Pericardial disease Medical Assignment Help

The normal pericardium lubricates the surface of the heart, prevents sudden deformation or dislocation of the heart, and acts as a barrier to the spread of infection.
There are three common presentations of pericardial disease:
1 Acute pericarditis
2 Pericardial effusion
3 Constrictive pericarditis

Acute pericarditis

Inflammation of the pericardium gives rise to chest pain that is substernal and sharp. It may be referred to the neck or shoulders. It is relieved by sitting forward and made worse by lying down and, lilce pleurisy, is aggravated by movement and respiration.
Acute pericarditis has numerous aetiologies, but Coxsackie viral infections and myocardial infarction are the commonest causes in the UK. Viral pericarditis can occur in epidemics. Other aetiologies include uraemia, connective tissue disease, trauma, postpericardiotorny, rheumatic fever, tuberculosis and malignancy.


The cardinal clinical sign is a pericardial friction rub. There is usually a fever when pericarditis is due to viral or bacterial infection, rheumatic fever or myocardial infarction.


During the first week of the illness the ECG shows ST segment elevation, concave upwards, in all leads facing the epicardial surface, i.e. the anterior, lateral and inferior leads. ST segment depression is only seen in the cavity leads (A VR and VI)’ Later, the ST segment falls and T wave inversion develops. As the illness improves the T waves become normal. Cardiac enzymes may be elevated if there is associated myocarditis.

ECGs associated with pericarditis.

ECGs associated with pericarditis.


Treatment consists of anti-inflammatory medication such as oral aspirin, naproxen or indomethacin. Occasionally, if pericarditis is severe or recurrent, systemic corticosteroids may be needed.


Viral pericarditis

This tends to affect young adults and is sudden in onset. Usually, the illness lasts for only a few weeks and the prognosis is good, although sudden deaths do occur. However, recurrences do occur.
Bacterial pericarditis Septicaemia or pneumonia may rarely be complicated by purulent pericarditis. Staphylococcus and Haemophilus influenzae account for two-thirds of such cases. Antibiotics and surgical drainage may be required. This form of pericarditis, especially when due to Staphylococcus, is usually fatal.

Tuberculous pericarditis

This is typified by a chronic low-grade fever, especially in the evening, associated with signs and symptoms of acute pericarditis, malaise and weight loss. Pericardial aspiration may be required to make the diagnosis. The pericardial effusion is usually serous but may be blood-stained. Specific antituberculous chemotherapy is needed.

Uraemic pericarditis

This is often asymptomatic. It usually develops in the terminal stages of uraemia. Pericarditis following myocardial infarction A pericardial friction rub and the recurrence of chest pain and fever occurs in about 20% of patients during the first few days after myocardial infarction, especially anterior wall infarction.

Dressler’s syndrome

This is pericarditis occurring 1 month to 1 year after an acute myocardial infarction.

Malignant pericarditis

Carcinoma of the bronchus, carcinoma of the breast and Hodgkin’s disease are the most common tumours to infiltrate the pericardium. Leukaemia and malignant melanoma are also associated with pericarditis.
Pericardiocentesis may be useful in diagnosing the malignancy.

Pericardial effusion

Although acute pericarditis is initially dry and fibrinous, almost all aetiologies of this inflammatory reaction also induce the formation of a pericardial effusion. The effusion collects in the closed pericardium. When the pericardium can distend no more, it may produce mechanical embarrassment to the circulation by preventing ventricular filling; this is called cardiac tamponade.


The clinical features include a raised jugular venous pressure, with sharp diastolic collapse-y descent (Friedreich’s sign), a paradoxical pulse (the blood pressure falls during inspiration), increased neck vein distension during inspiration (Kussmaul’s sign) and reduced cardiac output. Because of the effusion, the apex beat may not be palpable and heart sounds are soft. Although a friction rub is often heard, it may be quieter than before the fluid accumulated as the effusion separates the visceral from the parietal pericardium.


The ECG shows reduced voltages, and the chest X-ray may demonstrate an increasingly large globular heart with sharp outlines. The pulmonary veins are typically not distended. Echocardiography is the most useful technique for demonstrating a pericardial effusion.


When the effusion collects rapidly and the circulation is embarrassed, the effusion must be tapped. Pericardiocentesis is also indicated when a malignant, tuberculous or a purulent effusion is suspected. In the UK, malignancy is the most common cause of reaccumulation of pericardial effusion. Reaccumulation may require pericardial fenestration, i.e. the creation of a pericardial window, either transcutaneously via a balloon pericardiotomy under local anaesthesia or using a conventional surgical approach.

Constrictive pericarditis

Following tuberculous pericarditis, haemopericardium, or acute pericarditis due to viral infection, bacterial infection or rheumatic heart disease, the pericardium may become thick, fibrous and calcified. The heart is then encased in a solid shell and cannot fill properly.


There are signs of systemic venous congestion, i.e. ascites, dependent oedema, hepatomegaly and jugular venous distension, without much breathlessness or pulmonary venous distension. There are also signs of impaired ventricular filling, i.e. Kussmaul’s sign, Friedreich’s sign and pulsus paradoxus.
Atrial fibrillation is common (30%) and a loud heart sound, called a pericardial knock, due to rapid ventricular filling may be heard. This is an early third heart sound. Other causes of ascites must be excluded.


The chest X-ray shows a relatively small heart with obvious calcification seen on the lateral film and using fluoroscopy.
The ECG shows low QRS voltages and T wave inversion, and the echocardiogram will demonstrate the thickened pericardium and the relative immobility of the heart. CT is also good at detecting thickness and calcification of the pericardium.


Treatment involves the surgical removal of a substantial proportion of the pericardium. About half the patients do well, but in the others persistent constriction, atrial fibrillation and myocardial disease prevent full recovery.

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