The normal pericardium is a fibroelastic sac containing a thin layer of fluid (50 mL) that surrounds the heart and roots of the great vessels.
In the UK, acute inflammation of the pericardium is most commonly due to viral infection (Coxsackie B, echovirus, HIV infection) or follows myocardial infarction. Other causes include uraemia, autoimmune rheumatic diseases, trauma, infection (bacterial, tuberculosis, fungal), and malignancy (breast, lung, leukaemia and lymphoma).
There is sharp retrosternal chest pain which is characteristically relieved by leaning forward. Pain may be worse on inspiration and radiate to the neck and shoulders. The Cardinal clinical sign is a pericardial friction rub, which may be transient.
The ECG is diagnostic. There is concave upwards (saddle shaped) ST segment elevation across all leads and return towards baseline as inflammation sub-sides. ST segment elevation is convex upwards in myocardial infarction and limited to the leads that face the infarct.
Treatment is of the underlying disorder plus NSAIDs. Systemic corticosteroids are used in resistant cases. NSAIDs should not be used in the few days fol-lowing myocardial infarction as they are associated with a higher rate of myocardial rupture. Complications of acute pericarditis are pericardial effu-sion and chronic pericarditis (>6-12 months).
Pericardial effusion and tamponade
Pericardial effusion is an accumulation of fluid in the pericardial sac which may result from any of the causes of pericarditis. Hypothyroidism also causes a pericardial effusion which rarely compromises ventricular function. Pericardial tamponade is a medical emergency and occurs when a large amount of pericardial fluid (which has often accumulated rapidly) restricts diastolic ventricular filling and causes a marked reduction in cardiac output.
The effusion obscures the apex beat and the heart sounds are soft. The signs of pericardial tamponade are hypotension, tachycardia and an elevated jugular venous pressure, which paradoxically rises with inspiration (Kuss-maul's sign). There is invariably pulsus paradoxus (a fall in blood pressure of more than 10 mmHg on inspiration). This is the result of increased venous return to the right side of the heart during inspiration. The increased right ventricular volume thus occupies more space within the rigid pericardium and impairs left ventricular filling.
■ Chest X-ray shows a large globular heart.
■ ECG shows low-voltage complexes.
■ Echocardiography is diagnostic, showing an echo-free space around the heart.
■ Invasive tests to establish the cause of the effusion may only be neces-sary with a persistent effusion, if a purulent or tuberculous effusion is suspected, or if the eftusion is not known to be secondary to an underly-ing illness. Pericardiocentesis (aspiration of fluid under echocardiographic guidance) and pericardial biopsy for culture, cytology/histology and PCR (for tuberculosis) give a greater diagnostic yield with large effusions.
The treatment of tamponade is emergency pericardiocentesis. Pericardial fluid is drained percutaneously by introducing a needle into the pericardial sac. If the effusion recurs, in spite of treatment of the underlying cause, excision of a pericardial segment may be necessary. Fluid is then absorbed through the pleural and mediastinal lymphatics.
In the UK, most cases of constrictive pericarditis are idiopathic in origin or result from intrapericardial haemorrhage during heart surgery.
The heart becomes encased within a rigid fibrotic peri-cardial sac which prevents adequate diastolic filling of the ventricles. The clinical features resemble those of right-sided heart failure, with jugular venous distension, dependent oedema, hepatomegaly and ascites. Kussmaul's sign (JVP rises paradoxically with inspiration) is usually present and there may be pulsus paradoxus, atrial fibrillation and, on auscultation, a pericardial knock caused by rapid ventricular filling. Clinically, constrictive pericarditis cannot be dis-tinguished from restrictive cardiomyopathy (p. 478).
A chest X-ray shows a normal heart size and pericardial calcification (best seen on the lateral film). Diagnosis is made by CT or MRI, which shows pericardial thickening and calcification.
Treatment is by surgical excision of the pericardium.
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