ECG interpretation

Read the patient first — then read the tracing systematically.

A systematic 7-step method plus the patterns that change management in the next minutes.

Unstable? Treat the patient. Do not delay defibrillation or cardioversion for a prettier 12-lead.

Urgent ECG assessment · reference checklist

Confirm the tracing is real, then count the ventricular rate yourself.

Focus

Calibrated teaching diagramSynthetic lead II at 25 mm/s and 10 mm/mV. Grid and tracing share the same scale; screen millimetres vary with zoom.

Hover or tap: CAL 1mV · P wave · PR · QRS · ST · T wave · QT · RR rate.

Calibrated simulationSynthetic educational 12-lead; not a patient recording. Sequential 2.5-second columns plus a 10-second lead II strip. Swipe inside the paper on phones, or Enlarge to inspect.

Standard calibration: Paper speed 25 mm/s (1 small box = 40 ms; 1 large box = 200 ms). Voltage 10 mm/mV (1 small box = 0.1 mV; 2 large boxes = 1.0 mV). Check the calibration rectangle at the left edge.
Lead placement before diagnosis: V1–V2 in the 4th intercostal space at the sternal edge. High V1/V2 creates late RBBB-like rSR′ and can mimic Brugada or posterior OMI. Limb reversal: negative P and QRS in lead I with positive aVR.
Regular rate (300 rule): R wave on a heavy line, then 300 ÷ large boxes to the next R: 300, 150, 100, 75, 60, 50, 43, 37. Exact: 1500 ÷ small boxes.
Irregular rate (6-second rule): QRS count across 30 large boxes × 10. Mandatory in AF, flutter with variable block, or frequent ectopy.
ED rate meaning: Instability is perfusion, not a magic number. Cardiovert if the rate is causing shock, ischemia, heart failure, or AMS. Machine rates fail on artifact, tall T waves, and pacemaker spikes — count it yourself.

Pearl

Never trust a machine rate or axis on a tachycardic, paced, or artifact-laden tracing. Confirm speed and gain before you call low voltage or LVH.

Pitfall

Missing half-standard (5 mm/mV) or double-standard (20 mm/mV) calibration can mimic or hide low voltage and LVH. Document V1/V2 placement: accidental misplacement can alter morphology, while intentionally labelled high leads can reveal Brugada Type 1.

Rate · regularity · QRS width first. Then sinus vs not, then the frontal axis.

Focus

Paper-scaled teaching diagramSynthetic examples: sinus 75/min, a regular wide QRS rhythm at 86/min, and an irregularly irregular rhythm without discrete P waves. QRS width alone does not name a rhythm. I-positive/aVF-negative axis requires lead II.

Hover or tap: Narrow QRS · Wide QRS · Sinus P · Axis · Regularity.

The ED rhythm branch (do this before naming the rhythm): (1) Fast or slow? (2) Regular or irregular? (3) Narrow (<120 ms) or wide (≥120 ms)? That triad is the ACLS fork.
Sinus 4-point check: P before every QRS; QRS after every P; P upright in I, II, aVF and inverted in aVR; PR constant 120–200 ms.
Frontal axis (I and aVF, then confirm with II):
Normal (about −30° to +90°): Net positive in I and aVF. If aVF is negative, check lead II — positive II means 0° to −30° (physiologic), not pathologic LAD.
Pathologic LAD (−30° to −90°): I positive, aVF negative, II negative → LAFB, LVH, inferior infarct, or LBBB.
RAD (+90° to +180°): I negative, aVF positive → RVH, acute PE, LPFB, lateral infarct, COPD, sodium-channel toxicity, or limb reversal.
Extreme / northwest axis (−90° to ±180°): I and aVF both negative → VT, severe hyperK, or limb-lead reversal until proven otherwise.
If P in lead I is negative: arm-lead reversal (P and QRS positive in aVR) vs dextrocardia (whole precordial R-wave progression also reversed).

Pearl

Name the branch (narrow/wide, regular/irregular) before you name the rhythm. Extreme axis in a wide tachycardia is VT until proven otherwise.

Pitfall

Calling 0° to −30° “left axis” without checking lead II. Diagnosing a rhythm from a single 3-second snapshot when the strip shows something else.

PR (AV conduction), QRS (ventricular conduction), QTc (repolarization risk) — in that order.

Focus

Paper-scaled teaching diagramSynthetic lead II at 25 mm/s and 10 mm/mV. PR 160 ms, QRS 85 ms, and QT 380 ms to the drawn T-wave endpoint; Bazett QTc about 425 ms at 75/min.

Hover or tap: P wave · PR · QRS · ST · QT · RR rate.

PR (normal 120–200 ms / 3–5 small boxes):
Short (<120 ms): pre-excitation / WPW (delta wave) first. Isolated short PR without a delta wave is not an ED emergency label.
Long (>200 ms): first-degree AV block — note it, look harder if the patient is on AV-nodal blockers or has Lyme/ischemia.
Dropped beats: Mobitz I (Wenckebach — lengthening PR, usually AV-nodal) vs Mobitz II (fixed PR, unexpected drop — infranodal, pacing prep). 2:1 block cannot be typed on PR alone — treat as high-grade if the QRS is wide or the patient is unstable. Complete heart block: AV dissociation, regular escape.
PR depression: pericarditis (with PR elevation in aVR) — but territorial STE plus reciprocal STD is OMI, not pericarditis.
QRS (usually <110 ms; ACLS wide-complex threshold ≥120 ms): 110–119 ms requires morphology/context rather than a blanket normal label.
Wide (≥120 ms): LBBB/RBBB, VT, paced, hyperK, sodium-channel blockade (TCA, flecainide), WPW.
RBBB: rsR′ in V1–V2, wide slurred S in I, aVL, V5–V6.
LBBB: broad QS or rS in V1, broad notched R in I, aVL, V5–V6 without Q waves. New LBBB alone is not a STEMI equivalent (2025 ACC/AHA).
QTc: Bazett (QT/√RR) over-corrects when the rate is fast — use Fridericia (QT/∛RR) or a tachycardic-aware method. Practical prolonged-QTc thresholds: ≥450 ms in men and ≥460 ms in women; formula, age and QRS duration matter. ED danger zone ≥500 ms (TdP). Short QTc (<360 ms, especially <330 ms) raises SQTS/hypercalcemia/digoxin questions. With bundle branch block, consider JT/JTc rather than raw QTc.
Sustained polymorphic VT/TdP: immediate unsynchronized shock, including when a pulse is present; synchronization is unreliable. IV magnesium 2 g for TdP even if the magnesium is “normal”; overdrive pacing if pause-dependent and magnesium fails. Pull QT-prolonging drugs and replete K⁺/Mg²⁺.

Pearl

The half-RR rule is only a rough screen and can miss prolonged QT at slow rates or overcall it at fast rates. Measure QT and calculate QTc. QTc ≥500 ms is an ED action item, not a curiosity.

Pitfall

Measuring QT in a U-wave lead (pseudo-long QT), ignoring a wide QRS, or using Bazett alone at HR 130. Giving AV-nodal blockers to an irregular wide-complex tachycardia that is pre-excited AF.

LVH/RVH change the ST-T baseline. Low voltage and alternans change the next test.

Focus

Paper-scaled teaching diagramPaper-scaled voltage schematic. Top: V1 and V5 at 5 mm/mV, converted to standard-gain Sokolow–Lyon values. Bottom: representative low-voltage lead II at 10 mm/mV; confirm the criterion across every limb lead.

Hover or tap: V1 S wave · V5 R wave · Low voltage.

LVH voltage (supportive, not a stand-alone ED diagnosis): First confirm gain. At 10 mm/mV, Sokolow–Lyon is S in V1 + R in V5/V6 ≥35 mm, or R in aVL ≥11 mm. Cornell is R aVL + S V3 >28 mm (men) or >20 mm (women). Voltage has limited sensitivity/specificity: confirm suspected structural disease with echo, not the ECG alone.
LV strain: asymmetric down-sloping STD + inverted T in I, aVL, V5–V6. Chronic strain is not ACS — but new or changing ST/T is.
RVH: dominant R in V1 (R/S > 1, R > 7 mm) + RAD + RV strain (TWI/STD V1–V3 ± inferior). Differential of tall R in V1: RVH, RBBB, posterior OMI, WPW, lead misplacement, Duchenne, dextrocardia.
Atrial abnormality (an ECG clue, not a chamber-size diagnosis): RAE pattern — peaked P ≥2.5 mm in II. LAE pattern — notched P ≥120 ms in II, or a terminal negative P component in V1 that is ≥1 mm deep and ≥40 ms wide. Confirm anatomy with echo when it matters.
Low voltage: QRS <5 mm in all limb leads or <10 mm in all precordial leads; one small complex does not establish the diagnosis. Confirm gain first. Low voltage alone is nonspecific; low voltage + sinus tachycardia + electrical alternans should trigger immediate POCUS/echo for effusion/tamponade.
LV aneurysm vs acute STE: persistent STE with deep Q waves, no reciprocal depression, stable vs an old ECG. Acute OMI has reciprocal change and evolving T waves.

Pearl

Young, thin, or athletic chests often exceed Sokolow–Lyon without pathologic LVH. Pair voltage with LA enlargement and strain, and always compare with a prior ECG.

Pitfall

Calling anteroseptal MI from RVH (tall R V1), or calling lateral ischemia from chronic LV strain without looking at an old tracing. Missing tamponade because “the ECG is low voltage from obesity.”

Use the Fifth Universal Definition lead-by-lead: ≥1 mm in every standard lead except V2–V3; add posterior or right-sided leads when the 12-lead leaves a clinical gap.

Focus

Criteria diagramLead and threshold teaching map; not a patient ECG. Voltage examples share the paper scale, but isolated schematic beats do not establish a diagnosis.

Hover or tap: Anterior STE · Inferior STE · Mirror STD · Posterior mirror · Ischaemia STD/TWI.

Fifth Universal Definition (2026) — new J-point STE in two contiguous leads: ≥1.0 mm in every standard 12-lead except V2–V3 (I, aVL, II, III, aVF, V1, V4–V6). There is no single-lead STEMI rule; interpret anatomically contiguous lead groups and the clinical presentation. These thresholds do not apply unchanged in LBBB, paced rhythm, or LVH.
V2–V3 only: ≥2.5 mm in men <40 years, ≥2.0 mm in men ≥40 years, or ≥1.5 mm in women regardless of age.
Inferior (II, III, aVF): usually RCA or LCx. STE III > II supports RCA. Reciprocal STD in aVL is a high-yield clue; obtain right-sided leads when inferior injury is present.
Septal/anterior (V1–V4) and lateral (I, aVL, V5–V6): look for a contiguous distribution, reciprocal inferior change, and dynamic evolution. Isolated I/aVL change can be high-lateral/diagonal ischemia, but still needs context and comparison.
Supplemental leads — record, do not infer: with inferior OMI, record V3R–V6R (especially V4R) for RV involvement; STE ≥0.5 mm is supportive (≥1.0 mm in men <30 years). With V1–V3 depression or suspected LCx occlusion, record V7 (left posterior axillary), V8 (mid-scapular), and V9 (left paraspinal) in the V6 horizontal plane; STE ≥0.5 mm supports posterior infarction (use ≥1.0 mm in men <40 years for greater specificity).
Ischemic changes beyond STE (Fifth UDMI): new horizontal/downsloping STD ≥0.5 mm in ≥2 contiguous leads; new or dynamic T-wave inversion ≥1 mm in ≥2 contiguous leads; broad symmetric hyperacute T waves disproportionate to the QRS in ≥2 contiguous leads; pathologic Q waves ≥40 ms and/or ≥25% of the R wave in ≥2 contiguous leads.
Posterior and occlusion clues: posterior MI is suggested by STD ≥1 mm in V1, V2, and/or V3, particularly with a dominant R in V1/V2, with V7–V9 adding supportive evidence; negative posterior leads do not exclude occlusion. Acute occlusion can also present as de Winter, Wellens, Sgarbossa/modified Sgarbossa, Aslanger, or the South African flag pattern — these do not wait for a millimetre STEMI label.
Serial and prior ECGs: compare with an old tracing and repeat promptly with ongoing/recurrent symptoms or an initially nondiagnostic ECG. A normal or sub-threshold first ECG does not exclude an acute coronary occlusion.

Pearl

The core rule is simple: 1 mm in all standard leads except V2–V3. The work is recognizing a contiguous territory, adding V3R–V6R or V7–V9 when indicated, and acting on dynamic occlusion patterns before a textbook threshold appears.

Pitfall

Using one lead alone, treating V2–V3 as a 1 mm rule, or calling V1–V3 depression “anterior ischemia” without posterior leads. Do not give nitrate-dependent comfort false reassurance in an inferior MI before considering RV involvement.

Occlusion MI that misses millimetre STEMI criteria — and the patterns that are no longer automatic lab activations.

Paper-scaled teaching diagramSynthetic focused examples of hyperacute T waves, de Winter morphology and Wellens type B. Lead II below is a normal rhythm reference. These are separate teaching examples, not one patient ECG.

Paradigm: STEMI vs NSTEMI is a millimetre rule. OMI vs NOMI is whether the artery is occluded. More than 1 in 4 occlusions never meet STEMI millimetres. New or presumed-new LBBB alone is not a STEMI equivalent (2025 ACC/AHA/ACEP ACS) — use Smith-modified Sgarbossa plus the patient.
1. Wellens (high-risk anterior ischemic pattern): pain-free after resolved angina. Type A (~25%): biphasic T in V2–V3. Type B (~75%): deep symmetric inverted T in V2–V3 ± V4–V5. Preserved R waves, little or no STE, no pathologic Q. Stress testing is contraindicated. Recurrent pain or T-wave pseudonormalisation raises concern for recurrent ischemia and requires immediate reassessment.
2. de Winter T waves (high-risk coronary occlusion pattern): 1–3 mm upsloping J-point STD in precordial leads into tall, broad, symmetric T waves. STE in aVR is common but not required. Activate as anterior OMI.
3. Smith-modified Sgarbossa (LBBB or ventricular paced): positive if any of: (1) concordant STE ≥ 1 mm in a lead with a positive QRS; (2) concordant STD ≥ 1 mm in V1–V3; (3) discordant STE ≥1 mm with ST/S ratio ≤ −0.25 (STE ≥ 25% of S-wave depth). Original Sgarbossa’s 5 mm discordant rule missed many anterior occlusions.
4. Isolated posterior OMI: horizontal STD V1–V3, upright T, tall R (R/S > 1 in V2). V7–V9 STE ≥ 0.5 mm supports posterior infarction in the appropriate clinical context; ≥1 mm is more specific in men under 40. Do not call this “anterior ischemia.”
5. aVR STE + widespread STD: severe subendocardial ischemia from LMCA/3VD/proximal LAD or demand ischemia (shock, hypoxia, anemia, AS). Not automatic code STEMI if the patient is stable (2025 ACS: high-risk NSTE-ACS → urgent angiography). Immediate activation if unstable or the rest of the ECG is occlusive.
6. Hyperacute T waves: earliest OMI sign (minutes). Broad, bulky, symmetric T that dwarfs a small R; loss of normal ST-T concavity. Precedes millimetre STE. Serial ECGs.
7. Aslanger pattern: STE in III but not other inferior leads; STD in at least one of V4–V6, not V2, with a positive terminal T; ST in V1 higher than V2. This described pattern raises concern for inferior infarction with multivessel disease. It is not a standalone proof of occlusion.

Pearl

More than 25% of acute coronary occlusions never meet millimetre STEMI criteria. Wellens or de Winter during a pain-free interval is still an emergency.

Pitfall

Activating the lab for isolated new LBBB, or dismissing Wellens/de Winter as “nonspecific ST-T changes.” Treating stable aVR-STE + diffuse STD as automatic code STEMI without asking whether this is demand ischemia.

HyperK, channelopathy, PE strain, pericarditis vs BER, sodium-channel blockade, hypothermia, and tamponade.

Calibrated simulation · hyperkalemia examplesSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Three possible hyperkalemia appearances, not a predictable sequence or potassium-level scale.

Hover or tap: HyperK clue.

Hyperkalemia: peaked T, prolonged PR, diminished P, wide QRS or sine-wave changes may occur without a reliable sequence. A normal ECG does not exclude dangerous hyperkalemia. For life-threatening changes attributed to hyperkalemia, give IV calcium and potassium shifting/removal treatment using the local emergency protocol, with ECG and glucose monitoring. Cardiac arrest requires the ALS special-circumstances pathway.
Hypokalemia: flat T, ST depression, U waves (best V2–V3), apparent long QU, ectopy, TdP risk. Replete K⁺ and Mg²⁺. Looks a little like ischemia — check the potassium.
Calcium disorders: hypercalcemia shortens QT (short ST); hypocalcemia lengthens QT (long ST segment with a normal T).
Hypothermia: Osborn (J) waves — positive hump at the J point, biggest in V2–V5 — plus bradycardia, AF, long PR/QRS/QT, shivering artifact. VF risk during handling. Treatment is rewarming, not an antiarrhythmic chase.
Brugada Type 1: coved STE ≥2 mm with a negative T in at least one V1–V2 lead. Fever and sodium-channel drugs may unmask it. Record standard 4th ICS positions and, when indicated, labelled 2nd/3rd ICS right-precordial leads. A Type 1 pattern needs clinical evaluation and exclusion of phenocopies.
PE / RV strain: sinus tachycardia is the common finding. S1Q3T3 is neither sensitive nor specific. More useful: TWI in V1–V4 ± inferior leads, new RBBB, RAD. Normal ECG does not exclude PE.
Pericarditis vs BER vs OMI: pericarditis — diffuse concave STE, PR depression, PR elevation/STD in aVR, Spodick sign, no reciprocal STD except aVR/V1. BER — fish-hook J-point notching (often V4), ST/T ratio in V6 < 0.25. Any territorial STE + reciprocal STD is OMI until proven otherwise.
TCA / sodium-channel blockade: sinus tach, QRS > 100 ms (seizure risk) / > 160 ms (arrhythmia), terminal R in aVR ≥ 3 mm. Sodium bicarbonate 1–2 mEq/kg IV push, repeat toward QRS < 100 ms and pH ~7.50–7.55. Avoid class Ia/Ic agents.
Electrical alternans + low voltage + tachycardia: tamponade until bedside echo. Low voltage alone is not tamponade.
Digoxin effect vs toxicity: scooped STD is “digitalis effect,” not a diagnosis of toxicity. Toxicity: ectopy, bidirectional VT, atrial tach with block. Fab fragments; discuss calcium with toxicology if hyperK is from digoxin.

Pearl

If the ECG looks bizarre, wide, slow, or refuses to classify, treat hyperkalemia while the lab runs. Calcium for the membrane; insulin/albuterol/dialysis for the potassium.

Pitfall

Giving beta-blockers, diltiazem, or amiodarone to a wide-complex bradycardia that is actually hyperK. Calling territorial STE “pericarditis” because it is concave.

Jump to a pattern

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CriticalOMI / STEMI

Classic STEMI Millimetre Criteria

STEMI activation rule

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Convex STE II + III + aVF with mirror STD in aVL — territorial STE + mirror STD supports acute inferior occlusion.

Hover or tap: Inferior STE · Mirror STD.

Leads: II, III, aVF (STE) + aVL (mirror STD) — 2 contiguous at J point

Criteria: Inferior example: convex STE ≥1 mm in II + III + aVF with mirror STD in aVL. General rule: STE in V2–V3 ≥ 2.5 mm (men <40), ≥ 2.0 mm (men ≥40), ≥ 1.5 mm (women); ≥ 1.0 mm in all other leads ×2 contiguous. Posterior V7–V9 ≥ 0.5 mm. MIRROR — inferior up, aVL down.

Why it matters: Still the operational trigger for most cath-lab activations. Misses >25% of acute occlusions — that is why OMI equivalents exist.

Action: If millimetre STEMI + compatible symptoms/signs: immediate reperfusion pathway per local STEMI protocol. Add V4R for inferior STE and V7–V9 for isolated anterior STD.

Caution: A tracing that fails millimetre criteria can still be OMI (hyperacute T, Wellens, de Winter, posterior, Aslanger, Smith-modified Sgarbossa).

CriticalOMI / STEMI

Hyperacute T Waves

Earliest OMI sign

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Same V3 viewpoint, three T shapes: normal vs hyperacute vs hyperK tenting.

Hover or tap: T wave · Hyperacute T · HyperK clue.

Leads: One V3 viewpoint, three shapes: normal vs hyperacute vs hyperK

Criteria: Side-by-side in a single V3 viewpoint. Normal: smooth asymmetric T, R > T. Hyperacute: broad-based bulky ("inflated") T dwarfing QRS with straightened takeoff — always confirm territorial across 2+ adjacent leads in the patient, never all leads. HyperK tenting: narrow pointed peak with flat P, usually diffuse. May precede any millimetre STE. Compare with an old ECG, repeat in 10–15 minutes, and check potassium too — OMI and hyperK can coexist.

Why it matters: Minutes-old coronary occlusion. Waiting for millimetre STE loses myocardium.

Action: Treat as OMI: serial ECGs, old tracing, posterior/right-sided leads as indicated, immediate cardiology escalation. Do not wait for a “diagnostic” STEMI millimetre if the T waves are blowing up in a territorial distribution.

Caution: HyperK tented T waves are narrow-based and diffuse; hyperacute T waves are broad-based and territorial. HyperK and OMI can coexist — treat both possibilities.

CriticalOMI / STEMI

Wellens Syndrome (Type A & B)

High-risk ACS pattern

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Pain-free interval after resolved angina: Type A biphasic (+/−) vs Type B deep symmetric inversion in V2–V3. Strongly associated with critical LAD disease in the appropriate clinical setting.

Hover or tap: Wellens LAD.

Leads: V2–V3 (often V1–V5)

Criteria: Pain-free after resolved angina. Type A (~25%): biphasic T in V2–V3. Type B (~75%): deep symmetric inverted T in V2–V3. Preserved R-wave progression, isoelectric or minimally elevated ST, no pathologic Q waves.

Why it matters: Strongly associated with significant LAD disease and a high risk of anterior infarction. ECG alone does not establish exact lesion location or current artery patency.

Action: Urgent cardiology assessment and an invasive ACS pathway as indicated. Do not send for an exercise stress test.

Caution: Recurrent pain or T-wave pseudonormalisation may indicate recurrent ischemia and requires immediate reassessment. Repeat the ECG with every symptom change.

CriticalOMI / STEMI

de Winter T Waves

OMI equivalent

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Upsloping J-point ST depression with tall symmetric T waves across V2–V6. aVR elevation is supportive and may be absent.

Hover or tap: de Winter LAD.

Leads: V1–V6; aVR often

Criteria: 1–3 mm upsloping J-point STD in the precordial leads continuing into tall, prominent, symmetric T waves. STE in aVR is common but not required.

Why it matters: A high-risk occlusion pattern, commonly associated with LAD disease, that can occur without classic STE. The exact culprit anatomy cannot be inferred from the ECG alone.

Action: Immediate cath-lab activation. Treat as anterior OMI, not “nonspecific anterior ischemia.”

Caution: The pattern can evolve into frank anterior STE or appear only on the first tracing. Do not wait for millimetre STE.

CriticalOMI / STEMI

Smith-Modified Sgarbossa (LBBB & Paced)

OMI in LBBB / paced

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. LBBB-like wide complexes: concordant anterior ST depression and concordant lateral STE are abnormal.

Hover or tap: Concordant STE · Concordant STD · STE/S ≥25%.

Leads: Any lead with a positive QRS; V1–V3

Criteria: Positive if ANY of: (1) concordant STE ≥ 1 mm in a lead with a positive QRS; (2) concordant STD ≥ 1 mm in V1–V3; (3) discordant STE ≥1 mm, ST/S ratio ≤ −0.25 (STE ≥ 25% of S-wave depth).

Why it matters: Finds occlusion MI when the baseline is LBBB or a ventricular paced rhythm. New LBBB alone is not a STEMI equivalent (2025 ACC/AHA/ACEP).

Action: If any Smith-modified criterion is met in a compatible patient: immediate reperfusion pathway. Unmodified 5 mm discordant STE is obsolete as a standalone rule.

Caution: A paced or LBBB tracing that fails Sgarbossa can still be OMI clinically — use serial ECGs, old tracings, and the patient, not the millimetre rule alone.

CriticalOMI / STEMI

Isolated Posterior OMI

OMI equivalent

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. V1–V3 horizontal ST depression with dominant R and upright T raises concern for posterior occlusion. Record V7–V9 and interpret clinically.

Hover or tap: Posterior mirror.

Leads: V1–V3 (mirror); V7–V9 (true posterior)

Criteria: Horizontal STD in V1–V3 with upright T waves and prominent R waves (R/S > 1 in V2). Posterior leads: STE ≥ 0.5 mm in V7–V9 supports posterior infarction; ≥1 mm is more specific in men under 40.

Why it matters: Transmural posterior wall occlusion (LCx or distal RCA). Often labelled “anterior ischemia” and not activated.

Action: Place V7–V9 immediately. Use the urgent reperfusion pathway for a convincing posterior occlusion presentation; assess elevation in contiguous posterior leads with age-specific thresholds rather than one isolated measurement.

Caution: Turning the tracing over (or mentally flipping V1–V3) shows the STEMI hiding in the ST depression. Digitalis effect is scooped, not horizontal, and is not territorial.

CriticalOMI / STEMI

aVR STE with Diffuse ST Depression

High-risk ACS / demand ischemia

Calibrated synthetic ECGSynthetic educational strip · 6 seconds · selected leads, not a full 12-lead. Grid and waveform share a calibrated scale; on-screen millimetres depend on zoom. Selected morphology, not a clinically validated patient ECG.

Leads: aVR STE; widespread STD in I, II, aVL, V4–V6

Criteria: STE ≥ 1 mm in aVR (sometimes aVR > V1) plus horizontal STD in ≥ 6 other leads.

Why it matters: Severe subendocardial ischemia: LMCA / proximal LAD / triple-vessel disease, or demand ischemia from shock, hypoxia, anemia, or critical AS. True complete LM occlusion often presents in extremis.

Action: Resuscitate the cause (shock, hypoxia, anemia). Urgent cardiology. Immediate lab activation if unstable or the tracing is otherwise occlusive. Avoid heavy nitrates if hypotensive or RV/preload dependent.

Caution: 2025 ACC/AHA ACS: this is high-risk NSTE-ACS, not automatic code STEMI in a stable patient. Do not skip the bedside echo and the rest of the shock workup.

CriticalToxic-metabolic

Hyperkalemia Spectrum & Sine Wave

Metabolic emergency

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Three possible hyperkalemia appearances, not a predictable sequence or potassium-level scale.

Hover or tap: HyperK clue.

Leads: Diffuse

Criteria: Possible findings: peaked T waves, PR prolongation, diminished/absent P waves, QRS widening and a sine-wave appearance. They need not occur in sequence; a normal ECG does not exclude dangerous hyperkalemia.

Why it matters: Membrane instability. Once the QRS widens, VF/PEA/asystole can be minutes away.

Action: With life-threatening ECG changes attributed to hyperkalemia, obtain emergency senior help and give IV calcium under the local formulation-specific protocol; reassess the ECG. Begin potassium shifting/removal treatment with glucose monitoring and urgent renal input. In cardiac arrest, follow the ALS special-circumstances protocol; evidence for adjunct drugs is limited.

Caution: Do not wait for the lab if the tracing is already wide or sine-wave in a dialysis or oliguric patient. Do not mix calcium and bicarbonate in one line. Do not give AV-nodal blockers or amiodarone to a wide, slow, bizarre rhythm that is hyperK.

EmergentToxic-metabolic

Hypokalemia, U Waves & Long QU

Metabolic emergency

Leads: V2–V3 best; diffuse ST-T

Criteria: Flattened T waves, ST depression, prominent U waves (best V2–V3), apparent QT/QU prolongation, increased PVCs. Severe hypokalemia can precipitate VT/TdP, especially with low Mg²⁺ or QT drugs.

Why it matters: Arrhythmogenic and a common ACS mimic. The “ischemic” STD of hypokalemia is usually diffuse, not territorial.

Action: Replete potassium and magnesium on a monitored bed. Review diuretics, GI losses, and QT-prolonging drugs. Repeat the ECG after repletion before calling residual ischemia.

Caution: Do not send a hypokalemic patient with U waves and a long QU home on a QT-prolonging antiemetic. Apparent long QT is often QU.

CriticalToxic-metabolic

Hypothermia & Osborn (J) Waves

Environmental / metabolic

Leads: J waves biggest in V2–V5; rhythm strip

Criteria: Osborn J waves (positive hump at the J point) plus sinus bradycardia or AF, prolonged PR/QRS/QT, shivering artifact, and sometimes STE that mimics OMI.

Why it matters: Hypothermia can cause these findings and raises arrhythmia risk. J waves do not exclude coexisting coronary ischemia; assess core temperature and the clinical presentation.

Action: Confirm core temperature. Handle gently. Rewarm per local hypothermia protocol. Start CPR/defibrillation for arrest and follow the local temperature-specific ALS protocol for subsequent shocks and drugs; arrange ECLS rewarming when indicated.

Caution: J waves alone do not diagnose coronary occlusion. Ongoing ischemic symptoms, territorial changes or instability need urgent parallel assessment; do not defer suspected ACS solely while waiting for rewarming.

CriticalMimics

Brugada Type 1 ECG Pattern

Channelopathy

Leads: V1–V2 at 4th ICS; labelled recordings at 2nd/3rd ICS when indicated

Criteria: Coved STE ≥2 mm followed by a negative T wave in at least one of V1–V2 (Type 1), recorded at the 4th or intentionally at the 2nd/3rd intercostal space. A saddleback pattern alone is not diagnostic; assess clinical context and exclude phenocopies.

Why it matters: Risk of polymorphic VT/VF, often during sleep or fever. Sodium-channel drugs, cocaine, and fever unmask it.

Action: Treat fever aggressively. Avoid Brugada-unmasking drugs (flecainide, procainamide, bupivacaine, many TCAs — check brugadadrugs.org). Telemetry, EP/cardiology, ICD discussion for Type 1 with syncope or arrest.

Caution: Document lead placement. Standard V1/V2 use the 4th ICS; deliberate high right-precordial recordings at the 2nd/3rd ICS can reveal a true Type 1 pattern. Review ischemia, electrolytes, drug effects and the clinical history with cardiology/EP.

CriticalMimics

Acute PE & RV Strain

Cardiopulmonary

Leads: I, III, V1–V4, aVF

Criteria: Sinus tachycardia is the usual finding. RV strain: TWI in V1–V4 ± inferior leads, new RBBB, RAD, or S1Q3T3 (deep S in I, Q in III, TWI in III).

Why it matters: S1Q3T3 is neither sensitive nor specific (~10–20%). TWI V1–V4 is more useful when present. A normal ECG does not exclude PE.

Action: This tracing supports RV strain — it does not diagnose PE. Bedside echo (RV dilation, McConnell), then the PE pathway (PERC/Wells/YEARS ± CTPA). High-risk PE with shock: local reperfusion/PERT, not the ECG alone.

Caution: Do not delay the PE workup because S1Q3T3 is absent. Do not call every TWI V1–V4 “Wellens” — Wellens is pain-free LAD disease with preserved R waves and a coronary story.

EmergentMimics

Pericarditis vs BER vs OMI

Inflammatory / normal variant

Distinguish the patterns

Pericarditis: Often diffuse ST/PR changes with pleuritic positional pain; assess inflammation and effusion.
Early repolarization (BER): Prior stable pattern and J notching support it; ST/T ratios and concavity are clues, not exclusion tests for ACS.
OMI: New territorial or reciprocal changes and ischemic symptoms require urgent assessment even with concave STE.

Leads: Diffuse limb + precordial; aVR; V4 for BER notch

Criteria: Pericarditis: diffuse concave STE, PR depression, aVR PR elevation/STD, Spodick sign, no reciprocal STD except aVR/V1. BER: fish-hook J-point notching (often V4), ST/T amplitude ratio in V6 < 0.25 may support BER, particularly when stable versus an old ECG; neither feature alone excludes ACS.

Why it matters: The dangerous error is labelling OMI as pericarditis because the STE is concave.

Action: Territorial STE with reciprocal STD outside aVR/V1 strongly raises concern for coronary occlusion: arrange urgent ACS assessment. Pericarditis: echo (effusion/tamponade), NSAID + colchicine per local practice, review anticoagulation indications and bleeding/tamponade risk with cardiology; an effusion alone is not an absolute contraindication.

Caution: Reciprocal depression outside aVR/V1 is atypical for uncomplicated pericarditis. Read it with territorial ST elevation and symptoms; myocardial inflammation can also mimic ACS. When occlusion remains a concern, seek urgent cardiology assessment.

CriticalToxic-metabolic

TCA / Sodium-Channel Blockade

Toxicology

Leads: aVR and the rhythm strip

Criteria: Sinus tachycardia + QRS widening (>100 ms seizure risk, >160 ms ventricular arrhythmia risk) + terminal R in aVR ≥ 3 mm (or R/S in aVR > 0.7).

Why it matters: Fast sodium-channel blockade. The ECG is the dose of bicarbonate, not the drug level.

Action: For significant sodium-channel-blocker cardiotoxicity, give sodium bicarbonate 1–2 mEq/kg IV under the poison-centre protocol and reassess QRS, perfusion, sodium, potassium and pH. Repeat/infuse with expert guidance; avoid pH >7.55 or sodium >155 mmol/L. Do not keep dosing solely to force QRS below 100 ms. Avoid class Ia/Ic antiarrhythmics and physostigmine.

Caution: A “borderline” QRS of 110 ms in an overdose is already actionable. Do not wait for 160 ms. Flecainide, carbamazepine, and diphenhydramine can look identical.

CriticalRhythm

WPW and Pre-excited AF

Accessory pathway

Distinguish the patterns

Sinus pre-excitation (shown): Organized P waves, short PR, delta wave and widened QRS; arrange specialist risk assessment.
Pre-excited AF: Irregular RR and changing wide QRS morphology, often very fast. Cardioversion if unstable; avoid AV-nodal blockers and IV amiodarone.

Leads: All leads; the strip during tachycardia

Criteria: Sinus: short PR (<120 ms) + delta wave + wide QRS. Pre-excited AF: irregular, wide, bizarre, often >200–250 bpm with changing QRS morphology.

Why it matters: Rapid accessory-pathway conduction during AF can provoke VF. AV-nodal-blocking drugs can accelerate the ventricular response and are harmful in pre-excited AF.

Action: Unstable: immediate cardioversion. Stable pre-excited AF: IV procainamide or ibutilide with expert monitoring, or electrical cardioversion. Avoid adenosine, beta-blockers, diltiazem, verapamil, digoxin and IV amiodarone in pre-excited AF.

Caution: Delta waves fake Q waves (pseudo-infarct) and fake bundle-branch block. A very fast irregular wide tachycardia must raise concern for pre-excited AF. Consider AF with aberrancy and polymorphic VT as well; do not assume ordinary AF before assessing for pre-excitation.

CriticalRhythm

VT vs SVT with Aberrancy

Wide-complex tachycardia

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. A regular broad-complex tachycardia should be treated as VT until proved otherwise; seek AV dissociation, capture or fusion beats.

Distinguish the patterns

VT (shown): AV dissociation and capture/fusion support VT, but are often absent. Structural heart disease increases suspicion.
SVT with aberrancy: A supraventricular rhythm with abnormal ventricular conduction. A BBB-like shape alone cannot prove SVT; manage uncertain wide tachycardia as VT.

Leads: All leads, especially V1–V6

Criteria: Wide-complex tachycardia (QRS ≥120 ms, HR >100). Favours VT: AV dissociation, fusion/capture beats, extreme axis, precordial concordance, Brugada/Vereckei algorithms, history of MI or structural disease.

Why it matters: >80% of regular wide-complex tachycardias in the ED are VT; >90% if there is prior MI. The cost of treating VT as SVT is collapse.

Action: Treat as VT. Unstable: synchronized cardioversion (defibrillate if pulseless or truly polymorphic). Stable monomorphic: procainamide or amiodarone per local ACLS, or elective cardioversion. Adenosine only if regular, monomorphic, and you still think SVT with aberrancy — never if irregular.

Caution: Never give verapamil or diltiazem to an undifferentiated wide-complex tachycardia. Irregular and wide is not “SVT with aberrancy” — think AF + RBBB, pre-excited AF, or polymorphic VT.

CriticalRhythm

High-Grade AV Block & Complete Heart Block

Bradycardia emergency

Calibrated simulationSynthetic focused leads, not a patient recording or a full 12-lead. Each small box represents 40 ms / 0.1 mV at this setting. Regular P waves march through independently of a slow escape rhythm: complete AV block until proven otherwise.

Distinguish the patterns

Mobitz I: Progressively lengthening PR before a nonconducted P in the typical pattern.
Mobitz II: Intermittent nonconducted P with stable conducted PR intervals; exclude mimics and seek urgent pacing assessment.
2:1 AV block: Every other P conducts. PR alone cannot distinguish Mobitz I from II.
Complete block (shown): Independent atrial and slower ventricular rhythms with no consistent conduction; assess the full rhythm strip.

Leads: Rhythm strip plus full 12-lead

Criteria: Mobitz II: constant PR, sudden dropped QRS, often wide QRS (infranodal). Complete heart block: P waves and QRS independent; escape may be narrow (junctional) or wide (ventricular, slower, less stable). 2:1 block cannot be typed from PR alone.

Why it matters: Infranodal block can collapse to ventricular standstill. Atropine often fails when the escape is wide.

Action: ABCs, pads on, atropine 1 mg while preparing transcutaneous pacing if unstable. Dopamine/epinephrine infusion per ACLS if needed. Look for reversible causes: hyperK, ischemia (especially inferior vs anterior), Lyme, beta-blocker/calcium-channel/digoxin, post-cardiac surgery. Transvenous pacing / cardiology for persistent infranodal block.

Caution: Isorhythmic dissociation is not complete heart block. Do not send Mobitz II home because the patient “looks well” in the chair. Treat suspected hyperkalemia promptly while preparing pacing and circulatory support; do not delay stabilization of an unstable patient.

CriticalMimics

Low Voltage & Electrical Alternans

Tamponade warning

Leads: All leads; QRS amplitude beat-to-beat

Criteria: Low voltage: QRS < 5 mm in every limb lead or < 10 mm in every precordial lead. Electrical alternans: beat-to-beat QRS (sometimes P/T) amplitude change. Low voltage + alternans + sinus tachycardia raises concern for a large effusion and warrants prompt assessment for tamponade.

Why it matters: A large effusion can cause alternans through cardiac motion; alternans also occurs with tachyarrhythmias and other mechanisms and does not prove tamponade. Low voltage alone has a wide differential (COPD, obesity, infiltrative disease, anasarca).

Action: Bedside echo now. If tamponade physiology: IV fluid while arranging pericardiocentesis (or the local surgical pathway if type A dissection / post-op). Do not delay for a formal lab ECG repeat.

Caution: Electrical alternans is an insensitive clue and is not exclusive to tamponade. A normal ECG does not exclude tamponade; integrate hemodynamics and echocardiographic findings.

The jobRead the patient first — then read the tracing systematically.

Unstable? Treat the patient. Do not delay defibrillation or cardioversion for a prettier 12-lead.
Is the tracing usable? Speed 25 mm/s, gain 10 mm/mV, limbs not reversed, V1/V2 in the 4th intercostal space.
Branch the rhythm: rate · regular vs irregular · narrow vs wide QRS.
Scan the killers: OMI/STEMI equivalents, hyperK, VT, high-grade AV block, pre-excited AF, QTc ≥500 ms, Type 1 Brugada.
Pull an old ECG and repeat the tracing if symptoms persist, migrate, or return.

The ED ECG is a decision tool, not wallpaper. First: is the patient perfusing, and is this tracing technically real? Then branch the rhythm (rate, regularity, QRS width) and hunt the patterns that change management now — occlusion MI and its equivalents, hyperkalemia, unstable bradycardia or VT, pre-excited AF, and a dangerously long QT. Millimetre STEMI criteria still drive many cath-lab activations, but they miss a large fraction of acute coronary occlusions; that is the OMI skill. New or presumed-new LBBB alone is not a STEMI equivalent (2025 ACC/AHA/ACEP ACS). Compare with an old tracing and repeat the ECG if symptoms evolve.

These findings should move the patient to a different lane now.

Shock, pulmonary edema, severe ischemic pain, or altered mentation with any concerning tracing
STEMI millimetre criteria or an OMI equivalent (Wellens, de Winter, posterior, Smith-modified Sgarbossa, hyperacute T)
Wide-complex tachycardia — treat as VT until proven otherwise
Pre-excited AF (irregular, wide, very fast) — avoid AV-nodal blockers and IV amiodarone
Sine-wave, widening QRS, or disappearing P waves — hyperkalemia until proven otherwise
Complete heart block, Mobitz II, or long pauses
QTc ≥500 ms, pause-dependent polymorphic VT, or TdP
Type 1 Brugada pattern, especially with syncope or fever
Low voltage plus electrical alternans plus tachycardia — tamponade until echo says otherwise

Clinical Pearls

Patient first: an unstable wide-complex rhythm is shocked or cardioverted — the 12-lead can wait.
STEMI millimetres still activate labs; OMI equivalents catch the occlusions those millimetres miss.
New LBBB alone is not a STEMI equivalent (2025 ACC/AHA/ACEP). Use Smith-modified Sgarbossa.
Isolated STD V1–V3 with upright T waves is posterior OMI until V7–V9 are placed.
Bizarre, wide, slow, unclassifiable = hyperkalemia until calcium has gone in.
Irregular, wide and very fast raises concern for pre-excited AF: avoid AV-nodal blockers and IV amiodarone; seek expert rhythm treatment.
Territorial STE plus reciprocal STD is OMI, even if the STE is concave.

Pitfalls

Activating the lab for isolated new LBBB, or discharging Wellens because the patient is pain-free.
Calling aVR STE + diffuse STD automatic code STEMI in a stable, shocked, or hypoxic patient.
Treating VT as SVT with diltiazem or verapamil.
Skipping V4R in inferior STE and then giving nitrates to an RV infarct.
Trusting a machine QTc on tachycardia, artifact, or a wide QRS.
Labelling territorial STE “pericarditis” because it is concave.
Waiting for the potassium result on a sine-wave tracing.

PRACTICE REFRESHER

Rapid recall

Test your first action and the dangerous patterns before revealing the answer.

01 · First move

The patient is hypotensive with a wide-complex tachycardia. What happens before a prettier 12-lead?

02 · Killer patterns

Name three ECG patterns that should change management in the next minutes.

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Capture a weak point, a teaching pearl, or a question to take to your next shift.

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Selected guidance · source check 2026-09-07. These 5 source links support selected teaching points, not a complete review of this topic. Check population, setting and local protocol before applying a recommendation.

Rosen's Emergency Medicine, 10th ed. (2023) — ECG, ACS, dysrhythmia, and toxicology chapters
Fifth Universal Definition of Myocardial Infarction (2026) — current standard-lead ischemia/infarction criteria
Fourth Universal Definition of Myocardial Infarction (2018) — supplemental posterior/right-sided lead placement and thresholds
2025 ACC/AHA/ACEP ACS Guideline (new LBBB is not a STEMI equivalent; high-risk NSTE-ACS including aVR STE)
2023 ESC ACS Guidelines
Smith-modified Sgarbossa (Smith, Pendell Meyers, and OMI literature 2012–2026)
AHA ACLS: unstable tachycardia/bradycardia, hyperkalemia, and TdP
AHA/ACCF/HRS ECG standardisation Parts III–IV (Surawicz et al., Rautaharju et al., 2009) — QRS/BBB criteria, QT measurement method and limits
Educational ECG libraries: LITFL, Dr. Smith’s ECG Blog — pattern recognition adjuncts, not protocols

Diagrams above are original teaching drawings. For real 12-lead tracings see LITFL ECG Library — free for non-profit education with credit to litfl.com (CC BY-NC-SA 4.0).