Pericarditis

Cours DCEM

Most Common Causes of Acute Pericarditis

Infectious

Viral

Tuberculosis

Pyogenic Bacteria

Noninfectious

Postmyocardial infarction

Uremia

Neoplastic disease

Radiation induced

Connective tissue disease

Drug induced

Pathology of Acute PericarditisSerous 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

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

ECG in Pericarditis

• Diffuse ST elevation in multiple leads

• No “mirror” image

• PR segment depression

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…

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

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

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

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)

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

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

Cardiac Tamponade

Most common etiologies• Neoplastic• Postviral• Uremic• Acute pericardial hemorrhage

Cardiac Tamponade: Pathophysiology

Tamponade: Clinical Features

• Jugular venous distension• Hypotension• Quiet heart on examination• Sinus tachycardia• Dyspnea and tachypnea• Pulsus paradoxus• Clear lungs +++

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

Diagnostic Approach to Tamponade

• Echo

• Cardiac catheterization

Echocardiographic Findings in Tamponade

Hemodynamic Findings in Tamponade and Constrictive Pericarditis

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

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

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

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

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

Hemodynamic Findings in Constrictive Pericarditis