Pericarditis is inflammation of the pericardium (the double-layered membrane surrounding the heart). This disorder often leads to chest pain and fever. There may also be an increased amount of fluid( effusion) in the pericardial space, which separates the two smooth layers of the pericardium. The excess fluid may compress the heart and restrict its action. Long-term inflammation can cause a condition called constrictive pericarditis, in which the pericardium becomes scarred, thickens, and contracts, and as a result impedes the heart’ s action.


Causes of pericarditis include infection; myocardial infarction (heart attack); cancer spreading from another site; and injury to the pericardium. The disorder may accompany the autoimmune conditions rheumatoid arthritis and systemic lupus erythematosus, or kidney failure.


Pain, behind the sternum (breastbone) and sometimes in the neck and shoulders, may be more severe if the person takes a deep breath, changes position, or swallows. Pain may be relieved by sitting up and leaning forward. There may also be fever. Constrictive pericarditis causes oedema (fluid swelling) of the legs and abdomen.

Diagnosis and treatment 

Diagnosis is made from a physical examination, from an ECG (which records the electrical activity in the heart) and chest X-rays or echocardiography, which will show any excess fluid around the heart. If possible, treatment is aimed at the cause. Analgesic drugs (painkillers) or anti-inflammatory drugs may be given. If there is an effusion, the excess fluid may be drawn off through a needle. In severe constrictive pericarditis, the thickened part of the pericardium may be surgically removed so that the heart can pump freely.

Pericarditis in detail - technical



The most common causes of acute viral pericarditis are coxsackie B, flu, mumps, hepatitis B, rubella, echovirus 8, and HIV. The typical presentation is with ‘flu-like’ upper respiratory tract infection along with chest pain that is related to breathing. Sending blood tests for viral titres is not usually conclusive in routine clinical practice. The condition is usually self-limiting.

Bacterial infection (other than tuberculous) is a very rare cause of pericarditis, usually caused by staphylococci, pneumococci, or streptococci spreading directly from the lungs or pleura, particularly in patients with impaired immunity.

Tuberculous infection is an important cause of bacterial pericardial disease, particularly in developing countries. It may take the form of acute pericarditis, pericardial effusion, or constriction. The primary response is an acute pericarditis due to allergic reaction. Chronic pericardial effusion and constriction both reflect granulomatous disease complicated by fibrosis and calcification. Both parietal and visceral layers of the pericardium may be involved, including the epicardial layer of the myocardium. In sub-Saharan Africa most patients (>80%) with tuberculous pericarditis will be HIV positive. This needs to be established before treatment: antituberculous chemotherapy is the first line of management for all, but if there is pericardial effusion or constriction steroids are used for the first few weeks to limit the development of adhesions; hence the need for pericardiectomy in those who are HIV-negative.

Actinomycosis, coccidioidomycosis, histoplasmosis, and hydatid disease can rarely cause pericarditis in endemic areas.

Myocardial infarction

This may be complicated by acute pericarditis in 15% of cases, particularly in patients with transmural infarction, when the ECG demonstrates ST and T wave changes that are more generalized than the segmental distribution of the infarct. A friction rub may be heard and a small effusion may be seen on transthoracic echocardiographic examination. A delayed response 3 to 4 weeks after an acute infarct may present as Dressler’s syndrome, with fever and pericardial rub. Although this condition is self limiting it may respond to nonsteroidal anti-inflammatory medications (NSAIDs) and (if needed) steroids.

Autoimmune diseases

Pericardial involvement can be a serious manifestation of rheumatoid disease, systemic lupus erythematosus, systemic sclerosis, and Churg–Strauss syndrome. Presentation can be with pericardial pain, effusion, or even constriction. A small pericardial effusion is seen in most cases of rheumatic fever, but this hardly ever develops into a significant problem. If adhesions develop they may later mature in the form of constriction, a pathology which can be confirmed at the time of valve surgery.

Other medical conditions

Inadequately treated chronic renal failure may be complicated by pericarditis and pericardial effusion. Pericardial tamponade may develop if the effusion remains untreated. Hypothyroidism may be complicated by pericarditis, usually accompanied by a small fluid collection that is unlikely to require drainage.


Irradiation can cause pericarditis soon after treatment, with typical ECG presentation, fluid collection or even constriction. Late presentation can be seen years after irradiation, when the pericardium is thickened and fibrosed.

Clinical features

There are three main features of the clinical syndrome of acute pericarditis—chest pain, pericardial rub, and electrocardiographic changes.

The chest pain occurs at rest and varies with posture and respiration. It is typically sudden in onset (although often preceded by the nonspecific symptoms of a viral illness), retrosternal, continuous, sharp or ‘raw’ in character, worse on inspiration, radiating to the trapezius ridge, and relieved by sitting up. It needs to be distinguished from ischaemic cardiac pain (particularly in the context of recent myocardial infarction), oesophageal pain, and musculoskeletal pain.

On examination the main feature is the presence of a pericardial rub. This scratching or creaking sound, variably described as being like ‘walking on fresh snow’ or the ‘creaking of new leather’, is usually loudest at the left sternal border, but may be heard anywhere in the chest. It often changes with posture, may be louder with inspiration, and can be fleeting, coming and going over a matter of hours. Other elements of the cardiovascular examination are normal unless pericarditis is associated with the presence of sufficient pericardial fluid to cause tamponade, or with pericardial constriction.

The typical ECG change is generalized ST elevation, usually concave upwards, by 1 mm or more. Nonspecific T-wave changes may follow later, after the acute episode has resolved. These changes usually resolve, but they may persist for years afterwards in some cases.

The chest radiograph is not usually helpful in diagnosis: it may show cardiac enlargement, but may be completely normal. Echocardiography is the best technique to show any fluid collection around the heart and to assess its physiological significance.

Although the underlying cause of pericarditis should always be sought, the final diagnosis is often ‘idiopathic’ or ‘presumed viral’. Idiopathic pericarditis is self-limiting and needs only analgesics. Small effusions due to other causes rarely need drainage, but with symptoms the patient may benefit from NSAIDs.

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