Pathophysiology and Aetiology
| Idiopathic | Most likely to be viral in origin |
| Viral eg,
EchovirusEnterovirus, cocksackie virus, CMV, Hep B, Infections mononucleosis, HIV |
|
| Bacterial eg. Pneumococcus, staphylococcus,
streptococcus, mycoplasma |
Commonest cause would be from direct extension from a pneumonia. Characterized by purulent effusion |
| TB | Indolent course – non-specific symptoms of fever, malaise and dypsnoea (autoimmune) |
| Post-acute MI | Early (1-3 days) – transmural necrosis causing adjacent pericarditis
Late (1 week – a few months) – Dressler’s syndrome |
| Trauma/Post cardiac surgery | Blunt or penetration injury |
| Neoplastic | Secondary metastatic tumour |
| Uraemia | Pathophysiology unknown |
| Inflammatory/autoimmune | RA, SLE, Scleroderma |
| Chest wall irradiation | Early (acute illness), Late (years after exposure) |
| Drug induced | Isoniazid, Hydralazine |
Table 1: Causes of pericarditis – RCEM learning
Pericarditis
Pericarditis is caused by inflammation of the pericardial layers. The causes of pericarditis are widespread and can be separated into two different groups; non-infectious and infectious. However, around 80-90% are ‘idiopathic’ in nature.
Pericarditis can be split into 3 different categories:
- Acute pericarditis – no effusion seen in the acute phase
- Subacute pericarditis – no effusion, but transient constriction days to weeks after initial presentation
- Chronic pericarditis – >3 months in duration. Effusion may be present.
Acute and subacute pericarditis usually have the same aetiology (listed in Table 1). Chronic pericarditis can occur following an acute episode of pericarditis, or have its own aetiology, most commonly metastatic disease (lung cancer being the most common), but also rheumatological conditions (such as SLE, RA, and Behçet’s disease).
Pericardial effusion
These conditions (chronic or acute) if left untreated can lead to formation of a pericardial effusion. Normal volumes of fluid range from 15ml – 50ml. However, in pericarditis, this amount of fluid can increase. The fluid may be transudative, exudative or serosanguinous depending on the aetiology:
- Transudative – Heart failure, hypoalbuminaemia, cirrhosis, chest wall irradiation, renal insufficiency
- Exudative – viral/bacterial infection, malignancy, inflammatory/autoimmune
- Serosanguinous – blunt trauma, post cardiac surgery, uraemia, also malignancy
Cardiac Tamponade
Fluid accumulation from pericardial effusion causes increased pressure in the pericardial sac, causing impaired diastolic filling of the left and right heart. Reduced filling of the right heart can cause venous congestion, and reduced filling of the left heart can cause a drop in stroke volume. Increased pressure in the pericardial sac may cause compression of the heart, especially the right heart, due to a thinner wall. Impaired diastolic filling of the right heart causes venous congestion. Reduction in the diastolic filling of the left ventricle results in decreased cardiac output and eventually shock. This is a medical emergency called cardiac tamponade. Cardiac tamponade can occur with small rapid increases in volume of the pericardial fluid (around 100-150ml), with a classical example being from a traumatic cardiac injury (blunt or penetrating trauma). However, in chronic settings where there is gradual build-up such as in autoimmune disease, neoplasms or chronic pericarditis, the pericardial effusion may become 1L – 2L in size before it causes cardiac tamponade.
Constrictive Pericarditis
During healing of an acute/chronic pericarditis or resorption of pericardial effusion, granulation tissue forms on the pericardium. This granulation tissue gradually contracts over time and encases the heart and may get calcified. This creates pericardial noncompliance (stiff ventricle), leading to increased diastolic pressures and more rapid rise in ventricular pressures for a given venous return, causing reduced ventricular filling as compared to a normal pericardium. This results in decreased end diastolic volume and decreased stroke volume and cardiac output. Approximately 9% of patients with acute pericarditis develop constrictive physiology. In developed nations, the leading cause of this condition is idiopathic or post-viral infection with incidence being 40% to 60% of total cases.
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