Echocardiographic evaluation of

pericardium
Dr.Sruthi Meenaxshi.SR,
MBBS,MD,PDF
 Anatomy of pericardium
• The normal pericardium consists of two layers: a fibrous outer layer
and a serous inner layer.

• The serous layer is a closed sac with the visceral component lining
the epicardium and the parietal component lining the fibrous outer
layer.

• The outer fibrous pericardium produces one of the most strongly

reflective or echo-producing areas of the heart, and it normally
moves anteriorly with the epicardium.

• The pericardium is reflected from the pulmonary veins as they

enter the left atrium. The fibrous component has attachments to
the sternum and to the diaphragm
• Pericardial fat is also commonly seen on two-dimensional (2D)
echocardiography

• Accumulation is most common in the interventricular and

atrioventricular grooves and on the right ventricular (RV) free wall.

• This normal but highly variable finding is most commonly seen

anterior to the heart in the parasternal long axis view and in the
subcostal views

• The best clues to its identity as fat are its absence posteriorly,
normal motion of the pericardium, and low intensity echoes (often
seen as faint linear striations) within the pericardial space.
 Physiology
• In patients with a normal pericardium,
intrathoracic pressure decreases during
inspiration, leading to an increase in venous
return to the right heart and transient
increase in RV chamber size.
• Because the normal pericardium
accommodates the increased venous return
by expanding, this increase in venous return
does not impair left ventricular (LV) filling.
• When visualized on 2D echocardiography, the layers of the
pericardium appears as thin echogenic lines surrounding the
myocardium.

• The normal thickness of the visualized pericardial layers is less than

1 to 2 mm, but it can be difficult to make accurate measurements
on echocardiography due to motion throughout the cardiac cycle.

• In the normal healthy pericardium, there is less than 25 to 50 mL of

serous fluid in the pericardial sac formed by these layers .

• The interposition of this fluid between the pericardial layers results

in a very small physiological separation of the layers, best
appreciated on M-mode echocardiography only during systole
 PERICARDIUM
• The normal pericardium is a fibroelastic sac
containing a thin layer of fluid that surrounds
the heart.
• When larger amounts of fluid accumulate
(pericardial effusion) or when the pericardium
becomes scarred and inelastic,
• The pericardium consists of two layers that surround the
heart and proximal portions of the great vessels. The inner
layer, the visceral pericardium, is a thin membrane formed
by a single layer of mesothelial cells.
• The outer layer the parietal pericardium—a thick, fibrous
structure.
• A small amount (15–35 mL) of pericardial fluid separates
the two layers and serves a physiological lubricating
function. The fluid consists of a plasma ultrafiltrate
generated by the mesothelial lining of the pericardium and
is drained by the thoracic lymphatic system.
• Normally, a small amount of fluid (less than 25
to 50 mL) is contained within the closed sac of
the serous layer.

• Because of the pericardial reflection at the

level of the pulmonary veins, pericardial fluid
rarely accumulates in this area posterior to
the left atrium because the potential space
available decreases abruptly.
 Indications
• In general, transthoracic echocardiography (TTE) should be part of
the routine imaging evaluation in the following circumstances:
❖ All patients with suspected pericardial disease, including effusion,
constrictive pericarditis, or effusive-constrictive pericarditis.

❖ All patients with suspected bleeding into the pericardial space (eg,
trauma, perforation, post-operative).

❖ Follow-up study to evaluate recurrence of pericardial effusion

following treatment or to diagnose early constrictive pericarditis.

❖ Patients with pericardial friction rub developing in acute

myocardial infarction (MI) accompanied by symptoms such as
persistent pain, hypotension, and nausea.
 Ventricular interdependence
• The mechanical restraint of the pericardium
contributes to ventricular interdependence: the LV
and right ventricle (RV) share a common wall in the
interventricular septum and are surrounded by the
relatively noncompliant pericardium.
• Therefore, the volume in one ventricle can influence
the diastolic pressure and filling characteristics of the
opposite chamber. This physiology is accentuated in
states of pericardial pathology
 Acute pericarditis
• The echocardiogram is often normal in
patients with the clinical syndrome of acute
pericarditis unless it is associated with a
pericardial effusion, which is present in
approximately 60 percent of patients

• CMR is the preferred imaging method to

diagnose the pericardial inflammation seen in
pericarditis.
 Acute pericarditis
• Pericarditis is the most common affliction of the pericardium
and reflects inflammation that can result from abroad variety
of local and systemic disorders.
• Most causes can be assigned to one of six categories:
• infectious
• idiopathic
• metabolic
• collagen vascular/autoimmune
• postinjury
• neoplastic
 A 32 year old female with fever ,
dyspnea on exertion and chest pain .
Diagnosis
 Etiology
• Autoimmune disorders, including systemic lupus
erythematosus,rheumatoid arthritis, and scleroderma
may cause acute pericarditis as the first
manifestation of the systemic illness.
• Acute rheumatic fever can involve the pericardium as
part of a pancarditis.
• Certain drugs may cause pericarditis and/or pericardial
effusion either by inducing a lupus-like syndrome (e.g.,
hydralazine or procainamide), or by nonlupus,
unknown mechanisms
• (e.g., minoxidil, anthracycline antitumor agents).
Echocardiographic findings of
pericarditis
 Cardiac tamponade
• Cardiac tamponade, which may be acute or
subacute, is characterized by the
accumulation of pericardial fluid under
pressure.

• Variants include low pressure (occult) and

regional cardiac tamponade.
Cardiac tamponade
 Constrictive pericarditis
• Constrictive pericarditis is the result of
scarring and consequent loss of elasticity of
the pericardial sac.

• Pericardial constriction is typically chronic,

but variants include subacute, transient, and
occult constriction.
 Effusive-constrictive pericarditis
• Effusive-constrictive pericarditis is characterized by
underlying constrictive physiology with a coexisting
pericardial effusion, usually with cardiac tamponade.

• Such patients may be mistakenly thought to have only

cardiac tamponade

• Persistent elevation of the right atrial and pulmonary

wedge pressures after drainage of the pericardial fluid
points to the underlying constrictive process.
• Echocardiography is the initial method of choice for evaluating most
pericardial diseases, given its ability to provide both anatomic and
physiologic/hemodynamic information.

• When competently performed in patients with good acoustic

windows, echocardiography accurately detects pericardial effusions
and provides clinically relevant information about their size and
hemodynamic importance.

• The technique is less reliable than computed tomography (CT) for

detecting pericardial thickening/calcification, and both CT and
cardiac magnetic resonance (CMR) are superior for identifying small
loculated effusions.

• CMR is the preferred method to identify pericardial

inflammation/pericarditis.
Pericardial effusion
Loculated effusion with pericardial
thickening and calcification
M mode posterior wall diastolic
flattening
 Pericardial effusion
• Echocardiography has an important role in
diagnosing the presence of pericardial effusion,
estimating the size of the effusion, and evaluating
the hemodynamic importance of any effusion
• Key elements of the pericardial effusion which
should be described include
• size / Thickness
• location,
• circumferential versus loculated.
• Pericardial fluid appears on an echocardiogram as an echolucent space
between the pericardium and the epicardium.

• Small collections of pericardial fluid, which can be physiologic (25 to 50

mL), may be visible during ventricular systole. Effusions exceeding 25 to 50
mL are seen as an echo-free space throughout the cardiac cycle.

• Typically, a small (50 to 100 mL) free-flowing pericardial effusion is seen

posterior to the LV; this space diminishes and finally disappears as the
echo beam approaches the base of the LV and the left atrium

• Accumulation of pericardial fluid above the right atrium in the apical four
chamber view with the patient in the left lateral decubitus position is,
perhaps, the single most sensitive and specific indication of a pericardial
effusion

• 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 RV.
 Quantification of effusion
• The size of a pericardial effusion is graded semi-
quantitatively, and when measured, it is measured in
diastole.
●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
the echo-free space is greater than 20 mm at its greatest
width.
• The pericardial effusion should be described
as circumferential or loculated
• and transudative or exudative.
 Loculated effusion and other
postoperative sequelae
Pericardial fluid ceases to be circumferential and
free flowing and becomes loculated or
compartmentalized as a result of a variety of
disease processes, most commonly following
cardiac surgery or following pericardial
hemorrhage.

Pericardial stranding, suggestive of fibrous

material within the pericardial effusion, is easily
seen on echocardiographic imaging, often as a
precursor to loculation of the effusion
• A loculated, eccentric effusion or localized hematoma
can produce regional cardiac tamponade in which only
selected chambers are compressed.

• Regional cardiac tamponade is most often seen after

pericardiotomy or MI.
• Clinical suspicion should be heightened in these
settings. Establishing the diagnosis is challenging and
may require additional echocardiographic views (eg,
subcostal or transesophageal) and other advanced
imaging techniques (eg, CT).
 Differentiating between pleural and
pericardial effusions
• Left pleural effusions can present as large echo-free spaces
that resemble pericardial effusion

• These can be recognized because they appear as very large

posterior spaces often without any anterior component.

• Generally, in the parasternal long axis view, pleural

effusions are located posterior to the descending aorta,
while pericardial effusions are located anterior to the aorta.

• Additionally, pericardial effusions only rarely accumulate

posterior to the left atrium
Pericardial thickening and constrictive
pericarditis
Although pericardial thickening may be
appreciated on echocardiography, CMR and
CT are both superior techniques for detecting
pericardial thickening and for measuring the
thickness

CT is particularly beneficial for identifying

pericardial calcifications.
• If pericardial thickening fails to resolve, chronic pericardial
thickening with constrictive pericarditis can develop.

• Like cardiac tamponade, constrictive pericarditis is a

continuum of impairment of cardiac function that causes
restraint or restriction on ventricular filling sufficient to
raise filling pressures and decrease cardiac output or
cardiac reserve.

• One or more of the following echocardiographic findings

may be seen in patients with constrictive pericarditis
 Constrictive pericarditis
• Increased pericardial thickness with or without pericardial adhesion
(manifests as the absence of detectable motion between the layers
of the pericardium, which may be circumferential or occasionally
focal).

●Dilatation of the inferior vena cava and hepatic veins (plethora) with
absent or diminished inspiratory collapse.

●Moderate biatrial enlargement (although severe enlargement is more

compatible with restrictive cardiomyopathy).

●A sharp halt in ventricular diastolic filling (corresponding to the end

of early rapid diastolic filling as noted on Doppler).
●Septal bounce with inspiratory motion of the interventricular septum
toward the LV.

●Abnormal filling of the ventricles during early diastole. An increased E

velocity of RV and LV inflow is seen due to the abnormally rapid
early diastolic filling associated with the combination of a small
ventricular volume and rapid recoil.

●Annular early diastolic (E') velocities are lower in constrictive

pericarditis secondary to surgery or radiation than in other
etiologies but are typically higher than in patients with restrictive
cardiomyopathy. The mitral annular lateral/medial E' ratio is
reversed in the majority of patients with constrictive pericarditis,
with the medial E' velocity being higher than the lateral E' velocity;
typically, this is referred to as "annulus reversus."
Diastolic shudder or septal bounce
Respirophasic variation in tricuspid
and mitral valve
Diastolic collapse of RV
Right atrial systolic collapse
 Minor respirophasic changes with left
ventricular filling in contrast with
marked respirophasic changes in right
ventricular filling in cardiac tamponade
Pericardial effusion
Pericardial effusion vs pleural effusion
pleural effusion and its relation with
descending aorta
 Mechanical alternans corresponds to
swinging action of the heart in large
pericardial effusion similar to electrical
alternans
Dense adhesions in pericardium
Loculated effusion
Intrapericardial hematoma
 IVC loss of normal respirophasic changes
less than50 percent decrease in IVC diameter
during inspiration
reflection of increased right atrial pressures
❖ The propagation velocity of early diastolic transmitral flow on color M-mode is
normal or increased

❖ Pronounced respiratory variation in ventricular filling – Mitral inflow velocity falls

as much as 25 to 40 percent and tricuspid velocity greatly increases (>40 to 60
percent) in the first cardiac cycle following inspiration. The respiratory variation in
pulmonary venous flow is even more pronounced . These phenomena, which are
manifestations of ventricular interdependence, are not present in either normal
subjects or patients with restrictive cardiomyopathy.

❖ Hepatic venous flow reversal increases with expiration, reflecting the ventricular
interdependence and the dissociation of intracardiac and intrathoracic pressures.

❖ As with the distinction between cardiac tamponade and pericardial effusion, there
can be significant overlap between the findings in frank constriction and those in
extensive pericardial thickening without hemodynamic compromise.
• Partial or complete absence of the pericardium
may be suspected but cannot usually be
definitively diagnosed by echocardiography,
although most echocardiographic findings are
non-specific. The orientation and distance
between the transducer and the posterior wall on
TTE have been suggested as diagnostic
parameters, but in general, MRI and CT are
preferred for visualizing the pericardium and
confirming the diagnosis [1,12]. Typical findings
on echocardiography include:
 Absence of pericardium
• In patients with complete absence of the
pericardium, echocardiography may visualize
more of the RV than typically seen on routine left
parasternal echocardiogram, which is due to
enlargement of the RV, excessive motion of the
posterior LV wall, and shift of the heart to the
left.
• These changes may result in paradoxical motion
of the interventricular septum. All of these
findings mimic RV volume overload as seen in
atrial septal defect or tricuspid insufficiency
• In patients with partial absence of the
pericardium who have herniation of a chamber,
echocardiography may show a wall motion
abnormality along the line of demarcation.
• If the pericardial defect is left sided, it is the left
atrial appendage that is most likely involved.
However, if a coronary artery is compressed, a
true wall motion abnormality may indeed exist.
• Rare instances of sudden death and acute
ischemia resembling an acute ST elevation MI
have been reported
• No specific treatment is required for most patients
with complete congenital absence of the pericardium,
as such patients appear to have a normal life
expectancy.
• Partial defects may lead to herniation in which case
surgery is indicated. The pericardium can be removed if
the defect is large or closed if it is a smaller defect.
• Surgery in the absence of herniation can be
considered if the patient is symptomatic, while
occasionally prophylactic closure to prevent future
herniation is indicated.
Congenital partial absence of
pericardium
 Pericardial cyst
• Pericardial cysts which typically occur along the right heart border
but can occur anywhere, are generally asymptomatic, causing
symptoms only if adjacent structures (eg, coronary arteries) are
impacted.

• The primary clinical relevance of pericardial cysts relates to

distinguishing the cyst from other cardiac and mediastinal masses.

• The presence of a pericardial cyst is usually suggested by the chest

radiograph.
• Pericardial cysts, which echocardiographically appear as an echo-
free space that is more localized and spherical than a pericardial
effusion , are difficult to detect with TTE, although they may be
more readily visualized with transesophageal echocardiography