- Inflammation of the pericardium (e.g. following viral infection) produces characteristic chest pain (retrosternal, pleuritic, worse on lying flat, relieved by sitting forward), tachycardia and dyspnoea.
- There may be an associated pericardial friction rub or evidence of a pericardial effusion.
- Widespread ST segment changes occur due to involvement of the underlying epicardium (i.e. myopericarditis).
How To Recognise Pericarditis
- Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).
- Reciprocal ST depression and PR elevation in lead aVR (± V1).
- Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.
NB. ST- and PR-segment changes are relative to the baseline formed by the T-P segment. The degree of ST elevation is typically modest (0.5 – 1mm).
Stages of Pericarditis
Pericarditis is classically associated with ECG changes that evolve through four stages.
- Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (occurs during the first two weeks)
- Stage 2 – normalization of ST changes; generalized T wave flattening (1 to 3 weeks)
- Stage 3– Flattened T waves become inverted (3 to several weeks)
- Stage 4 – ECG returns to normal (several weeks onwards)
NB. Less than 50% of patients progress through all four classical stages and evolution of changes may not follow this typical pattern.
Causes of Pericarditis
- Infectious – mainly viral (e.g. coxsackie virus); occasionally bacterial, fungal, TB.
- Immunological – SLE, rheumatic fever
- Post-myocardial infarction / Dressler’s syndrome
- Following cardiac surgery (post pericardiotomy syndrome)
- Paraneoplastic syndromes
- Drug-induced (e.g. isoniazid, cyclosporin)
- Widespread concave ST elevation and PR depression is present throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF).
- There is reciprocal ST depression and PR elevation in aVR.
- Sinus tachycardia
- Widespread concave STE and PR depression (I, II, III, aVF, V4-6).
- Reciprocal ST depression and PR elevation in V1 and aVR.
Another typical example of pericarditis with:
- Widespread ST elevation and PR depression
- Reciprocal ST depression and PR elevation in V1 and aVR
- Marked sinus tachycardia (145 bpm)
- Widespread subtle concave ST elevation with PR depression, most obvious in the precordial (V2-6) and inferior leads (II, III, aVF).
- There is reciprocal ST depression and PR elevation in aVR.
This (sadly slightly faded) ECG was taken from a 6-year old child with viral pericarditis, hence the tachycardia is age-appropriate. The child also had evidence of myocardial involvement with elevated cardiac enzymes (i.e. myopericarditis) .
Pericarditis vs Benign Early Repolarisation
Pericarditis can be difficult to differentiate from BER as both conditions are associated with concave ST elevation.
One useful trick to distinguish between these two entities is to look at the ST segment / T wave ratio:
- The vertical height of the ST segment elevation (from the end of the PR segment to the J point) is measured and compared to the amplitude of the T wave in V6.
- A ratio of > 0.25 suggests pericarditis
- A ratio of < 0.25 suggests BER
Example 1: Benign Early Repolarisation
- ST segment height = 1 mm
- T wave height = 6 mm
- ST / T wave ratio = 0.16
- The ST / T wave ratio < 0.25 is consistent with BER.
- ST segment height = 2 mm
- T wave height = 4 mm
- ST / T wave ratio = 0.5
- The ST / T wave ratio > 0.25 is consistent with pericarditis.
Fish Hook Pattern
Another clue that suggests BER is the presence of a notched or irregular J point: the so-called “fish hook” pattern. This is often best seen in lead V4.
- Notched J-point elevation in V4 with a “fish hook” morphology, characteristic of BER.
The main differences between pericarditis and BER are summarised below. For more information visit the BER library page.
Features suggesting BER
- ST elevation limited to the precordial leads
- Absence of PR depression
- Prominent T waves
- ST segment / T wave ratio < 0.25
- Characteristic “fish-hook” appearance in V4
- ECG changes usually stable over time (i.e non-progressive)
Features suggesting pericarditis
- Generalised ST elevation
- Presence of PR depression
- Normal T wave amplitude
- ST segment / T wave ratio > 0.25
- Absence of “fish hook” appearance in V4
- ECG changes evolve slowly over time
NB. These features have limited specificity, therefore it may not always be possible to tell the difference between these two conditions.
Look at this ECG example:
Is this BER or pericarditis?
- There is widespread concave ST elevation suggesting pericarditis.
- However, the ST elevation is markedly more prominent in the precordial leads (esp. V2-5), consistent with BER.
- There appears to be some subtle downsloping PR depression in the limb (I, aVL) and precordial leads (V3-6), with subtle PR elevation in aVR, suggesting pericarditis.
- The J wave notching (fish-hook pattern) in V3-V4 is highly suggestive of BER.
- There are prominent T waves in the precordial leads, suggestive of BER.
- The ST / T wave ratio of 0.16 is also consistent with a diagnosis of BER.
- These ECG appearances could be caused by BER alone, although it is possible that this ECG represents BER with superimposed pericarditis. This ECG demonstrates the difficulty in differentiating between these two very similar conditions.
- Remember that it is possible for a patient with BER to get pericarditis!
Benign Early Repolarisation plus Pericarditis
The following two ECGs demonstrate what happens when a patient with BER develops pericarditis.
- The baseline ECG was taken from a fit 23-year old male military recruit during a routine health evaluation.
- The subsequent ECG was taken from the same patient several months later when he presented with pleuritic chest pain and was found to have pericarditis…
Baseline ECG: Benign Early Repolarisation
- Widespread minor ST elevation and J-point notching consistent with BER
Follow-up ECG: Benign Early Repolarisation + Pericarditis!
- Relatively tachycardic heart rate (95 bpm) for a fit young man.
- Widespread concave ST elevation, noticeably increased compared to previous ECG.
- New widespread PR depression with PR elevation in aVR.
Pericarditis vs STEMI
- classic teaching of generalised concave up ST elevation and PR elevation in aVR is not reliable for distinguishing pericarditis from ST elevation myocardial infarction (STEMI).
- Pericarditis can cause localised ST elevation but there should be no reciprocal ST depression (except in AVR and V1).
- STEMI, like pericarditis, can also cause concave up ST elevation.
- Only STEMI causes convex up or horizontal ST elevation.
- ST elevation greater in III than II strongly suggests a STEMI.
- PR segment depression is only reliably seen in viral pericarditis, not by other causes. It is often only an early transient phenomenon (lasting only hours). MI can also cause PR segment depression due to atrial infarction (or PR segment elevation in aVR).
- You can’t rely on history either — STEMI can also cause positional or pleuritic pain. A pericardial friction rub
- Steps to distinguish pericarditis from STEMI:
- Is there ST depression in a lead other than AVR or V1? This is a STEMI
- Is there convex up or horizontal ST elevation? This is a STEMI
- Is there ST elevation greater in III than II? This is a STEMI
- Now look for PR depression in multiple leads… this suggests pericarditis (especially if there is a friction rub!)
- Get serial ECGs on any patient with chest pain — things may become more obvious with time!
- ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
- ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
- ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
- ECG Reference Sites on the WEB – the best of the rest
- Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in Emergency Medicine and Acute Care. Elsevier 2005
- Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.