pericardial disease

1. Pericardial disease
Dr.Abdulilah Alshenghiti

2. Learning Objectives
• Acute pericarditis and recurrent Pericarditis
• Pericardial effusion
• Cardiac Tamponade
• Constrictive pericarditis
• Pericardial tumors and metastatic disease

3. Anatomy
Pericardium
is an avascular sac surrounding the heart
composed of a double layer with thickness
1mm.
- Outer fibrous pericardium
- Inner serous pericardium
- Parietal and visceral layer
The cavity normally contain from 10 to 50
ml of clear plasma ultrafiltrate between the
two layers.

4. Function of pericardium
• 1.Stabilization of the heart within the thoracic cavity .It is attached to
the diaphragm, sternum and the cartilage of the ribs which limiting
the heart’s motion.
• 2.Protection of the heart from mechanical trauma and infection from
adjoining structures.
• 3.The pericardial fluid functions as a lubricant and decreases friction
of cardiac surface during systole and diastole.
• 4.Prevention of excessive dilation of heart especially during sudden
rise in intra-cardiac volume (e.g. acute aortic or mitral regurgitation)

5. Acute pericarditis
Acute inflammation of pericardium usually due to idiopathic, viral infection.
It is the most common form of pericardial disease and represents around 5 % of
non-ischemic chest pain attending in the ER .

6. Etiology

7. Typical features of Acute Pericarditis
• Chest Pain < 85-90 %
• Friction Rub < 40% ( disappear when effusion
develop)
• Classic ECG 60 %
• Effusion ( Echo) 60 %
Not useful in early stage of dry pericarditis.
The presence of any 2 of these in context of the appropriate clinical
history is needed to diagnose acute pericarditis.

8. Presentation
Chest pain :
Pericardium is well innervated such that pericardial inflammation may
produce severe pain and trigger vagally mediated reflexes. The pericardium
also secretes prostaglandins that modulate cardiac reflexes and coronary
tone.
Acute onset , Sharp, Stabbing, continues precordial chest pain radiating to
the shoulder
Relieved by sitting up and leaning foreword and aggravated by laying down
and cough.
Pain originated from 2 places either from big vessels or apex of the heart
from the diaphragm innervation.

9. Pericardial rub
(disappear when effusion develop)

10. Investigation (ECG)

12. Investigation
Labs
CBC: May shows Leukocytosis
Inflammatory markers : ESR and CRP may be elevated
Elevated Cardiac enzyme may indicate associate Myocarditis.
(So Cardiac enzyme and troponin trending and is important If still positive do Echo and if there no abnormal
wall motion then treated as pericarditis ,and if positive then it is a mandatory to cath the patient to confirm the
Dx. )

13. When do you admit the
patient ?

14. Predictors of poor prognosis
• Major:
• Fever < 38 C
• Subacute onset
• Large pericardial effusion
• Cardiac tamponade
• No response to NSAID in 1 w
• Minor:
• Myopericarditis
• Immunosuppression
• Trauma
• Oral anticoagulation therapy
• d
Improved
Acute
Pericarditis
Risk
Markers
Absent
Risk
Markers
Present
Admi
t
Start
Empiric
Therapy
No
Improvemen
t
Search
Alterati
ve
Etiology
Continue
OP
Follow-
up

15. Aspirin 750 – 1000 mg every 8h 1 – 2 weeks
Ibuprofen 600 mg every 8h 1 – 2 weeks
Indomethacin 50 mg every 8h 1 – 2 weeks
Acute Pericarditis Therapy
Colchicine 0.5 mg* 3 months
*Once (<70 kg) or twice daily (≥70 kg)
One from each
box
Use gastric
protection (PPI)
Duration of
therapy can be
guided by
symptoms and
CRP

16. Acute Pericarditis therapy

17. Recurrent Pericarditis
1st Line: NSAID + Colchicine Guided by CRP taper NSAID over several weeks,
Colchicine x 6m
2nd Line: Triple therapy with
steroid
Taper steroid over 6 – 12m
Taper NSAID next, then Colchicine x 6m
3rd Line: Immunomodulation IVIG, Anakinra or AZT taper agent one at a time
4th Line: Pericardiectomy

18. Myopericarditis
(So Cardiac enzyme and troponin trending and is important If still positive do Echo and if there no abnormal wall motion then treated as pericarditis ,and if positive then it is a mandatory to cath the patient to confirm the Dx. )
• Hospitalization
• MRI to Confirm no extensive myocarditis
• Consider coronary angio to exclude CAD
• Return to competition (6 months after onset )

19. Pericardial effusion
Accumulation of fluid between the
visceral and parietal layers of serous
pericardium
• Trivial : 50 – 100 cc fluid is only seen in
systole
• Small : 100 cc
• Moderate : 500 cc
•Large : 1000 cc

20. Etiology
1. Inflammation from infection, immunologic process.
2. Trauma causing bleeding in pericardial space.
3. Noninfectious conditions such as:
a. increase in hydrostatic pressure e.g. congestive heart failure.
b. increase in capillary permeability e.g. hypothyroidism
c. decrease in plasma oncotic pressure e.g. cirrhosis.
d. Uremic pericarditis
1. 4. Decreased drainage of pericardial fluid due to obstruction of
thoracic duct as a result of malignancy or damage during surgery.

21. Pericardial effusion without Tamponade

23. How much Fluid should be in the pericardium
to produce tamponade ?

24. Pericardial effusion
Hemodynamic compromised in pericardial Effusion is related to the Rate
rather than the amount .

25. Cardiac tamponade -- Pathophysiology

26. Etiology
Pericardial pressures > intracardiac pressures
• Most common causes :
– Malignancy
– Idiopathic pericarditis (Viral ? )
– Renal failure.
– Bleeding following cardiac Surgery ,early post MI (before fibrosis
formation while the wall is weak ) and
- trauma .
- TB.

28. Clinical Features
Symptoms
Acute : confusion / agitation
Tachycardia (sensitivity, 77%)
• Signs ( Becks triad)
- hypotension
- elevated JVP (sensitivity, 76%)
- muffled heart sounds
Pulsus paradoxus : insp drop in SBP > 10 mmhg Pulsus paradoxus also seen in CP,
COPD, asthma (with pericardial effusion) >10mmHg (sensitivity, 82%).
Cardiomegaly on chest radiograph (sensitivity, 89%).

29. Kussmaul’s sign
What is Kussmaul's sign of JVP?
is the paradoxical increase in JVP that occurs
during inspiration. Jugular venous pressure
normally decreases during inspiration
because the inspiratory fall in intrathoracic
pressure creates a “sucking effect” on venous
return.
It is a good tool to differentiate it with severe
Right HF.

30. Investigation
ECHO
findings suggestive of cardiac tamponade –
examine the right side of the heart and IVC
- A pericardial effusion >25mm (but smaller
pericardial effusions can cause tamponade)
- Diastolic right ventricular collapse (high
specificity clip in mobile)
- Systolic right atrial collapse (earliest sign clip
in computer)
- A Dilated inferior vena cava with minimal
respiratory variation (high sensitivity clip in
mobile ).

31. Echo
- Diastolic right ventricular
collapse (high specificity clip

32. Echo
- Dilated inferior vena cava
with minimal respiratory
variation (high sensitivity clip
in mobile ).

33. Investigation
JVP

34. CVP wave

35. Cardiac tamponade
Absent Y wave is due to ventricular
relaxation.
Ventricles can't relax when the
pericardium is full of fluid, leading
to the absence of y descent.

36. Constrictive pericarditis
• Constrictive pericarditis (CP) is a chronic inflammatory process, often
characterized by chronic scarring, fibrosis and calcification of the
pericardium.
• associated with diastolic dysfunction, eventually leading to low
cardiac output and heart failure.

38. Investigation
Chest CT has sensitivity 93 %

39. JVP wave

40. Treatment
• Treat the underline couse ex : TB , Malignancy
• Surgical pericardiectomy is the definitive management the earliest the
better.

41. Take away…
• Symptoms may be non cardiac
• Chronic Pericarditis and Pericardial effusion will mimic right heart
failure.
• In any RHF symptoms rule out pericardial disease
• Because treatment is completely different (diuretics, digoxin)
• Clinical suspicion is essential for diagnosis
• Correct diagnosis is imperative
• Potential for permanent cure

42. Thank you