EKG Library

Classic ECG patterns with teaching points and management pearls

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All Patterns

Full ECG pattern library — ischemia, arrhythmia, conduction, electrolytes

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Ischemia

STEMI, NSTEMI, ischaemic patterns, reciprocal changes, equivalents

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Arrhythmia

AFib, VT, SVT, WPW, flutter, bradycardias, tachycardias

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Conduction

AV blocks, LBBB, RBBB, fascicular blocks, hemiblocks

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Electrolytes

Hyperkalemia, hypokalemia, hypocalcemia, hypomagnesemia

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Normal Variants

Patterns that look abnormal but are benign — critical to recognize

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Select a category above

Choose All Patterns or a specific category to browse the EKG library

Anterior STEMI

Essential Ischemia

ST elevation ≥2mm in V1–V4 (anterior leads). Loss of R wave progression. Q waves may develop if presentation is delayed. Reciprocal ST depression in inferior leads (II, III, aVF).

STE V1–V4 Reciprocal II/III/aVF Loss R progression Q waves late

📚 Teaching: The LAD supplies approximately 40–50% of the left ventricle. Anterior STEMI has the highest mortality of all STEMI locations. Time is muscle — every 30-minute delay increases mortality by 7.5%.

Management

→Activate cath lab immediately

→Door-to-balloon time <90 min

→Dual antiplatelet + anticoagulation

Inferior STEMI

Essential Ischemia

ST elevation ≥1mm in II, III, aVF. ST elevation III > II suggests RCA occlusion. Reciprocal ST depression in I and aVL. Check V4R for RV involvement.

STE II/III/aVF III > II = RCA Reciprocal I/aVL Check V4R

📚 Teaching: Always get right-sided leads (V4R) in inferior STEMI. ST elevation in V4R confirms RV involvement. RV infarction requires volume loading, NOT nitroglycerin (drops preload and causes hypotension).

Management

→Get V4R for RV involvement

→Avoid nitrates if RV involved

→Volume resuscitation if hypotensive

Lateral STEMI

Essential Ischemia

ST elevation in I, aVL, V5–V6. Reciprocal depression in inferior leads (II, III, aVF). May be subtle — LCx occlusion is often missed on standard 12-lead.

STE I/aVL/V5-V6 Reciprocal inferior LCx territory Often subtle

📚 Teaching: LCx occlusion is the most commonly missed STEMI because it may only show subtle lateral changes or posterior changes. If clinical suspicion is high but standard ECG is nondiagnostic, get posterior leads (V7–V9).

Management

→Consider posterior leads V7–V9

→Serial ECGs if initial nondiagnostic

→Low threshold for cath

Wellens Syndrome

Advanced Ischemia

Biphasic (Type A) or deeply inverted (Type B) T waves in V2–V3. Occurs in pain-FREE interval. No significant ST elevation. Preserved R waves (no Q waves yet).

Biphasic/deep T V2-V3 Pain-free pattern No STE Preserved R waves

📚 Teaching: Wellens syndrome is a warning sign of critical proximal LAD stenosis. These patients often feel fine when the pattern is seen. Stress testing is CONTRAINDICATED — it may precipitate complete occlusion and anterior MI.

Management

→Urgent cardiology consult

→Plan for angiography — no discharge

→NO STRESS TEST (contraindicated)

de Winter T-Waves

Advanced Ischemia

Upsloping ST depression at J-point in V1–V6. Tall, symmetric T waves in precordial leads. Slight ST elevation in aVR. No classic ST elevation — this is a STEMI equivalent.

Upsloping STD J-point Tall symmetric T waves STE in aVR No classic STE

📚 Teaching: Found in ~2% of acute LAD occlusions. This is a STEMI equivalent — do not wait for classic ST elevation. Requires emergent cath lab activation. Often missed because providers look for ST elevation.

Management

→Activate cath lab — STEMI equivalent

→This IS an acute LAD occlusion

→Do not wait for classic STE

Atrial Fibrillation

Essential Arrhythmia

Irregularly irregular R-R intervals with no discrete P waves. Fibrillatory baseline (f waves), especially in V1. Variable ventricular rate.

Irreg. irregular No P waves Fibrillatory baseline Variable rate

📚 Teaching: AF management triad: (1) Rate control, (2) Rhythm control consideration, (3) Anticoagulation based on CHA₂DS₂-VASc score. Per 2025 guidelines, early rhythm control may improve outcomes in recent-onset AF.

Management

→CHA₂DS₂-VASc for anticoagulation

→Cardioversion if <48h (or anticoagulated)

→Rule out reversible causes

Atrial Flutter

Essential Arrhythmia

Sawtooth flutter waves at ~300 bpm. Best seen in inferior leads (II, III, aVF). Regular ventricular rate — typically 150 bpm with 2:1 block. Flutter waves may be hidden in QRS/T waves.

Sawtooth waves ~300/min Regular rate (150 = 2:1) Best in inferior leads Flutter may hide in QRS

📚 Teaching: A regular tachycardia at exactly 150 bpm should ALWAYS raise suspicion for atrial flutter with 2:1 block. Flutter waves may be hidden — adenosine can unmask them by transiently blocking the AV node.

Management

→Adenosine to unmask (diagnostic)

→Rate control: beta-blocker or CCB

→Cardioversion + anticoagulation

Ventricular Tachycardia

Essential Arrhythmia

Wide complex tachycardia (QRS >120ms). Rate typically 150–250 bpm. AV dissociation — independent P waves (if visible). Fusion beats and capture beats (pathognomonic).

Wide QRS >120ms Rate 150–250 AV dissociation Fusion/capture beats

📚 Teaching: Rule #1: Wide complex tachycardia is VT until proven otherwise. Treating SVT with aberrancy as VT is safe. Treating VT as SVT (with adenosine or CCBs) can be fatal. When in doubt, it is VT.

Management

→Unstable: immediate cardioversion

→Stable: amiodarone or procainamide

→Do NOT give adenosine if VT suspected

LBBB

Essential Conduction

QRS ≥120ms. Broad notched R wave in I, aVL, V5–V6 (mnemonic: WiLLiaM). Deep S wave in V1–V3. No septal Q waves in lateral leads. Appropriate ST-T discordance.

QRS ≥120ms Broad R I/aVL/V5-6 Deep S in V1-V3 No septal Q waves

📚 Teaching: LBBB masks typical STEMI findings. New LBBB + chest pain = STEMI equivalent → activate cath lab. In old LBBB, use Sgarbossa/Smith modified criteria to detect superimposed MI.

Management

→New LBBB + chest pain = STEMI

→Sgarbossa criteria for old LBBB

→Compare to prior ECG

RBBB

Essential Conduction

QRS ≥120ms. rsR' pattern in V1–V2 (M-shaped, "rabbit ears"). Wide slurred S wave in I and V5–V6 (mnemonic: MaRRoW). ST-T changes opposite to terminal QRS deflection.

QRS ≥120ms rsR' in V1-V2 Wide S in I/V5-6 Discordant ST-T

📚 Teaching: RBBB is often benign in the absence of heart disease. However, new RBBB + chest pain is concerning. Can still assess ST changes in non-affected leads. Look for associated LAFB or LPFB (bifascicular block).

Management

→New RBBB + chest pain = concerning

→Assess ST in unaffected leads

→Look for bifascicular block

Complete Heart Block

Essential Conduction

Complete AV dissociation — P waves and QRS complexes march independently. Regular P-P intervals, regular R-R intervals. Atrial rate > ventricular escape rate. No relationship between P and QRS.

AV dissociation P and QRS independent Atrial rate > ventricular Escape rhythm

📚 Teaching: In complete heart block, the ventricles are maintained by an escape rhythm. Junctional escape = narrow QRS at 40–60 bpm. Ventricular escape = wide QRS at 20–40 bpm (less reliable, more dangerous). Requires pacing.

Management

→Transcutaneous pacing on standby

→Atropine (often ineffective)

→Emergent transvenous pacing

WPW Pattern

Advanced Conduction

Short PR interval (<120ms). Delta wave — slurred upstroke of QRS. Wide QRS (>100ms). Secondary ST-T changes. Pseudo-infarct Q waves may be present.

Short PR <120ms Delta wave Wide QRS Pseudo-Q waves

📚 Teaching: In AF with WPW (pre-excited AF), the accessory pathway has no rate-limiting properties — very fast ventricular rates (>200 bpm) can occur and degenerate to VF. AV nodal blockers (adenosine, beta-blockers, CCBs, digoxin) are absolutely contraindicated.

Management

→Avoid ALL AV nodal blockers in AF

→Procainamide for rate control

→DC cardioversion if unstable

Hyperkalemia

Essential Electrolytes

Peaked narrow symmetric T waves (early). Prolonged PR, flattened P waves. Progressive QRS widening. Sine wave pattern (pre-arrest). Progression: peaked T → wide QRS → sine wave → VF.

Peaked narrow T waves Flat P waves Wide QRS Sine wave late

📚 Teaching: Hyperkalemia is a great ECG mimicker — can look like STEMI, VT, or asystole. The classic progression: peaked T waves → PR prolongation → P wave loss → QRS widening → sine wave → VF/asystole. Treat early!

Management

→Calcium gluconate (membrane stabilization)

→Insulin + glucose (shift K⁺ in)

→Kayexalate/Lokelma (remove K⁺)

Pericarditis

Essential Ischemia

Diffuse saddle-shaped (concave up) ST elevation in all leads except aVR and V1 (which show ST depression). PR depression — specific sign. No focal reciprocal changes. Spodick sign: downsloping TP segment.

Diffuse saddle STE PR depression No reciprocal changes Spodick sign

📚 Teaching: Key differentiators from STEMI: (1) Diffuse STE without focal reciprocal depression, (2) PR depression in II and lateral leads, (3) Concave/saddle-shaped ST, (4) Clinical context — pleuritic, positional pain. When in doubt, treat as STEMI.

Management

→NSAIDs + colchicine (first-line)

→Echo to rule out effusion

→Consider STEMI if any doubt

Posterior STEMI

Advanced Ischemia

ST depression in V1–V3 with tall, broad R waves in V1 (mirror image of posterior wall injury). May have upright T waves in V1-V2. Often accompanies inferior STEMI. Confirm with posterior leads V7–V9.

STD + tall R in V1-V3 Mirror image STE Often with inferior STEMI Confirm V7-V9

📚 Teaching: Posterior STEMI is the most commonly missed MI because the standard ECG shows only reciprocal (mirror image) changes. The clue: horizontal ST depression + tall R in V1-V2. Simply flip the ECG upside-down and mirror image — you will see classic STE.

Management

→Order posterior leads V7-V9

→Treat as STEMI if confirmed

→Avoid missing this — LCx or RCA

Brugada Syndrome

Advanced Arrhythmia

Type 1 (diagnostic): Coved ST elevation ≥2mm with downsloping morphology in V1–V2, followed by negative T wave. RBBB-like pattern. Types 2 and 3 are saddle-shaped — NOT diagnostic without provocation testing.

Coved STE ≥2mm V1-V2 Negative T wave RBBB-like pattern Unmask with fever/NaChannel blockers

📚 Teaching: Brugada is a channelopathy (SCN5A mutation, ~30% of cases). Fever, sodium channel blockers, and cocaine can UNMASK the pattern. Always ask: did the patient have syncope? Family history of sudden death? These are high-risk features requiring EP referral.

Management

→EP referral for risk stratification

→Avoid fever (antipyretics aggressively)

→ICD if high risk or symptomatic

SVT / AVNRT

Essential Arrhythmia

Regular narrow complex tachycardia at 140–280 bpm. P waves absent or hidden in QRS (AVNRT) or immediately after QRS (AVRT). Pseudo-R' in V1 or pseudo-S in inferior leads — retrograde P waves. Abrupt onset and termination.

Regular narrow tachycardia Rate 140-280 No/retrograde P waves Pseudo-R in V1

📚 Teaching: AVNRT is the most common regular SVT. The retrograde P wave is buried in the QRS, producing a pseudo-R' in V1 or pseudo-S in inferior leads. Vagal maneuvers first, then adenosine. Always compare to prior ECG for delta wave (WPW).

Management

→Vagal maneuvers first (modified Valsalva)

→Adenosine 6mg IV push

→Cardioversion if unstable

Mobitz I (Wenckebach)

Essential Conduction

Progressive PR prolongation with each beat until a P wave is non-conducted (dropped QRS). PR is shortest after the dropped beat. Group beating pattern. PP interval constant; RR interval progressively shortens before the drop.

Progressive PR lengthening Dropped QRS (non-conducted P) Shortest PR after drop Group beating

📚 Teaching: Wenckebach is a benign AV block located at the AV node. Common in athletes (high vagal tone), inferior MI, digitalis toxicity. Almost never requires pacing. Often intermittent — look for the group beating pattern.

Management

→Usually no treatment required

→Monitor for progression

→Atropine if symptomatic

Mobitz II

Essential Conduction

Constant PR interval with sudden unexpected non-conducted P wave (dropped QRS). Often has wide QRS (infranodal block). PR never lengthens before the drop. May have 2:1, 3:1, or higher degree block.

Constant PR Sudden dropped QRS Often wide QRS Infranodal block

📚 Teaching: Mobitz II is a dangerous AV block located below the Bundle of His. High risk of sudden progression to complete heart block. Wide QRS is common (RBBB or LBBB morphology). Requires pacemaker placement — even if asymptomatic.

Management

→Cardiology/EP consult urgently

→Prepare for temporary pacing

→Permanent pacemaker required

LVH with Strain

Essential Conduction

Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35mm. Cornell: R in aVL ≥11mm (or R aVL + S V3 ≥28mm men). Strain pattern: ST depression + T-wave inversion in lateral leads (I, aVL, V5-V6).

S(V1)+R(V5/V6) ≥35mm R in aVL ≥11mm Lateral ST depression ST-T discordance

📚 Teaching: LVH strain pattern is secondary repolarization abnormality — NOT primary ischemia. However, strain pattern significantly increases cardiovascular risk. Always evaluate for underlying cause: hypertension (most common), aortic stenosis, HCM. May obscure ischemic changes.

Management

→Evaluate for HTN, aortic stenosis, HCM

→Echo for structural assessment

→BP control reduces LVH over time

Pulmonary Embolism

Advanced Arrhythmia

Sinus tachycardia (most common finding). S1Q3T3 pattern (S wave in I, Q wave in III, inverted T in III) — classic but insensitive (~20%). New RBBB. T-wave inversions in V1–V4. Right axis deviation. AF or flutter.

Sinus tachycardia (most common) S1Q3T3 (classic, insensitive) New RBBB TWI V1-V4 (RV strain)

📚 Teaching: The ECG in PE is frequently normal or just shows sinus tachycardia. S1Q3T3 is specific but only present in ~20% of cases. The most diagnostically useful pattern is new RBBB or T-wave inversions V1-V4 with sinus tachycardia — suggests RV strain from massive PE.

Management

→CT pulmonary angiography is gold standard

→Anticoagulation if high probability

→Thrombolytics if massive PE + hemodynamic compromise

Hypokalemia

Essential Electrolytes

T wave flattening (T amplitude <1mm in limb leads). Prominent U waves (especially V2–V3) — may exceed T wave amplitude. Apparent QT prolongation (actually QU prolongation). ST depression. In severe cases: wide QRS, VT, torsades.

Flat T waves Prominent U waves (V2-V3) Apparent long QT (QU) ST depression

📚 Teaching: The U wave — a positive deflection after the T wave, best seen in V2–V3 — is the hallmark of hypokalemia. When K⁺ falls below 3.0, risk of torsades rises significantly. Always check magnesium — concurrent hypomagnesemia must be corrected or you cannot correct hypokalemia.

Management

→Replace K⁺ to ≥4.0 mEq/L

→Always check and replace Mg²⁺

→Monitor QTc — risk of torsades

Cardiac Tamponade

Advanced Arrhythmia

Sinus tachycardia. Electrical alternans — alternating QRS amplitude (heart swinging in effusion). Low voltage throughout (QRS <5mm in limb leads, <10mm in precordials). PR depression if associated with pericarditis.

Electrical alternans Low voltage Sinus tachycardia Beck's triad

📚 Teaching: Electrical alternans is SPECIFIC for tamponade — caused by the heart swinging back and forth inside a large pericardial effusion, changing the cardiac axis with each beat. Beck's triad: hypotension, muffled heart sounds, JVD. Immediate pericardiocentesis for tamponade.

Management

→Emergent echocardiogram

→Pericardiocentesis if hemodynamically compromised

→IV fluids as temporizing measure

Torsades de Pointes

Advanced Arrhythmia

Polymorphic VT with QRS complexes twisting around the isoelectric baseline. Preceded by long-short RR sequence (long QTc). Rate 200–250 bpm. Often self-terminating but can degenerate to VF.

Twisting QRS morphology Long-short RR initiator Rate 200-250 Self-terminating often

📚 Teaching: Torsades requires a prolonged QTc substrate (drug-induced, electrolyte, or congenital LQTS). Treatment is magnesium sulfate 2g IV (regardless of serum Mg level) — it works by shortening the QT and suppressing after-depolarizations. AVOID all QT-prolonging drugs.

Management

→Magnesium sulfate 2g IV immediately

→Overdrive pacing if recurrent

→Remove all QT-prolonging drugs

Normal Sinus Rhythm

Essential Normal Variants

Rate 60–100 bpm. Regular P waves before every QRS. P-wave axis 0–75° (upright in I and aVF). Constant PR interval 120–200ms. QRS narrow (<120ms). This is the baseline against which all abnormalities are compared.

Rate 60-100 bpm P before every QRS PR 120-200ms QRS <120ms

📚 Teaching: Every abnormality you will ever see on an ECG is defined relative to normal sinus rhythm. Know this pattern deeply — rate, rhythm, P morphology, PR, QRS, QT, and ST baseline. Most ECGs you will read in practice are normal or near-normal.

Management

→No treatment required

→Establish your baseline knowledge

→Document clearly as "Normal sinus rhythm"

Sinus Arrhythmia

Essential Normal Variants

Phasic variation in R-R interval >160ms or >10% with respiration. P wave morphology constant — same P before every QRS. Rate increases on inspiration (vagal withdrawal), decreases on expiration.

Variable R-R with breathing Constant P morphology Rate ↑ inspire / ↓ expire Young/athletes common

📚 Teaching: Sinus arrhythmia is a physiological variant, most prominent in young adults and athletes. The P-wave morphology is constant — this is the key feature distinguishing it from atrial ectopics. If you can't see the P waves, compare inspiration vs expiration — the rate variation reveals the mechanism.

Management

→No treatment required

→Reassure patient — benign

→Document: physiological variant

Early Repolarization

Essential Normal Variants

J-point elevation 1–3mm in lateral leads (I, aVL, V4–V6) with concave upward ST. Slurred or notched J point (fishhook). T waves remain upright and tall. Common in young males and athletes.

J-point STE 1-3mm lateral Concave (smiley) ST Notched J point Young male/athlete

📚 Teaching: Early repolarization is one of the most important normal variants — it is the most common cause of ST elevation misdiagnosed as STEMI. Key differentiators from STEMI: (1) Diffuse lateral, not focal, (2) Concave (smiley face) ST, not convex (frowning), (3) Tall T waves in same leads as STE, (4) No reciprocal depression, (5) Stable on serial ECGs. However, inferolateral ER in older patients with syncope carries slight risk.

Management

→No treatment for typical ER

→Serial ECGs if acute presentation

→Compare to prior ECG always

Athlete's Heart

Essential Normal Variants

Sinus bradycardia (HR 40–60 bpm). Increased QRS voltage (LVH by voltage criteria). Incomplete RBBB. Early repolarization pattern. First-degree AV block. Sinus arrhythmia. All due to increased vagal tone and cardiac remodeling.

Sinus bradycardia High voltage (vagal/LVH) Incomplete RBBB Sinus arrhythmia/1° AVB

📚 Teaching: Athlete's heart is a collection of ECG findings caused by intense endurance training — high vagal tone and structural cardiac adaptation. None of these findings are pathological in a true athlete. The challenge is distinguishing athlete's heart from genuine HCM or channelopathy. Key: athletic ECG findings normalize after deconditioning; pathological findings do not. International criteria (2017 Seattle Criteria, 2017 International Criteria) guide interpretation.

Management

→No treatment required

→Use Seattle/International criteria

→Deconditioning test if uncertain

Juvenile T-Wave Pattern

Essential Normal Variants

T-wave inversions in V1–V3 (or V1–V4) in patients under 30. Normal variant in children. Should resolve by adulthood. T-wave inversions isolated to right precordial leads with no other abnormality.

TWI V1-V3 (young patients) Normal in children Resolves by adulthood No other abnormality

📚 Teaching: Juvenile T-wave pattern is a normal variant in children that persists into young adulthood in some individuals, especially women. It becomes abnormal if it extends beyond V3 or appears de novo in an adult. When you see T-wave inversions in V1–V3 in a young patient with no symptoms — consider this variant before diagnosing RV strain, ischemia, or Brugada.

Management

→Benign in children/young adults

→Abnormal if >V3 in adults

→Serial ECG and comparison to prior

Benign Notched QRS

Essential Normal Variants

Slurring or notching of the QRS complex in one or two leads without meeting RBBB or LBBB criteria. QRS duration <120ms. Most common in V3–V4. No association with axis deviation or ST changes.

QRS slurring/notching QRS <120ms (not BBB) 1-2 leads only No ST changes

📚 Teaching: QRS notching is extremely common and usually has no clinical significance. It becomes relevant only if the QRS is ≥120ms (then it is a bundle branch block) or if there is delta wave morphology (then consider pre-excitation). Isolated QRS notching in a young asymptomatic patient requires no workup.

Management

→No treatment required

→Confirm QRS <120ms

→Not a bundle branch block

Voltage Criteria for LVH (False Positive)

Advanced Normal Variants

Tall QRS voltage meeting LVH criteria (S V1 + R V5/V6 ≥35mm) in a young, thin patient without structural disease. Normal PR, narrow QRS. No ST-T changes. Normal axis.

High QRS voltage Meets Sokolow-Lyon criteria No strain pattern Young/thin patients

📚 Teaching: Voltage criteria for LVH have poor specificity — up to 50% of young thin adults and athletes meet voltage criteria without true LVH. Actual LVH requires repolarization changes (strain pattern) or echocardiographic confirmation. Never diagnose LVH on voltage alone in a young patient without corroborating evidence.

Management

→Voltage alone is insufficient

→Need echo for true LVH diagnosis

→Young thin patients: likely normal

TCA / Sodium Channel Blocker Toxicity

Advanced Arrhythmia

Sinus tachycardia + wide QRS (>100ms) + terminal R wave in aVR ≥3mm + right axis deviation. QT prolongation. Anticholinergic features (tachycardia, dry skin, dilated pupils). Caused by TCAs, cocaine, flecainide, propafenone.

Wide QRS (>100ms) Terminal R in aVR ≥3mm Sinus tachycardia Right axis deviation

📚 Teaching: The terminal R wave in aVR is the most specific ECG sign of TCA toxicity (Na+ channel blockade). QRS >100ms = high seizure risk; QRS >160ms = high VF risk. Sodium bicarbonate IV narrows the QRS and reverses toxicity by two mechanisms: (1) alkalinization shifts the drug from Na+ channels, (2) extra sodium load restores conduction. Target pH 7.45–7.55.

Management

→IV sodium bicarbonate 1–2 mEq/kg

→Target QRS <100ms and pH 7.45–7.55

→Avoid Class IA/IC antiarrhythmics

Digoxin Toxicity

Advanced Electrolytes

Characteristic scooped/sagging ST depression ("Salvador Dalí moustache") in lateral leads. Bidirectional VT (alternating QRS axis — nearly pathognomonic). Bradyarrhythmias, PAT with block, accelerated junctional rhythm. Baseline digoxin effect: short QT + scooped ST.

Scooped ST ("Dalí moustache") Bidirectional VT (pathognomonic) Bradyarrhythmias Any arrhythmia possible

📚 Teaching: Digoxin toxicity is a common clinical emergency — especially in elderly patients with renal impairment, hypokalemia, or drug interactions (clarithromycin, amiodarone, verapamil double digoxin levels). The bidirectional VT (beat-to-beat alternating QRS axis from alternating fascicular activation) is essentially pathognomonic. Avoid calcium in digoxin toxicity (worsens Ca2+ overload). Do NOT cardiovert — risks precipitating refractory VF.

Management

→Digibind (Fab antibodies) — definitive

→Hold digoxin, correct K+/Mg2+

→Avoid calcium and cardioversion

Drug-Induced Long QT

Advanced Electrolytes

Prolonged QTc (>500ms or increase >60ms from baseline). T-wave changes: broadening, notching, bifid morphology. U waves. "Short-long-short" sequence triggers Torsades (PVC → pause → long QT → TdP). Major culprits: class IA/III antiarrhythmics, macrolides, fluoroquinolones, antipsychotics, methadone, antiemetics (ondansetron).

QTc >500ms T-wave notching/broadening U waves visible Short-long-short trigger

📚 Teaching: Drug-induced QT prolongation is the leading cause of drug withdrawal from the market. The "short-long-short" sequence triggers TdP: a PVC creates a compensatory pause (short-long), and the next sinus beat lands on a prolonged QT (setting up TdP). Risk factors: bradycardia, hypokalemia, hypomagnesemia, renal/hepatic failure, female sex (longer baseline QTc), structural heart disease. Check CredibleMeds (www.crediblemeds.org) before combining multiple QT-prolonging drugs.

Management

→Magnesium sulfate 2g IV (first-line)

→Stop ALL QT-prolonging drugs

→Correct K+ (target >4.5 mEq/L)

🔺

ST Elevation

STEMI, pericarditis, BER, de Winter, Wellens, LV aneurysm

📉

ST Depression

Subendocardial ischaemia, reciprocal changes, digoxin, RVH strain

⚡

Arrhythmias

AFib, VT, SVT, WPW, atrial flutter, torsades, AVNRT

🔗

Heart Blocks

1°/2°/3° AV block, SA block, escape rhythms, BBB

📐

Morphology

LVH, RVH, LBBB, RBBB, P-wave changes, axis deviation

⏱

Intervals

QT prolongation, short QT, PR changes, Brugada pattern, delta waves

🧪

Metabolic

Hyperkalemia, hypokalemia, hypercalcemia, drug effects on ECG

🔬

Select a category above

Choose a differential category to browse ECG criteria and teaching pearls

STEMI — ST-Elevation Myocardial Infarction

⚠ CRITICAL ▾

Diagnostic Criteria

≥1 mm STE in ≥2 contiguous limb leads (I+aVL, II+III+aVF)
≥2 mm STE in V2–V3 (men ≥40 yrs); ≥2.5 mm (men <40 yrs); ≥1.5 mm (women)
New LBBB in setting of chest pain = STEMI equivalent
Reciprocal ST depression in mirror territory (high sensitivity)

Territory / Vessel

Inferior (II, III, aVF) — RCA (80%) or LCx; always check V3R/V4R for RV involvement
Anterior (V1–V4) — LAD; proximal = wider territory + worse prognosis
Lateral (I, aVL, V5–V6) — LCx or diagonal; may be high lateral only (I + aVL)
Posterior — Look for tall R + ST depression V1–V3 (mirror); confirm V7–V9
aVR elevation + diffuse ST↓ — Left main or 3-vessel disease; emergent cath

Pearl: The bigger the territory, the more leads involved. Inferior + lateral STE = wrap-around LCx or dominant RCA. Always check for RV MI with inferior STEMI (STE V1 + V3R/V4R → RV; treat with fluids, avoid nitrates).

Wellens' Syndrome — Critical LAD Stenosis

⚠ CRITICAL ▾

Diagnostic Criteria

Type A: Biphasic T waves in V2–V3 (initial positive deflection → negative)
Type B: Deep symmetric T-wave inversion in V2–V3 (more common, ≥2mm)
ECG change seen during pain-FREE interval (ominous — reperfusion pattern)
No significant Q waves, minimal STE, preserved R waves

Pearl: Wellens' is a pre-infarction warning. Do NOT stress test — risk of massive anterior MI. Needs urgent angiography. Missing it = potentially fatal delay. The T changes represent intermittent LAD reperfusion after near-total occlusion.

de Winter T-Wave — Proximal LAD Occlusion

⚠ CRITICAL ▾

Diagnostic Criteria

Upsloping ST depression ≥1mm at J-point in V1–V6
Tall, prominent, symmetrically positive T waves following the depression
STE in aVR (reciprocal to diffuse anterior ischaemia)
No classic STE in any precordial lead (STEMI equivalent)

Pearl: de Winter pattern = proximal LAD occlusion in ~2% of anterior MIs. The cath lab team may not recognise it as a STEMI — YOU must call it. Treat as cath lab activation. Static pattern (unlike Wellens', it doesn't evolve).

Acute Pericarditis

▲ HIGH ▾

Diagnostic Criteria

Diffuse saddle-shaped STE in multiple leads (spares V1, aVR)
PR depression in same leads that have STE (reciprocal PR elevation in aVR)
No reciprocal ST depression (unlike STEMI)
T-wave inversion appears AFTER STE resolves (unlike STEMI where it appears during)
Spivak's sign: STE/T-wave amplitude ratio >0.25 in V6 → pericarditis

Pearl: 4 stages of pericarditis ECG: (1) diffuse STE + PR↓; (2) STE normalises; (3) T inversion; (4) normalisation. If effusion develops, look for low voltage + sinus tachycardia + electrical alternans (tamponade triad).

Brugada Pattern (Type 1)

▲ HIGH ▾

Diagnostic Criteria

Type 1 (diagnostic): Coved ST elevation ≥2mm + T-wave inversion in V1–V2
Type 2 (saddle-back): STE ≥2mm + positive/biphasic T wave — requires provocation
Spontaneous Type 1 = high risk; drug-induced or fever-unmasked = intermediate
RBBB morphology pattern (incomplete or complete)

Pearl: Brugada is a sodium channelopathy (SCN5A mutation). Fever unmasks it — check ECG during febrile illness in all young VF survivors. High intercostal lead placement (V1–V2 in 2nd/3rd ICS) increases sensitivity. ICD if symptomatic.

Early Repolarisation (Benign / High-Risk)

✓ NOTE ▾

Diagnostic Criteria

J-point elevation ≥1mm in ≥2 contiguous leads
Notching or slurring at end of QRS (J-wave or Osborn wave)
Most prominent V2–V5; concave STE; T waves often tall and upright
High-risk features: inferior + lateral distribution, horizontal/descending ST, amplitude ≥2mm

Pearl: Most early repolarisation is benign (seen in young athletes, African Americans). High-risk variant: inferior leads + horizontal ST slope + amplitude ≥2mm — associated with idiopathic VF. If VF survivor with this pattern, ICD evaluation needed.

NSTEMI / Unstable Angina

⚠ CRITICAL ▾

Diagnostic Criteria

Horizontal or downsloping ST depression ≥0.5mm in ≥2 contiguous leads
Dynamic changes: new ST depression during chest pain that resolves with relief
Troponin elevated (NSTEMI) vs normal (UA)
T-wave inversion in multiple leads is common

Pearl: Upsloping ST depression is generally benign; horizontal and downsloping are concerning. The deeper and more widespread, the more likely significant ischaemia. Serial ECGs and troponins are essential — a single normal ECG does NOT rule out ACS.

Posterior STEMI (Reciprocal Pattern)

⚠ CRITICAL ▾

Diagnostic Criteria

Horizontal ST depression V1–V3 (mirror image of posterior STE)
Tall, broad, upright R wave in V1 (mirror of posterior Q wave)
Tall upright T wave in V1–V2 (mirror of posterior T inversion)
Confirm with V7–V9: STE ≥0.5mm diagnostic

Pearl: Posterior MI is the most commonly missed STEMI. Any V1–V3 "NSTEMI" pattern with tall R in V1 should prompt posterior leads. Flip V1–V3 upside down — you'll see a STEMI. RCA or LCx territory. Often coexists with inferior STEMI.

LVH Strain Pattern

◆ CONSIDER ▾

Diagnostic Criteria

ST depression + T-wave inversion in lateral leads (I, aVL, V5–V6)
Seen in leads with tall R waves (strain is discordant — depression in high R leads)
Voltage criteria for LVH present (Sokolow-Lyon, Cornell)
Concave or downsloping morphology of T-wave inversion

Pearl: LVH strain = secondary repolarisation change from prolonged pressure overload. It does NOT indicate ischaemia by itself. But when a patient with known LVH presents with chest pain, new or dynamic strain changes should raise concern for superimposed ischaemia.

Digoxin Effect ("Salvador Dali" sign)

— NOTE ▾

Diagnostic Criteria

Scooped (Salvador Dali moustache) downsloping ST depression in lateral leads
Shortened QT interval (digoxin effect, not toxicity)
Flattened or inverted T waves in same lateral leads
PR prolongation common

Pearl: Digoxin effect ≠ toxicity. Effect = therapeutic level producing characteristic ECG changes. Toxicity = elevated serum levels causing arrhythmias (PAT with block, regularised AFib, ventricular bigeminy/trigeminy). Hypokalemia potentiates toxicity.

Left Main / 3-Vessel Disease

⚠ CRITICAL ▾

Diagnostic Criteria

aVR ST elevation ≥1mm (reflecting subendocardial ischaemia of LMCA territory)
Diffuse ST depression in multiple leads (≥6 leads) simultaneously
ST depression maximal in V4–V6 (subendocardial circumferential ischaemia)
May have anterior STE + diffuse lateral ST depression

Pearl: aVR is the "forgotten lead" that faces the right shoulder / left main ostium. Elevation here mirrors diffuse subendocardial ischaemia. aVR STE + diffuse depression = left main or proximal LAD or 3-vessel disease. Needs emergent cath.

Atrial Fibrillation

◆ CONSIDER ▾

Diagnostic Criteria

Irregularly irregular R-R intervals (no two consecutive RR intervals equal)
No distinct P waves — replaced by fibrillatory (f) waves of varying amplitude/frequency
Atrial rate 400–600 bpm (f waves), ventricular rate variable 100–180 bpm (uncontrolled)
QRS usually narrow; wide if BBB, accessory pathway, or aberrant conduction

Pearl: Irregularly irregular rhythm + absent P waves = AFib until proven otherwise. Pre-excited AFib (WPW + AFib) is life-threatening — NEVER give AV nodal blockers (adenosine, diltiazem, digoxin, amiodarone) → facilitates accessory pathway conduction → VF. Cardiovert immediately.

Atrial Flutter

◆ CONSIDER ▾

Diagnostic Criteria

Sawtooth flutter waves (F waves) at ~300 bpm in II, III, aVF (inverted) and V1 (upright)
Regular or regularly irregular ventricular rate (usually 2:1 = 150 bpm)
2:1 block: ventricular rate ~150 bpm → ALWAYS think flutter first
Variable block: 3:1, 4:1, or Wenckebach-type variable conduction

Pearl: Rate exactly 150 bpm = atrial flutter with 2:1 block until proven otherwise. The flutter waves may be buried in the QRS — use adenosine (slow conduction, unmask F waves transiently). Carotid sinus massage has same unmasking effect.

Multifocal Atrial Tachycardia (MAT)

◆ CONSIDER ▾

Diagnostic Criteria

≥3 distinct P wave morphologies in the SAME lead
Irregular R-R intervals (can mimic AFib, but P waves ARE present)
Heart rate >100 bpm (if <100, called wandering atrial pacemaker)
Isoelectric baseline between P waves (unlike flutter/AFib)

Pearl: MAT = COPD exacerbation or critical illness (sepsis, respiratory failure) until proven otherwise. Multiple ectopic atrial foci firing irregularly due to metabolic stress. Treat the underlying cause. Calcium channel blockers (verapamil) can help rate control. AF cardioversion is ineffective — it's not AFib.

Ventricular Tachycardia (VT)

⚠ CRITICAL ▾

Diagnostic Criteria

Wide complex tachycardia ≥120ms, rate 100–250 bpm
AV dissociation (P waves at different rate from QRS) = pathognomonic of VT
Fusion beats (sinus + ectopic = hybrid QRS) — diagnostic of VT
Capture beats (narrow QRS during wide tachycardia) — diagnostic of VT
Concordance: positive (all precordials same direction) → VT; negative concordance → VT

Pearl: Brugada algorithm: (1) No RS in any precordial? → VT. (2) RS >100ms in any precordial? → VT. (3) AV dissociation? → VT. (4) Classic LBBB/RBBB morphology criteria met? → if not → VT. When in doubt = VT. Treating VT as SVT can be fatal. Wide complex tachycardia in a patient with structural heart disease = VT until proven otherwise.

Junctional Rhythm / AVNRT

◆ CONSIDER ▾

Diagnostic Criteria

Retrograde P waves: inverted in II, III, aVF — may appear before, during, or after QRS
Junctional escape: narrow QRS at 40–60 bpm, no preceding P wave
AVNRT: short RP interval (<70ms); P often buried in QRS (pseudo-R in V1, pseudo-S in II)
AVRT: P wave >70ms after QRS (long RP — retrograde via accessory pathway)

Pearl: AVNRT is the most common paroxysmal SVT in women (2:1 female predominance). Vagal manoeuvres terminate it by blocking AV node. Adenosine 6mg IV → terminates in >90%. Distinguishing AVNRT (short RP) from AVRT (long RP) and atrial tachycardia (variable RP) requires looking at retrograde P wave position.

1st Degree AV Block

✓ NOTE ▾

Diagnostic Criteria

PR interval >200ms (5 small squares) in ALL beats
Every P wave is followed by a QRS (1:1 conduction maintained)
PR interval is constant beat-to-beat

Pearl: 1st degree block is not truly a "block" — every impulse conducts, just slowly. Usually AV nodal disease. Important clinically: PR >300ms can cause "pacemaker syndrome" physiology (atrial kick lost if P overlaps preceding T wave). Lyme carditis classically presents with high-degree AV block.

Mobitz I — Wenckebach AV Block

◆ CONSIDER ▾

Diagnostic Criteria

Progressive PR lengthening with each beat until one QRS is dropped
After dropped beat: PR resets to shortest interval and cycle repeats
RR intervals progressively shorten before the dropped beat (paradox of Wenckebach)
Block is at AV node level — usually benign, rarely progresses

Pearl: Wenckebach is the "kind" 2nd degree block. AV nodal location = responds to atropine, beta-blocker/CCB effect. Common in inferior MI (RCA → AV nodal artery), vagotonic states (athletes, sleep). Usually doesn't need pacing unless symptomatic.

Mobitz II AV Block

⚠ CRITICAL ▾

Diagnostic Criteria

Fixed, constant PR interval — then sudden QRS dropout WITHOUT prior PR lengthening
Block is infra-Hisian (below AV node) — His bundle or bundle branches
QRS often wide (coexisting BBB) due to infra-Hisian disease
Can degenerate unpredictably to complete heart block

Pearl: Mobitz II = pacemaker indication even if asymptomatic. It's an electrical ticking time bomb — can abruptly progress to complete heart block with ventricular escape (20–40 bpm) without warning. Does NOT respond to atropine (infra-Hisian). Seen in anterior MI (LAD → proximal conduction system).

Complete (3°) AV Block

⚠ CRITICAL ▾

Diagnostic Criteria

P waves and QRS march at INDEPENDENT rates (AV dissociation)
Atrial rate > ventricular rate (atria faster, ventricles slower)
Escape rhythm: junctional (40–60 bpm, narrow) or ventricular (20–40 bpm, wide)
No consistent PR relationship — PR interval varies randomly

Pearl: AV dissociation ≠ always complete block (isorhythmic dissociation exists). Complete block: atrial rate ALWAYS faster than ventricular. Use calipers — march out P waves, then QRS separately, confirm they're independent. Wide complex escape = lower, less reliable pacemaker = higher risk = emergent TCP.

WPW — Wolff-Parkinson-White Syndrome

▲ HIGH ▾

Diagnostic Criteria

Short PR interval <120ms (accessory pathway bypasses AV node delay)
Delta wave: slurred initial QRS upstroke (ventricular pre-excitation)
Wide QRS >120ms (fusion of normal + pre-excited ventricular activation)
Secondary ST-T changes discordant with delta wave direction

Accessory Pathway Location

Left lateral: negative delta V1, positive I/aVL
Posteroseptal: negative delta II/III/aVF
Anteroseptal: negative delta V1–V3

Pearl: WPW risk stratification matters. If ERP of accessory pathway <250ms → rapid pre-excited conduction → VF risk. Shortest pre-excited RR in AFib <250ms → high risk → ablation urgently. Avoid AV nodal blockers in pre-excited AFib (adenosine, verapamil, digoxin) — they paradoxically increase ventricular rate via accessory pathway.

Left Bundle Branch Block (LBBB)

▲ HIGH ▾

Diagnostic Criteria (William Morrow — WiLLiaM)

QRS ≥120ms
Broad monophasic R wave in I, aVL, V5–V6 (no septal Q waves)
QS or rS pattern in V1 (broad S wave)
Discordant ST-T changes (ST/T opposite to main QRS deflection)

Sgarbossa Criteria (LBBB + MI)

Concordant STE ≥1mm (ST same direction as QRS) — 5 points
Concordant ST depression ≥1mm in V1–V3 — 3 points
Discordant STE ≥5mm — 2 points (modified: STE/S ratio ≥0.25)
Score ≥3 = highly specific for MI; modified Sgarbossa more sensitive

Pearl: New LBBB + chest pain = STEMI equivalent (activate cath lab). Old LBBB + chest pain = apply modified Sgarbossa. LBBB alone does NOT diagnose ischaemia — it makes it HARDER to see. Without Sgarbossa criteria, the ECG is "uninterpretable for ischaemia" in LBBB.

Right Bundle Branch Block (RBBB)

◆ CONSIDER ▾

Diagnostic Criteria (MaRRoW)

QRS ≥120ms (complete); 110–119ms (incomplete)
RSR' pattern (bunny ears) in V1–V2
Broad, slurred S wave in I, aVL, V5–V6
ST-T discordant with terminal QRS deflection

Pearl: RBBB in the right clinical context: new RBBB post-anterior MI → infra-Hisian disease (LAD territory includes right bundle). RBBB + LAFB = bifascicular block = pacing evaluation if new. RBBB alone in young person with coved STE V1 = Brugada (get sodium channel blocker provocation). PE can cause new RBBB (right heart strain).

Left Ventricular Hypertrophy (LVH)

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Voltage Criteria

Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35mm (or R in aVL ≥11mm)
Cornell voltage: R in aVL + S in V3 >28mm (men) or >20mm (women)
Cornell product: Cornell voltage × QRS duration >2440mm·ms

Associated Features

Left axis deviation (not alone diagnostic)
Lateral strain pattern: ST depression + T inversion in I, aVL, V5–V6
Left atrial enlargement: P-mitrale (notched P ≥120ms in II), negative P terminal V1 >40ms×1mm

Pearl: Voltage criteria have poor sensitivity (~50%) but good specificity (~90%). Increased voltage alone is NOT sufficient — Cornell product or strain pattern greatly increases diagnostic confidence. Young athletes have high voltage from training (athlete's heart) — NOT LVH pathology.

Right Ventricular Hypertrophy (RVH)

◆ CONSIDER ▾

Diagnostic Criteria

Tall R wave in V1 (R:S ratio >1 in V1)
Right axis deviation (>+90°)
Deep S waves in I, aVL, V5–V6
RV strain: ST depression + T inversion V1–V3 (right precordial leads)
P pulmonale: peaked P wave >2.5mm in II (right atrial enlargement)

Pearl: Causes: pulmonary hypertension (chronic), PE (acute), mitral stenosis, COPD (cor pulmonale), congenital (ASD, PS). Acute cor pulmonale (massive PE): S1Q3T3 — S wave in I, Q wave in III, T inversion in III. This is seen in only ~20% of PE — normal ECG does NOT rule out PE.

Prolonged QTc — Torsades de Pointes Risk

▲ HIGH ▾

Diagnostic Criteria

QTc (Bazett: QT/√RR) >440ms men, >460ms women — borderline
QTc >500ms — high risk for Torsades de Pointes (TdP)
TdP on ECG: polymorphic VT with sinusoidal twisting of QRS axis around baseline
Often initiated by short-long-short RR sequence (pause-dependent)

Common Causes (MUDPILES-QT)

Drugs: antipsychotics, macrolides, fluoroquinolones, methadone, antiarrhythmics (IA, III)
Electrolytes: ↓K⁺, ↓Mg²⁺, ↓Ca²⁺
Congenital: Romano-Ward (autosomal dominant), Jervell-Lange-Nielsen (+ deafness)
Acquired: hypothyroidism, hypothermia, severe bradycardia, intracranial events

Pearl: Management: IV magnesium sulfate 2g over 5 min (drug of choice for TdP). Increase heart rate (temporary pacing or isoproterenol) to suppress pause-dependent TdP. Stop all QT-prolonging agents. Correct K⁺ to 4.5–5 mEq/L and Mg²⁺ to 2+ mEq/L.

Short PR — Pre-excitation / WPW

▲ HIGH ▾

Diagnostic Criteria

PR <120ms with delta wave = WPW (accessory AV connection)
PR <120ms WITHOUT delta wave = enhanced AV nodal conduction (LGL pattern)
PR <120ms due to high sympathetic tone (sinus tachycardia) — not pathological

Pearl: WPW delta wave polarity maps to pathway location. Negative delta in V1 → left-sided pathway (commonest). Negative delta in inferior leads → posteroseptal. Right-sided pathways: positive delta in V1. Radiofrequency catheter ablation is curative (>95% success, low risk).

1st Degree AV Block (PR >200ms)

✓ NOTE ▾

Diagnostic Criteria

PR interval consistently >200ms (5 small squares at 25mm/s)
Every P wave conducts to a QRS (1:1 relationship maintained)

Pearl: PR >300ms = "long PR" — may cause haemodynamic compromise if atrial kick is lost (diastolic MR, reduced CO). Causes include AV nodal disease, inferior MI, Lyme carditis, drug effect (digoxin, beta-blockers, CCBs, amiodarone). Check all medications before calling it primary AV nodal disease.

Hyperkalemia

⚠ CRITICAL ▾

ECG Progression with Rising K⁺

K⁺ 5.5–6.0: Peaked, narrow, symmetric T waves (earliest sign — "tent-like")
K⁺ 6.0–6.5: PR prolongation, QRS widening begins
K⁺ 6.5–7.0: P wave flattening/disappearance ("sinoventricular conduction")
K⁺ >7.0: Sine wave pattern (QRS merges with T), VF, asystole

Pearl: Treat any K⁺ >6.5 as emergency. ECG changes lag behind serum K⁺ — can have deadly K⁺ with minimal ECG changes. Calcium gluconate (membrane stabiliser) acts in minutes; insulin+glucose shifts K⁺ in 20 min; sodium bicarbonate helpful in acidosis. Dialysis is definitive.

Hypokalemia

◆ CONSIDER ▾

Diagnostic Criteria

T-wave flattening or inversion (widespread)
U waves: positive deflection after T wave, best seen V2–V3; U > T amplitude = significant
Apparent QT prolongation (actually QU interval — T+U fused)
ST depression in multiple leads

Pearl: Hypokalemia + hypomagnesaemia are co-dependent: can't replete K⁺ without fixing Mg²⁺. Always check both. U waves in hypokalemia are best seen in precordial leads V2–V3. If U wave amplitude > T wave amplitude → significant hypokalemia. Risk for TdP with any QT-prolonging drug escalates dramatically when K⁺ is low.

Cardiac Tamponade

⚠ CRITICAL ▾

Diagnostic Criteria

Sinus tachycardia (often first sign, compensatory)
Low voltage: QRS amplitude <5mm in all limb leads or <10mm all precordial leads
Electrical alternans: alternating QRS amplitude (beat-to-beat swinging of the heart in effusion)
All three together = Beck's ECG triad = highly specific for tamponade

Pearl: Electrical alternans is pathognomonic when present, but sensitivity is low (~20%). Low voltage + tachycardia in a patient with pericarditis history = tamponade until proven otherwise → urgent echo. Bedside POCUS is faster than formal echo. Pericardiocentesis is life-saving — don't wait.

Hypothermia — Osborn / J Waves

▲ HIGH ▾

Diagnostic Criteria

Osborn (J) waves: notch at the junction of QRS and ST segment, positive deflection
Best seen in inferior leads (II, aVF) and lateral precordial leads (V4–V6)
Amplitude increases as core temperature falls
Bradycardia, PR/QRS/QT prolongation, muscle tremor artifact

Pearl: Hypothermia ECG: Bradycardia → J waves appear → QRS widens → VF risk at <28°C. "J wave" amplitude inversely correlates with temperature — bigger J wave = colder patient. Atrial fibrillation is common at moderate hypothermia. Rewarm actively if core temp <32°C. "Not dead until warm and dead."

ARVC — Arrhythmogenic RV Cardiomyopathy

▲ HIGH ▾

Diagnostic Criteria

Epsilon wave: small notch at end of QRS in V1–V3 (delayed RV depolarisation)
T-wave inversion in V1–V3 (with complete RBBB)
Prolonged terminal activation duration >55ms in V1–V3
LBBB-morphology PVCs or VT (RV origin conducts via LBB territory)

Pearl: ARVC = fibrofatty replacement of RV myocardium (desmosomal mutations — plakophilin, desmoglein). Presents as VT/VF in young athletes — exercise triggers arrhythmia. Diagnosis requires Task Force Criteria (ECG + imaging + biopsy + history). Competitive sport restriction is mandatory. ICD for all high-risk patients.