving tamponade will outweigh the risks of the procedure.
Contributor Disclosures
Brian D Hoit, MD Speaker's Bureau: Philips Medical [Heart valve disease]. All of the relevant financial
relationships listed have been mitigated. Martin M LeWinter, MD Grant/Research/Clinical Trial
Support: Kiniksa Pharmaceuticals [Pericarditis]. Consultant/Advisory Boards: Kiniksa Pharmaceuticals
[Pericarditis]. All of the relevant financial relationships listed have been mitigated. Daniel J Sexton,
MD Equity Ownership/Stock Options: Magnolia Medical Technologies [Medical diagnostics].
Grant/Research/Clinical Trial Support: Centers for Disease Control and Prevention [Healthcare
epidemiology]; National Institutes of Health [Healthcare epidemiology]. Consultant/Advisory Boards:
Magnolia Medical Technologies [Medical diagnostics]; Johnson & Johnson [Mesh-related infections]; CVS
Pharmacy [COVID testing]. All of the relevant financial relationships listed have been mitigated. Susan
B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.