Pericarditis vs. Myocardial Infarction: Recognizing ECG Differences

ST elevations on the ECG are among the findings that immediately trigger alarm in the emergency department – and rightly so. The consequence of a missed STEMI can be fatal. At the same time, reflexive activation of the cardiac catheterization lab for every ST elevation leads to unnecessary invasive procedures when the cause is acute pericarditis. Studies show that a relevant proportion of coronary angiographies performed for suspected STEMI reveal "clean" coronary anatomy – with corresponding resource consumption and patient risk. Systematic knowledge of the ECG differences between pericarditis and myocardial infarction is therefore a core clinical competency that should be regularly trained in the ACLS context.

Pathophysiological Basis of ECG Changes

To understand the ECG differences, it's worth taking a brief look at the underlying pathophysiology – because it explains why the ST elevations in both entities look so different.

STEMI

In acute myocardial infarction with ST elevation, a thrombotic occlusion of a coronary artery occurs. The downstream myocardium becomes ischemic, creating a regional injury current. This projects onto those ECG leads that face the affected vascular territory. Therefore, a regional ST elevation with reciprocal ST depressions in the opposing leads is typical. The elevation usually has a convex ("tombstone") or obliquely ascending morphology.

Acute Pericarditis

In pericarditis, there is diffuse inflammation of the pericardium and the epicardial myocardial layers. The resulting injury current is not confined to a single coronary vascular territory but affects the epicardium diffusely. The ECG therefore shows ST elevations in many leads simultaneously, not attributable to a single vascular territory. Reciprocal ST depressions are absent – with one important exception: aVR and occasionally V1.

The Six Decisive ECG Criteria

The following systematic checklist helps you perform the differentiation in a structured manner in clinical practice. No single criterion is definitive on its own – but the combination of multiple features significantly increases diagnostic certainty.

1. Distribution of ST Elevations

• STEMI: Regional, attributable to a coronary territory (e.g., II, III, aVF in inferior STEMI; V1–V4 in LAD occlusion; I, aVL, V5–V6 in lateral STEMI).
• Pericarditis: Diffuse, in many leads simultaneously, not corresponding to a single vascular territory. Simultaneous elevations in I, II, III, aVF, aVL, and V2–V6 are typical.

Clinical tip: If you find ST elevations in leads that don't anatomically fit together (e.g., simultaneously inferior AND anterior AND lateral), pericarditis should be at the very top of your differential list.

2. Reciprocal ST Depressions

• STEMI: Present. Reciprocal depressions are a strong indicator of regional infarction. Example: ST elevation in II, III, aVF with reciprocal depression in I and aVL.
• Pericarditis: Absent. The only exception is aVR (and sometimes V1), where ST depression occurs as a "mirror image" of the diffuse epicardial injury currents.

Remember: The presence of reciprocal ST depressions (other than in aVR) is one of the strongest arguments against pericarditis and for a STEMI.

3. ST Elevation Morphology

• STEMI: Convex ST elevation (upwardly bowed, "tombstone" configuration) or horizontal elevation, often transitioning into a broad, monophasic curve.
• Pericarditis: Concave ST elevation (upwardly hollowed, "smiley face" or "saddle shape"). The elevation looks like an upwardly open bowl.

Caution: This criterion has limitations. Early STEMI stages can also show concave ST elevations, and not every pericarditis has a textbook concave morphology. Never rely on this criterion alone.

4. PR Segment Depression (Key Finding!)

• STEMI: PR segment is usually isoelectric.
• Pericarditis: PR segment depression in most leads, PR elevation in aVR. This finding reflects concomitant inflammation of the atrial epicardium and is highly specific for pericarditis.

Clinical tip: PR depression is subtle and easily overlooked. Look for it deliberately – especially in lead II, where it is most pronounced. A systematic look at the PR segment should be routine with every ST elevation.

5. Pathological Q Waves

• STEMI: Q waves can develop over time and indicate transmural necrosis. Often not yet present in the early phase, but already detectable when presentation is delayed.
• Pericarditis: No pathological Q waves. The myocardium does not become necrotic in pure pericarditis.

6. T Wave Changes and Temporal Progression

The temporal progression of ECG changes differs fundamentally:

Pericarditis – the four stages according to Spodick:

1. Stage I: Diffuse concave ST elevation + PR depression (acute phase)
2. Stage II: ST segments normalize, T waves flatten (pseudo-normalization)
3. Stage III: Diffuse T wave inversions (without concurrent ST elevation!)
4. Stage IV: Normalization of the ECG

STEMI: ST elevation and T wave inversions occur simultaneously or in rapid succession. In pericarditis, by contrast, T waves invert only after resolution of ST elevations. This sequential pattern is another important differentiating point.

The Spodick Sign: An Underappreciated Detail

A subtle but valuable sign in pericarditis is the so-called Spodick sign: a depression of the TP segment that manifests as a downsloping baseline of the ST segment (from the J point toward the T wave). This "downsloping" of the ST segment before the transition into the T wave is found preferentially in the lateral leads and is relatively specific for pericarditis. It is frequently overlooked but can provide the decisive clue in ambiguous cases.

The Ratio Method: Quantitative Assistance

When visual assessment is inconclusive, the ST/T ratio can serve as a quantitative tool. In lead V6 (alternatively lead I), the amplitude of the ST elevation (at the J point) is divided by the amplitude of the T wave:

• Ratio ≥ 0.25: Favors pericarditis
• Ratio < 0.25: Argues against pericarditis (i.e., favors another cause of ST elevation)

This method has good specificity but should always be interpreted in the overall context.

Summary of ECG Criteria at a Glance

Criterion	STEMI	Pericarditis
ST elevation distribution	Regional (vascular territory)	Diffuse (multiple territories)
Reciprocal ST depressions	Present	Absent (except aVR/V1)
ST morphology	Convex ("tombstone")	Concave ("smiley")
PR segment	Isoelectric	Depressed (aVR: elevated)
Q waves	Possible	Absent
T wave inversion	Concurrent with ST elevation	Only after ST normalization
Spodick sign	Absent	Possible

Additional Clinical Signs: More Than Just the ECG

ECG analysis never occurs in a vacuum. Clinical context information is crucial for overall assessment:

History and Pain Characteristics

• STEMI: Retrosternal pressure or tightness, radiation to arm/jaw/back, autonomic symptoms (nausea, diaphoresis, sense of impending doom). Pain is often exertion-independent but can also occur at rest.
• Pericarditis: Sharp, pleuritic chest pain, worsening when supine, improvement when leaning forward and sitting upright. Often preceded by a viral infection. Typical patients are younger and have fewer cardiovascular risk factors.

Auscultation

• A pericardial friction rub is pathognomonic for pericarditis, but it is only heard in a proportion of affected patients and is position-dependent. It is most reliably auscultated with the patient sitting and leaning forward.

Biomarkers

• Troponin: Can be elevated in both entities! In pericarditis with epicardial myocardial involvement (perimyocarditis), troponin levels rise. An elevated troponin therefore by no means excludes pericarditis.
• CRP and ESR: Often significantly elevated in pericarditis and can serve as markers for monitoring disease course.
• Troponin kinetics: In STEMI, typically a steep rise with a clear peak. In perimyocarditis, often a more moderate rise.

Imaging

• Echocardiography can reveal a pericardial effusion in pericarditis and exclude or confirm regional wall motion abnormalities (which would suggest a STEMI). It should be performed early in every unclear case.

Typical Pitfalls and Gray Areas

Pitfall 1: The Young Patient with Chest Pain and ST Elevation

The temptation is great to automatically think of pericarditis in young patients without risk factors. However: myocardial infarctions also occur in young people (cocaine users, thrombophilias, spontaneous coronary artery dissections). Careful ECG analysis remains indispensable – regardless of age.

Pitfall 2: Early Repolarization

Early repolarization (benign ST elevation, particularly in V2–V4 in young men) is another important differential diagnosis. It typically shows J-point elevation with a notch or slur morphology, but no PR depression and no dynamic changes over time.

Pitfall 3: Multivessel Disease Mimicking Pericarditis

Theoretically, a left main occlusion or severe multivessel disease could cause diffuse ST changes. In practice, however, this situation typically shows diffuse ST depressions (with elevation in aVR) and does not present a picture that could be confused with pericarditis.

Pitfall 4: Perimyocarditis

Perimyocarditis – pericarditis with involvement of the adjacent myocardium – can cause troponin elevations and regional wall motion abnormalities. Here the boundaries become blurred, and invasive workup may be indicated despite a pericarditis-typical ECG.

Pitfall 5: Time Pressure and Decision Pressure

In reality, the clock is ticking with ST elevation: "Time is muscle." If you are uncertain whether a STEMI or pericarditis is present, the safer decision in many cases is activation of the cardiac catheterization lab. An unnecessary coronary angiography is less dangerous than a missed STEMI. Nevertheless, systematic analysis helps identify clear pericarditis cases and spare these patients invasive diagnostics.

A Structured Algorithm for Clinical Practice

When you are facing an ECG with ST elevations in an acute setting, the following checklist can help:

1. Check distribution: Does the ST elevation correspond to a coronary territory? → If yes: suspect STEMI.
2. Look for reciprocal depressions: Present (other than aVR)? → If yes: STEMI likely.
3. Analyze the PR segment: PR depression in multiple leads? → If yes: pericarditis likely.
4. Assess ST morphology: Convex? → More likely STEMI. Concave? → More likely pericarditis (but caution: early phase of STEMI).
5. Incorporate clinical context: Pleuritic pain? Preceding infection? Young age? → Suspicious for pericarditis. Risk factors? Typical infarction pain? → Suspicious for STEMI.
6. When in doubt: STEMI management until proven otherwise. Better one angiography too many than a delayed treatment of an occluded vessel.

What Changes Once You've Made Your Decision

The therapeutic consequences are fundamentally different:

• STEMI: Immediate reperfusion therapy (primary PCI or fibrinolysis if applicable), dual antiplatelet therapy, anticoagulation, hemodynamic monitoring.
• Pericarditis: NSAIDs (ibuprofen as first-line, commonly used in Austria), colchicine for recurrence prophylaxis, activity restriction. No anticoagulation (risk of hemorrhagic pericardial tamponade!).

These diametrically opposed treatment strategies underscore why correct differentiation on the ECG is so clinically relevant.

Practical Training

Distinguishing pericarditis from STEMI on the ECG is a skill that is sharpened through repeated practice with real and simulated ECGs. In the ACLS course by Simulation Tirol, you train systematic ECG interpretation under realistic time pressure – including the differential diagnoses described here. The AHA-certified courses offer you the opportunity to work through such decision-making situations in a safe simulation environment and solidify your algorithms before it matters in a real emergency.