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Now I have a thorough understanding of the ECG findings and the relevant textbook content. Let me carefully analyze the ECG image and compile the full Major/Long Case.
ECG Analysis from the image:
Looking carefully at the ECG (25 mm/s, appears to be a long-format 12-lead or rhythm strip ECG):
- Rate: The complexes appear regular, approximately 75-90 bpm
- Rhythm: Regular
- QRS: Wide complexes visible - appears broad (>120 ms)
- Morphology: The QRS complexes show a pattern consistent with Left Bundle Branch Block (LBBB) - broad, notched, monophasic R waves in lateral leads (I, aVL, V5-V6), with rS or QS pattern in right precordial leads
- ST-T: Secondary ST-T changes (discordant) typical of LBBB
- P waves: Appear present before each QRS - sinus rhythm
- Axis: Left axis deviation
The ECG shows a complete Left Bundle Branch Block (LBBB) in sinus rhythm.
π MAJOR / LONG CASE: Complete Left Bundle Branch Block (LBBB)
PART 1: CASE PRESENTATION
Patient: Male, 62 years old
Chief Complaint: Exertional breathlessness and fatigue for 3 months, with recent onset of bilateral ankle swelling
History of Presenting Illness
A 62-year-old male with a known history of hypertension presents with a 3-month history of progressively worsening exertional dyspnea (now NYHA Class II-III), easy fatigability, and orthopnea (2 pillows). He also reports bilateral ankle swelling for the past 3 weeks. He denies chest pain at rest, palpitations, or syncope. There is no history of fever, cough, or wheeze. He has been on amlodipine 5 mg for hypertension for 8 years but admits poor compliance.
Past History
- Hypertension (8 years)
- No known diabetes, dyslipidemia, or prior cardiac events
- No history of rheumatic fever
Family History
- Father died of "heart attack" at age 68
Social History
- Smoker: 20 pack-years (quit 5 years ago)
- No significant alcohol use
Medications
- Amlodipine 5 mg OD (irregular compliance)
Allergies
- None known
Review of Systems
- Dyspnea on exertion: Yes (NYHA II-III)
- Orthopnea: Yes (2 pillows)
- PND: Yes (twice in last month)
- Ankle swelling: Yes (bilateral, pitting)
- Chest pain: No
- Syncope/pre-syncope: No
- Palpitations: No
PART 2: PHYSICAL EXAMINATION
| System | Finding |
|---|---|
| General | Middle-aged male, comfortable at rest, mildly dyspnoeic on minimal exertion |
| Vitals | BP 158/96 mmHg, HR 82 bpm (regular), RR 18/min, SpO2 96% on air, Temp 37Β°C |
| Pulse | Regular, 82 bpm, normal volume, no radio-radial delay |
| JVP | Elevated ~5 cm above angle of Louis |
| Apex Beat | Displaced to 6th ICS, anterior axillary line - heaving character |
| Heart Sounds | S1 normal, S2 normal, S3 gallop present, no murmurs |
| Lungs | Bibasal fine crepitations |
| Abdomen | Mild hepatomegaly (2 cm below costal margin), no ascites |
| Lower Limbs | Bilateral pitting edema to mid-shin |
PART 3: ECG FINDINGS - SYSTEMATIC ANALYSIS
Technical Details: Paper speed 25 mm/s | Gain 10 mm/mV (standard)
Step-by-Step ECG Interpretation
1. Rate
- R-R interval appears approximately 3-4 large squares β Heart rate ~75-85 bpm
- Normal rate (normocardic)
2. Rhythm
- P waves present and regular before each QRS complex
- Regular sinus rhythm
3. P Wave
- Upright in leads I and II
- Broad, possibly notched in lead II - suggesting left atrial abnormality
- PR interval: ~160-180 ms (normal)
4. QRS Complex - THE KEY FINDING
- Duration: β₯120 ms (β₯3 small squares) - WIDE
- Morphology:
- Broad, monophasic, notched (M-shaped) R wave in lateral leads (I, aVL, V5, V6)
- Absent septal q waves in I, V5, V6
- QS or rS pattern in right precordial leads (V1, V2)
- No secondary R wave (no R') in V1 - distinguishes from RBBB
- CONCLUSION: COMPLETE LEFT BUNDLE BRANCH BLOCK (LBBB)
5. ST Segment and T Waves
- Discordant ST-T changes (opposite to the main QRS deflection) - this is EXPECTED and SECONDARY in LBBB
- ST elevation in V1-V2 (leads with negative QRS)
- ST depression + T-wave inversion in V5-V6, I, aVL (leads with positive QRS)
- These are the "appropriate discordant" changes of LBBB - they do NOT represent ischemia on their own
6. QT Interval
- Prolonged (secondary to widened QRS) - corrected QTc assessment is unreliable in LBBB
7. Axis
- Left axis deviation (QRS predominantly positive in I, negative in aVF)
π ECG Diagnosis:
Sinus rhythm with Complete Left Bundle Branch Block (LBBB)
- Rate ~80 bpm
- QRS duration β₯120 ms
- Broad monophasic R in I, aVL, V5-V6
- QS in V1-V2
- Absent septal q waves in lateral leads
- Secondary (discordant) ST-T changes
Criteria for Complete LBBB (All must be met):
| Criterion | Present? |
|---|---|
| QRS duration β₯120 ms | β |
| Broad monophasic R in I, aVL, V6 | β |
| No septal q waves in I, V5, V6 | β |
| QS or rS in V1 | β |
| Discordant ST-T changes | β |
(Harrison's Principles of Internal Medicine 22E, p. 1914-1916)
PART 4: PATHOPHYSIOLOGY OF LBBB
Normal conduction: SA node β AV node β Bundle of His β Left and Right bundle branches β Purkinje fibers β simultaneous ventricular activation.
In LBBB:
- The left bundle branch is blocked (diseased, fibrosed, ischemic)
- The left ventricle is activated late - via slow cell-to-cell conduction from the right ventricle
- This produces the wide, aberrant QRS morphology
- Septal activation reversal: Normally the septum activates left-to-right (producing small septal q waves in lateral leads). In LBBB, this is reversed - hence no septal q waves
- The major QRS vector is directed left and posteriorly β tall R in I, aVL, V5-V6
- The delayed, abnormal repolarization produces secondary discordant ST-T changes
(Harrison's Principles of Internal Medicine 22E, p. 1915)
PART 5: CAUSES OF LBBB
Cardiac Causes (most common):
| Cause | Mechanism |
|---|---|
| Hypertensive heart disease | Most common cause - LV hypertrophy β bundle fibrosis |
| Ischemic heart disease / CAD | Infarction or ischemia of septal/bundle tissue |
| Dilated cardiomyopathy | Diffuse fibrosis, bundle disruption |
| Aortic valve disease | Proximity of left bundle to AV ring |
| Post-cardiac surgery / TAVR | Direct trauma to conduction system |
| Lev's disease | Age-related fibrosis of left-sided conduction |
| Lenegre's disease | Primary sclerodegenerative disease of conduction |
Non-Cardiac:
- Hyperkalemia (severe)
- Drug toxicity (class Ic antiarrhythmics - flecainide)
- Brugada syndrome (sometimes)
In this patient: Most likely cause is hypertensive heart disease with LV hypertrophy progressing to LBBB.
PART 6: INVESTIGATIONS
Bedside / Immediate:
| Investigation | Expected Finding |
|---|---|
| 12-lead ECG | LBBB as described above |
| SpO2 | 96% (mildly reduced) |
| Blood glucose | Rule out DM |
Blood Tests:
| Test | Rationale | Expected |
|---|---|---|
| CBC | Anaemia as cause/aggravator of heart failure | Mild normocytic anaemia possible |
| Serum electrolytes (Na, K, Cr, Urea) | Baseline for diuretic therapy; hyperkalemia causing LBBB | K may be mildly elevated due to RAAS activation |
| LFT | Cardiac hepatopathy, drug interactions | Mildly elevated enzymes if hepatic congestion |
| Serum BNP / NT-proBNP | Diagnostic and prognostic in heart failure | Markedly elevated (>400 pg/mL) |
| Troponin I/T (high-sensitivity) | Exclude acute MI as cause of new LBBB | May be mildly elevated in HF |
| Thyroid function (TSH) | Hypothyroid cardiomyopathy | To rule out |
| Fasting lipid profile | CAD risk factor assessment | Likely elevated |
| HbA1c | Screen for DM | To rule out |
| Chest X-Ray | Cardiomegaly, pulmonary venous congestion, pleural effusions | Cardiomegaly + pulmonary venous congestion |
Key Imaging:
| Test | Rationale | Expected Finding |
|---|---|---|
| Echocardiogram (TTE) | MOST IMPORTANT - assess LV size, EF, wall motion, valves, RWMA | Dilated LV, reduced EF (~30-40%), global hypokinesia, no RWMA (suggests non-ischemic) |
| Coronary angiography / CT coronary angiography | Exclude ischemic cardiomyopathy (IHD) | May show non-obstructive CAD or normal coronaries |
| Cardiac MRI | If etiology unclear; assess fibrosis (LGE) | Diffuse LGE-free pattern in hypertensive/idiopathic DCM; subendocardial LGE in ischemic DCM |
| Nuclear stress test (if no invasive angiography) | Assess for ischemia (LBBB makes exercise stress ECG unreliable) | ADENOSINE nuclear stress preferred |
β οΈ Important: Exercise stress ECG is unreliable for ischemia detection in LBBB because LBBB itself causes ST changes. Use pharmacologic (vasodilator) nuclear stress testing or stress echo instead.
Holter Monitor / Device:
- 24-hour Holter: To assess for paroxysmal arrhythmias, AV block, or rate response
PART 7: DIAGNOSIS
Primary Diagnosis:
New-onset Complete Left Bundle Branch Block in the setting of Hypertensive Heart Disease with Systolic Heart Failure (HFrEF)
Supporting Evidence:
- 62M with longstanding hypertension
- Symptoms of HF (dyspnea, orthopnea, PND, oedema)
- Displaced, heaving apex beat
- S3 gallop
- Bibasal crepitations
- JVP elevated
- LBBB on ECG - a marker of advanced hypertensive/ischemic cardiomyopathy
PART 8: MANAGEMENT
Acute / Initial Stabilization:
- Oxygen if SpO2 <94%
- Furosemide IV 40-80 mg if pulmonary edema present (loop diuretic for decongestion)
- Upright positioning
- IV access, continuous monitoring (ECG, SpO2, BP)
- Rule out ACS: If new LBBB + ischemic symptoms β treat as STEMI equivalent (Sgarbossa criteria apply - see below)
Long-term Medical Management (HFrEF with LBBB):
The "Fantastic Four" / GDMT for HFrEF (EF <40%):
| Drug Class | Drug | Dose | Evidence |
|---|---|---|---|
| ACE inhibitor / ARB | Ramipril 5-10 mg OD or Sacubitril/Valsartan (ARNI) | Titrate to max tolerated | Reduces mortality, reverse remodeling |
| Beta-blocker | Carvedilol 3.125 mg BD β titrate OR Bisoprolol 1.25 mg OD | Titrate to max tolerated | Reduces mortality, rate control |
| MRA (aldosterone antagonist) | Spironolactone 25-50 mg OD | Titrate | Reduces mortality |
| SGLT2 inhibitor | Dapagliflozin 10 mg OD OR Empagliflozin 10 mg OD | Fixed dose | Reduces hospitalization and CV death |
Other:
- Loop diuretic: Furosemide 20-40 mg OD for symptom relief (decongestion) - NOT shown to reduce mortality
- Treat hypertension: Target BP <130/80 mmHg
- Anticoagulation: If AF develops - consider CHAβDSβ-VASc-guided anticoagulation
Device Therapy - THE CRITICAL COMPONENT IN LBBB:
Cardiac Resynchronization Therapy (CRT)
π LBBB + HFrEF = Major indication for CRT
Indication (Class I, Level A evidence):
- LBBB with QRS β₯150 ms
- EF β€35%
- NYHA II-IV despite optimal medical therapy
- Sinus rhythm
Mechanism: CRT delivers simultaneous pacing to both ventricles, resynchronizing LV contraction, improving EF and reducing functional MR
Options:
- CRT-P (pacemaker function only)
- CRT-D (with defibrillator - preferred if EF <35% for SCD prevention)
ICD alone (if no CRT indication but EF <35%):
- Indicated if EF β€35% and NYHA II-III despite 3+ months GDMT
The Sgarbossa Criteria - LBBB and ACS:
When a patient with LBBB presents with chest pain, standard STEMI criteria are unreliable. Use Sgarbossa criteria to identify AMI in LBBB:
| Criterion | Points | Specificity |
|---|---|---|
| ST elevation β₯1 mm concordant with QRS (same direction) | 5 | High |
| ST depression β₯1 mm in V1-V3 | 3 | Moderate |
| ST elevation β₯5 mm discordant with QRS | 2 | Lower |
Modified Sgarbossa (Smith): ST/S ratio >0.25 in any lead with discordant ST elevation (more sensitive)
Score β₯3 = High probability of AMI - treat as STEMI equivalent
Non-Pharmacological / Lifestyle:
- Salt restriction (<2 g/day sodium)
- Fluid restriction (1.5 L/day if hyponatremia)
- Daily weight monitoring (report >2 kg gain in 2 days)
- Cardiac rehabilitation
- Smoking cessation counselling
- Vaccinations (influenza, pneumococcal)
PART 9: PROGNOSIS
- Isolated LBBB in an otherwise healthy person: relatively benign
- LBBB + reduced EF: Significantly worse prognosis - associated with:
- Higher risk of sudden cardiac death (SCD)
- Progressive heart failure
- Increased all-cause mortality
- CRT-D improves survival, EF, and quality of life in LBBB-HFrEF
- ECG evidence of LVH/LBBB is "a major noninvasive marker of increased risk of cardiovascular morbidity and mortality rates, including sudden cardiac death" (Harrison's, p. 1915)
PART 10: DIFFERENTIALS FOR WIDE QRS
| Condition | Differentiating Features |
|---|---|
| LBBB | Broad R in I/aVL/V5-V6, no septal q, QS in V1-V2, discordant ST-T |
| RBBB | rSR' in V1, wide S in I/V6, T-wave inversion V1-V3 |
| Left anterior fascicular block (LAFB) | Normal QRS duration, left axis deviation (-45 to -90Β°), small q in I/aVL |
| Pre-excitation (WPW) | Short PR, delta wave, secondary ST-T changes |
| Ventricular paced rhythm | Pacing spikes before QRS, LBBB morphology (if RV pacing) |
| Ventricular tachycardia | AV dissociation, fusion beats, very wide (>160 ms), hemodynamic instability |
| Hyperkalemia | Peaked T, widened QRS, sine wave pattern |
PART 11: VIVA VOCE / EXAMINER QUESTIONS
Q1: What is the most common cause of LBBB?
A: Hypertensive heart disease (due to LV hypertrophy and subsequent fibrosis of the conduction system). Ischemic heart disease is also common.
Q2: Why is stress ECG unreliable in LBBB?
A: LBBB itself produces ST depression (discordant changes) in lateral leads, which mimics exercise-induced ischemia. Pharmacologic stress testing (adenosine/dobutamine nuclear scintigraphy or stress echocardiography) should be used instead.
Q3: What is the difference between new LBBB and old LBBB in the context of chest pain?
A: New LBBB in the context of ischemic symptoms is treated as a STEMI equivalent (primary PCI indicated). Known old LBBB requires application of Sgarbossa criteria to identify concurrent AMI.
Q4: What device therapy is indicated in this patient?
A: CRT-D (Cardiac Resynchronization Therapy with Defibrillator) if EF β€35%, LBBB with QRS β₯150 ms, NYHA II-IV despite 3+ months of optimal medical therapy. This improves LV function, symptoms, and reduces SCD risk.
Q5: What is the mechanism of CRT benefit in LBBB?
A: LBBB causes interventricular and intraventricular dyssynchrony - the RV contracts before the LV, causing inefficient LV contraction, functional mitral regurgitation, and paradoxical septal motion. CRT delivers synchronized biventricular pacing (RV + LV coronary sinus lead), restoring synchronized ventricular contraction, improving stroke volume, reducing functional MR, and promoting reverse cardiac remodeling.
Q6: Mention voltage criteria for LVH.
A:
- Sokolow-Lyon: SV1 + RV5 or V6 β₯35 mm
- Cornell: RaVL + SV3 >28 mm (men), >20 mm (women)
- aVL criterion: RaVL >11 mm
- LVH can progress to LBBB (Harrison's, p. 1915)
Q7: What is the difference between Lev's disease and Lenegre's disease?
A: Both are causes of idiopathic bundle branch block in the elderly. Lev's disease involves calcification and fibrosis spreading from adjacent cardiac structures (mitral/aortic valves, central fibrous body) into the conduction system. Lenegre's disease is a primary sclerodegenerative disease of the bundle branches themselves, not related to adjacent structures.
SUMMARY BOX
| Parameter | Finding |
|---|---|
| ECG Diagnosis | Complete LBBB in Sinus Rhythm |
| Rate | ~80 bpm |
| Key Feature | QRS β₯120 ms, monophasic R in I/aVL/V5-V6, QS in V1-V2, no septal q, discordant ST-T |
| Likely Cause | Hypertensive heart disease β HFrEF |
| Key Investigation | Echocardiogram (EF), BNP, Coronary angiography |
| Medical Treatment | GDMT: ACE-I/ARNI + Beta-blocker + MRA + SGLT2i + Furosemide |
| Device Therapy | CRT-D (if EF β€35%, QRS β₯150 ms, NYHA II-IV) |
| Prognosis | Guarded - improved with CRT-D and GDMT |
| Critical Rule | New LBBB + chest pain = STEMI equivalent until proven otherwise |
Sources: Harrison's Principles of Internal Medicine 22E (2025) - Chapter 247: Electrocardiography; Braunwald's Heart Disease; ESC Guidelines for HF 2021
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now read this ecg and give interpreatations
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I can now see this ECG clearly. This is a very striking tracing. Let me do a full systematic read.
π ECG INTERPRETATION
Technical Details: 25 mm/s | Standard calibration 10 mm/mV | 12-lead ECG with visible leads: I, II, III, aVR, aVL, aVF, V1, V2, V3, V4, V5, V6
STEP-BY-STEP SYSTEMATIC ANALYSIS
1. RATE
- R-R interval: approximately 3 large squares β Heart rate ~100 bpm (borderline tachycardia)
- Rate is regular
2. RHYTHM
- P waves are present and precede every QRS
- Rhythm is regular
- Sinus rhythm (sinus tachycardia, ~100 bpm)
3. P WAVE
- Upright in lead I and II - normal sinus origin
- P wave appears broad/notched in inferior leads - possible left atrial abnormality
- PR interval: ~160-180 ms - normal
4. QRS COMPLEX - THE DOMINANT FINDING
Duration:
- QRS appears narrow (~80-100 ms) - importantly, this is a narrow complex ECG
Morphology - Lead by Lead:
| Lead | Morphology | Interpretation |
|---|---|---|
| I | Small positive QRS, flat/inverted T | Low voltage, flat T |
| II | Upright QRS with tall R, ST changes | Inferior territory |
| III | Deep Q wave + elevated ST | Pathological Q + ST elevation |
| aVR | Negative complex (normal) | - |
| aVL | Small QRS, reciprocal ST depression | Reciprocal change |
| aVF | Deep Q wave + ST elevation | Pathological Q + ST elevation |
| V1 | rS pattern, ST changes | - |
| V2 | Tall R wave, ST changes | Posterior involvement? |
| V3 | Tall R, prominent ST elevation | Anterior ST elevation |
| V4 | Tall R, massive ST elevation with upward convexity | Anterior STEMI - ST elevation |
| V5 | Tall R, ST elevation | Anterior-lateral ST elevation |
| V6 | Upright, ST elevation visible | Lateral ST elevation |
5. ST SEGMENT - THE CRITICAL FINDING
ST ELEVATION present in:
- Inferior leads: II, III, aVF - with deep Q waves (especially III and aVF)
- Anterior-lateral leads: V3, V4, V5, V6 - massive ST elevation with upward convexity ("tombstone" pattern)
- V4 shows the most dramatic elevation - dome-shaped, tombstone ST segment
Reciprocal ST DEPRESSION in:
- aVL - reciprocal to inferior leads
- V1-V2 may show reciprocal changes
Q Waves:
- Deep Q waves in III and aVF - pathological (>40 ms wide, >25% R wave height)
- Suggests evolving or established inferior infarction
6. T WAVES
- Hyperacute T waves (tall, broad, peaked) in V3-V5 - characteristic of hyperacute phase of MI
- T wave inversion in aVL (reciprocal)
7. QTc
- Likely prolonged (secondary to ST elevation and acute ischemia)
8. AXIS
- Normal to right axis (QRS positive in I, II, aVF)
π΄ ECG DIAGNOSIS
ACUTE EXTENSIVE ANTERIOR + INFERIOR STEMI
(Anteroinferior STEMI - likely proximal LAD or dominant RCA occlusion with wraparound, OR proximal LAD with inferior extension)
Summary of Findings:
| Finding | Location | Significance |
|---|---|---|
| Massive ST elevation with tombstone morphology | V3, V4, V5, V6 | Acute anterior-lateral STEMI |
| ST elevation + deep Q waves | II, III, aVF | Acute/evolving inferior STEMI |
| Reciprocal ST depression | aVL | Confirms inferior STEMI |
| Hyperacute T waves | V3-V5 | Early/hyperacute phase |
| Pathological Q waves | III, aVF | Evolving infarction (Q already formed) |
| Sinus tachycardia ~100 bpm | - | Sympathetic activation / cardiogenic stress |
TERRITORY AND CULPRIT VESSEL
Pattern Analysis:
Anterior + Inferior simultaneous ST elevation is a classical pattern of:
| Culprit Vessel | Pattern |
|---|---|
| Proximal/Mid LAD (wrap-around type) | LAD wraps around apex and supplies inferior wall β anterior + inferior ST elevation |
| Large Dominant RCA + separate LAD lesion | Less likely (both territories simultaneously) |
| Left Main Coronary Artery (LMCA) occlusion | Can cause massive anterior + lateral + inferior involvement - very high risk |
Most likely: Proximal LAD occlusion (wrap-around LAD) OR LMCA involvement
β οΈ The simultaneous anterior AND inferior ST elevation with the tombstone pattern in V3-V5 and Q waves already in inferior leads makes this a large territory, high-risk, potentially LMCA or proximal LAD event with likely significant LV territory at risk.
CLINICAL URGENCY
This ECG = STEMI Equivalent β CODE STEMI / CATH LAB ACTIVATION
Immediate Steps (Time-Critical):
- Activate cardiac catheterization lab - primary PCI target door-to-balloon β€90 minutes
- Aspirin 300 mg loading dose (chew)
- P2Y12 inhibitor loading: Ticagrelor 180 mg OR Clopidogrel 600 mg
- IV access x2 + continuous ECG monitoring
- Anticoagulation: UFH bolus (60-70 U/kg, max 5000 U) OR Enoxaparin
- O2 therapy if SpO2 <90%
- IV morphine (cautiously) for pain
- GTN if BP permits and no right ventricular infarction (check right-sided leads V3R-V4R!)
β οΈ Critical: If inferior STEMI is confirmed, right-sided ECG (V4R) is mandatory to rule out Right Ventricular Infarction (RVI) before giving nitrates - GTN is CONTRAINDICATED in RVI as it can cause severe hypotension.
RISK STRATIFICATION
| Feature | Risk |
|---|---|
| Tombstone ST elevation in anterior leads | High - large territory |
| Simultaneous inferior + anterior STEMI | Very High - proximal/LMCA occlusion |
| Q waves already formed in inferior leads | Evolving (not hyperacute-only) - time elapsed |
| Sinus tachycardia | Sympathetic activation / early hemodynamic compromise |
| Lack of significant precordial Q waves yet | Some myocardium potentially salvageable |
Killip Classification: Likely Killip II-III depending on clinical exam
COMPARISON WITH PREVIOUS ECG (from first ECG in this session)
| Feature | Previous ECG | This ECG |
|---|---|---|
| QRS width | Wide (LBBB) | Narrow |
| ST changes | Secondary/discordant | Primary ST elevation - STEMI |
| Rhythm | Sinus ~80 bpm | Sinus tachycardia ~100 bpm |
| Diagnosis | LBBB (chronic cardiomyopathy) | Acute anteroinferior STEMI |
These are two different patients with different ECG diagnoses.
FINAL SUMMARY BOX
| Parameter | Finding |
|---|---|
| Rate | ~100 bpm (sinus tachycardia) |
| Rhythm | Regular sinus rhythm |
| QRS | Narrow (~90 ms) |
| Axis | Normal-right |
| Key ST Finding | Tombstone ST elevation V3-V5; ST elevation II, III, aVF |
| Q Waves | Pathological Q in III, aVF |
| Reciprocal Changes | ST depression aVL |
| Diagnosis | Acute Anteroinferior STEMI (proximal LAD / LMCA occlusion) |
| Action | STEMI activation - Primary PCI immediately |
| Do Not Forget | Right-sided leads for RV infarction before nitrates |
π΄ This ECG represents a large, life-threatening acute STEMI. Immediate primary PCI is the treatment of choice. Every minute of delay = additional myocardium lost ("time is muscle").
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