Pericardial Disease — Structured clinical teaching for the UKMLA: acute inflammation, effusion, tamponade and constriction.
8.01 Pericardial Anatomy and Physiology
The pericardium comprises a fibrous sac and a thin, lubricated serous cavity. It limits sudden cardiac expansion; inflammation produces pain, fluid accumulation may impair filling, and chronic scarring can cause constriction.
- Inflammation: Irritation of pain-sensitive parietal pericardium causes pleuritic, positional pain.
- Effusion: Both volume and rate of accumulation determine haemodynamic risk; rapidly developing haemopericardium may cause tamponade even when the volume is modest.
- Constriction: A rigid pericardium restricts diastolic filling despite preserved intrinsic myocardial contractility early in the disease.
8.02 Acute Pericarditis: Presentation and Diagnosis
Acute pericarditis is inflammation of the pericardial layers, most often idiopathic or presumed viral in the UK. The clinical pattern is usually distinctive, but acute coronary occlusion and other dangerous causes of chest pain must be excluded when appropriate.
Clinical presentation
- Pain: Sharp retrosternal or left-sided chest pain, worse with inspiration, coughing or lying flat; improves when sitting forwards. May radiate towards the trapezius ridge.
- Associated features: Recent viral illness, low-grade fever, malaise, tachycardia, occasional dyspnoea.
- Examination: A superficial scratchy pericardial friction rub, best sought at the left sternal edge with the patient leaning forwards; absence does not exclude the diagnosis.
Diagnostic assessment
- Traditional clinical criteria: At least two of characteristic pain, rub, new widespread ST elevation/PR depression, or new/worsening pericardial effusion; inflammatory markers and pericardial imaging provide additional evidence.
- ECG: Often diffuse concave ST elevation and PR depression, with reciprocal PR elevation in aVR; the ECG may be normal or atypical.
- Bloods: CRP/ESR, FBC, U&E/eGFR and troponin (myocardial involvement or alternative ACS).
- Echocardiography: Look for an effusion, signs of tamponade and LV function; normal echo does not exclude uncomplicated pericarditis.
- Differential diagnosis: STEMI/ACS, PE, aortic dissection, pleurisy and musculoskeletal pain. Regional ST changes, reciprocal depression or ongoing ischaemic symptoms mandate proper ACS assessment.
Clinical pearl: Do not diagnose pericarditis from a concave ST segment alone; correlate the history, serial ECGs, troponin and clinical risk.
8.03 Causes of Pericarditis and Red Flags
Causes
- Common: Idiopathic/presumed viral; post-cardiac injury (post-MI, after surgery or intervention); systemic inflammatory disease.
- Important alternatives: Tuberculosis, purulent bacterial infection, malignancy, uraemia, autoimmune disease, chest radiotherapy and trauma.
High-risk features — assess urgently and usually admit
- Fever above 38°C, insidious/subacute presentation or failure to respond to anti-inflammatory treatment.
- Large effusion, suspected tamponade or significant myocardial involvement.
- Immunosuppression, anticoagulation, trauma, suspected bacterial infection or underlying neoplasia.
These features change the pre-test probability of a specific cause and the risk of complications; additional imaging, microbiology and specialist investigations should be selected accordingly.
8.04 Treatment of Acute and Recurrent Pericarditis
Treat the underlying cause when identified. For uncomplicated presumed inflammatory pericarditis, treatment targets pain, inflammatory remission and recurrence prevention.
- First-line: Full anti-inflammatory-dose ibuprofen or aspirin plus colchicine (usually for at least three months after a first episode); give gastroprotection with anti-inflammatory therapy and check contraindications and interactions.
- Review before prescribing: Renal function, peptic ulcer or bleeding risk, anticoagulant use, pregnancy and colchicine interactions or hepatic impairment; dose and duration are individualised.
- Activity: Avoid strenuous exercise until pain has settled and objective inflammatory activity has resolved; myocardial involvement requires a more restrictive specialist plan.
- Monitoring: Reassess symptoms and CRP; use repeat echocardiography when effusion or complications are a concern.
- Avoid routine first-line corticosteroids: They can predispose to relapses and are reserved for selected indications or treatment-resistant disease.
- Recurrence: Confirm the diagnosis, check adherence and aetiology, and use a longer colchicine course (commonly at least six months); specialist options for refractory inflammatory disease include IL-1 blockade.
MLA pearl: NSAID/aspirin plus colchicine is the expected first-line combination for uncomplicated acute pericarditis; urgent drainage, not anti-inflammatory medication alone, is needed if tamponade develops.
8.05 Pericardial Effusion
Pericardial effusion is fluid in the pericardial space. It may be inflammatory, malignant, uraemic, haemorrhagic or associated with hypothyroidism, systemic illness or cardiac surgery.
- Symptoms: May be absent; progressive effusions cause breathlessness, chest fullness, fatigue or orthopnoea.
- Assessment: Echocardiography defines distribution, size and haemodynamic effects; ECG may show low QRS voltage or electrical alternans but neither is diagnostic.
- Critical principle: A rapidly developing small effusion may be more dangerous than a chronic large one.
- Management: Treat the cause, investigate unexplained or symptomatic effusions and follow with echocardiography as appropriate. Drain urgently if there is haemodynamic compromise; specialist drainage may also be indicated for suspected purulent or malignant disease.
8.06 Cardiac Tamponade: Recognition and Emergency Treatment
Cardiac tamponade is obstructive shock. Rising intrapericardial pressure prevents ventricular filling, reducing stroke volume, cardiac output and organ perfusion.
Recognition
- Tachycardia, dyspnoea, hypotension, cool peripheries, raised JVP and narrow pulse pressure.
- Pulsus paradoxus: Exaggerated inspiratory fall in systolic BP (classically more than 10 mmHg).
- Beck triad: Hypotension, raised JVP and quiet heart sounds — often incomplete, so its absence does not exclude tamponade.
- Echo: Pericardial fluid, right-sided chamber collapse, plethoric IVC and marked respiratory flow variation in a supportive clinical setting.
Immediate management
- ABCDE, monitoring, IV access and urgent senior/cardiology or cardiothoracic assistance.
- Definitive treatment: Emergency image-guided pericardiocentesis or surgical drainage according to the cause (surgical assessment is especially important with trauma, suspected aortic dissection or postoperative bleeding).
- While arranging drainage: Maintain adequate preload and perfusion; avoid unnecessary diuresis or vasodilatation. Positive-pressure ventilation can precipitate further cardiovascular collapse.
Do not miss: Hypotension with a raised JVP and relatively clear lungs suggests obstructive rather than left-ventricular pulmonary-oedema physiology.
8.07 Constrictive Pericarditis versus Restrictive Cardiomyopathy
Both conditions impede ventricular filling and can present with prominent right-sided congestion, but the pathological compartment differs: pericardium in constriction versus myocardium in restriction.
- Clinical features: Oedema, ascites, hepatomegaly and raised JVP; a pericardial knock or Kussmaul sign may be present.
- Constrictive physiology: Septal bounce and exaggerated ventricular interdependence on echo; CT may show thickened/calcified pericardium and CMR can demonstrate inflammation.
- Restrictive physiology: Myocardial infiltration or fibrosis (especially amyloid) causes stiff ventricles, often with biatrial enlargement and characteristic CMR findings.
- Management distinction: Chronic symptomatic constriction may require pericardiectomy; transient inflammatory constriction may respond to anti-inflammatory treatment, whereas restrictive cardiomyopathy requires aetiology-specific care.
MLA pearl: In a patient with oedema, ascites and raised JVP but apparently reasonable LV systolic function, consider constrictive pericarditis as well as HFpEF.