Constrictive Pericarditis Flashcards
What is constrictive pericarditis?
- Inflammation, thickening, scarring and/or calcification of the pericardium
- Results in fusion of visceral and parietal pericardial layers
- Encasement of heart within a solid, non-compliant sac
- Impaired diastolic filing (due to fixed total intra-pericardial volume)
Restricted diastolic filling in CP?
- Early diastole: rapid ventricular filling as normal
- Mid diastole: rapid termination of diastolic flow occurs when the limits of pericardial compliance reached (i.e. pericardium can stretch no further)
Haemodynamic hallmark of CP?
- Equalisation of diastolic pressures in all 4 chambers
- “Square root sign” seen in cardiac catheterisation
Right and left heart filling with respiration in CP?
- Exaggerated
- Dissociation between ITP and ICP = haemodynamic effects similar to tamponade
Ventricular interdependence in CP?
- Enhanced
- Dissociation between ITP and ICP = haemodynamic effects similar to tamponade
What are the clinical signs of CP?
- Kussmaul’s sign
- Pericardial knock
- Not specific for CP, also seen when right heart failure
What is Kussmaul’s sign?
Paradoxical rise in JVP on inspiration (normally falls)
What is a pericardial knock?
- High pitch heart sounds in early diastole
- Occurs when rapid ventricular filling is abruptly halted by the constricting pericardium
Anatomic features of CP?
- Thickened and calcified pericardium
- Fibrosis and adhesion of pericardial layers
CP vs Tamponade: Low CO state
- CP: Yes
- Tamponade: Yes
CP vs Tamponade: JVD
- CP: Present
- Tamponade: Present
CP vs Tamponade: Restricted Diastolic Filling
- CP: Mid-late diastole
- Tamponade: Entire diastolic period
CP vs Tamponade: Dissociation between ITP and ICP
- CP: Isolation of heart by constrictive pericardial shell
- Tamponade: Increased IPP (impedes transmission of ITP to pericardial sac and heart)
CP vs Tamponade: Kussmaul’s Sign
- CP: Present
- Tamponade: Absent
CP vs Tamponade: Pulsus Paradoxus
- CP: Absent
- Tamponade: Present
CP vs Tamponade: Heart Sounds
- CP: Pericardial knock
- Tamponade: Decreased
Echo signs of CP?
- Notching of IVS (as seen on m-mode)
- Pericardial thickening (increased echo-genicity of pericardium)
- Absence of pericardial slippage (thickened pericardium tethered to the heart)
- Septal bounce (exaggerated ventricular interdependence)
Enhanced Ventricular Interdependence in CP?
- Inspiration: septum moves left = increased RV cavity size = decreased LV cavity size
- Expiration: septum moves right = increased LV cavity size = decreased RV cavity size
Mitral inflow variation in CP?
- Decreased E velocity on 1st beat of inspiration
- Same as tamponade
IVRT in CP?
Prolonged IVRT 1st beat of inspiration
Tricuspid inflow variation in CP?
Increased E velocity on 1st beat inspiration
Hepatic venous variation in CP?
- Increased peak D velocity on 1st beat inspiration
- Marked increase AR velocity with expiration
Formula to calculate respiratory change?
(Expiration - inspiration) / expiration x 100
Transmitral significance of respiratory change in CP?
Inspiratory decrease in E velocity ≥ 25%
Tricuspid significance of respiratory change in CP?
Inspiratory increase in E velocity > 40%
Hepatic venous significance of respirator change in CP?
- Expiratory increase in AR velocity ≥ 25% of forward flow
Transmitral and tricuspid inflow in CP?
- May show restrictive filling
- E:A is high, > 2, and deceleration time is very short
What is the normal relationship between lateral and septal e’?
Medial/septal e’ < lateral e’
What is the relationship between lateral and septal e’ in CP?
- Annulus reverses
- Lateral e’ < septal e’
What is the normal relationship between E/e’ ratio and LVFP?
The higher the E/e’ ratio, the higher the LV filling pressure
What is the relationship between E/e’ ratio and LVFP in CP?
- Annulus paradoxus
- E/e’ ratio decreases as LV filling pressures increase
Why does annulus reversus occur in CP?
Tethering of adjacent fibrotic and scarred pericardium which impedes diastolic lateral longitudinal motion (lateral e’ < medial e’)
Why does annulus paradoxus occur in CP?
Compensatory increase in diastolic medial longitudinal motion (e’ preserved or accentuated despite increased LVFP)
Calculating E/e’ in CP?
- Use medial e’
- Lateral e’ affected by calcification or adhesions of the pericardium
Challenging cases in CP?
- Chronic obstructive airways disease (COAD)
- Ventilated patients
- CP without respiratory variation
What is COAD?
- Exaggerated changes due to exaggerated respiratory changes in ITP
- In COAD patients with pericardial thickening; may be difficult to determine cause for respiratory variation in MV/TV inflow
How to distinguish COAD from CP?
Look at SVC flow profile
COAD vs CP SVC Flow Profile?
- COAD: marked augmentation of SD forward flow with inspiration
- CP: minimal variation in S forward flow with respiration
CP in ventilated patients?
- Respiratory changes are opposite to spontaneously breathing patients
- ITP increases (rather than decreases) with inspiration
What can cause reduced respiratory variation?
- Localised construction
- Combined restrictive CM and CP
- Markedly raised atrial pressure
What to do when you suspect CP but no respiratory variations?
Sit or stand patient up and repeat mitral inflow to unmask characteristic respiratory variation
What is effusive-constrictive pericarditis?
Pericardial effusion + constrictive physiology
Echo features of effusive-constrictive pericarditis?
- Small-moderate PE
- Fibrous strands within PE
- Classic 2D/Doppler features of CP
What is the gold standard for effusive-constrictive pericarditis?
- Cardiac MRI
- Can identify pericardial thickening and location of thickening (characterised by white rim around the heart)
