Covers the classification of pericardial diseases, then acute pericarditis: its definitions, causes, clinical features, a staged ECG table, differential diagnosis, admission criteria and drug treatment with doses. It also covers pericardial effusion by size and content, and cardiac tamponade with its pathophysiology, Beck triad, pulsus paradoxus, echo and ECG signs, and drainage. A brief section on constrictive pericarditis closes the note.
Topic 18 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 6 sections, about 1,890 words (14 min of reading), with 16 flashcards.
In this note
Anatomy and physiology
Classification of pericardial diseases
Acute pericarditis
Pericardial effusion
Cardiac tamponade
Constrictive pericarditis (briefly)
Anatomy and physiology
The pericardium is a double sac: a tough outer fibrous layer and a serous layer (parietal and visceral; the visceral layer is the epicardium). Between them lies 10–50 mL of serous fluid that lubricates the heart.
It fixes the heart in the chest, protects it from infection and from sudden over-distension, and couples the filling of the two ventricles (ventricular interdependence).
The parietal pericardium is innervated by the phrenic nerves (C3–C5): pericardial pain radiates to the trapezius ridge.
Its pressure–volume curve is steep: it stretches slowly over weeks, but acute filling quickly raises the pressure inside it.
Classification of pericardial diseases
The European Society of Cardiology (ESC) 2025 guideline groups pericarditis and myocarditis as one spectrum, the inflammatory myopericardial syndrome: pure pericarditis, myopericarditis (pericarditis with raised troponin but normal ventricular function), perimyocarditis and pure myocarditis (topic 19).
Acute pericarditis
Definition and epidemiology
Inflammation of the pericardial layers, with or without effusion. About 5% of emergency visits for non-ischaemic chest pain; more in young and middle-aged men.
Etiology
Idiopathic or viral: 80–90% of cases in developed countries. Viruses: enteroviruses (Coxsackie A and B, echovirus), adenovirus, herpesviruses (Epstein–Barr virus, cytomegalovirus, human herpesvirus 6), parvovirus B19, influenza, SARS-CoV-2, HIV.
Tuberculosis: the leading cause in developing countries, often with HIV; frequently leads to constriction.
Bacterial (purulent): rare; staphylococci, streptococci, pneumococci; spread from pneumonia, empyema, surgery, endocarditis or sepsis.
Post-cardiac injury syndromes: early infarct-associated pericarditis (days after a transmural myocardial infarction), late post-infarction (Dressler) syndrome (weeks later, immune), post-pericardiotomy syndrome after heart surgery, after trauma, percutaneous coronary intervention (PCI), pacemaker insertion or catheter ablation.
Systemic autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, vasculitis, sarcoidosis, familial Mediterranean fever and other autoinflammatory diseases.
Physical: radiotherapy (acute or years later), chest trauma.
Drugs: drug-induced lupus (procainamide, hydralazine, isoniazid), immune checkpoint inhibitors, anthracyclines, rarely mRNA vaccines. Anticoagulants cause bleeding into the pericardium rather than pericarditis.
Aortic dissection (type A) bleeding into the pericardium.
Clinical features
Chest pain (over 85–90%): sharp, retrosternal or left-sided, pleuritic, worse lying flat and better sitting up and leaning forward; radiates to the trapezius ridge, neck or shoulders.
Often a viral prodrome (fever, malaise, myalgia, upper respiratory or gastrointestinal symptoms); dyspnoea, dry cough, palpitations.
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