Pericarditis and ST-elevation myocardial infarction both lift the ST segment, the stretch of the electrocardiogram (ECG) between the end of ventricular depolarisation and the start of repolarisation. They do not call for the same treatment: giving fibrinolysis, a clot-dissolving drug, for pericarditis is harmful, and treating an occluded coronary artery as pericarditis is worse. The ECG therefore carries much of the diagnostic weight in the first hours, even though pericarditis remains a clinical diagnosis that no single test confirms.
The ECG and its four stages
The ECG records the heart from several viewpoints called leads. In acute pericarditis the tracing evolves through four stages, and the evolution itself is informative. Besides the ST segment, the PR segment, the stretch between the end of the P wave and the start of the QRS complex, is also affected:
- Stage 1. Diffuse, concave-upward ST elevation with PR-segment depression in most leads. Leads aVR and V1 show the mirror image: ST depression and PR elevation. PR depression in V5–V6 reflects atrial injury.
- Stage 2. The ST and PR deviations normalise and the tracing briefly looks unremarkable.
- Stage 3. Diffuse T-wave inversion in all leads except aVR.
- Stage 4. The tracing either returns to normal or the T waves stay inverted indefinitely.
The ST segments return to baseline about 2–5 days after presentation, and T-wave inversion follows over the next weeks. The boundaries between stages are approximate, not sharp: stage 1 typically lasts days, stage 2 a few days, stage 3 up to several weeks, and stage 4 may be permanent in some patients.
Separating pericarditis from ST-elevation infarction
Because confusing the two is consequential in both directions, the most useful bedside test is where the elevation sits.
In ST-elevation myocardial infarction (STEMI), the changes map onto one vascular territory: anterior leads V2–V4 with a left anterior descending occlusion, inferior leads II, III and aVF with a right coronary occlusion, lateral leads I, aVL, V5–V6 with a circumflex occlusion. Elevation in that territory comes with reciprocal ST depression, a mirror-image lowering of the ST segment, in leads facing the opposite wall. In pericarditis the elevation is diffuse and crosses non-contiguous territories at once — inferior together with anterior together with lateral — and there is no reciprocal ST depression. The reciprocal change in pericarditis is PR depression instead, which reflects atrial injury and is highly specific for the condition and uncommon in the acute phase of STEMI. The shape helps as well: pericardial elevation is usually concave upward, while infarct elevation is often convex, the tombstone pattern.
Two cautions keep this rule honest. First, not every patient follows the typical pattern — a minority show only PR depression or only T-wave changes, so a normal or atypical ECG does not exclude pericarditis. Second, early repolarisation, a benign variant common in young athletic men, produces ST elevation that can look similar; it is recognised by J-point notching (a notch at the junction of the QRS complex and the ST segment) without PR depression and by the absence of evolution through the four stages. When the picture stays ambiguous, troponin (a marker of myocardial injury), echocardiographic wall motion and, where doubt persists, coronary angiography or cardiac magnetic resonance settle it.
Making the diagnosis
The diagnosis rests on clinical criteria rather than on a single test, and the ECG is one part of them. Acute pericarditis is diagnosed when at least two of four features are present: characteristic chest pain, a pericardial friction rub, new widespread ST elevation or PR depression, and a new or worsening pericardial effusion. Supportive findings are a raised white cell count, erythrocyte sedimentation rate or C-reactive protein, and imaging evidence of pericardial inflammation.
Once the criteria are applied, further tests are chosen for specific questions. Echocardiography shows whether fluid has accumulated, how much, and whether it is compromising the heart. It does not make or exclude the diagnosis. An echo without a pericardial effusion does not rule out pericarditis, and an incidental effusion in a patient with no pain and no ECG changes is not pericarditis — it belongs to a different differential with a different set of causes.
Blood tests answer specific questions: renal function for uraemia, C-reactive protein and full blood count for the intensity of inflammation, troponin for a myocardial component, antinuclear antibodies when SLE is suspected, and viral serology on the rare occasions when the result would change management. When malignancy is suspected, it is pursued directly. Pericardiocentesis, drainage of pericardial fluid through a needle, has a low yield as a routine diagnostic test and is usually performed therapeutically, to drain fluid that is compressing the heart; when a bacterial or malignant cause is suspected, the fluid is nevertheless sent for cell count, culture and cytology, because those results change treatment.
Whether an individual episode can be managed at home or needs hospital assessment is decided by the high-risk features listed in Pericarditis: Management and Risk Stratification.