Pericarditis

The classic sign of pericarditis is a friction rub heard with a stethoscope on the cardiovascular examination, usually on the lower left sternal border.[11] Other physical signs include a person in distress, positional chest pain, diaphoresis (excessive sweating); possibility of heart failure in form of pericardial tamponade causing pulsus paradoxus, and the Beck's triad of low blood pressure (due to decreased cardiac output), distant (muffled) heart sounds, and distension of the jugular vein (JVD).

Pericarditis can progress to pericardial effusion and eventually cardiac tamponade. This can be seen in people who are experiencing the classic signs of pericarditis but then show signs of relief, and progress to show signs of cardiac tamponade which include decreased alertness and lethargy, pulsus paradoxus (decrease of at least 10 mmHg of the systolic blood pressure upon inspiration), low blood pressure (due to decreased cardiac index), (jugular vein distention from right sided heart failure and fluid overload), distant heart sounds on auscultation, and equilibration of all the diastolic blood pressures on cardiac catheterization due to the constriction of the pericardium by the fluid.

In such cases of cardiac tamponade, EKG or Holter monitor will then depict electrical alternans indicating wobbling of the heart in the fluid filled pericardium, and the capillary refill might decrease, as well as severe vascular collapse and altered mental status due to hypoperfusion of body organs by a heart that can not pump out blood effectively.

The diagnosis of tamponade can be confirmed with trans-thoracic echocardiography (TTE), which should show a large pericardial effusion and diastolic collapse of the right ventricle and right atrium. Chest X-ray usually shows an enlarged cardiac silhouette ("water bottle" appearance) and clear lungs. Pulmonary congestion is typically not seen because equalization of diastolic pressures constrains the pulmonary capillary wedge pressure to the intra-pericardial pressure (and all other diastolic pressures).

Pericarditis may be caused by viral, bacterial, or fungal infection.

In the developed world, viruses are believed to be the cause of about 85% of cases.[6] In the developing world tuberculosis is a common cause but it is rare in the developed world.[6] Viral causes include coxsackievirus, herpesvirus, mumps virus, and HIV among others.[4]

Pneumococcus or tuberculous pericarditis are the most common bacterial forms. Anaerobic bacteria can also be a rare cause.[13] Fungal pericarditis is usually due to histoplasmosis, or in immunocompromised hosts Aspergillus, Candida, and Coccidioides. The most common cause of pericarditis worldwide is infectious pericarditis with tuberculosis.

• Idiopathic: No identifiable cause found after routine testing.[4]
• Autoimmune disease: systemic lupus erythematosus, rheumatic fever,[4] IgG4-related disease[14][15]
• Myocardial infarction
  • Dressler's syndrome)[4]
  • Peri-Myocardial Infarction Pericarditis[16]
• Trauma to the heart[4]
• Uremia (uremic pericarditis)[4]
• Cancer[4]
• Side effect of some medications, e.g. isoniazid, cyclosporine, hydralazine, warfarin, and heparin
• Radiation induced[4]
• Aortic dissection[4]
• Postpericardiotomy syndrome—such as after CABG surgery[4]
• Vaccines-such as smallpox[17][18] and Covid-19 Vaccines[19] in rare yet documented instances.

Diffuse ST elevation in a young male due to myocarditis / pericarditis

An ECG showing pericarditis. Note the ST elevation in multiple leads with slight reciprocal ST depression in aVR.

Laboratory values can show increased urea (BUN), or increased blood creatinine in cases of uremic pericarditis. Generally, however, laboratory values are normal, but if there is a concurrent myocardial infarction (heart attack) or great stress to the heart, laboratory values may show increased cardiac markers like Troponin (I, T), CK-MB, Myoglobin, and LDH1 (lactase dehydrogenase isotype 1).

The preferred initial diagnostic testing is the ECG, which may demonstrate a 12-lead electrocardiogram with diffuse, non-specific, concave ("saddle-shaped"), ST-segment elevations in all leads except aVR and V1[11] and PR-segment depression possible in any lead except aVR;[11] sinus tachycardia, and low-voltage QRS complexes can also be seen if there is subsymptomatic levels of pericardial effusion. The PR depression is often seen early in the process as the thin atria are affected more easily than the ventricles by the inflammatory process of the pericardium.

Since the mid-19th century, retrospective diagnosis of pericarditis has been made upon the finding of adhesions of the pericardium.[20]

When pericarditis is diagnosed clinically, the underlying cause is often never known; it may be discovered in only 16–22 percent of people with acute pericarditis.

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  Ultrasounds showing a pericardial effusion in someone with pericarditis
• 
  A pericardial effusion as seen on CXR in someone with pericarditis

On MRI T2-weighted spin-echo images, inflamed pericardium will show high signal intensity. Late gadolinium contrast will show uptake of contrast by the inflamed pericardium. Normal pericardium will not show any contrast enhancement.[21]

Pericarditis can be classified according to the composition of the fluid that accumulates around the heart.[22]

Types of pericarditis include the following:

• serous
• purulent
• fibrinous
• caseous
• hemorrhagic

Depending on the time of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or even as a result of a heart attack (myocardial infarction), as Dressler's syndrome. Chronic pericarditis however is less common, a form of which is constrictive pericarditis. The following is the clinical classification of acute vs. chronic:

• Clinically: Acute (<6 weeks), Subacute (6 weeks to 6 months) and Chronic (>6 months)