Contents
Pericarditis is inflammation of the pericardium and can occur as an isolated entity or as a manifestation of an underlying systemic disease.
Pericarditis is inflammation of the pericardium (the fibrous sac surrounding the heart).

Etiopathogenesis
Acute pericarditis is diagnosed in approximately 0.1% of hospitalized patients and in 5% of patients admitted to the emergency department with noncardiac chest pain.
- Idiopathic (85% cases): Most cases of acute pericarditis are idiopathic because the yield of diagnostic tests to confirm etiology has been relatively low
- Infections due to various viral and bacterial (eg, tuberculous) microorganisms:
- Viral (M/C known cause): Coxsackie B virus
- Bacterial: Tuberculosis
- Parasitic: Trichinosis
- Systemic diseases: Autoreactive or immune-mediated diseases
- Neoplastic invasion of pericardium
- Uremic pericarditis (kidney failure with excessive blood urea nitrogen): ↑ BUN → Irritates pericardium → Thick pericardial fluid (fibrous strands + WBC) “Buttered-bread appearance”
- Cardiovascular comorbidities:
- Previous acute myocardial infarction; aortic dissection and chest wall trauma
- Previous cardiotomy or thoracic surgery

Complications
- Pericardial effusion → Cardiac tamponade
- Chronic constrictive pericarditis
- Myocarditis

Relapsing pericarditis:
Pericarditis is defined as “recurrent” in case of relapse after a minimum symptom-free interval of 4–6 weeks.
- Incessant type: Relapse in < 6 weeks; usually in corticosteroid therapy
- Intermittent type: Symptom-free intervals of > 6 weeks without treatment

Presentation
Acute pericarditis usually appears in the form of a clinical triad of Chest pain + friction rub + serial ECG changes
Pleuritic chest pain:
The chest pain of acute pericarditis is usually sudden in onset, retrosternal, and pleuritic in that it is exacerbated by inspiration. Dull, oppressive pain can also occur in pericarditis, making it difficult to distinguish from myocardial ischemia.
- Tripod position: Lessening of the pain when they lean forward or are in the upright position
- Radiation to neck, arms, or left shoulder (similar to myocardial infarction)
Pericardial Friction Rub:
Generated by friction of the 2 inflamed layers of the pericardium, corresponds to the movement of the heart within the pericardial sac. The rub tends to vary in intensity over time, and thus patients should be examined repeatedly.
- Audible friction rub (85% cases & highly specific for pericarditis): High-pitched, scratchy or squeaky sound heard best at the left sternal border
- Classic friction rub consists of 3 phases that correspond to the movement of the heart during 3 phases of the cardiac cycle:
- Atrial systole
- Ventricular systole
- Rapid ventricular filling during early diastole
- However, some rubs are present in only 1 (monophasic) or 2 (biphasic) components of the cardiac cycle,11 and it is difficult to know whether these rubs are truly due to pericardial disease
Physical signs of cardiac tamponade:
- Pulsus paradoxus
- Kussmaul sign with elevated jugular venous pressure

Diagnosis
Because most cases of acute pericarditis follow a benign course, a full diagnostic evaluation is not needed for all patients with acute pericarditis. However, the initial evaluation should identify patients with high-risk features of acute pericarditis, including significant effusion and cardiac tamponade. In addition, tuberculous, purulent, uremic, or neoplastic causes of acute pericarditis should be adequately investigated.

ECG:
Typical ECG changes in acute pericarditis include wide-spread upward concave ST-segment elevation and PR-segment depression. However, 4 stages of ECG abnormalities have been described previously. Typical ECG evolution in acute pericarditis has been shown in up to 60% of patients in a clinical series, and stage 1 changes have been observed in 80% of patients with pericarditis.
- Stage 1 (hours to days):
- Diffuse ST-elevation secondary to epicardial inflammation
- PR-depression
- Reciprocal ST-segment depression in the aVR and V1 leads.
- Stage 2: ST and PR segments normalize
- Stage 3: Development of widespread T-wave inversions
- Stage 4: ECG may become normal or T-wave inversions may persist indefinitely

Chest Radiography:
Cardiomegaly with clear lung fields suggests a significant pericardial effusion and indicates at least 200 mL of pericardial fluid. However, cardiomegaly is an uncommon finding, and most findings on chest radiography are normal in patients with acute pericarditis.
- Cardiomegaly: Large cardiac silhouette “Bottle water shaped“

Echocardiography:
Transthoracic echocardiography is recommended in patients with suspected acute pericarditis who have evidence of hemodynamic compromise.

Cardiac computed tomography (CT) and cardiac magnetic resonance imaging (CMR):
Cardiac computed tomography (CT) and cardiac magnetic resonance imaging (CMR) are increasingly being used in the diagnosis of pericarditis. Both imaging modalities are very sensitive in the detection of generalized or loculated effusions and can also be used to measure pericardial thickness. Normal pericardial thickness is less than 4 mm and is usually 1 to 2 mm
- Cardiac CT: Increased pericardial thickness (not diagnostic for pericarditis)
- Cardiac MR: Delayed enhancement of pericardium (most sensitive method for the diagnosis of acute pericarditis)
- On CMR, the pericardium normally appears black because of its low water content; however, in patients with pericarditis, enhanced gadolinium uptake in the inflamed pericardium is delayed


Differential diagnosis:
Characteristic | Pericarditis | Myocardial infarction |
---|---|---|
Pain description | Sharp, pleuritic, retrosternal (under the sternum) or left precordial (left chest) pain | Crushing, pressure-like, heavy pain. Described as “elephant on the chest.” |
Radiation | Pain radiates to the trapezius ridge (to the lowest portion of the scapula on the back) or no radiation. | Pain radiates to the jaw or left arm, or does not radiate. |
Exertion | Does not change the pain | Can increase the pain |
Position | Pain is worse in the supine position or upon inspiration (breathing in) | Not positional |
Onset/duration | Sudden pain, that lasts for hours or sometimes days before a patient comes to the ER | Sudden or chronically worsening pain that can come and go in paroxysms or it can last for hours before the patient decides to come to the ER |
Management
When the identified etiology of acute pericarditis is not viral or idiopathic, management should be directed toward treating the underlying cause. Patients with no high-risk features can be managed as outpatients.
Hospitalization for high-risk cases:
Patients with high-risk features should be hospitalized. High-risk features include the following:
- Fever (temperature >38°C), leukocytosis
- Large pericardial effusion (echo-free space >20 mm)
- Cardiac tamponade
- Acute trauma
- Immunosuppressed state
- Concurrent oral anticoagulation
- Failure of nonsteroidal anti-inflammatory drug (NSAID) therapy
- Elevated troponin levels
- Recurrent or incessant pericarditis
Medical management:
Medical management for viral or idiopathic acute pericarditis has been centered on 3 major agents—NSAIDs, colchicine, and corticosteroids. The management and prognosis of patients with myopericarditis are similar to those of patients with acute pericarditis.
- Aspirin + NSAID (Indocin) + PPI ± Colchicine ± Corticosteroids (Prednisolone)

Pericardiocentesis:
Fluid aspiration from pericardium. It is indicated in severe effusion and in cardiac tamponade
Summary