ESC guidelines

Management
of pericardial
diseases
Ahmed Elborae
Assistant Lecturer of Cardiology, Cairo University
Etiology
Etiology
Etiology
 Positional
> Persist after holding breath
 Knuckle sign
Diffuse ST ↑ infero-lateral leads
(PR elevation aVr)

Spodick sign
Down sloping TP in Lead II

N.B: Pericarditis: T wave become inverted after ST normalize

In STEMI: T wave become inverted while ST is still elevated, + reciprocation +Convex ST
COPE-CORP-ICAP RCTs

Only 10%

Recurrent pericarditis 38%

 Pregnancy:
-Colchicine is contraindicated
-Avoid aspirin/NSAID after 20 weeks (Premature duct closure)
-So, low dose steroid might be used in this scenario
Etiology
 Two layers : Visceral and outer fibrous parietal

Normally:
Volume: 25 ml
Pressure: < 5 mmHg
 Cardiac tamponade

as little as 50 cc
May exceed 1000 cc
can
without
cause tamponade
tamponade

Rate dependent not volume dependent

 Signs of tamponade

Inspiration

Beck’s triad
Electrical

alternans

Volume: Variable
Pressure: “15-20 mmHg”
Pulsus paradoxus
> 10 mmHg drop

Absent Y descend
Late diastole Inspiration Early diastole Inspiration

A4 A4 view+ PWD
view

Hemodynamic significance is what really matter

At least 300 ml
Settings:

-Emergency
-Semi-urgent
-Elective
TB
CKD
 Constrictive pericarditis

20% of constrictive pericarditis occurs with normal pericardial thickness,

So, it is a pathophysiological phenomena rather than anatomical one
 Two important pathophysiological
characteristics
Normally
(ventricular interdependence)
• Both ventricles are contained in the
same sac “pericardium”, so changes
of pressure in one ventricle could be
transmitted to the other (Minute
effect)
Constrictive pericarditis
(Exaggerated ventricular interdependence)
• Being contained in a rather more tight
sac, so this effect become exaggerated
• During inspiration, increase systemic
venous return to RV> shift septum to left
“septal bouncing”
• During expiration, increase pulmonary
venous return to LV> shift septum to the
right, and this could be transmitted to
hepatic veins causing ” expiratory flow
reversal”
 Inspiratory
Septal shift left

Expiratory
Septal shift to right
(Expiratory hepatic
 Second characteristic

Normally Constrictive pericarditis

(Changes in intrathoracic pressure during respiration (Halting of intrathoracic pressure changes
are reflected similarly to venous return and during respiration on the ventricle ) :
ventricles)

• Systemic venous return increase with • Ventricles isolated by calcium shield

inspiration , while pulmonary venous return
increases with expiration

• Similar changes in the intraventricular

pressure of the RV, LV.

• So, net result, no significant changes in the

flow at the level of mitral and tricuspid • So, net result, significant changes in the
valves with respiration. flow at the level of mitral and tricuspid
valves with respiration.
Ventricles are isolated from intrathoracic pressure changes by thick pericardium
pulmonary veins are extra-pericardial

X
early diastolic

-Rapid Y descend (Friedreich sign)

-M shaped JVP (Absent in AF, TR)
-Inspiratory rise of JVP (Kussmaul sign)
 Hemodynamic study

Exaggerated ventricular interdepence “The most specific sign”

Constrictive pericardial syndromes
Percutaneous balloon pericardiotomy