1. Pericardial diseases

2. 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.

3. 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.

4. 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.

5. 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).

6. 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).

7. 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.

8. Subcostal echocardiogram recorded in a patient with constrictive pericarditis revealing a dilated inferior vena cava (IVC).

9. 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.

10. Mitral inflow showing respiratory variation in e velocity

11. Restrictive mitral inflow velocity with respiratory variation in early diastolic velocities (arrow).

12. Tricuspid valve inflow
Early diastolic flow velocity increases with inspiration.
Mitral valve inflow
Early diastolic flow velocity increases with expiration.

13. Prominent diastolic expiratory flow reversals in the hepatic veins (arrow).

14. 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.

15. 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.

16. 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.

17. 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.

18. Constrictive Pericarditis Versus Restrictive Cardiomyopathy

19. Restriction
Constriction
Dilated
Normal
Atrial size
Thick/bright
Pericardial appearance
Respiratory shift
Septal motion
> 1.5
Mitral E/A
Short (<160 ms)
Deceleration time
Usually > 7 cm/s
Usually < 7 cm/s
Mitral annular septal E’
Higher than septal Eʼ
Lower than septal Eʼ
Mitral annular lateral E’
Frequent
Rare
Pulmonary hypertension

20. Restriction
Constriction
Normal
Left ventricular size and function
Frequent (TR > MR)
Infrequent
Mitral/tricuspid regurgitation
Stable with respiration
Varies with respiration
Isovolumic relaxation time
Exaggerated (≥25%)
Mitral inflow respiratory vriation
Reduced
Normal (≥55 cm/sec)
Color M-mode mitral valve Vp
Inspiratory diastolic flow reversal
Expiratory diastolic flow reversal
Hepatic vien doppler
Usually normal
Ventricular septal strain

21. 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).