The document discusses constrictive pericarditis, providing details on: 1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity. 2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes. 3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.

1. Constrictive
Pericarditis
Secrete parlour

2. Pathology
 Pericardium
 Thickened > 5mm by
CT
 Scarred
 Loss of elasticity

3. No thickening
28% -CT scan
18% -Histopathology
Ref:Talreja et al,circulation,2003

4. Effusive-constrictive
pericarditis
Constrictive pericarditis Cardiac tamponade
 JVP remain elevated
despite lowering of the
pericardial pressure to
near zero with peri-
cardiocentesis
 Rapid y descent
appears
 No inspiratory decline
in RAP
 Thickened ,scarred
and consequent loss
of the normal elasticity
of the pericardial sac
 Typically chronic
 Variants
 Subacute
 Transient
 occult constriction
 Acute
 Subacute
 Accumulation of
pericardial fluid under
pressure
 Variants
 Low pressure
(occult)
 Regional
tamponade

5. What went wrong
Normal pericardium Pericardium in constriction
The normal pericardium can stretch to
accommodate physiologic changes in cardiac
volume
 Keep up with intra thoracic pressure
Inelastic, resulting in minimal ability to adapt
to volume changes
Cardiac filling is impeded by an external
force(constriction)
 Pathophysiologic
 Entry and exit of external volume is
handled by enhanced ventricular
interdependence= exaggerated
coupling
 Pericardial space has no communication
with intra thoracic pressure change

6. A little more
Normal pericardium Constriction
With a normal pericardium,
intrathoracic pressure decreases
during inspiration, leading to an
increase in venous return to the right
heart and transient increase in right
ventricular chamber size. Because the
normal pericardium accommodates the
increased venous return by expanding,
this increase in venous return does not
impair left ventricular filling or
influences to bare minimum
 Upper limit of cardiac volume is constrained
 Intrathoracic pressure is not transmitted to the heart chambers
 Pericardium does not expand to accommodate increased venous return to
the right heart during inspiration
 PCWP fall but not LVEP in inspiration, leading to a reduction in LV volume
 Ventricular filling thrives on interdependence
 Compression does not occur until the cardiac volume approximates that of
the pericardium, which begins in mid-diastole
 Early diastolic filling is even more rapid than normal
 Ventricular filling occurs in early diastole with little or no filling subsequently
 Stroke volumes are reduced

7. Tuberculosis is the most common cause in
INDIA
Idiopathic or viral – 42 to 49 percent
Post-cardiac surgery – 11 to 37
percent
Post-radiation therapy – 9 to 31
percent, primarily after Hodgkin
disease or breast cancer
Connective tissue disorder – 3 to 7
percent
Postinfectious (tuberculous or purulent
pericarditis) – 3 to 6 percent
Miscellaneous causes (malignancy,
trauma, drug-induced, asbestosis,
sarcoidosis, uremic pericarditis) – 1 to
10 percent
Idiopathic/viral – 0.76 cases per 1000
person-years
Connective tissue/pericardial injury
syndrome – 4.40 cases per 1000
person-years
Neoplastic pericarditis – 6.33 cases
per 1000 person-years
Tuberculous pericarditis – 31.65 cases
per 1000 person-years
Purulent pericarditis – 52.75 cases per
1000 person-years

8. Out of Subject

9. Respiratory variations

10. You know all of them
The " a " wave corresponds to right Atrial contraction and
ends synchronously with the carotid artery pulse. The peak
of the 'a' wave demarcates the end of atrial systole.
The " c " wave corresponds to right ventricular Contraction
causing the tricuspid valve to bulge towards the right
atrium.
The " x " descent follows the 'a' wave and corresponds to
atrial relaxation and rapid atrial filling due to low pressure.
The " x' " (x prime) descent follows the 'c' wave and occurs
as a result of the right ventricle pulling the tricuspid valve
downward during ventricular systole. (As stroke volume is
ejected, the ventricle takes up less space in
pericardium, allowing relaxed atrium to enlarge). The x' (x
prime) descent can be used as a measure of right ventricle
contractility.
The " v " wave corresponds to Venous filling when the
tricuspid valve is closed and venous pressure increases
from venous return - this occurs during and following the
carotid pulse.
The " y " descent corresponds to the rapid emptying of the
atrium into the ventricle following the opening of the
tricuspid valve.

11. How does normal pericardium response?
Rapid vs slow accumulation

12. Transmural pressure gradient
(TPG)
Normal pericardial pressure is -5 to +5 mmHg
RVEDP or LVEDP minus intra-pericardial
pressure=TPG
Normal Transmural pressure gradient is zero
Negative in Tamponade
Positive in CP

13. Some beautiful features of CP

14. Features……
Increased right atrial pressure
Prominent x and y descents of venous in atrial pressure tracings
Kussumal's sign
Increased RV end-diastolic pressure, usually to a level one-third or more of RV systolic
pressure
"Square root" signs in the RV and LV diastolic pressure tracings A greater inspiratory fall in
pulmonary capillary wedge pressure compared to left ventricular diastolic pressure
Equalization of LV and RV diastolic plateau pressure tracings, with little separation with
exercise, since filling, and therefore diastolic pressure, in both ventricles is constrained by the
inelastic pericardium
Mirror-image discordance between RV and peak LV systolic pressures during inspiration,
another sign of increased ventricular interdependence
 During peak inspiration, an increase in RV pressure occurs when LV pressure is lowest

15. Pulsus Paradoxus not in CP
Normally intrapericardial pressure tracks intrathoracic pressure
Inspiration:
→ -ve intrathoracic pressure is transmitted to the pericardial space
→ ↓ IPP
→ ↑ blood return to the right ventricle
→ ↑ right ventricular volume & shifting of IVS towards the LV
→ ↓ left ventricular volume
→ ↓ LV stroke volume.
↓ blood pressure (>10mmHg) during inspiration.

16. Kussumal’s sign +ve in CP
Kussumal’s Sign is no reduction of mean
column height JVP in inspiration
RV fills only in early diastole irrespective of
respiratory phase
Because no communication between
pericardial space and intra thoracic pressure
change

17. CT vs. CP

18. Clinical

19. M-Mode: Constriction
Septum-
Abnormal Rapid
movements- notching in
early diastole.
Post LV wall-
Abrupt postr motion in early
diastole and flat in remaining
diastole
IVC and hepatic vein
dilatation

20. 2D: Constriction
Increased echogenicity of the pericardium from thickening
May see effusion (effusive-constrictive)
Septal bounce
Abrupt septal shift toward LV in early diastole and bounce back
toward RV following atrial contraction.

21. Echo Doppler- mitral inflow:
Constriction
1. RV and LV inflow show
prominent E wave due to
rapid early diastolic filling
2. Short deceleration time of E
wave as filling abruptly stops
3. Small A wave as little filling
occurs in late diastole
following atrial contraction
4. E/A ratio >1.5:1
5. DT<160ms
6. IVRT: <60ms

22. Echo Doppler- mitral inflow: RCM
Early disease E<A.
Late disease: E>A
Constant IVRT

23. Respiratory Mitral Inflow velocity
IN CP:
Mitral peak E velocity >25 %
increase in exp.
IN RCM:
velocity varies by <10%.

24. Tissue Doppler of mitral annulus
Constrictictive pericarditis:
Annular paradox:
E’ increases as severity of CP increase[as increased filing pressure]
Peak E’ ≥ 8 cm/s
89% senstive for constriction
100% specific.
RCM:
E’ decreases as severity ↑
E’< 8 cm/s.

25. Respiratory Mitral Inflow & TD of mitral
annulus

26. HV diastolic flow reversal:CP vs
RCM
VS

27. Pulmonary Venous flow

28. Right Heart Catheterization
Equalization of pressures
< 5 mm hg difference between
mean RA, RV diastolic, PA
diastolic, PCWP, LV diastolic and
pericardial pressures in CP.
Diagnostic for CP (also seen in
tamponade).

29. Right & Left Heart
Catheterization
Dip and plateau pattern in diastolic waveform (square root
sign)
Constrictive pericarditis
Restrictive cardiomyopathy
RV ischemia

30. Right & Left Heart
Catheterization
RVSP < 35-45 mm
Hg
RVEDP / RVSP >
1/3
LVEDP-RVEDP < 5
• PASP = RVSP very high(>55 - 60 mm
Hg)
• RVEDP / RVSP < 1/3
• LVEDP-RVEDP > 3-5 mm Hg
CP RCM

31. RV- LV discordance vs.
concordance
CP RCM

32. Conclude with some comparison

33. Pericardium failed to relax