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 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

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