ECG Interpretation

Rate & Rhythm

• Rate: Approximately 75-85 bpm (estimated from R-R intervals)
• Rhythm: Sinus rhythm - P waves are present and appear to precede every QRS complex
• P wave axis: Upright in I and II - confirms normal sinus origin

Intervals

• PR interval: Appears within normal limits (~160-180 ms) - no overt first-degree block, though borderline prolongation possible
• QRS duration: Narrow (<120 ms) - no bundle branch block
• QTc: Difficult to measure precisely from image, but appears within normal range

Axis

• QRS appears predominantly positive in I and aVF - normal axis (roughly 0° to +90°)

P Waves

• Morphology appears normal; no obvious bifid or peaked P waves to suggest atrial enlargement

QRS Complexes

• Septal Q waves present in lateral leads (I, aVL, V5-V6) - normal finding
• R wave progression: R wave appears to increase from V1 to V4/V5 - normal precordial progression
• No pathological Q waves identified (no wide/deep Q in inferior or anterior leads suggesting prior infarction)

ST Segments & T Waves

• ST segment: Appears isoelectric across the precordium and limb leads - no obvious ST elevation or depression
• T waves: Upright in I, II, and precordial leads V3-V6; inverted in aVR (normal); T wave morphology in V1-V2 appears flat/biphasic - this can be normal but warrants clinical correlation

Voltage

• No obvious criteria for left ventricular hypertrophy (LVH), though image resolution limits precise measurement

Summary

• Normal rate, axis, and intervals
• No pathological Q waves
• No ST elevation or depression
• No bundle branch block

Important disclaimer: This is an educational ECG interpretation only and does not constitute medical advice or a clinical diagnosis. All ECGs must be interpreted in the context of the patient's clinical presentation by a qualified clinician.

ECG Interpretation: Guidelines & Criteria

The Systematic 14-Step Approach

1. Standardization and calibration (paper speed, gain, lead placement, artifacts)
2. Rhythm
3. Heart rate
4. PR interval / AV conduction
5. QRS interval
6. QT/QTc interval
7. Mean QRS electrical axis
8. P waves
9. QRS voltages
10. Precordial R-wave progression
11. Abnormal Q waves
12. ST segments
13. T waves
14. U waves

Normal ECG Intervals

QTc = QT / √RR (RR in seconds)

P Wave Criteria

• Normal duration: < 120 ms
• Upright in leads I, II, and aVF; inverted in aVR
• Broad/bifid P wave ("P mitrale"): suggests left atrial enlargement
• Tall peaked P wave ("P pulmonale", >2.5 mm in II): suggests right atrial enlargement

PR Interval

• Normal: 90-200 ms
• > 200 ms = first-degree AV block (delayed AV conduction)
• Short PR = ventricular preexcitation (WPW), junctional rhythm, or enhanced AV nodal conduction
• Delay usually localized to the AV node, though other sites are possible

QRS Complex

• Normal width: 75-110 ms
• Capital letters (Q, R, S): amplitudes ≥ 5 mm (0.5 mV)
• Lowercase letters (q, r, s): amplitudes < 5 mm (0.5 mV)
• Q waves preceding an R wave are initial negative deflections; S waves follow positive deflections
• Wide QRS (≥ 120 ms) = intraventricular conduction delay / bundle branch block

Bundle Branch Block Criteria

ST Segment - STEMI Criteria by Territory

• Reciprocal ST depression in leads away from the injury zone indicates larger infarct territory and increased mortality risk.
• New LBBB with chest pain was historically treated as STEMI-equivalent, but < 10% of new LBBB cases have AMI - the Sgarbossa criteria are used to identify MI in LBBB.

Chamber Hypertrophy Criteria

• Cornell criterion (preferred): SV3 + RaVL > 2.8 mV (men) or > 2.0 mV (women)
• Sokolow-Lyon criterion: SV1 + RV5 or V6 > 3.5 mV
• Sensitivity only 30-50%; specificity 85-95%
• "Strain pattern": ST depression + T-wave inversion in lateral leads (I, aVL, V5-V6)

• Sokolow-Lyon for RVH: RV1 + SV5 or V6 ≥ 1.05 mV
• Sensitivity very poor (10-20%); specificity similar to LVH criteria
• Supporting features: right axis deviation, dominant R in V1, P pulmonale

Low QRS Voltage

• Defined as: peak-to-peak amplitude < 5 mm in all limb leads, or < 10 mm in all precordial leads
• Common causes: pericardial effusion, myocardial infarction, cardiomyopathy, COPD/emphysema, obesity, hypothyroidism

Repolarization / ST-T Abnormalities

• T waves should be concordant with QRS direction
• Early repolarization: ST elevation with an "upward concave" morphology, often a normal variant - but associated with slightly increased risk of idiopathic ventricular fibrillation; absolute risk remains low
• Wellens' T-wave sign: deep symmetrical T-wave inversions in V1-V4 (± I, aVL) = high-grade LAD stenosis
• Posterior MI: prominent tall R waves in V1-V2 without anterior ST elevation

Conditions That Make ECG Interpretation Difficult

• LBBB (masks ischemia patterns)
• Ventricular pacing
• WPW pre-excitation
• LVH with strain
• Hyperkalemia
• Early repolarization pattern (can mimic STEMI)

Key References

• Goldman-Cecil Medicine International Edition, Ch. 42 (ECG Intervals, Hypertrophy, Bundle Branch Blocks)
• Harrison's Principles of Internal Medicine 22E (2025), Ch. 247 (Clinical Interpretation)
• Tintinalli's Emergency Medicine, Ch. 49 (Table 49-4, STEMI criteria)
• AHA/ACCF/HRS Scientific Statement: Recommendations for Standardization and Interpretation of the Electrocardiogram (Parts I-VI) - available via HRS
• Goldberger AL: Goldberger's Clinical Electrocardiography: A Simplified Approach, 10th ed. Elsevier, 2024

Disclaimer: ECG interpretation must always be correlated with the patient's clinical presentation, symptoms, and history by a qualified clinician. No automated or reference-based interpretation replaces bedside clinical judgment.

Acute Ischemia vs. Chronic MI: ECG Patterns

The Core Concept: Why the ECG Changes Over Time

• Transmural (full-thickness, epicardial) - causes ST elevation
• Subendocardial (inner-layer only) - causes ST depression
• Chronic/healed (necrosis and fibrosis) - leaves permanent Q waves

The Sequential ECG Evolution of Acute MI

Stage 1 - Hyperacute Phase (Minutes to ~30 min)

• Appear within 5 minutes of coronary occlusion
• Large, broad-based, asymmetric (gradual upstroke, rapid descent)
• Disproportionately tall relative to the preceding QRS complex
• Often described as "bulky" - you could nearly "fit the QRS inside the T wave"
• Transient - typically evolve into overt ST elevation within 30 minutes
• Key distinction from hyperkalemia: hyperkalemic T waves are narrow-based, symmetrical, and sharply peaked; hyperacute T waves are wide-based and asymmetric

Stage 2 - Acute Phase: ST Elevation (Hours)

• Transmural ischemia (epicardial involvement): ST vector directed outward → ST elevation in overlying leads
• Subendocardial ischemia: ST vector directed inward toward ventricular cavity → ST depression in overlying leads (with ST elevation in aVR)

• ST elevation in the territory of the affected artery (see regional criteria from previous session)
• Reciprocal ST depression in contralateral leads (larger infarct, worse prognosis)
• ST elevation is typically convex upward ("tombstone" shape) in fully developed STEMI
• The more ST segments elevated and the higher the elevation, the more extensive the injury

Stage 3 - Developing Q Waves + T Wave Inversion (Hours to Days)

• Represent myocardial necrosis - loss of viable depolarizing tissue
• Criteria: duration ≥ 40 ms (≥ 0.04 sec) OR amplitude ≥ 25% of the R wave amplitude in the same lead
• Can appear within the first hour but most commonly develop at 8-12 hours
• Presence of Q waves with ST elevation does NOT preclude reperfusion - patient history of symptom onset is the key guide

• As ST elevation begins to resolve, the T wave typically inverts in the same leads
• Following successful reperfusion, T wave inversions may be deep and symmetrical - resembling Wellens' syndrome pattern (this is called "reperfusion T waves")
• Following failed reperfusion: T wave inversions tend to be shallower

Stage 4 - Subacute / Evolving Phase (Days to Weeks)

• ST segment returns toward isoelectric baseline
• Pathological Q waves persist (permanent marker of necrosis)
• T wave inversions persist but may begin to normalize
• R wave amplitude in the infarcted territory is typically reduced or lost ("poor R-wave progression")

Stage 5 - Chronic / Old MI Pattern (Weeks to Months - Permanent)

• Pathological Q waves - the most enduring marker of old infarction. May be permanent, or may partially resolve (especially with smaller infarcts or after successful reperfusion).
• T waves - may normalize (become upright again) over weeks to months
• Reduced R wave amplitude in the affected leads
• ST segment - usually returns fully to baseline. Persistent ST elevation >4-6 weeks after MI suggests ventricular aneurysm

The Wellens' Pattern - High-Grade LAD Stenosis

• Type A (25%): Biphasic T waves in V2-V3 (initial positive deflection, terminal negative)
• Type B (75%): Deeply and symmetrically inverted T waves in V2-V3 (± V1-V4, I, aVL)
• No significant Q waves; minimal or no ST elevation
• Represents critical stenosis (not yet complete occlusion) of the proximal LAD
• If misidentified as old ischemia and the patient undergoes stress testing, it can precipitate full anterior STEMI

Key Differential: Acute vs. Chronic - Summary Table

STEMI Equivalents (Do Not Miss)

1. Posterior MI - tall R in V1-V2, ST depression V1-V3 (reciprocal); confirm with posterior leads
2. Hyperacute T waves - before ST elevation develops
3. de Winter pattern - upsloping ST depression in V1-V6 + tall symmetric T waves; no ST elevation; represents proximal LAD occlusion
4. LBBB with modified Sgarbossa criteria - ST elevation > 1 mm concordant with QRS; ST depression ≥ 1 mm in V1-V3; discordant ST elevation > 5 mm
5. T wave pseudonormalization - a previously inverted T wave becomes "normal-looking" during an acute ischemic episode

Practical Pitfalls

• Serial ECGs are essential - a single normal or non-diagnostic ECG does not exclude acute MI; repeat at 15-30 min intervals in high-risk patients
• LBBB and paced rhythms mask ischemic changes - use Sgarbossa criteria
• Q waves can disappear over time, especially after successful reperfusion of small infarcts - their absence does not rule out prior MI
• Persistent ST elevation beyond 4-6 weeks after MI suggests left ventricular aneurysm, not ongoing acute ischemia

• Harrison's Principles of Internal Medicine 22E (2025), Ch. 247 - Myocardial Ischemia and Infarction
• Rosen's Emergency Medicine, Ch. 64 - Q wave formation, T wave inversion, Wellens' pattern
• Tietz Textbook of Laboratory Medicine 7E, Figure 48.4 - Serial ECG evolution of AMI
• Turkish Journal of Emergency Medicine (2025) - High-risk ECG presentations in ACS beyond STEMI

Disclaimer: This is educational content only. ECG interpretation must always incorporate the full clinical context and be performed by a qualified clinician.