Pericardium & diseases

Pericardium &
diseases
Vidyasagar Reddy
Meesala
Cardiac Sonographer
M.Sc/PGDES
KIMS -Hyderabad

Normal pericardial anatomy&
physiology
➢ It’s a sac like structure surrounding the heart
➢ Pericardium consists of 2 layers
1.fibrous pericardium: it is superficial layer of the
pericardium. It is made up of dense and loose connective
tissue
2.Serous pericardium: it is devided in to parietal
layer and visceral layer (Epicardium)
➢ Pericardial cavity is deviding them
➢ Pericardial cavity is filled with about 10-40ml of normal
pericardial fluid
2pericardial diseases/Vidyasagar Reddy

Pericardium layers illustration

• Intrapericardial parts:
• All 4 Chambers except posterior part of LA
• Almost entire Asc. Aorta, MPA, all 4 Pulmonary
Veins
• In case of TAPVC, PV confluence is intrapericardial
• Extrapericardial parts:
❖ Right and Left Pulmonary Artery
❖ Ductus Arteriosus
❖ Aortic arch & thoracic aorta
❖ In TAPVC schemitar vein & vertical vein is extra
pericardial
pericardial diseases/Vidyasagar Reddy 4

Pericardial sac anterior view
(heart removed)

Normal Functions:
▶ keeps heart in mediastinum and limits its
motion
▶ Protects heart from infections coming from
other organs (such as lungs)
▶ Prevents excessive dilation of the heart in
cases of acute volume overload
▶ Lubricates the heart
▶ Reducing the friction between beating heart
and adjacent structures

Pericardial desease types:
▶ Congenital defect
(partial or complete absent pericardium)
▶ Pericardial tumors
(1) mesothelioma
(2) pericardial lipomas
(3) pericardial cysts
▶ pericardial effusion & cardiac tamponade
▶ Pericarditis
▶ constrictive pericarditis
▶ uremic pericarditis

Congenital defect:
▶ Congenital absence of the pericardium is a rare
cardiac malformation and is most often
asymptomatic.
▶ Happens by Defective development of the
pleuropericardial membranes
▶ Partial defect is more common than complete
absence of pericardium
▶ It is usually discovered as an incidental finding
during chest radiography, and electrocardiogram
▶ Here Echocardiography provides valuable
information in diagnosis

Echocardiography features of
Absent pericardium:
▶ Displacement of the heart
▶ Enlargement of LA appendage
▶ Excessive cardiac motion
▶ Abnormal septal motion
*But CT/MRI is needed for subsequent
confirmation

Pericardial tumours:
▶ Primary pericardial tumours are rare and may be
classified as benign or malignant
▶ Mesothelioma is the most common primary malignant
pericardial neoplasm.
▶ Other malignant tumors include a wide variety of
sarcomas, lymphomas.
▶ The most common benign lesions are
(1)pericardial lipomas
(2)pericardial cysts

➢ signs and symptoms are generally nonspecific.
Patients often present with dyspnea, chest
pain, palpitations, fever, or weight loss.
➢ Although the imaging approach usually begins
with chest X ray or echocardiography. But
Needs to confirm with CT/MRI
➢ Both benign and malignant tumors may result
in compression of vital mediastinal structures.
Malignant lesions may also directly invade
structures, such as the myocardium and great
vessels

Pericardial Mesothelioma
▶ Most pericardial mesothelioma patients
experience no symptoms when the cancer
initially develops
▶ Symptoms in chronic stage are
palpitations,fatigue,dyspnea,fever,SOB,chestpai
n,nightsweats
▶ Mesothelioma may encroaches or partially
compress cardiac chambers
▶ Usually presents as constrictive pericarditis
histology confirms the diagnosis

Mesothelioma
mesothelioma

Pericardial lipomas:
▶ Pericardial lipomas are rare clinical findings
account for 10% of all primary cardiac tumors
▶ Lipomas usually mimic the malignant tumors
▶ lipoma mass showes an echostructure identical to
that of subcutaneous adipose tissue.
▶ Can externally compress cardiac chambers
▶ Needs CT/MRI and Histology report to confirm
lipoma

Lipoma in AP4CH view
Lipoma→

Pericardial cysts:
▶ Pericardial cysts are rare congenital abnormalities
with a reported incidence rate of 1/100,000
▶ Most common location for these cysts is right
cardiophronic angle
▶ Usually asymptomatic unless a complication or
rapid growth occurs.
▶ Diagnosis is generally made incidentally by using
Echocardiography,X-ray,CT
▶ Treatment is needle aspiration, and surgical
excision of the cysts.
▶ Recurrence of the disease is common when
aspiration approach is selected

cyst→

Differential diagnosis of P.cyst:
▶ The differential diagnosis includes other solid
tumors and cysts of the mediastinum
▶ Diaphragmatic hernia or tumors
▶ Aneurysms of the heart or great vessels*
_____________________________________________
▶ sometimes bubble contrast with agitated saline
may useful to rule out connection from right heart
chambers
▶ We should make sure that there is no phasic flow
with the help of low velocity color/PW Doppler to
exclude anomalous systemic veins

Pericardial effusion

Forms of PEF
▶ Transudative :Congestive heart failure,
Myxedema, nephrotic syndrome
▶ Transudate is fluid pushed through the
capillary due to high pressure within the
capillary.
▶ Exudative:Tuberculosis etc
▶ Exudate is fluid that leaks around the cells of
the capillaries caused by inflammation
▶ Hemorrhagic: trauma, rupture of aneurysms,
malignant effusion

Causes of PEF
▶ Idiopathic:No cause if founf despite full diagnostic investigation
▶ Infectious: common in viral, bacterial& fungal infection
▶ Autoimmune disease: particularly systemic lupus erythematodes
▶ Rheumatic: usually minimal PEF
▶ Surgery:pacemaker catheter procedures, biopsy, post cardiac
surgery(usually hematoma) often localized
▶ Radiation: usually seen in post chemo pts and some patients may
develop constrictive pericarditis
▶ Traumatic:chest trauma,aourtic rupture
▶ Post MI:myocardial rupture
▶ Renal failure:uremia/dialysis associated
▶ Miscellaneous: pregnancy, downs syndrome, right heart failure,
CHF, severe PAH,

Minimal PE video

Echo in Pericardial effusion
▶ Echocardiography can provide an estimate of the size of effusions.
▶ Always measure echofree space in end diastole
▶ Usually pericardium highly reflective to ultrasound
▶ Using multiple views,apical view focusing RV especially subcostal
view gives more information
▶ Hemopericardium with blood clots identifiable by echocardiography
▶ Small effusions: less than 8mm
▶ Mild effusions:8 to 14mm
▶ Moderate effusions:14 to 20mm
▶ Large effusions:more than 20mm
▶ Very large:more than 30mm

Minimal PEF

Location of pericardial effusion

Hemopericardium
thrombus

Differential diagnosis
▶ Pleuraleffusion:PEF is anterior to the desc Aorta while
pleural effusions are posterior to it
▶ Pericardial cyst
▶ ascitis
▶ Epicardial fat:

Cardiac tamponade
▶ Pericardial tamponade ,constriction
&effusive constriction shares many
common features
▶ But cardiac tamponade is a medical
emergency that occurs when fluid
accumulates with high pressures than
intracardiac pressures

Clinical symptoms of tamponade
▶ Chest pain (positional/oppressive
precordial)
▶ Dyspnoea
▶ Dry cough
▶ Hoarseness
▶ Dysphagia
▶ Nausea/abdominal pain

Cardiac tamponade : 2 types
▶ Acute cardiac tamponade: occurs with in
minutes, due to trauma or rupture of heart
or aorta, or complication of invasive
diagnostic or therapeutic procedure this
resembling cardiogenic shock that requires
urgent reduction in pericardial pressure
▶ Subacute cardiac tamponade: occurs over
days to weeks and can be associated with
infection or idiopathic pericarditis. May be
asymptomatic in early in course

Key diagnostic finding
Pulsus paradoxus/Kussmaul sign:
kussumaul sign paradoxical rise in jugular
venous pressure (JVP) on inspiration, or a
failure in the appropriate fall of the JVP
with inspiration. It can be seen in some
forms of heart disease and is usually
indicative of limited right ventricular
filling due to right heart dysfunction

Echo in tamponade
➢ Detected on either M-mode or two- dimensional
echocardiography
➢ simply a marker of a large pericardial effusion in
which the four cardiac chambers are free to float
within the pericardial space in a phasic manner
indirect evidence of elevated pressure.
➢ RV early diastolic collapse/RA collapse/inversion
/IVC plethora
➢ In Doppler Exaggerated respiratory variation in
mitral and tricuspid inflow velocities
➢ Phasic variation in right ventricular outflow
tract/left ventricular outflow tract flow

➢ RA free-wall collapse during late diastole
➢ IVC is usually greater than 2.2 cm in diameter with less than 50%
inspiratory compression
➢ Exaggerated inspiratory effects, especially with pulsus paradoxus,
may include RV expansion, interventricular septum shift to the
left, and LV compression
➢ Mitral changes, with reduced D-E amplitude or E-F slope and
delayed mitral opening time
➢ Aortic valve with premature closure
➢ RV epicardial notching during isovolumic contraction
➢ Course vibrations of LV posterior wall
➢ Exaggerated respiratory variation in inferior vena cava flow
➢ mitral and/or tricuspid pseudoprolapse, mitral valve systolic
anterior motion
➢ Pseudohypertrophy or apparent wall thickening due to
compression

RV Diastolic Collapse ,Most commonly involves
the RV outflow tract (more compressible area of
RV) Occurs in early diastole, immediately after
closure of the pulmonary valve, at the time of
opening of the tricuspid valve
When collapse extends form outflow tract to the
body of the right ventricle, this is evidence that
intrapericardial pressure is elevated more
substantially Circulation.

Right atrial collapse / RA inversion:
❖ Right atrium normally contracts in volume
with atrial systole,In the presence of marked
elevation of intrapericardial pressure, RA
wall will remain collapsed throughout atrial
diastole (early ventricular systole),Isolated
RA inversion occurs during late diastole

Parasternal long axis view

PLAX M-mode
RVOT collapse in early diastole

Parasternal short axis view

Rt heart collapse in diastole
❑ Right ventricular diastolic collapse is a highly
sensitive and specific indicator of Cardiac
Tamponade.
❑ Right atrial collapse although specific for Cardiac
Tamponade was less sensitive for the detection
of Cardiac Tamponade.
❑ Right heart collapse may not be seen in patients
with pulmonary HTN and Cardiac Tamponade

PLAX view

Subcostal view

Apical 4 chamber view

Pathophysiology of tamponade
interventricular interdependence

Septum shifting in short axis view
towards LV side during inspiration

Doppler imaging in tamponade
▶ Generally reduced flows and stroke volumes
▶ Exaggerated inspiratory augmentation of right-sided flows and
reduction in left-sided flows
▶ >25 -40% inspiratory change in peak transvalvular Doppler of
Tricuspid valve, >25% at Mitral valve
▶ Respiratory variation in superior and inferior vena caval flow
velocities, particularly marked in tamponade
▶ Hepatic vein expiratory effects: marked atrial flow reversal (AR
wave), marked decrease or reversal of diastolic forward flow
▶ Marked inspiratory decrease in LV ejection time occurs, along
with increased RV ejection time
▶ Marked inspiratory increase in LV isovolumic relaxation time is
encountered, in association with decreased RV isovolumic
relaxation time
▶ On transesophageal echocardiography (TEE), expiratory increase
in pulmonary vein diastolic forward flow can be appreciated
pericardial diseases/Vidyasagar Reddy
47

Doppler variations across
Mitral &Tricuspid Valves

Mitral PW spectral doppler

Pw imaging of the hepatic vein recorded in a pt with
hemodynamically significant pericardial effusion
Note the loss of forward flow in H.V during expiration
(E-phase)

AV valves PW spectral doppler

Constrictive pericarditis
▶ It is aCondition in which thickened scarred inelastic
noncompliance calcified pericardium limits the diastolic filling of
ventricle
▶ Charectarised by impaired & elevated Lv diastolic filling
pressures
▶ The etiologies of CP are diverse, including viral pericarditis,
cardiac surgery, collagen vascular disease, radiation,
tuberculosis, and sometimes idiopathic.
▶ Clinically, patients with CP usually present with fluid retention
(ascites and leg edema), dyspnea, fatigue, abdominal discomfort,
and sometimes persistent pleural effusion. Characteristic physical
findings are increased jugular venous pressure with rapid ‘‘y’’
descent and Kussmaul’s sign, peripheral edema, hepatomegaly, a
diastolic gallop soon after the second heart sound (pericardial
knock), and ascites
54

▶ . M-Mode and 2D Echocardiography.– Echocardiography is
usually the initial diagnostic procedure in patients with
suspected CP. Pericardial thickening and calcification and
abnormal ventricular filling produce characteristic
changes on M-mode echocardiography (Figure 42).
Increased pericardial thickness is suggested by parallel
motion of the visceral and parietal pericardium, which is
separated by a relatively echo-free space.
Echocardiographic correlates of the hemodynamic
abnormalities of CP include diastolic flattening of the LV
posterior wall endocardium, abrupt posterior motion of
the ventricular septum in early diastole with inspiration
(septal shudder and bounce), and, occasionally,
premature opening of the pulmonary valve.
55

▶ Two-dimensional echocardiography reveals dilation and
absent or diminished collapse of the IVC and hepatic
veins (plethora, a sign of elevated RA pressure),
moderate biatrial enlargement (restrictive
cardiomyopathy is more often associated with severe
atrialenlargement), a sharp halt in ventricular diastolic
filling, and abnormal ventricular septal motion that
results from interventricular dependence
▶ Atrial septal notch seen
56

▶ . Doppler Flow Velocity Recordings.–Doppler echocardiography is
essential for establishing the diagnosis and usually shows a restrictive
LV and RV diastolic filling pattern, characterized by a high early (E)
velocity, a shortened deceleration time, and a reduced atrial (A) wave.
Mitral inflow velocity usually, but not always, falls by as much as 25%
to 40%, and tricuspid velocity greatly increases (>40%–60%) in the first
beat after inspiration
▶ In summary, the key points using Doppler echocardiography in CP are
the following:
▶ The consensus for the calculation of percentage respiratory variation
in CP for mitral and tricuspid inflow is (expiration
inspiration)/expiration.
▶ For peak mitral E inflow, the maximal drop occurs with the first beat
of inspiration and the first beat of expiration and usually exceeds 25%
respiratory variation.
▶ For peak tricuspid E inflow, the maximal drop is on the first beat in
expiration at the same time as the hepatic vein atrial reversal and
usually exceeds 40% respiratory variation. The calculated % will be a
negative value.
60

▶ The respiratory variation in pulmonary venous
(particularly diastolic) flow is often pronounced similar
to mitral inflow, but not always necessary for the
diagnosis of constriction.
▶ Hepatic vein diastolic flow reversal increases with
expiration, reflecting the ventricular interaction and
the dissociation of intracardiac and intrathoracic
pressures which is essential in the diagnosis of
constriction.
▶ inspiratory hepatic vein diastolic flow reversals suggest
restrictive cardiomyopathy
61

▶ Doppler tissue imaging is particularly useful in differentiating
between CP and restrictive cardiomyopathy.140-143 Tissue
Doppler shows a prominent early diastolic velocity (e0 ) from the
medial mitral annulus, which is an important point of distinction
from restrictive cardiomyopathy in which transmitral E is tall and
narrowbut tissue e0 is reduced (<7cm/sec)
▶ The usually positive linear relation between E/e0 ratio and left
atrial pressure, which is useful for assessing left atrial pressure in
cardiomyopathy, is reversed (‘‘annulus paradoxus’’) in most
patients with CP
▶ because medial e0 increases progressively as the severity of
constriction becomes worse. Lateral mitral annular e0 is usually
lower than e0 from the medial annulus (‘‘annulus reversus’’) in
patients with CP
▶ The finding of annulus reversus appears to be related to the
tethering of the lateral mitral annulus to the thickened
pericardium.
▶ After pericardiectomy, the lateral and medial mitral annulus
normalizes 63

▶ The propagation velocity of early diastolic transmitral
flow on color M-mode is normal or increased and is
often >100 cm/sec
64

Strain imaging
▶ –Differences in longitudinal and circumferential deformation
may be useful to distinguish CP from restrictive
cardiomyopathy. Usually, circumferential strain, torsion, and
early diastolic untwisting are reduced, and global longitudinal
strain, displacement, and early diastolic tissue velocities are
unchanged in constriction, whereas circumferential strain and
early diastolic untwisting are preserved and longitudinal strain
is reduced in restrictive cardiomyopathy
▶ Recent work using speckle-tracking showed that there are
significant differences in regional longitudinal systolic strain in
constriction compared to restriction. The ratio of LV lateral
wall strain to LV septal wave strain was more robust than
regional annular velocity using tissue Doppler in differentiating
constriction from restriction. Removal of the pericardial
constraint by pericardiectomy led to improvement in
longitudinal strain in the RV and LV free walls as well the
circumferential strain
65

Uremic pericarditis:
(loculated pericardial effusion)
▶ Also called fibrinous pericarditis
▶ Uremic pericarditis (fibrinous pericarditis) more
commonly seen in chronic renal failure.
▶ Fibrinous pericarditis is an exudative
inflammation
▶ The pericardium is infiltrated by the fibrinous
exudate. This consists of fibrin strands
and leukocytes.

Effusive Constrictive pericarditis
▶ Effusive CP is the most uncommon of the pericardial constraint
syndromes. It is a distinct entity with transitional and concomitant
pathophysiologic features of acute effusive pericarditis with cardiac
tamponade and chronic CP. Effusive CP occurs when pericardial
fluid accumulates between a thickened, edematous, or fi- brotic
parietal and visceral pericardium
▶ Echocardiography. The echocardiographic findings of effusive CP
depend on the stage ofthe M-mode, 2D, and Doppler features are
consistent with a sizable PEff and cardiac tamponade. Later stages
of effusive pericarditis may have features more suggestive of CP
the disease, although most often.
▶ 3 Within the effusion, there may be bandlike fibrinous strands that
traverse the pericardial cavity from visceral to parietal surfaces,
resulting in regions of loculation
68

Uremic pericarditis:
(loculated pericardial effusion)
▶ Also called fibrinous pericarditis
▶ Uremic pericarditis (fibrinous pericarditis) more
commonly seen in chronic renal failure.
▶ Fibrinous pericarditis is an exudative
inflammation
▶ The pericardium is infiltrated by the fibrinous
exudate. This consists of fibrin strands
and leukocytes.
71

Fibrin strands→

▶ When dialysis is not employed, uremic pericarditis
is usually a preterminal event and is characterized
by a serofibrinous exudation of an amount
inadequate to cause cardiac tamponade.
▶ Nevertheless, cardiac tamponade may
uncommonly be observed in nondialyzed patients
with CKD which maybe life-threatening

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