# How to Read an ECG (EKG) for USMLE Step 1 & 2

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

An eight-step ECG reading order with normal values, the 2026 STEMI cut-offs, a lead-to-artery map, and the first move for each arrhythmia, electrolyte and drug pattern.

Read every USMLE ECG in one order: rate, rhythm, axis, intervals, P waves, QRS, ST segment, then T and U waves, checking each against its normal: rate 60 to 100/min, PR 120 to 200 ms, QRS under 120 ms, axis −30° to +90°. Step 1 asks the mechanism; Step 2 CK asks the next step.

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

A fixed order keeps one dramatic finding from hiding a second. At the standard 25 mm/s, a large box is 200 ms and a small box 40 ms.

| Step | Normal | Quick method | Abnormal finding |
| --- | --- | --- | --- |
| 1. Rate | 60-100/min | 300 / large boxes between R waves (300, 150, 100, 75, 60, 50); if irregular, QRS count in 6 seconds x 10 | Over 100 tachycardia, under 60 bradycardia |
| 2. Rhythm | P before every QRS, upright in I, II and aVF | March out P waves and R-R intervals | Irregularly irregular, no P waves: atrial fibrillation |
| 3. Axis | −30° to +90° | I and aVF positive: normal. I positive, aVF negative: II positive is still normal, II negative is left deviation | Left −30° to −90°; right beyond +90° |
| 4. Intervals | PR 120-200 ms; QRS under 120 ms; QTc up to 440 ms (men) or 460 ms (women) per StatPearls | Bazett: QTc = QT / √RR, in seconds | PR over 200 ms: first-degree block; QRS 120 ms or more: bundle branch block, ventricular origin, hyperkalemia or sodium-channel blockade |
| 5. P waves | 0.11 s or shorter | Lead II for width, V1 for the terminal dip | Wide or notched: left atrial enlargement; tall and peaked: right atrial enlargement |
| 6. QRS | No pathologic Q waves; normal voltage | V1 and V6 for a bundle branch pattern | Q 40 ms or more, or 25% of the R, in two contiguous leads: infarction |
| 7. ST segment | At baseline at the J point | Compare lead groups and find the mirror image | Regional with reciprocal depression: occlusion; diffuse: pericarditis or early repolarization |
| 8. T and U waves | New T inversion over 1 mm in two contiguous leads suggests ischemia | V2-V3 and the tall-R lateral leads | Peaked T: hyperkalemia; U waves: hypokalemia; biphasic or deep V2-V3 T: Wellens |

Sources differ on QTc: the Merck Manual puts the male limit at 450 ms, and StatPearls ties a QTc above 500 ms to torsades risk.

## Axis deviation, chamber enlargement and LVH criteria

Causes of left axis deviation (−30° to −90°): left anterior fascicular block, LVH, inferior MI, WPW, hyperkalemia, pacing, pregnancy or ascites. Right axis deviation (beyond +90°): RVH, left posterior fascicular block, lateral MI, pulmonary embolism, COPD with cor pulmonale, dextrocardia, swapped arm electrodes, and normal children and young adults.

- **LVH:** Sokolow-Lyon is S in V1 plus the taller R in V5 or V6 of 35 mm or more, or R in aVL of 11 mm or more; Cornell is R in aVL plus S in V3 above 28 mm in men or 20 mm in women. The ECG is specific but insensitive, so echocardiography decides ([HFrEF vs HFpEF](/blog/hfref-vs-hfpef-usmle)).
- **RVH:** right axis deviation, R/S above 1 in V1, R in V1 above 6 mm.
- **Left atrial enlargement:** a P wave longer than 0.11 s, a notched P in II (P mitrale), or a terminal negative P in V1 deeper than 1 mm and wider than 0.04 s. Mitral valve disease is a classic cause, so read it with the [murmur in the stem](/blog/valvular-heart-disease-murmur-usmle).
- **Right atrial enlargement:** tall, peaked P waves in II, III and aVF (P pulmonale).

## Bundle branch blocks, fascicular blocks and WPW

A complete bundle branch block lasts 120 ms or more; a fascicular block keeps the QRS under 120 ms and shifts the axis.

| Pattern | QRS | Defining leads | Exam point |
| --- | --- | --- | --- |
| RBBB | 120 ms or more (incomplete 100-119) | rSR' in V1-V2; S wider than 40 ms in I and V6 | PE or cor pulmonale; does not hide a STEMI |
| LBBB | 120 ms or more | Broad notched R in I, aVL, V5-V6; no q in I, V5, V6; ST-T opposite the QRS | Masks STEMI, so use Sgarbossa |
| Left anterior fascicular block | Under 120 ms | Axis beyond −45°; qR in aVL | With RBBB: bifascicular block |
| Left posterior fascicular block | Under 120 ms | Axis beyond +120°; rS in aVL, qR in II and aVF | Bifascicular block needs no treatment unless intermittent second- or third-degree block appears |
| WPW | Widened by a delta wave | Short PR, slurred QRS upstroke | No AV nodal blockers in pre-excited AF |

In WPW an accessory pathway bypasses the AV node and pre-excites part of the ventricle. When atrial fibrillation conducts down it, the tracing becomes an irregular wide-complex tachycardia of shifting QRS shapes. AV nodal blockers (adenosine, verapamil, diltiazem, beta-blockers) favor conduction down the pathway and can precipitate ventricular fibrillation, and IV amiodarone has done so in reports. Give procainamide or ibutilide if stable, synchronized cardioversion if unstable, and ablation for symptomatic patients. See [WPW in depth](/blog/2026-05-26-everything-you-need-to-know-about-wolff-parkinson-white-for-step-1) and [LBBB vs RBBB](/blog/2026-05-25-comparison-table-bundle-branch-blocks-lbbb-rbbb).

## Which leads localize a STEMI to which coronary artery?

Under the Fifth Universal Definition of Myocardial Infarction (ESC, ACC, AHA and World Heart Federation, 28 August 2026), a working diagnosis of STEMI needs new J-point ST elevation in two or more contiguous leads: 1 mm or more in any lead other than V2-V3, where the cut-off is 2.5 mm in men under 40, 2 mm in men 40 or older and 1.5 mm in women, without LVH or LBBB.

| Leads with ST elevation | Wall | Usual culprit | Supporting clue |
| --- | --- | --- | --- |
| II, III, aVF | Inferior | RCA in most; circumflex in a minority | Reciprocal depression in I and aVL; III above II favors the RCA |
| V1-V2 | Septal | LAD, septal branches | V1-V4 together: anteroseptal |
| V2-V5 | Anterior | LAD | V1-V6 plus I and aVL: extensive anterior |
| I, aVL, V5-V6 | Lateral | Circumflex (obtuse marginal) or an LAD diagonal | Reciprocal depression in III and aVF |
| I and aVL | High lateral | First diagonal of the LAD | South African flag: elevation in I, aVL and V2, depression in III |
| V7-V9 (ST depression in V1-V3) | Posterior | RCA via the posterior descending artery, or the circumflex | Tall R and upright T waves in V1-V3 |
| V4R | Right ventricle | Proximal RCA | Above 1 mm (StatPearls); check it in every inferior STEMI |

New horizontal or downsloping ST depression of 0.5 mm or more in two contiguous leads suggests ischemia, and diffuse depression with elevation in aVR may mean left main or three-vessel disease. Late presenters more often show Q waves and T inversion than ST shifts.

About 40% of inferior MIs involve the right ventricle, so record right-sided leads; V4R elevation with hypotension and clear lungs calls for fluid, not nitrates ([STEMI vs NSTEMI management](/blog/2026-05-26-everything-you-need-to-know-about-stemi-vs-nstemi-management-for-step-1)). The Fifth UDMI replaces numbered types: primary MI (type 1 plus other acute coronary causes, such as dissection or vasospasm), secondary MI (a narrower type 2) and procedure-related MI (within 30 days of a cardiac procedure, replacing types 4 and 5); type 3 is removed.

## STEMI equivalents and the Wellens warning

Up to 1 in 4 patients managed as NSTEMI have an occluded culprit artery, so the Fifth UDMI lists STEMI equivalents for the right clinical setting.

- **Posterior MI:** ST depression of 1 mm or more in V1-V3 with a dominant R wave and upright T waves, confirmed by V7-V9 elevation (above 0.5 mm per StatPearls). Treat it as a STEMI.
- **de Winter pattern:** 1 to 3 mm of upsloping J-point ST depression across the precordial leads with tall, symmetric T waves, often with elevation in aVR. It signals acute LAD occlusion and needs emergent catheterization.
- **Hyperacute T waves:** broad, symmetric T waves too large for their QRS in two contiguous leads.
- **LBBB or a paced rhythm (Sgarbossa):** concordant ST elevation of 1 mm or more, ST depression of 1 mm or more in V1-V3, or discordant elevation of 5 mm or more. The modified rule replaces 5 mm with discordant elevation of 25% or more of the S-wave depth. A new bundle branch block with other signs of ischemia can also qualify.

Wellens syndrome, which the definition also lists, is a warning sign: in a pain-free patient with recent angina, biphasic or deep, symmetric T inversion in V2-V3 with little ST elevation and no Q waves marks a critical proximal LAD stenosis. In the original series, three-quarters of medically treated patients had an anterior MI within weeks, and stress testing can precipitate one, so the answer is catheterization.

## Arrhythmia recognition and the first step

QRS width and regularity sort a tachycardia, and stability picks the first move. The 2025 AHA adult algorithms call a patient unstable with hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort or acute heart failure, usually at 150/min or more, or under 50/min. Unstable tachycardia with a pulse gets synchronized cardioversion (an unsynchronized shock for polymorphic VT); unstable bradycardia gets atropine 1 mg every 3 to 5 minutes up to 3 mg, then pacing or a dopamine or epinephrine infusion.

| Rhythm | ECG clue | First step |
| --- | --- | --- |
| Sinus tachycardia | Over 100/min, normal P before each QRS | Treat the cause: fever, pain, hypovolemia, hypoxia, PE, hyperthyroidism |
| Atrial fibrillation | Irregularly irregular, no P waves | Unstable: synchronized cardioversion. Stable: beta-blocker or diltiazem; anticoagulate by CHA2DS2-VASc |
| Atrial flutter | Sawtooth waves in II, III, aVF; often 2:1 at 150/min | As for AF; isthmus ablation cures most typical flutter |
| Multifocal atrial tachycardia | 3 or more P-wave shapes, irregular, over 100/min | Treat the lung disease, K and Mg; verapamil or diltiazem; no cardioversion |
| AVNRT | Regular, narrow, 140-250/min; P hidden or a pseudo-r' in V1 | Vagal maneuver, then adenosine 6 mg, then 12 mg |
| Orthodromic AVRT | Regular, narrow; retrograde P visible after the QRS | As for AVNRT; ablate the pathway |
| Pre-excited AF | Irregular wide QRS complexes of varying shape | Procainamide or ibutilide; no AV nodal blockers |
| Monomorphic VT | 3 or more wide beats over 100/min; AV dissociation, capture or fusion beats | Unstable: synchronized cardioversion. Stable: procainamide, amiodarone or sotalol |
| Torsades de pointes | Polymorphic VT twisting around the baseline, long QT | Unsynchronized shock if sustained; IV magnesium 2 g may be considered for recurrences |
| Ventricular fibrillation | Chaotic waves, no P, QRS or T | CPR and immediate defibrillation |
| First-degree AV block | PR over 200 ms, every P conducted | None |
| Mobitz I | PR grows until one P fails to conduct; AV node | None, or atropine if symptomatic |
| Mobitz II | Fixed PR, sudden dropped QRS; below the node | Pace, then a permanent pacemaker |
| Third-degree AV block | P waves and QRS unrelated; escape rhythm | Unstable: atropine, then pacing; permanent pacemaker |

Treat a wide-complex tachycardia as VT, which it is about 80% of the time: adenosine may be considered for a stable, regular, monomorphic one, and verapamil or diltiazem is harmful. Manage a fixed 2:1 block like Mobitz II; the [AV block cheat sheet](/blog/2026-05-25-one-page-cheat-sheet-av-blocks-1st-2nd-3rd-degree) compares all four.

## Electrolytes, drugs and look-alike patterns

Electrolytes, drugs and mimics change the ST segment, T wave and QT too.

| Condition | ECG pattern | Exam pivot |
| --- | --- | --- |
| Hyperkalemia | Peaked T (5.5-6.5 mEq/L), flat or lost P waves (6.5-7.5), wide QRS (7-8), sine wave (8-10) | IV calcium gluconate first; the speed of the rise matters more than the level |
| Hypokalemia | Flat T, ST depression, U waves, long QT | Replace potassium and magnesium |
| Calcium | Hypocalcemia lengthens the QT; hypercalcemia shortens it | IV calcium gluconate for symptomatic hypocalcemia |
| Digoxin effect | Scooped ST depression in lateral leads | Expected on digoxin, not toxicity |
| Digoxin toxicity | PVCs, bidirectional VT, atrial tachycardia with block, AV block | Digoxin immune Fab; potassium above 5.5 mEq/L in acute poisoning is ominous |
| TCA overdose | Sinus tachycardia, QRS over 100 ms, R in aVR over 3 mm | IV sodium bicarbonate |
| QT-prolonging drugs | Long QTc, torsades | Class IA and III antiarrhythmics, macrolides, fluoroquinolones, antipsychotics, TCAs |
| Hypothermia | Osborn (J) wave, bradycardia, long PR, QRS and QT | Slow AF, then VF or asystole |
| Acute pericarditis | Diffuse concave ST elevation, PR depression; reciprocal depression only in aVR and V1 | NSAID or aspirin plus colchicine |
| Pulmonary embolism | Sinus tachycardia, nonspecific ST-T changes; S1Q3T3 uncommon | The ECG cannot rule PE in or out |
| Brugada type 1 | Coved ST elevation of 2 mm or more in a right precordial lead, then T inversion | SCN5A; fever and sodium-channel blockers unmask it; ICD after arrest or syncope |
| Early repolarization | Concave V2-V5 elevation, notched J point, no reciprocal depression | Usually benign; ST/T ratio in V6 under 0.25 |

ST elevation also occurs with myocarditis, Takotsubo syndrome and raised intracranial pressure; for the channelopathies see [long QT syndrome](/blog/2026-05-26-everything-you-need-to-know-about-long-qt-syndrome-for-step-1).

## How Step 1 and Step 2 CK test ECGs

USMLE says Step 1 tests principles and mechanisms underlying health, disease and modes of therapy, while Step 2 CK tests the clinical science needed for patient care under supervision.

**Step 1** asks what each wave means and which current a drug changes. P is atrial depolarization, PR mostly AV nodal delay, QRS ventricular depolarization and T ventricular repolarization; the U wave is attributed to late repolarization of papillary muscles or Purkinje fibers. In ventricular myocytes, phase 0 is sodium influx, phase 1 a potassium notch, phase 2 a plateau of calcium in and potassium out, phase 3 potassium repolarization and phase 4 rest. Nodal cells rely on calcium for the upstroke, and the funny current through HCN channels largely drives their phase 4 drift.

| Class | Drugs | Action | ECG effect |
| --- | --- | --- | --- |
| IA | Quinidine, procainamide, disopyramide | Sodium and potassium block | Longer QRS and QT |
| IB | Lidocaine, mexiletine | Fast-kinetic sodium block | Little change; QT may shorten |
| IC | Flecainide, propafenone | Marked sodium block | Longer PR and QRS |
| II | Beta-blockers | Beta block | Longer PR |
| III | Amiodarone, sotalol, dofetilide, ibutilide | Potassium block | Longer QT |
| IV | Verapamil, diltiazem | Calcium channel block | Longer PR |

**Step 2 CK** shows the tracing and asks the next step: right-sided leads and fluid for an inferior STEMI with hypotension, procainamide for pre-excited AF, calcium for peaked T waves, pacing for Mobitz II, magnesium for torsades, bicarbonate for a tricyclic's wide QRS. More on the [Cardiology](/topics/cardiology) hub.

> **10-second ECG check:** 1) Rate and regularity. 2) Narrow or wide QRS. 3) P before every QRS? 4) Axis from I, aVF, then II. 5) PR, QRS, QTc against 200, 120, 440-460 ms. 6) ST change regional with a mirror image, or diffuse? 7) Peaked T, U waves, deep V2-V3 T inversion.

## Worked vignette: an inferior STEMI with hypotension

A 62-year-old man has 40 minutes of crushing chest pain with sweating. Blood pressure is 86/54 mm Hg and pulse 54/min, with distended neck veins and clear lung fields. On the ECG: sinus bradycardia, a normal axis and normal intervals, and 3 mm of ST elevation in II, III and aVF, larger in III than II, with reciprocal depression in I and aVL. V4R shows 1.5 mm of elevation. The catheterization laboratory is activated. Which additional step is most appropriate now?

- A. Sublingual nitroglycerin
- B. IV furosemide
- C. IV normal saline bolus
- D. IV metoprolol
- E. Delay reperfusion until the troponin result returns

**Answer: C.** One contiguous inferior group with reciprocal change, larger in III than II, points to the right coronary artery, and V4R elevation above 1 mm marks right ventricular infarction. A preload-dependent right ventricle explains hypotension with clear lungs and a raised JVP, so give IV fluid while reperfusion proceeds. Nitroglycerin (A) and furosemide (B) cut preload and deepen the hypotension. Metoprolol (D) worsens the bradycardia and hypotension. Waiting for troponin (E) delays reperfusion the ECG already justifies.

## Common wrong-answer traps

- **Calling diffuse ST elevation a STEMI.** No reciprocal depression plus PR depression suggests pericarditis.
- **AV nodal blockers in pre-excited AF.** Use procainamide or ibutilide.
- **Atropine for Mobitz II.** Block below the node often ignores it; pace.
- **Waiting for a sine wave in hyperkalemia.** Give calcium once the ECG shows toxicity.

## Sources

- Fifth Universal Definition of MI (2026): [AHA summary](https://professional.heart.org/en/science-news/fifth-universal-definition-of-myocardial-infarction-2026), [top things to know](https://professional.heart.org/en/science-news/fifth-universal-definition-of-myocardial-infarction-2026/top-things-to-know), [PubMed](https://pubmed.ncbi.nlm.nih.gov/42661421/)
- 2025 AHA adult advanced life support: [guideline page](https://professional.heart.org/en/guidelines-statements/part-9-adult-advanced-life-support-2025-american-heart-association-guidelinescir0000000000001376), [PubMed](https://pubmed.ncbi.nlm.nih.gov/41122884/)
- StatPearls: [ECG](https://www.ncbi.nlm.nih.gov/books/NBK549803/), [axis](https://www.ncbi.nlm.nih.gov/books/NBK470532/), [LVH](https://www.ncbi.nlm.nih.gov/books/NBK557534/), [RVH](https://www.ncbi.nlm.nih.gov/books/NBK499876/), [LAE](https://www.ncbi.nlm.nih.gov/books/NBK553096/), [RBBB](https://www.ncbi.nlm.nih.gov/books/NBK507872/), [LBBB](https://www.ncbi.nlm.nih.gov/books/NBK482167/), [WPW](https://www.ncbi.nlm.nih.gov/books/NBK554437/), [inferior](https://www.ncbi.nlm.nih.gov/books/NBK470572/), [anterior](https://www.ncbi.nlm.nih.gov/books/NBK562234/), [lateral](https://www.ncbi.nlm.nih.gov/books/NBK537228/), [posterior](https://www.ncbi.nlm.nih.gov/books/NBK553168/) and [RV](https://www.ncbi.nlm.nih.gov/books/NBK431048/) MI, [de Winter](https://www.ncbi.nlm.nih.gov/books/NBK557573/), [Wellens](https://www.ncbi.nlm.nih.gov/books/NBK482490/), [SVT](https://www.ncbi.nlm.nih.gov/books/NBK441972/), [AVNRT](https://www.ncbi.nlm.nih.gov/books/NBK499936/), [MAT](https://www.ncbi.nlm.nih.gov/books/NBK459152/), [VT](https://www.ncbi.nlm.nih.gov/books/NBK532954/), [VF](https://www.ncbi.nlm.nih.gov/books/NBK537120/), [AV block](https://www.ncbi.nlm.nih.gov/books/NBK482359/), [hyperkalemia](https://www.ncbi.nlm.nih.gov/books/NBK470284/), [hypokalemia](https://www.ncbi.nlm.nih.gov/books/NBK482465/), [digoxin](https://www.ncbi.nlm.nih.gov/books/NBK459165/), [TCA](https://www.ncbi.nlm.nih.gov/books/NBK430931/), [long QT](https://www.ncbi.nlm.nih.gov/books/NBK441860/), [Brugada](https://www.ncbi.nlm.nih.gov/books/NBK519568/), [PE](https://www.ncbi.nlm.nih.gov/books/NBK560551/), [antiarrhythmics](https://www.ncbi.nlm.nih.gov/books/NBK482322/)
- USMLE: [Step 1](https://www.usmle.org/step-exams/step-1), [Step 2 CK](https://www.usmle.org/step-exams/step-2-ck)

Make the eight steps automatic on real tracings before test day: [Practice ECG-based questions on StepGenie](https://dashboard.stepgenie.app/sign-up).

## Frequently asked questions

### How do you calculate heart rate on an ECG?

At the standard paper speed of 25 mm/s, divide 300 by the number of large boxes between two R waves, giving 300, 150, 100, 75, 60 and 50 for one to six boxes, or divide 1,500 by the number of small boxes. For an irregular rhythm, count the QRS complexes on the 10-second rhythm strip and multiply by 6, or count for 6 seconds and multiply by 10. Normal sinus rate is 60 to 100/min.

### What are the normal ECG intervals for the USMLE?

The PR interval runs 120 to 200 ms, three to five small boxes; a longer PR is first-degree AV block, and a short PR with a delta wave means pre-excitation. The QRS should be under 120 ms, so 120 ms or more points to a bundle branch block, a ventricular rhythm, hyperkalemia or sodium-channel blockade. StatPearls calls a QTc above 440 ms in men or 460 ms in women prolonged, and torsades risk rises above 500 ms.

### What are the ECG criteria for a STEMI?

The Fifth Universal Definition of Myocardial Infarction, published in August 2026, requires new ST elevation at the J point in at least two contiguous leads: 1 mm or more in any lead other than V2 and V3, where the threshold is 2.5 mm in men under 40, 2 mm in men 40 or older and 1.5 mm in women. These cut-offs apply without LVH or LBBB; with LBBB or ventricular pacing, the Sgarbossa criteria are used instead.

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

Acute pericarditis gives diffuse, concave ST elevation that crosses coronary territories, often with PR depression, and reciprocal ST depression appears only in aVR and V1, with no pathologic Q waves. A STEMI keeps its elevation within one regional lead group, such as II, III and aVF, and usually brings reciprocal depression in the opposite leads. Early repolarization also lacks reciprocal change but shows a notched J point and an ST-to-T ratio in V6 under 0.25.

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

Hyperkalemia typically produces tall, peaked T waves first, around 5.5 to 6.5 mEq/L, then flattening or loss of P waves at 6.5 to 7.5, QRS widening at 7 to 8, and a sine-wave pattern before asystole at 8 to 10. The speed of the rise matters more than the absolute level, so a chronic patient may show little change. Once the ECG shows cardiac toxicity, IV calcium gluconate comes first to stabilize the myocardium, followed by insulin with glucose.

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Canonical page: [How to Read an ECG (EKG) for USMLE Step 1 & 2](https://www.stepgenie.app/blog/how-to-read-ecg-usmle)
Topic hub: [Cardiology](https://www.stepgenie.app/topics/cardiology)