Pathophysiology and Aetiology | Medibuddy
10th May 2025

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:  

  1. Acute pericarditis – no effusion seen in the acute phase  
  2. Subacute pericarditis – no effusion, but transient constriction days to weeks after initial presentation  
  3. 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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