1. Pericarditis
Cours DCEM

2. Most Common Causes of Acute Pericarditis
Infectious
Viral
Tuberculosis
Pyogenic Bacteria
Noninfectious
Postmyocardial infarction
Uremia
Neoplastic disease
Radiation induced
Connective tissue disease
Drug induced

3. Pathology of Acute Pericarditis
Serous pericarditis
Few PMN, lymphcytes and histiocytes
The exudate is a thin fluid secreted by mesothelial cells
Serobibrinous pericarditis
Most common form
Exsudate is rich in plasma proteins including fibrinogen
Appearance of “bread and butter”
Portions of the visceral and parietal pericardium may become thickened and fused
May lead to constrictive pericarditis
Suppurative (or purulent) pericarditis
Hemorrhagic pericarditis

4. Clinical Features Chest pain Fever
Dyspnea: reluctance of the patient to breathe deeply because of the pleuritic pain
Pericardial friction rub: sharp; best heard with patient leanign forward while exhaling; evanescent

5. ECG in Pericarditis Diffuse ST elevation in multiple leads
No “mirror” image
PR segment depression

6. Additional Tests in Pericarditis
Echo: May or may not show a pericardial effusion
ESR and CRP: Frequently elevated, but non specific
Chest X-Ray: May or may not show a pericardial effusion; may show etiology of pericarditis: pneumonia, pleural effusion, cancer…
Serological tests: ANA, Rheumatic factor…

7. The yield of diagnostic pericardiocentesis in uncomplicated acute pericarditis is low, and should be reserved for patients with very large effusions or evidence of cardiac chamber compression

8. Treatment of Acute Pericarditis
Idiopathic or viral pericarditis
Self-limited disease (runs its course in 1-3 weeks)
Rest + pain relief (analgesics, aspirin, anti-inflammatory drugs)
Oral corticosteroids are often effective for severe or recurrent pericardial pain, but should not be used in uncomplicated cases, because of potentially devastatin side effects and because of increased risk of recurrence
Post-MI pericarditis rest + aspirin
Purulent pericarditis catheter drainage + antibiotics
Uremia Intensive dialysis
Neoplastic

9. Pericardial Effusion
3 factors determine whether a pericardial effusion remains clinically silent, or whether symptoms of cardiac compression ensue:
The volume of fluid
The rate at which the fluid accumulates
The compliance characteristics of the pericardium

10. Clinical Features of Pericardial Effusion
Asymptomatic
Dull constant ache in the left side of the chest
Symptoms of cardiac tamponade
Compression of adjacent structures: dysphagia, dyspnea, hoarseness, hiccups
Decrease in intensity of heart sounds
No friction rub
Dullness to percussion of the left lung over the angle of the scapula (Ewart’s sign)

11. Diagnostic Studies of Pericardial Effusion
Chest X ray: normal; if > 250 ml, enlarged cardiac silhouette in a globular, symmetric fashion
ECG: Decrease voltage; electrical alternans
Echo: Most important test; gives the diagnosis; can identify pericardial collections as small as 20 ml; determine whether ventricular filling is compromised

12. Treatment of Pericardial Effusion
Treatment of the cause
An asymptomatic effusion may be left for years without specific intervention
If hemodynamic compression occurs, pericardiocenthesis should be performed

13. Cardiac Tamponade Most common etiologies Neoplastic Postviral Uremic
Acute pericardial hemorrhage

14. Cardiac Tamponade: Pathophysiology

15. Tamponade: Clinical Features
Jugular venous distension
Hypotension
Quiet heart on examination
Sinus tachycardia
Dyspnea and tachypnea
Pulsus paradoxus
Clear lungs +++

16. Pulsus paradoxus Inspiration Decrease intra-thoracic pressure
Increase in venous return to the RV
The RV cannot expand because of the external compression by pericardial fluid
Bulging of the interventricular septum to the LV
Decrease LV filling
Decrease blood pressure

17. Diagnostic Approach to Tamponade
Echo
Cardiac catheterization

18. Echocardiographic Findings in Tamponade

19. Hemodynamic Findings in Tamponade and Constrictive Pericarditis

20. Constrictive Pericarditis
Etiology:
Any cause of acute pericarditis
Most common: idiopathic pericarditis
In the past, the most common form was tuberculous pericarditis
Pathology:
Following acute pericarditis, there is resorption of pericardial fluid
In some patients (rare), the fluid undergoes organization with fusion of the 2 layers followed by fibrous scar formation
Sometimes, calcification of the layers may ensue, leading to further stiffening of the pericardium

21. Constrictive Pericarditis: Pathophysiology
Abnormality occurs during diastole
Systolic contraction of the ventricle is normal
The scarred pericardium inhibits normal filling of the cardiac chambers
As blood passes from the RA into the RV, the RV size expands and quickly reaches the limit imposed by the constricting pericardium
At that point, further filling is suddently arrested and venous return to the RV ceases
Systemic venous pressure increases and signs of right-sided heart failure
In addition, impaired filling of the LV causes a reduction in stroke volume, cardiac output and blood pressure

22. Clinical Features of Constrictive Pericarditis
Reduced cardiac output: fatigue, hypotension, tachycardia
Elevated systemic venous pressure: jugular distension, hepatomegaly, ascites, peripheral edema
On auscultation: early diastolic “knock” may follow S2. It represents the sudden cessation of ventricular diastolic filling imposed by the rigid pericardial sac
No pulsus paradoxus
Kussmaul’s sign: during inspiration the increased venous return accumulates in the intrathoracic systemic veins because the negative intrathoracic pressure cannot be transmitted to the RV through the rigid pericardial sac. This causes the jugular veins to become more distended during inspiration

23. Hemodynamic effects and effects of respiration on cardiac tamponade vs constrictive pericarditis

24. Diagnostic Approach to Constrictive Pericarditis
Chest X Ray: normal or mildly increased cardiac silhouette. Calcifications of the pericardium in 50%
ECG: non specific ST/T abnormalities, atrial arrythmia
Echo: The ventricular cavities are small and contract vigorously; diastolic ventricular filling terminates abruptly in early diastole
CT or MRI: Increased pericardial thickness
Cardiac catheterization:
Elevation and equalization of diastolic pressures in the 4 cardiac chambers
LV and RV: dip and plateau
Prominent y descent in right atrial tracing

25. Hemodynamic Findings in Constrictive Pericarditis