Download Constrictive Pericarditis

A normal pericardium consists of an outer sac called the fibrous
pericardium and an inner double-layered sac called the serous
pericardium.
The visceral layer of the serous pericardium, or epicardium, covers
the heart and proximal great vessels. It is reflected to form the
parietal pericardium.
There is 5 to 10 mL of normal buffering fluid within the pericardial
space.
Constrictive Pericarditis
Pericardial constriction is a relatively uncommon
In constrictive pericarditis the pericardium is stiff and fibrotic and
restricts diastolic filling.
The classic form of pericardial constriction is calcific constriction
secondary to tuberculous pericarditis.
More commonly in today's practice, constrictive pericarditis is the
result of infectious or inflammatory processes such as connective
tissue disease or radiation therapy or develops several years after
cardiac surgery.
Early diastolic filling is normal but late diastolic filling is impaired
(terminated abruptly when the limits of the pericardium are reached).
In late stages of the disease the pericardium may calcify.
In patients with endstage pericardial constriction, symptoms of
ascites, peripheral edema, and hepatic insufficiency predominate
and can mimic RV failure.
Echo Findings of Constrictive Pericarditis
1. M-mode and 2-D Echo
• Thickened pericardium
Detection of a thickened pericardium is often difficult with TTE
(especially if pericardial fluid and pleural fluid are both present).
The normal pericardium is no more than 1-2 mm in thickness.
Pericardial thickening >3 mm or calcification is highly predictive
of constrictive pericarditis,
but up to 18% of patients with proven constriction have
histologically abnormal pericardium with normal thickness.
If calcific pericardial disease is present, ultrasound shadowing may
occur.
cardiac multislice CT and cardiac MRI can be used for accurate
assessment of pericardial thickness.
• Dilation and lack of respiratory variation of IVC.
• Exaggerated septal shift with inspiration.
• Hepatic vein doppler flow:
Usually dilated and show prominent diastolic flow
reversal during expiration.
M-mode abnormalities
• Flattened diastolic left ventricular posterior wall
motion
(early diastolic motion is normal, followed by
flattening in late diastole).
• Abnormal septal motion
Early diastolic notching may be seen (Abrupt septal
shift toward LV in early diastole), followed by
paradoxical (bowing toward the RV).
M-mode echocardiogram recorded in a patient with constrictive pericarditis.
Note the flat position of the posterior wall during diastole after initial rapid filling.
Also note the abnormal motion of the ventricular septum (double arrows).
M-mode echocardiogram through the right ventricular free wall, ventricular septum, and
posterior wall showing marked phasic respiratory-dependent downward motion of the
ventricular septum (arrow).
Note that with inspiration (I), there is expansion of the right ventricular cavity with abrupt
posterior motion of the ventricular septum consistent with exaggerated interdependence.
Subcostal echocardiogram recorded in a patient with constrictive pericarditis revealing
a dilated inferior vena cava (IVC).
2. Doppler findings
• An exaggerated E/A ratio of mitral valve inflow with
a short deceleration time.
• exaggerated respiratory variation in E-wave
velocity:
mitral inflow: variation of 25% or more.
The total intracardiac volume is limited by the
constrictive pericardium >> This results in an
exaggerated respiratory variation in septal position >>
any inspiratory increase in right-sided filling must be
accompanied by a reciprocal decrease in left-sided
filling >>> exaggerated respiratory variation in E-wave
velocity.
Mitral inflow showing respiratory variation in e velocity
Restrictive mitral inflow velocity with respiratory variation in early diastolic velocities
(arrow).
Tricuspid valve inflow
Early diastolic flow velocity
increases with inspiration.
Mitral valve inflow
Early diastolic flow velocity increases
with expiration.
Prominent diastolic expiratory flow reversals in the hepatic veins (arrow).
The classic findings of constriction are usually most
prominent when the patient is euvolemic (normal
volume).
This findings may not be present in patients with
depleted volume or overloaded volume.
Also, these classic findings may not be present in
patients with :
Noncalcific pericardial constriction,
Localized forms of constriction,
Patients with significant concurrent valvular or
myocardial disease.
Key Point. Restrictive LV filling, prominent diastolic
flow reversal during expiration in the hepatic veins,
and normal or increased tissue Doppler annular
velocities should raise suspicion of constrictive
pericarditis in patients with heart failure and normal
EFs, even when the respiratory variation in mitral
inflow is absent or not diagnostic.
Effusive Constrictive Pericarditis
It is a combination of constrictive and tamponade
physiology.
The most common causes are malignancy and radiation
therapy.
The diagnosis is confirmed when, after pericardiocentesis,
a decrease in the intrapericardial pressure is associated
with a persistently elevated intracardiac pressure.
Patients with effusive constrictive pericarditis will present
with pericardial effusion, often with evidence of marked
inflammation.
Although tamponade may be present, the thickening of
the visceral pericardium may prevent right ventricular or
right atrial free wall collapse.
After pericardiocentesis, the effusive component resolves
and hemodynamics appear more similar to constriction.
• From a clinical standpoint, the diagnosis is often
established in a patient with hemodynamic compromise
and moderate pericardial effusion in whom jugular vein
distention and hemodynamics persist after
pericardiocentesis.
• After pericardiocentesis, the effusive component
resolves and hemodynamics appear more similar to
constriction.
Constrictive Pericarditis Versus
Restrictive Cardiomyopathy
Constriction
Restriction
Atrial size
Normal
Dilated
Pericardial appearance
Thick/bright
Normal
Septal motion
Respiratory shift
Normal
Mitral E/A
> 1.5
> 1.5
Deceleration time
Short (<160 ms)
Short (<160 ms)
Mitral annular septal E’
Usually < 7 cm/s
Usually > 7 cm/s
Mitral annular lateral E’
Lower than septal Eʼ
Higher than septal Eʼ
Pulmonary hypertension
Rare
Frequent
Constriction
Restriction
Left ventricular size and function
Normal
Normal
Mitral/tricuspid regurgitation
Infrequent
Frequent (TR > MR)
Isovolumic relaxation time
Varies with respiration
Stable with respiration
Mitral inflow respiratory
vriation
Exaggerated (≥25%)
Normal
Color M-mode mitral valve Vp
Normal (≥55 cm/sec)
Reduced
Hepatic vien doppler
Expiratory diastolic flow
reversal
Inspiratory diastolic flow
reversal
Ventricular septal strain
Usually normal
Reduced
Hepatic vein Doppler recordings from patients with restriction, constriction, pulmonary
hypertension, and severe tricuspid regurgitation
A: Restrictive cardiomyopathy. Systolic (S) forward flow velocity is smaller than diastolic
(D) forward flow velocity. Inspiratory (Insp) diastolic flow reversal is larger than expiratory
(Exp) diastolic flow reversal.
B: The recording of constriction is similar to that of restriction except that Exp diastolic
flow reversal is larger than Insp diastolic reversal.
C: Pulmonary hypertension. Diastolic flow reversal (arrows) does not change much with
respiration.
D: Severe tricuspid regurgitation with late systolic flow reversal (arrow).