Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Confirm acute pericardial inflammation, exclude lethal chest-pain mimics, triage high-risk features and prescribe evidence-based anti-inflammatory treatment.
Acute pericarditis is an inflammatory chest-pain syndrome with ECG, rub or effusion evidence. The opening task is to exclude ACS, PE, dissection and tamponade before accepting a usually benign idiopathic/viral explanation.
Risk stratification separates low-risk outpatient care from admission and cause-directed investigation. Fever, large effusion, haemodynamic effect, myocardial involvement and immunocompromise should change disposition.
Treatment suppresses symptoms and recurrence while the cause is addressed. Aspirin/NSAID plus colchicine is standard for suitable patients; steroids are reserved for defined indications or contraindications after infection is excluded.
Many uncomplicated cases have no proven organism and are labelled idiopathic, often after a viral syndrome. The label should follow consideration of dangerous and specific secondary causes rather than assumption from the pain pattern alone.
Systemic lupus erythematosus, rheumatoid arthritis and other immune-mediated conditions can inflame the pericardium. Recurrent disease or accompanying systemic features should prompt a directed rather than indiscriminate immune work-up.
Myocardial infarction, cardiac surgery, catheter procedures, trauma or radiotherapy can expose antigens or directly injure the pericardium, producing an immediate or delayed inflammatory syndrome.
Bacterial or tuberculous infection, cancer and advanced kidney failure with uraemia are less common but clinically important causes. Fever, immunosuppression, a large effusion or subacute onset increases concern.
An infectious, immune or injury signal inflames the visceral and parietal pericardium. Their movement against each other generates pleuritic positional pain and sometimes a transient friction rub.
When inflammation involves the superficial myocardium and atrial epicardium, it can alter repolarisation across broad territories, producing widespread ST elevation and PR-segment change rather than a single coronary distribution.
Inflammatory capillary leakage adds fluid to the pericardial space. Slowly accumulating fluid may become large before causing pressure, whereas a smaller rapid collection can impair filling.
Rising intrapericardial pressure restricts diastolic chamber filling and can cause tamponade. Myocardial involvement ranges from troponin release with preserved ventricular function to dysfunction or arrhythmia, changing risk and follow-up.
Acute sharp retrosternal pain worsened by inspiration or lying flat and relieved by sitting forward; radiation to trapezius ridge is suggestive.
A superficial scratchy, often triphasic sound can be transient; repeat auscultation with the patient leaning forward.
New widespread concave ST elevation and PR depression, reciprocal PR elevation in aVR, then T-wave inversion; focal change or reciprocal ST depression should heighten ACS concern.
May be absent, small or large; muffled sounds or enlarging cardiac silhouette are late/non-specific clues.
Tachycardia, hypotension, raised JVP, pulsus paradoxus or echo chamber collapse requires emergency drainage assessment.
Troponin rise, ventricular dysfunction, heart-failure signs or ventricular arrhythmia requires admission and myocarditis-level evaluation.
Pressure-like pain, territorial ST change, reciprocal ST depression beyond aVR or V1, or a coronary-pattern wall-motion abnormality favours myocardial infarction. Troponin elevation alone cannot distinguish ACS from myopericardial injury.
Sudden dyspnoea, hypoxaemia, venous thromboembolism risk or right-heart strain suggests PE. Pleuritic pain may be identical, so probability-based pulmonary vascular assessment remains necessary.
Abrupt maximal chest or back pain, pulse or blood-pressure asymmetry, aortic regurgitation or neurological deficit points towards dissection and requires time-critical aortic imaging.
Heart failure, ventricular arrhythmia, significant LV dysfunction or myocardial oedema and non-ischaemic scar suggest myocardial involvement dominates; overlap with pericarditis is common rather than binary.
Pneumonia, pleurisy and costochondritis may give respiratory or reproducible pain, but do not explain a pericardial rub, characteristic widespread ECG change or a new effusion. Absence of any one of those findings does not exclude pericarditis.
Rapid or large fluid accumulation raises intrapericardial pressure, reduces venous return and cardiac output, and can progress to obstructive shock requiring urgent drainage assessment.
Troponin elevation with preserved ventricular function is often termed myopericarditis; new ventricular dysfunction suggests predominant myocardial involvement or perimyocarditis. Either pattern can change monitoring and activity advice after ACS has been considered.
Persistent immune activation can produce repeated painful episodes and cumulative disability. Inadequate initial treatment or withdrawal before clinical and inflammatory remission may contribute to recurrence and the need for more complex anti-inflammatory strategies.
Chronic scarring and loss of pericardial compliance can restrict diastolic filling, causing raised venous pressure and right-sided heart failure; risk is higher with bacterial or tuberculous disease.
Pain alone is insufficient, and an effusion is not required when another criterion is present.
Classic ECG changes can coexist with effusion or myocardial injury; disposition depends on risk, not pattern beauty.
Clinical remission and normal inflammation reduce rebound risk better than an arbitrary rapid stop.
It signals myocardial involvement and need for ventricular/rhythm assessment, but does not by itself distinguish myocarditis from ACS.
When needed, use a defined indication, exclude infection and taper very slowly after remission rather than giving an early high-dose burst.
Diagnosing pericarditis from positional pain without two criteria or dangerous-differential assessment.
Discharging fever, a large effusion, anticoagulation or troponin-positive disease as low risk.
Prescribing colchicine without renal/hepatic and CYP3A4/P-gp interaction review.
Stopping anti-inflammatory treatment while symptoms or CRP remain active.
Allowing early intense exercise after myopericardial involvement.
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A patient has classic pleuritic positional pain and a pericardial rub. ECG, CRP and echo are normal. Which statement is correct?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Avoid/modify with active ulcer or bleeding, severe renal disease, decompensated HF, NSAID hypersensitivity and late pregnancy; review anticoagulants and cardiovascular risk.
In mild or moderate renal or hepatic impairment use 0.5 mg once daily; severe impairment is contraindicated. Do not combine with strong CYP3A4/P-gp inhibitors when renal or hepatic function is impaired, and reduce or interrupt treatment even with normal function according to the interacting medicine. Stop and assess diarrhoea, vomiting, cytopenia or myopathy.