# How to Read an ECG: USMLE Approach

> How do you read an ECG for USMLE Step 1 and Step 2?

A systematic eight-step method for USMLE ECG questions, with the interval cutoffs, the high-yield patterns and the lead-to-artery map for STEMI localisation.

Read every USMLE ECG in the same eight steps: rate, rhythm, axis, P waves, PR interval, QRS width, QT interval, then ST segments, T waves and chamber enlargement. Calculate rate as 300 divided by the number of large boxes between consecutive R waves, then match the pattern to the vignette's clinical story before answering.

## How do you read an ECG for USMLE Step 1 and Step 2?

USMLE ECG items pair one dominant abnormality with a stem that either confirms it or quietly contradicts it. Reading in a fixed order stops you anchoring on the first striking wave, the error distractors are built to exploit.

1. **Rate** -- 300, 150, 100, 75, 60, 50 for one to six large boxes.
2. **Rhythm** -- one P per QRS, regular R-R intervals.
3. **Axis** -- leads I and aVF give the quadrant.
4. **P waves** -- morphology and amplitude for atrial enlargement.
5. **PR interval** -- short with a delta wave, or long with dropped beats.
6. **QRS** -- width, then bundle branch block, Q waves, voltage.
7. **QT interval** -- corrected for rate.
8. **ST segments and T waves** -- elevation, depression, reciprocal change.

Step 1 stops at the mechanism or lesion: the electrolyte, the accessory pathway, the infarcted wall. Step 2 CK pushes into management, so the same inferior ST elevation becomes a question about right-sided leads, nitrate avoidance or reperfusion timing.

## The numbers behind each of the eight steps

**Rate.** Normal sinus rate is 60-100 bpm. Use the large-box rule when regular; if irregular, count QRS complexes in a six-second strip and multiply by ten.

**Rhythm.** Sinus rhythm needs upright P waves in I, II and aVF, an inverted P in aVR, and one P per QRS. Irregularly irregular with absent P waves is atrial fibrillation.

**Axis.** Normal axis spans −30° to +90°. Positive QRS in I and aVF is normal; positive in I with negative in aVF and II is left axis deviation (left anterior fascicular block, LVH, inferior infarct); the reverse is right axis deviation (RVH, pulmonary embolism, COPD).

**PR interval.** Normal is 120-200 ms. Constant PR above 200 ms with every beat conducted is first-degree AV block. Progressive lengthening before a dropped QRS is Mobitz I; constant PR with dropped beats is Mobitz II, which needs a pacemaker.

**QRS duration.** Normal is under 120 ms. Widening means bundle branch block, ventricular origin, pacing, hyperkalaemia or sodium-channel blockade such as tricyclic overdose. Pathologic Q waves, at least 40 ms wide or a quarter of R-wave height, mean old infarct.

**QT interval.** Correct for rate with Bazett's formula, RR in seconds:

$$QTc = \frac{QT}{\sqrt{RR}}$$

Upper limits are roughly 440 ms in men and 460 ms in women; above 500 ms torsades risk is real. Hypokalaemia, hypomagnesaemia, hypocalcaemia, macrolides, antipsychotics and class IA or III antiarrhythmics all prolong it.

**ST segments.** ST elevation counts at 1 mm in two contiguous leads anywhere except V2-V3, where the cutoff is 2 mm in men and 1.5 mm in women. Horizontal or downsloping depression of at least 0.5 mm means subendocardial ischaemia; reciprocal depression separates occlusion from pericarditis.

**T waves.** Tall, narrow, symmetric peaked T waves are the earliest hyperkalaemia sign, and broad hyperacute T waves precede ST elevation in the first minutes of occlusion. Flat T waves with U waves suggest hypokalaemia. Biphasic or deeply inverted T waves in V2-V3 in a pain-free patient are Wellens syndrome, a critical proximal LAD lesion.

**Hypertrophy and chamber enlargement.** LVH means S in V1 plus R in V5 or V6 above 35 mm, or R in aVL above 11 mm, often with lateral strain; hypertensive LVH underlies [HFpEF](/blog/hfref-vs-hfpef-usmle). RVH gives R taller than S in V1 with right axis deviation. A broad notched P in lead II is left atrial enlargement, classically mitral stenosis, so read it beside the [murmur in the stem](/blog/valvular-heart-disease-murmur-usmle); a peaked P above 2.5 mm is right atrial enlargement.

## High-yield ECG patterns and the diagnosis each one signals

Each row below pairs a tracing pattern with its single best diagnosis.

| ECG finding | Diagnosis to pick |
| --- | --- |
| Peaked narrow T waves, then flat P waves, wide QRS, sine wave | Hyperkalaemia, in rising severity |
| Short PR interval with a delta wave (slurred QRS upstroke) | Wolff-Parkinson-White pre-excitation |
| Epsilon wave, a terminal notch after the QRS in V1-V2 | Arrhythmogenic right ventricular cardiomyopathy (ARVC) |
| Electrical alternans with diffusely low voltage | Large pericardial effusion or cardiac tamponade |
| Diffuse concave ST elevation with PR depression | Acute pericarditis |
| S1Q3T3 with sinus tachycardia | Acute pulmonary embolism with right heart strain |
| Osborn (J) wave, a positive deflection at the J point | Hypothermia |
| Prolonged QTc above 500 ms | Torsades risk from drugs, electrolytes or congenital LQTS |
| Sawtooth waves at an atrial rate near 300 bpm | Atrial flutter, usually 2:1 conducted at 150 bpm |
| Irregularly irregular rhythm with absent P waves | Atrial fibrillation |
| QRS >=120 ms with RSR' in V1 and wide slurred S in I and V6 | Right bundle branch block |
| QRS >=120 ms with broad monophasic R in V5-V6 and QS in V1 | Left bundle branch block |
| Downsloping "scooped" ST depression with a short QT | Digoxin effect at therapeutic levels |

> **10-second exam strategy:** before reading the answer choices, state the rate, the rhythm and whether the QRS is narrow or wide. Those three facts eliminate most distractors on a rhythm question.

## Which leads localise a STEMI to which coronary artery

Contiguous means anatomically adjacent, not adjacent on the printed page: II, III and aVF belong together.

| Leads with ST elevation | Wall infarcted | Culprit artery |
| --- | --- | --- |
| II, III, aVF | Inferior | Right coronary artery (circumflex in a minority) |
| V1-V2 | Septal | Left anterior descending, septal branches |
| V3-V4 | Anterior | Left anterior descending |
| I, aVL, V5-V6 | Lateral | Left circumflex or first diagonal |
| V4R (right-sided lead) | Right ventricle | Proximal right coronary artery |
| Tall R with ST depression in V1-V3, elevation in V7-V9 | Posterior | Left circumflex or right coronary artery |

Inferior ST elevation obliges right-sided leads: RV infarction is preload-dependent, so give fluids and withhold nitrates.

## Normal variants written to look like pathology

**Early repolarisation** gives concave ST elevation with a notched J point, largest in V2-V5, in a young healthy patient, no reciprocal depression, unchanged over years. **Sinus arrhythmia** is vagal rate variation with respiration, normal in the young. **An isolated Q wave in lead III** is positional and often disappears on deep inspiration, whereas an inferior infarct needs Q waves across II, III and aVF. Athletes also show sinus bradycardia and first-degree AV block without disease.

## Worked example: putting the sequence together

A 62-year-old man has 40 minutes of crushing substernal chest pain with nausea and diaphoresis. Blood pressure is 88/54 mm Hg, heart rate 52 bpm, lungs clear. The ECG is regular at 52 bpm, normal axis, PR 180 ms, QRS 90 ms, with 3 mm ST elevation in II, III and aVF and reciprocal depression in I and aVL.

Walk the steps: bradycardic rate, sinus rhythm, normal axis and intervals, narrow QRS -- not a conduction or ventricular problem. The elevation sits in one contiguous inferior group with genuine reciprocal change, excluding pericarditis and early repolarisation. Inferior STEMI with bradycardia, hypotension and clear lungs means proximal right coronary occlusion involving the right ventricle. Obtain right-sided leads, give fluids rather than nitroglycerin, then reperfuse. More pathways sit in the [Cardiology](/topics/cardiology) hub.

## How ECG reading is tested on the exam

- **Stem:** young man collapses while exercising, family history of sudden death, epsilon wave in V1. **Answer:** arrhythmogenic right ventricular cardiomyopathy.
- **Stem:** missed dialysis, weakness, peaked T waves with a widening QRS. **Answer:** hyperkalaemia; calcium gluconate first to stabilise the myocardium.
- **Stem:** pleuritic pain relieved by sitting forward, diffuse ST elevation with PR depression. **Answer:** pericarditis; NSAIDs plus colchicine.

## Common wrong-answer traps

**Calling every ST elevation a STEMI.** Pericarditis elevates ST segments across several territories with PR depression and no reciprocal change except in aVR, which shows PR elevation. Territory plus reciprocal depression is the discriminator.

**Reading V1-V3 ST depression as anterior ischaemia.** Tall R waves with anterior ST depression mirror a posterior infarct, which needs reperfusion, not medical management.

**Waiting for a sine wave to diagnose hyperkalaemia.** Peaked T waves come first; by sine wave the patient is near arrest, so act at the T-wave stage.

## Sources

- [NBME exam content outlines and practice materials](https://www.nbme.org/)
- [American College of Cardiology clinical guidelines](https://www.acc.org/Guidelines)

Pattern recognition only becomes automatic against real vignettes. [Practice ECG-based questions on StepGenie](https://dashboard.stepgenie.app/sign-up) and drill tracings paired with the stems, management steps and explanations the exam rewards.

## Frequently asked questions

### What are the normal ECG interval values tested on the USMLE?

Normal sinus rate is 60 to 100 bpm. The PR interval runs 120 to 200 ms, three to five small boxes; longer means first-degree AV block, and shorter with a delta wave means pre-excitation. QRS duration should be under 120 ms, and anything wider suggests bundle branch block, a ventricular origin, hyperkalaemia or sodium-channel blockade. Corrected QT is normal up to roughly 440 ms in men and 460 ms in women.

### How do you distinguish acute pericarditis from a STEMI on an ECG?

Pericarditis produces concave ST elevation spread across several vascular territories, with PR depression in the limb leads, PR elevation in aVR, and no reciprocal ST depression. A STEMI confines its elevation to one contiguous group, such as II, III and aVF, and produces reciprocal depression in the opposite leads. Pleuritic pain relieved by leaning forward favours pericarditis; crushing pain with diaphoresis favours coronary occlusion.

### What is the order of ECG changes in hyperkalaemia?

Hyperkalaemia changes the ECG in a predictable sequence: tall, narrow, symmetric peaked T waves first, then PR prolongation with flattening and loss of P waves, then progressive QRS widening, and finally a sine-wave pattern that precedes asystole. Peaked T waves are the earliest finding and are enough to act on. The exam answer is intravenous calcium gluconate to stabilise the myocardium, before insulin with glucose shifts potassium into cells.

### Which ECG findings suggest a pulmonary embolism?

Sinus tachycardia is the most common ECG finding in pulmonary embolism, so a fast but otherwise unremarkable tracing does not exclude it. The classic board pattern is S1Q3T3: a deep S wave in lead I, a Q wave in lead III, and T-wave inversion in lead III. Other markers of acute right heart strain include a new right bundle branch block, right axis deviation, and T-wave inversions in V1 to V4.

### Which leads show an inferior MI, and which artery is usually responsible?

Leads II, III and aVF face the inferior wall, and ST elevation there is most often a right coronary artery occlusion, with the left circumflex responsible in a minority of patients. Reciprocal depression appears in I and aVL. Because the right coronary artery also supplies the right ventricle, obtain right-sided leads: if V4R is elevated, the patient is preload-dependent, so give fluids and withhold nitrates.

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Canonical page: [How to Read an ECG: USMLE Approach](https://www.stepgenie.app/blog/how-to-read-ecg-usmle)
Topic hub: [Cardiology](https://www.stepgenie.app/topics/cardiology)