ECG Practice Test Questions with Verified Answers

Master electrocardiography with realistic, exam-style practice and build unshakable confidence before your next test or clinical shift.

If you want fast, exam-ready skills in electrocardiography, this ECG practice test is built for clinicians, students, and paramedics who need realistic, clinically relevant questions with clear, evidence-based explanations. Each question mirrors scenarios you’ll see on boards and in the ward — from acute STEMI recognition to device troubleshooting — so you don’t just memorize answers, you learn to act.

What is ECG (Electrocardiography)?

Electrocardiography (ECG or EKG) is the noninvasive recording of the heart’s electrical activity. It converts cardiac depolarization and repolarization into waveforms — P waves, QRS complexes, T waves, and intervals — that tell a story about rhythm, conduction, ischemia, electrolyte disturbance, and mechanical complications. Mastery of ECG interpretation speeds diagnosis and improves patient outcomes; our ECG practice exam helps you get there faster.

About our ECG Exam (What you’ll get)

This ECG practice exam is a comprehensive, clinically focused bank of practice ecg questions designed from dozens of real-world scenarios. Each item includes four answer choices and a robust, plain-language explanation that walks you through the ECG findings, pathophysiology, and evidence-based management steps. The exam emphasizes active decision-making: when to call for immediate reperfusion, when to give IV calcium for hyperkalemia, when electrical cardioversion is mandatory, and when definitive therapies like ablation or device implantation are indicated.

Key features:

• Realistic case vignettes that simulate emergency, inpatient, and outpatient ECG decision points.
• Clear rationale for each answer that teaches pattern recognition and clinical actions.
• Coverage of high-yield ECG patterns and emergencies so you can confidently interpret and intervene.
• Perfect for timed practice or self-paced learning — ideal as a pre-test boost or long-term review.

Searchers also like to try our interactive ecg practice game — a rapid-fire mode built from the same question bank for speed and retention.

Our Topic Coverage

Our ECG exam covers the full spectrum of essential topics you’ll encounter in exams and clinical care:

Ischemia & Infarction

• Anterior, inferior, lateral, posterior STEMI localization; recognizing reciprocal changes and using posterior leads (V7–V9).
• ECG patterns suggesting left main or severe multivessel ischemia (diffuse ST depression with aVR elevation).
• New LBBB and application of Sgarbossa/modified criteria for suspected MI.

Arrhythmias & Acute Management

• Narrow-complex SVT (AVNRT, AVRT): recognition, vagal maneuvers, IV adenosine, and ablation options.
• Atrial fibrillation: rate vs rhythm control, CHA₂DS₂-VASc stroke risk consideration, and cardioversion for instability.
• Atrial flutter, multifocal atrial tachycardia (MAT), and specific management pearls.
• Ventricular tachycardia (monomorphic, polymorphic, torsades), differentiation from SVT with aberrancy, and immediate management (defibrillation, antiarrhythmics, ablation).
• Inherited channelopathies: Brugada pattern, Long QT syndromes, and Catecholaminergic Polymorphic VT (CPVT) — recognition, family screening, and first-line therapies.

Conduction Abnormalities & Devices

• First-, second- (Mobitz I & II), and third-degree AV block: localization, prognosis, and pacing indications.
• Bundle branch blocks (LBBB/RBBB), bifascicular and alternating blocks — when to refer for pacemaker.
• Pacemaker troubleshooting: failure to capture/sense, pacing modes (AAI, DDD), and temporary vs permanent pacing strategies.
• CRT and ICD indications for heart failure and primary/secondary prevention of sudden death.

Electrolytes & Drug Effects

• Hyperkalemia and classic progressive ECG changes; emergent stabilization with IV calcium, insulin/glucose, β-agonists, and dialysis.
• Hypokalemia ECG findings and replacement strategy.
• Drug-induced QT prolongation (sotalol, methadone, macrolides) and torsades prevention.

Structural & Mechanical Complications

• Pericarditis and myopericarditis: diffuse ST elevation/PR depression, pericardial rub, effusion assessment.
• Cardiac tamponade: electrical alternans and urgent pericardiocentesis.
• Post-MI mechanical complications: papillary muscle rupture, ventricular septal defect, and left ventricular aneurysm.

Toxicity & Special Cases

• Digoxin toxicity (bidirectional VT) and antidote use.
• WPW syndrome and management of preexcited AF.
• Practical bedside priorities (who to cardiovert, when to call cath lab, when to stabilize and dialyze).

Who can take this ECG practice exam?

This exam is ideal for:

• Medical and nursing students preparing for clinical exams.
• Resident physicians (internal medicine, emergency medicine, cardiology) honing acute ECG decision-making.
• Paramedics, physician assistants, and critical care staff who interpret ECGs under pressure.
• Practicing clinicians refreshing skills or prepping for credentialing.
• Anyone who wants an honest, practical way to practice ecg questions and track improvement.

Benefits — what you’ll gain

• Faster, more accurate ECG interpretation under pressure.
• Confidence to act: know when to cardiovert, when to call for reperfusion, and when to stabilize first.
• Improved exam performance on both multiple-choice and case-based assessments.
• Practical clinical readiness: less hesitation, more correct early interventions, and better patient outcomes.

Smart study tips to beat the ECG exam

1. Practice daily in short blocks. Ten focused questions with review beats one long marathon.
2. Active review: After each question, summarize the ECG pattern and the immediate clinical action in one sentence.
3. Mix learning modes: Alternate full practice tests with the ecg practice game to build speed and accuracy.
4. Master core algorithms: Learn immediate responses — ischemia (PCI), hyperkalemia (IV calcium → insulin/glucose), unstable arrhythmia (cardioversion).
5. Log mistakes: Keep a short error log; revisit weak areas weekly.
6. Simulate exam conditions: Time yourself and practice decision making with limited data — that’s what clinical care often looks like.

If you’re serious about mastering ECGs, this ECG practice exam delivers focused, clinically relevant practice with clear explanations and practical management steps. Buy now, start practicing, and convert confusion into confidence — one ECG at a time.

ECG Sample Questions and Answers

A 55-year-old patient’s ECG shows a regular rhythm at 72 bpm, P waves before every QRS, PR interval 0.18 s, QRS 0.08 s. What is the rhythm?
A. Sinus bradycardia
B. Normal sinus rhythm
C. Atrial fibrillation
D. Junctional rhythm
Answer: B. Normal sinus rhythm
Explanation: The ECG shows P waves preceding each QRS with a PR interval within the normal range (0.12–0.20 s) and a narrow QRS (<0.12 s), and the rate is normal (~60–100 bpm). These features define normal sinus rhythm — the sinus node is pacing, conduction through AV and ventricles is normal, no axis or interval abnormalities are noted.

PR interval is measured at 0.28 seconds on an ECG. What is the most likely diagnosis?
A. First-degree AV block
B. Second-degree Mobitz I AV block
C. Second-degree Mobitz II AV block
D. Third-degree AV block
Answer: A. First-degree AV block
Explanation: First-degree AV block is defined by a prolonged PR interval >0.20 seconds with each atrial impulse conducted to the ventricles (every P is followed by a QRS). It’s a conduction delay through the AV node or proximal His bundle, not a dropped beat. Mobitz blocks involve progressive PR changes or dropped QRS complexes, and complete heart block has AV dissociation.

An ECG shows more P waves than QRS complexes with a steadily lengthening PR interval until a drop occurs, then the cycle repeats. This describes:
A. Mobitz II AV block
B. Mobitz I (Wenckebach) AV block
C. Complete AV block
D. Sinus exit block
Answer: B. Mobitz I (Wenckebach) AV block
Explanation: Mobitz I (Wenckebach) is characterized by progressive PR prolongation until a nonconducted P wave (dropped QRS), then the cycle restarts. It usually stems from AV nodal dysfunction and is often benign in young patients or due to medications, vagal tone, or ischemia. Mobitz II has fixed PRs with sudden dropped beats, which is more dangerous.

A patient’s ECG has P waves that march independently from QRS complexes; ventricular rate is 40 bpm, atrial rate 90 bpm. What is the rhythm?
A. Atrial flutter with variable block
B. Third-degree (complete) AV block
C. Ventricular tachycardia
D. Multifocal atrial tachycardia
Answer: B. Third-degree (complete) AV block
Explanation: Complete AV block shows AV dissociation — atria and ventricles beat independently. Atrial rate (sinus) continues at its own pace while the ventricles escape at a slow rate (often 30–50 bpm). The PR intervals vary because there is no conduction relationship. This is a potentially life-threatening block often requiring pacing.

ECG shows a sawtooth pattern in leads II, III, aVF at atrial rate ~300 bpm with ventricular response around 150 bpm. What is the diagnosis?
A. Atrial fibrillation
B. Atrial flutter with 2:1 block
C. Multifocal atrial tachycardia
D. Sinus tachycardia
Answer: B. Atrial flutter with 2:1 block
Explanation: Typical atrial flutter produces regular atrial activity ≈300/min; with a 2:1 conduction ratio, every second flutter wave conducts to the ventricles, giving a ventricular rate ≈150/min. The classic sawtooth flutter waves are most apparent in inferior leads. Atrial fibrillation has irregular baseline and irregularly irregular R-R intervals rather than sawtooth waves.

Which ECG finding is most indicative of acute transmural anterior STEMI?
A. ST elevation in leads II, III, aVF
B. ST depression in V1–V3
C. ST elevation in V1–V4 with reciprocal changes in inferior leads
D. Widespread ST elevation in all leads with PR depression
Answer: C. ST elevation in V1–V4 with reciprocal changes in inferior leads
Explanation: Anterior STEMI typically shows ST elevation in precordial leads V1–V4 (anteroseptal/anterior territory), reflecting transmural injury to the anterior wall (LAD territory). Reciprocal ST depression may appear in inferior leads. ST elevation in II, III, aVF indicates inferior STEMI; diffuse ST elevation with PR depression suggests pericarditis.

A wide QRS (>0.12 s), regular tachycardia at 170 bpm with AV dissociation and capture beats on ECG indicates:
A. SVT with aberrancy
B. Ventricular tachycardia (VT)
C. Atrial flutter with 2:1 block
D. Torsades de pointes
Answer: B. Ventricular tachycardia (VT)
Explanation: VT often presents as a regular wide QRS tachycardia with AV dissociation; capture or fusion beats (intermittent normal QRS due to a supraventricular impulse conducting) are specific clues. Differentiating VT from SVT with aberrancy is critical; features like age, structural heart disease, AV dissociation, and concordance in precordial leads favor VT and prompt urgent management.

ECG shows polymorphic ventricular tachycardia with twisting of QRS around baseline and prolonged QTc of 560 ms. What is the term?
A. Monomorphic VT
B. Torsades de pointes
C. Ventricular fibrillation
D. Accelerated idioventricular rhythm
Answer: B. Torsades de pointes
Explanation: Torsades de pointes is polymorphic VT with QRS complexes that appear to twist around the baseline, classically associated with prolonged QTc (>500 ms increases risk). It can be drug-induced, electrolyte-related, or congenital. Immediate management centers on magnesium, correcting electrolytes, and treating the arrhythmia aggressively due to risk of degeneration into ventricular fibrillation.

A patient with hyperkalemia often shows which progressive ECG change as K+ rises?
A. Tall peaked T waves → PR prolongation → wide QRS → sine wave
B. ST elevation → Q waves → T wave inversion
C. Shortened QT interval → U waves
D. Peaked P waves and short PR
Answer: A. Tall peaked T waves → PR prolongation → wide QRS → sine wave
Explanation: Hyperkalemia causes classic ECG progression: early tall, peaked T waves, then PR prolongation and P wave flattening, followed by widening of QRS complexes. Severe hyperkalemia can produce a sine-wave appearance and lead to ventricular fibrillation or asystole. Rapid recognition and treatment (calcium, insulin/glucose, bicarbonate, dialysis) are critical.

Left ventricular hypertrophy (LVH) on ECG is best suggested by:
A. Low QRS voltage in limb leads
B. Sokolow-Lyon criteria: S in V1 + R in V5 or V6 ≥ 35 mm
C. Diffuse ST elevation in precordial leads
D. New pathologic Q waves in V1–V3
Answer: B. Sokolow-Lyon criteria: S in V1 + R in V5 or V6 ≥ 35 mm
Explanation: Sokolow-Lyon is a common voltage criterion for LVH: S in V1 plus R in V5 or V6 ≥ 35 mm (35 mm = 3.5 mV). LVH often also has repolarization changes (ST depression/T wave inversion) in lateral leads due to strain. Low voltages argue against hypertrophy. ECG criteria have limitations and should be correlated with imaging when possible.

On ECG the frontal plane QRS axis is approximately −45°. How is this described?
A. Normal axis
B. Left axis deviation (LAD)
C. Right axis deviation (RAD)
D. Extreme axis deviation (northwest)
Answer: B. Left axis deviation (LAD)
Explanation: Normal QRS axis ranges roughly −30° to +90° (some definitions −30° to +100°). An axis of −45° falls into left axis deviation territory. LAD can result from left anterior fascicular block, inferior MI, LVH, or anatomical variation. Always interpret in clinical context; mild LAD may be normal in some older adults.

A 12-lead ECG shows diffuse ST elevation in multiple leads with PR depression in the same leads. Most likely cause?
A. Early repolarization
B. Acute pericarditis
C. Anteroseptal MI
D. Hyperkalemia
Answer: B. Acute pericarditis
Explanation: Acute pericarditis classically causes diffuse concave ST elevation across many leads along with PR segment depression (especially V leads and limb leads) due to atrial current injury. Reciprocal ST depression is typically absent except in aVR and V1. Clinical correlation with chest pain relieved by leaning forward and friction rub supports the diagnosis.

A narrow complex tachycardia at 180 bpm with sudden onset and termination, no visible P waves, most consistent with:
A. Atrial fibrillation
B. Paroxysmal supraventricular tachycardia (PSVT) — AVNRT/AVRT
C. Ventricular tachycardia
D. Multifocal atrial tachycardia
Answer: B. Paroxysmal supraventricular tachycardia (PSVT) — AVNRT/AVRT
Explanation: PSVT (commonly AV nodal reentry tachycardia or orthodromic AVRT) presents as a sudden, regular, narrow QRS tachycardia typically 150–250 bpm, often with absent or retrograde P waves. It has abrupt onset/termination. Treatment includes vagal maneuvers and adenosine diagnostically/therapeutically, or longer-term ablation if recurrent.

Which of the following leads best reflects the electrical activity of the right ventricle and is useful in detecting right ventricular infarction?
A. V1
B. V4R (right-sided V4)
C. I and aVL
D. V6
Answer: B. V4R (right-sided V4)
Explanation: Right-sided chest leads such as V4R (placed in the mirror position on the right chest) are most helpful to detect right ventricular infarction, which can accompany inferior MI. V1 can give hints but V4R is more sensitive for RV involvement. Right ventricular infarction may present with ST elevation in right-sided leads and requires careful volume management.

An ECG shows peaked T waves and a shortened QT interval. Which electrolyte disturbance best fits?
A. Hypokalemia
B. Hyperkalemia
C. Hypercalcemia
D. Hypocalcemia
Answer: C. Hypercalcemia
Explanation: Hypercalcemia shortens the QT interval primarily by shortening the ST segment; T waves may appear tall. Severe hypercalcemia can produce arrhythmias. Hypocalcemia prolongs QT. Hyperkalemia produces peaked T waves but typically prolongs QRS and PR as it worsens; however the combination of short QT plus ECG features points to hypercalcemia.

A pacemaker spike is seen just before every QRS complex, producing narrow QRS complexes. This indicates:
A. Ventricular demand pacemaker with failure to capture
B. Atrial pacemaker with retrograde conduction
C. Ventricular pacing with good capture (paced ventricular rhythm)
D. A malfunctioning pacemaker producing undersensing
Answer: C. Ventricular pacing with good capture (paced ventricular rhythm)
Explanation: Pacemaker spikes immediately preceding QRS complexes with resulting QRS complexes indicate successful capture. If QRS is narrow, the ventricular pacing lead may be located close to the conduction system or synchronous intrinsic conduction is occurring; typically ventricular paced QRS are wide, but capture is the key. Failure to capture would show spikes without subsequent QRS.

Which ECG sign suggests previous (old) myocardial infarction in a specific territory?
A. Tall R waves in V1–V3 with Q waves in V5–V6
B. Pathologic Q waves (>40 ms or >25% of R wave) in contiguous leads
C. Diffuse T wave inversion across all leads
D. Peaked T waves in precordial leads
Answer: B. Pathologic Q waves (>40 ms or >25% of R wave) in contiguous leads
Explanation: Pathologic Q waves that are deep/wide in contiguous leads often indicate transmural necrosis from a prior MI in that territory (e.g., Q waves in II, III, aVF suggest inferior wall MI). Criteria generally consider width >0.04 s or depth >25% of the subsequent R wave. Q waves must be interpreted alongside clinical history and prior ECGs.

A 24-lead ambulatory monitor reports multifocal P wave morphologies, irregular R-R intervals, and rate ~110 bpm in a patient with severe COPD. Likely rhythm?
A. Atrial fibrillation
B. Multifocal atrial tachycardia (MAT)
C. Atrial flutter
D. Sinus tachycardia with PACs
Answer: B. Multifocal atrial tachycardia (MAT)
Explanation: MAT shows at least three different P wave morphologies, irregularly irregular rhythm, and atrial rate >100 bpm. It is classically associated with severe pulmonary disease (COPD) and hypoxemia. Management focuses on treating underlying pulmonary disease and controlling rate; it is distinct from AF because distinct P wave morphologies are present rather than chaotic baseline.

Which pattern on ECG suggests a posterior wall MI?
A. ST elevation in leads V1–V3
B. ST depression in V1–V3 with tall R waves and upright T waves (reciprocal of posterior elevation)
C. New left bundle branch block only
D. Widespread low voltage QRS
Answer: B. ST depression in V1–V3 with tall R waves and upright T waves (reciprocal of posterior elevation)
Explanation: Posterior MI often presents with ST depression, tall R waves, and upright T waves in V1–V3 — these are reciprocal changes to ST elevation that would be seen on posterior leads (V7–V9). Recognizing this pattern is crucial; obtaining posterior leads may unmask ST elevation and guide reperfusion therapy.

QT interval varies with heart rate. Which corrected QT (QTc) is generally considered prolonged and increases risk of torsades?
A. QTc > 350 ms
B. QTc > 440–450 ms (male/female general threshold)
C. QTc < 340 ms
D. QTc = 400 ms
Answer: B. QTc > 440–450 ms (male/female general threshold)
Explanation: A QTc >440 ms in men and >460 ms in women is commonly used as a threshold for prolonged QT, and values >500 ms confer a higher risk of torsades de pointes. QTc should be calculated (Bazett or other formulas) because raw QT shortens at higher heart rates. Medication review and electrolyte correction are critical when QTc is prolonged.

An ECG shows a left bundle branch block (LBBB) pattern. Which of the following is true?
A. QRS < 0.10 s, R wave in V1
B. QRS ≥ 0.12 s with broad, notched R waves in lateral leads and deep S in V1
C. Peaked T waves in precordial leads only
D. Always benign and does not mask ischemia
Answer: B. QRS ≥ 0.12 s with broad, notched R waves in lateral leads and deep S in V1
Explanation: LBBB is defined by wide QRS (≥0.12 s), absent Q waves and broad, often notched R waves in leads I, aVL, V5–V6, and a dominant S in V1. LBBB can mask ischemic ST changes and complicate STEMI diagnosis; new LBBB in chest pain should raise concern for acute MI. Clinical correlation and further testing (troponins, imaging) are key.

In Wolff-Parkinson-White (WPW) syndrome, which ECG feature is characteristic during sinus rhythm?
A. Short PR interval with a delta wave and widened QRS
B. Peaked T waves and prolonged QT
C. Deep Q waves in V1–V3
D. Low amplitude P waves in limb leads
Answer: A. Short PR interval with a delta wave and widened QRS
Explanation: WPW features ventricular preexcitation via an accessory pathway, producing a short PR interval, a slurred initial upstroke of the QRS called a delta wave, and a slightly widened QRS. WPW predisposes to reentrant tachycardias; during tachycardia, managing conduction down the accessory pathway is essential because some drugs that slow the AV node can paradoxically facilitate conduction via the accessory pathway.

Atrial rate ~300/min with sawtooth waves, ventricular rate irregularly irregular due to varying conduction — what is the rhythm?
A. Atrial flutter with variable block
B. Atrial fibrillation
C. Multifocal atrial tachycardia
D. Sinus tachycardia with PACs
Answer: A. Atrial flutter with variable block
Explanation: Atrial flutter produces regular atrial activity ≈300/min (sawtooth). If the AV conduction ratio varies (e.g., sometimes 2:1, 3:1, 4:1), the ventricular response becomes irregular. This differs from AF, which has chaotic atrial activity without discrete flutter waves. Identifying flutter versus AF has treatment implications including cardioversion and ablation strategies.

Which lead pair best represents the inferior ECG territory?
A. V1–V2
B. II, III, aVF
C. I and aVL
D. V5–V6
Answer: B. II, III, aVF
Explanation: Leads II, III, and aVF view the inferior wall of the heart (usually right coronary artery territory). ST changes or Q waves in these leads suggest inferior ischemia/infarction. Lateral leads (I, aVL, V5–V6) and anterior leads (V1–V4) correspond to other myocardial regions, so lead grouping helps localize ischemic events.

ECG shows a regular rhythm 50 bpm, narrow QRS, absent P waves replaced by inverted P waves after QRS in leads II and aVF. Likely origin?
A. Sinus bradycardia
B. Junctional escape rhythm
C. Ventricular escape rhythm
D. Atrial fibrillation with slow ventricular response
Answer: B. Junctional escape rhythm

Explanation: A junctional escape rhythm originates near the AV junction and typically produces narrow QRS complexes. P waves may be absent, inverted before, during, or after the QRS depending on retrograde atrial activation; a rate around 40–60 bpm is typical. This rhythm occurs when sinus node fails and the junction takes over as the pacemaker.

Which ECG artifact commonly mimics ventricular tachycardia and can mislead clinicians?
A. Muscle tremor (shivering) artifact
B. Low amplitude baseline wander from respiration
C. U waves due to hypokalemia
D. Left axis deviation
Answer: A. Muscle tremor (shivering) artifact

Explanation: Muscle tremor or movement artifact can produce rapid, irregular baseline oscillations that may be mistaken for VT or VF. Distinguishing true arrhythmia from artifact involves checking pulse/clinical status, lead integrity, and correlating with the patient. If artifact is suspected, repositioning leads or stopping movement will clarify the tracing.

Which of the following best describes the J point?
A. The onset of the QRS complex
B. The end of the QRS complex and the beginning of the ST segment
C. The peak of the T wave
D. The end of the T wave
Answer: B. The end of the QRS complex and the beginning of the ST segment

Explanation: The J point is the junction between the termination of the QRS complex and the start of the ST segment. It is the reference point for measuring ST elevation or depression. Accurate identification of the J point is crucial when assessing for acute ST-elevation myocardial infarction versus other causes of ST changes.

In a patient with chest pain, which ECG finding is most specific for left main coronary artery occlusion?
A. ST elevation in V2–V4
B. ST-segment depression in multiple leads with ST elevation in aVR
C. Tall R waves in V1–V2 only
D. Diffuse PR depression
Answer: B. ST-segment depression in multiple leads with ST elevation in aVR

Explanation: Diffuse ST depression with ST elevation in aVR can indicate left main coronary or severe proximal triple-vessel ischemia and is associated with high risk. It reflects widespread subendocardial ischemia. This pattern requires urgent evaluation and frequently emergent revascularization. Clinical context and troponin testing guide management.

Which of these best describes Brugada syndrome ECG features?
A. ST elevation in V1–V3 with coved or saddleback morphology and risk of sudden cardiac death
B. Diffuse ST elevation with PR depression
C. Tall peaked T waves from hyperkalemia
D. Low voltage QRS in all leads
Answer: A. ST elevation in V1–V3 with coved or saddleback morphology and risk of sudden cardiac death

Explanation: Brugada syndrome is characterized by right precordial ST elevation patterns (type 1 coved morphology is diagnostic) in V1–V3 and predisposes to ventricular arrhythmias and sudden cardiac death, often in structurally normal hearts. Diagnosis sometimes requires pharmacologic challenge and has important implications for family screening and ICD consideration.

A 70-year-old has new onset chest pain and his ECG shows new left bundle branch block (LBBB). What is the immediate clinical significance?
A. New LBBB in chest pain may indicate acute MI and should prompt urgent evaluation for reperfusion.
B. LBBB rules out myocardial infarction.
C. LBBB indicates hyperkalemia.
D. LBBB is always chronic and benign in elders.
Answer: A. New LBBB in chest pain may indicate acute MI and should prompt urgent evaluation for reperfusion.

Explanation: A new LBBB in the setting of chest pain may mask ST changes and can represent an acute infarction, historically considered equivalent to STEMI in some protocols. Although not all new LBBB indicates MI, it warrants urgent evaluation with serial ECGs, cardiac biomarkers, and consideration for reperfusion strategies as clinically appropriate.