---

🫀 40 ECG Cases: ICU + OPD Practice Guide

ECG Kaise Dekhe — Systematic Approach + Cases with Photos & Treatment

---

📋 ECG DEKHNE KA SYSTEMATIC APPROACH (How to Read an ECG)

---

🔴 ICU LEVEL CASES (Cases 1–20)

---

CASE 1 — Anterior STEMI (LAD Occlusion)

ECG Findings:

• ST elevation: V1–V6 (anterior leads) — convex/tombstone morphology
• Reciprocal ST depression: aVR, aVL (lateral reciprocal)
• Hyperacute T waves: V2–V4 (tall, broad)
• QS waves: V2–V3 (necrosis if established)
• Rate: Sinus, may have bradycardia (vagal) or tachycardia (shock)

Territory:

V1–V4 = LAD (anterior) | V4–V6, I, aVL = Cx (lateral) | II, III, aVF = RCA (inferior)

Treatment (ICU):

• STEMI Protocol: Door-to-balloon <90 min
• Aspirin 325mg + Clopidogrel/Ticagrelor
• Heparin UFH bolus IV
• PCI (Primary — gold standard) / Thrombolysis if PCI not available (Streptokinase/Tenecteplase)
• Morphine 2–4mg IV for pain
• Oxygen if SpO2 <90%
• Beta-blocker (if HR >60, no shock, no AV block)
• ACE inhibitor start within 24h

---

CASE 2 — Anterolateral STEMI

ECG Findings:

• ST elevation: V1–V6, Lead I, aVL — proximal LAD occlusion
• Reciprocal depression: II, III, aVF (inferior leads)
• Hyperacute T waves: V2–V4
• Wide QRS in leads with max ST elevation

Key Teaching Point:

Reciprocal changes (ST depression in opposite leads) confirm STEMI diagnosis. If V1–V6 + I + aVL involved → proximal LAD = worst prognosis, may need emergency CABG.

Treatment:

---

CASE 3 — Inferolateral STEMI (RCA/Circumflex)

ECG Findings:

• ST elevation: II, III, aVF (inferior) + V4–V6 (lateral)
• Reciprocal ST depression: aVL, Lead I
• Hyperacute T waves: merging with ST segment
• Bradycardia: common with inferior MI (vagal + SA node ischemia)

Key Teaching Point:

Always do right-sided leads (V3R–V4R) in inferior MI to rule out Right Ventricular infarction (ST elevation V4R = RV MI → avoid nitrates, give IV fluids).

Treatment:

• PCI/thrombolysis
• Atropine 0.5mg IV for symptomatic bradycardia
• Avoid nitrates if RV involvement
• IV fluid bolus for hypotension with RV MI

---

CASE 4 — Tombstone STEMI (LAD, Extensive)

ECG Findings:

• Massive ST elevation V2–V5 — "tombstone" pattern
• Convex-upward (coved) morphology
• Reciprocal: II, III, aVF with ST depression
• Indicates proximal LAD occlusion with large territory at risk

Tombstone Pattern:

ST elevation so prominent it merges with QRS and T wave, forming a "tombstone" shape. Very high mortality. Associated with cardiogenic shock.

Treatment:

• Immediate PCI (emergent)
• IABP/Impella for cardiogenic shock
• Targeted temperature management if post-cardiac arrest (33–36°C for 24h)

---

CASE 5 — Atrial Fibrillation with Rapid Ventricular Response (RVR)

ECG Findings:

• No P waves — replaced by irregular fibrillatory baseline (f waves)
• Irregularly irregular R-R intervals (key feature)
• Narrow QRS <120ms (supraventricular origin)
• Rate: ~134 bpm (RVR = >100 bpm)
• Poor R-wave progression (PRWP) V1–V3

ECG Kaise Pehchaanein (How to identify AF):

Rule of 3 "Irregulars": Irregular rhythm + Irregular baseline + Irregular QRS intervals = AF until proven otherwise

Treatment (ICU — hemodynamically unstable):

• Synchronized cardioversion 120–200J (if unstable)
• Rate control if stable: IV Metoprolol 5mg slow, or Diltiazem 0.25mg/kg
• Rhythm control: Amiodarone IV 150mg over 10 min, then infusion
• Anticoagulation: Heparin if >48h or unknown duration
• Treat cause: thyroid, infection, hypoxia, electrolytes

---

CASE 6 — Atrial Fibrillation with Complete Heart Block

ECG Findings:

• Atrial activity: Fibrillatory waves ~180 bpm (no organized P waves)
• Ventricular rate: ~43 bpm — slow, regular
• AV dissociation: Atrial and ventricular activity completely independent
• Narrow QRS: Junctional escape focus (supra-Hisian)

Key Teaching Point:

In AF, the rhythm is always irregularly irregular. If you see AF with a regular ventricular response — think Complete Heart Block with escape rhythm. This is a high-grade emergency.

Treatment:

• Temporary pacemaker (transcutaneous → transvenous)
• Atropine 0.5–1mg IV (may not work in complete block)
• Dopamine/Adrenaline infusion as bridge
• Permanent pacemaker implantation

---

CASE 7 — Complete AV Block + VT

ECG Findings:

• P waves: Regular, independent of QRS
• Wide QRS complexes at slow escape rate
• Runs of VT: Broad, bizarre QRS complexes at rapid rate
• AV dissociation: Complete

Treatment:

• Immediate temporary pacing
• Amiodarone for VT suppression
• Defibrillation if degenerates to VF
• Urgent electrophysiology consultation

---

CASE 8 — Atrial Fibrillation with RBBB

ECG Findings:

• Irregularly irregular rhythm
• No P waves (AF)
• Wide QRS >120ms
• RBBB morphology: rsR' (M-shape) in V1 + broad S waves in I, aVL, V5, V6
• T-wave inversions in right precordial leads (normal with RBBB)

RBBB vs LBBB Quick Tip:

Treatment:

• Treat AF (rate control/anticoagulation)
• RBBB alone: usually no specific treatment unless symptomatic
• Investigate for structural cause

---

CASE 9 — Torsades de Pointes (TdP)

ECG Findings:

• Panel A: Complete AV block with bradycardia
• Panel B: Prolonged QT + notched T waves (warning sign)
• Panel C: TdP — wide QRS complexes twisting around the isoelectric baseline, varying amplitudes and cycle lengths — pathognomonic!

Causes of Long QT (mnemonic: ABCDE):

• Antiarrhythmics (amiodarone, sotalol)
• Bradycardia
• Congenital (Romano-Ward, Jervell-Lange-Nielsen)
• Drugs (antipsychotics, antibiotics — azithromycin, antimalarials)
• Electrolytes (↓K, ↓Mg, ↓Ca)

Treatment (ICU Emergency):

• IV Magnesium Sulfate 2g over 5–15 min (first-line even if Mg normal)
• Stop offending drugs
• Correct electrolytes (K >4.5, Mg >2)
• Overdrive pacing at 90–100 bpm to shorten QT
• Isoproterenol infusion (acquired TdP, bradycardia-dependent)
• NOT amiodarone (prolongs QT further)

---

CASE 10 — Pulmonary Embolism (S1Q3T3)

ECG Findings:

• Sinus tachycardia ~116 bpm (most common finding in PE)
• S1Q3T3 pattern (McGinn-White sign):
  • S wave in Lead I (prominent)
  • Q wave in Lead III
  • T inversion in Lead III
• T-wave inversions V1–V3 (right precordial) = RV strain
• Incomplete RBBB (QRS 110ms, S in V5–V6)

PE ECG Quick Memory Aid:

"SI QIII TIII" = S in I, Q in III, T-inversion in III + sinus tachycardia = Think PE!

Treatment:

• Anticoagulation: Heparin UFH bolus + infusion (or LMWH/DOAC if stable)
• Massive PE + hemodynamic instability: Systemic thrombolysis (Alteplase 100mg over 2h)
• CDT (catheter-directed therapy) if thrombolysis contraindicated
• Surgical embolectomy (last resort)
• Oxygen, IV fluids (cautious — RV overload)
• Vasopressors (Norepinephrine) for shock

---

CASE 11 — PE with More Extensive RV Strain

ECG Findings:

• S1Q3T3 labeled
• Deep T-wave inversions V1–V6 (severe RV strain)
• Sinus tachycardia
• T inversions extending across ALL precordial leads = submassive/massive PE

Severity Classification of PE by ECG:

---

CASE 12 — Hyperkalemia (Peaked T Waves → Sine Wave)

ECG Findings:

• Peaked (tented) T waves V4–V5 — narrow base, symmetric (first sign)
• Prolonged PR interval (1st degree AV block)
• Wide QRS >120ms (RBBB morphology)
• Progressive changes with rising K+:

Hyperkalemia ECG Progression (K+ levels):

Treatment (ICU Emergency):

1. Calcium gluconate 1g IV over 5 min (cardiac membrane stabilization — works in 5 min, lasts 30–60 min)
2. Insulin 10 units + Dextrose 50% 50mL (shifts K intracellularly — works in 30 min)
3. Salbutamol nebulization 10–20mg (works in 30 min)
4. Sodium bicarbonate 50mEq IV (if acidotic)
5. Furosemide IV (if urine output present)
6. Kayexalate/Patiromer (GI excretion — slow)
7. Emergency dialysis (definitive — if oliguric/anuric)

---

CASE 13 — Electrolyte ECG Comparison Chart

All 4 Electrolyte Patterns:

---

CASE 14 — Hypokalemia (with U Waves)

ECG Findings:

• Diffuse ST depression
• T-wave flattening (V2–V6)
• Prominent U waves after T waves (best seen V3–V5)
• Prolonged QU interval (appears as long QT)
• T inversion in aVR

U Wave Tips:

U waves are normally present but small. When they become larger than T wave → hypokalemia, bradycardia, digitalis. U waves in V2–V3 best seen at 25mm/s.

Treatment:

• IV KCl replacement max 40mEq/h via central line
• Oral K if mild (K>3.0 and asymptomatic)
• Replace Magnesium first (hypoMg causes refractory hypoK)
• Monitor ECG continuously

---

CASE 15 — Hypokalemia with VPCs (Before/After K Replacement)

ECG Findings:

• Top panel: Sinus rhythm + multifocal VPCs + R-on-T phenomenon, QTc 485ms
• Bottom panel: After K+ replacement — VPCs completely resolved, QTc normalized to 422ms

R-on-T Phenomenon:

When a premature ventricular beat falls on the vulnerable period of T wave (relative refractory period) → can trigger VF. Very dangerous with hypokalemia!

Treatment:

• Aggressive K replacement + Magnesium
• Continuous ECG monitoring
• Avoid QT-prolonging drugs

---

CASE 16 — Hypokalemia with Annotated Features

ECG Findings (Annotated with Arrows):

• Blue arrows: ST depression (V1–V4)
• Black arrows: T-wave inversion
• Red arrows: Prominent U waves
• Double arrow: Prolonged QU interval in V2

---

CASE 17 — Dilated Cardiomyopathy: AF + Complete AV Block + CRTD

ECG Findings (Panels a–c):

• Panel a: AF + complete AV block (bradycardia 40 bpm)
• Panel b: NSVT (non-sustained VT runs)
• Panel c: Regular paced rhythm after CRTD implantation

Indications for Device Therapy (ICU/Cardiology):

---

CASE 18 — Atrial Fibrillation with PVC

ECG Findings:

• AF baseline: Irregular rhythm, no P waves, fine fibrillatory waves (inferior leads, V1)
• Narrow QRS majority (normal conduction)
• Single wide, bizarre QRS at end = PVC (premature ventricular complex)
• Compensatory pause after PVC
• T waves concordant with QRS

PVC on ECG — Identification:

Wide QRS >120ms, bizarre morphology, no preceding P wave, compensatory pause = PVC

---

CASE 19 — AF with RVR (Rapid Rate, Fine Fibrillation)

ECG Findings:

• Irregularly irregular rhythm, HR ~123 bpm
• No P waves — undulating fibrillatory (f) waves in V1 baseline
• Narrow QRS (<120ms) — normal conduction
• No ST changes suggesting acute ischemia

Thyrotoxicosis + AF Treatment:

• Beta-blocker (propranolol preferred — also controls thyroid symptoms)
• Digoxin (less effective in high-adrenergic states)
• Carbimazole/PTU for hyperthyroidism
• Cardioversion only after euthyroid state achieved

---

CASE 20 — AF with Auto-Interpretation (Outpatient Telemetry)

ECG Findings:

• AF — absent P waves, irregularly irregular
• RVH (right ventricular hypertrophy) — reported by auto-interpretation
• HR: 79–84 bpm
• Clinical correlation required — auto-interpretation is a screening tool only

---

🟡 OPD-LEVEL CASES (Cases 21–40)

---

CASE 21 — Sinus Tachycardia

ECG Findings:

• Rate: >100 bpm
• P wave: Present, upright in II, inverted in aVR
• PR interval: Normal
• QRS: Narrow, normal
• Rhythm: Regular

Causes (FLATED):

• Fever, Low BP (hypovolemia), Anemia, Thyroid (↑), Emotion/pain, Drugs (salbutamol, caffeine)

Treatment:

• Treat underlying cause
• Beta-blocker if symptomatic (anxiety, thyrotoxicosis)

---

CASE 22 — Sinus Bradycardia

ECG Findings:

• Rate: <60 bpm
• P wave: Normal, present before each QRS
• Rhythm: Regular
• QRS: Narrow

Causes:

• Athlete's heart, hypothyroidism, inferior MI, beta-blockers, vagal tone, hypothermia

Treatment:

• Asymptomatic + athlete → reassure
• Symptomatic: Atropine 0.5mg IV, consider pacemaker

---

CASE 23 — First-Degree AV Block

ECG Findings:

• PR interval: >0.20s (>1 large square = >200ms)
• All P waves conducted
• Normal QRS (narrow)
• Rate: Normal

Causes:

• Beta-blockers, digoxin, inferior MI, Lyme disease, elderly/fibrosis

Treatment:

• Usually benign, no treatment
• Stop offending drug if symptomatic

---

CASE 24 — Second-Degree AV Block Mobitz Type I (Wenckebach)

ECG Findings:

• Progressive PR lengthening until one P wave NOT followed by QRS
• Grouped beating pattern
• Narrowing R-R before dropped beat

Memory Aid:

"Longer, longer, longer — DROP, then shorter" = Wenckebach

Treatment:

• Often benign (especially in inferior MI — usually reversible)
• Atropine if symptomatic
• Temporary pacemaker if persistent/symptomatic

---

CASE 25 — Second-Degree AV Block Mobitz Type II

ECG Findings:

• Constant PR interval — suddenly a P wave not followed by QRS
• No warning (unlike Wenckebach)
• Often with wide QRS (infranodal block)
• 2:1, 3:1 conduction ratios may occur

Key Difference:

Treatment:

• Requires pacemaker (high risk of complete heart block)

---

CASE 26 — Left Bundle Branch Block (LBBB)

ECG Findings:

• QRS >120ms (wide)
• V1: QS or rS (W-shaped)
• V6, I, aVL: Broad, notched R wave, no Q or S wave
• Lead I: Broad M-shaped R
• Concordant ST/T changes (ST/T opposite to QRS direction = normal for LBBB)

Clinical Significance:

New LBBB + chest pain = STEMI equivalent (Sgarbossa criteria) → treat as STEMI!
Sgarbossa Criterion 1: ST elevation >1mm concordant with QRS = very specific for MI

Treatment:

• If new LBBB + symptoms: urgent cardiology
• Old LBBB: investigate for cardiomyopathy, CAD
• Symptomatic + EF<35% + QRS>150ms: CRT consideration

---

CASE 27 — Right Bundle Branch Block (RBBB)

ECG Findings:

• QRS >120ms
• V1: rsR' (M or "rabbit ears" pattern)
• V6, I: Broad S wave (slurred)
• T inversions V1–V3 (secondary — normal)

Causes:

• Normal variant (isolated RBBB common)
• PE, RV pressure overload, ASD, ischemia, Brugada syndrome

Treatment:

• Isolated RBBB without symptoms: no treatment
• Investigate for PE if new onset + dyspnea

---

CASE 28 — Left Ventricular Hypertrophy (LVH)

ECG Findings:

• Sokolow-Lyon criteria: S in V1 + R in V5 or V6 >35mm
• Cornell criteria: R in aVL >11mm, or S in V3 + R in aVL >20mm (F) / >28mm (M)
• ST depression + T inversion in I, aVL, V5–V6 (strain pattern)
• Left axis deviation

Memory Aid:

"Deep S in V1 + Tall R in V5/V6" = LVH

Treatment:

• Aggressive BP control (target <130/80)
• ACE inhibitor / ARB (best for LVH regression)
• Lifestyle modification

---

CASE 29 — Right Ventricular Hypertrophy (RVH)

ECG Findings:

• Tall R in V1 (R>S in V1)
• Deep S in V5, V6, I (right axis deviation >+90°)
• T inversion V1–V3 (strain)
• P pulmonale: Peaked P wave >2.5mm in II, III, aVF (RA enlargement)

Causes:

• PAH, COPD, MS, ASD, VSD, Tetralogy of Fallot

Treatment:

• Treat underlying cause
• PAH: phosphodiesterase inhibitors, prostacyclin, endothelin antagonists

---

CASE 30 — Wolff-Parkinson-White (WPW) Syndrome

ECG Findings (Baseline):

• Short PR interval <120ms
• Delta wave: Slurred initial upstroke of QRS
• Wide QRS (>120ms due to delta wave)
• Pseudo-ST changes and T-wave changes (secondary)

WPW Quick Identification:

"Short PR + Wide QRS + Delta wave" = WPW

Danger:

WPW + AF = Most dangerous combination. Accessory pathway conducts fast → VF!
Never give AV nodal blockers (Adenosine, Verapamil, Diltiazem, Digoxin) in WPW+AF → may cause VF!

Treatment:

• SVT in WPW: Adenosine (if no AF), Procainamide/Flecainide
• WPW + AF: DC cardioversion or Procainamide IV
• Definitive: Radiofrequency ablation of accessory pathway (curative ~95%)

---

CASE 31 — Supraventricular Tachycardia (SVT / AVNRT)

ECG Findings:

• Rate: 150–250 bpm
• Regular narrow complex tachycardia
• P waves: Hidden in QRS or just after QRS (retrograde P)
• No visible P wave before QRS

Vagal Maneuvers:

Carotid sinus massage, Valsalva, ice-water face immersion → may terminate SVT

Treatment:

• Vagal maneuvers first
• Adenosine 6mg IV rapid push (flush with 20mL saline) → if no response: 12mg
• Verapamil 5mg IV (if no WPW, no hypotension)
• DC cardioversion if hemodynamically unstable
• Long-term: Beta-blocker, flecainide, or catheter ablation

---

CASE 32 — Atrial Flutter

ECG Findings:

• Sawtooth baseline (flutter waves) — best in II, III, aVF
• Atrial rate: ~300 bpm
• 2:1 block most common → ventricular rate ~150 bpm
• Regular rhythm (unless variable block)
• No isoelectric baseline between flutter waves

Memory Aid:

"Regular HR of 150 in older patient" = Think flutter 2:1 block

Treatment:

• Rate control: Beta-blocker, Diltiazem, Digoxin
• Cardioversion: Synchronized DC shock (low energy 50–100J — very responsive)
• Ablation: Cavotricuspid isthmus ablation (highly effective, >95% cure)
• Anticoagulation similar to AF

---

CASE 33 — Premature Ventricular Complexes (PVCs)

ECG Findings:

• Premature, wide QRS (>120ms)
• No preceding P wave
• Compensatory pause after PVC
• Bizarre morphology — different from sinus beats
• T wave opposite to QRS direction

Benign vs Malignant PVCs:

Treatment:

• Isolated PVCs, no structural disease: reassure, avoid caffeine/alcohol
• Frequent symptomatic PVCs: Beta-blocker
• PVCs >10,000/day causing cardiomyopathy: ablation

---

CASE 34 — Pericarditis

ECG Findings (4 Stages):

Pericarditis vs STEMI Differentiation:

Treatment:

• NSAIDs (Ibuprofen 600mg TID or Aspirin 750–1000mg TID) for 1–2 weeks
• Colchicine 0.5mg BD × 3 months (reduces recurrence)
• Avoid anticoagulants (risk of hemorrhagic tamponade)
• Steroids only if recurrent/refractory

---

CASE 35 — Early Repolarization Syndrome

ECG Findings:

• J-point elevation ≥1mm with concave ST elevation
• Notching/slurring at terminal QRS
• Best seen in lateral leads (V4–V6)
• No reciprocal changes
• Tall peaked T waves

Early Repolarization vs STEMI:

Early repolarization: concave, benign, young athletes
STEMI: convex, focal territory, reciprocal changes, symptoms

Management:

• Young athlete, no symptoms: reassure
• If associated with VF/cardiac arrest → ICD implantation (rare, malignant form)

---

CASE 36 — Digitalis (Digoxin) Toxicity

ECG Findings:

• "Salvador Dali moustache" / Reverse tick: ST segment scooping/sagging (typical digoxin effect — not toxicity per se)
• PR prolongation
• Regularization of AF (AV block increasing)
• Bidirectional VT (pathognomonic for severe toxicity)
• Various arrhythmias: PAT with block, junctional rhythms, AV blocks

Digoxin ECG Effects vs Toxicity:

Treatment:

• Digoxin immune Fab (Digibind) — specific antidote
• Treat hyperkalemia (worsens toxicity)
• Temporary pacemaker for severe bradycardia
• Avoid cardioversion (induces VF in digoxin toxicity)

---

CASE 37 — Hypothermia

ECG Findings:

• Osborn (J) waves: Positive deflection at J-point (junction of QRS and ST) — pathognomonic!
• PR prolongation, QRS widening
• Prolonged QT
• Bradycardia
• AF common
• Shivering artifact

Temperature Correlation with ECG:

Treatment:

• Passive rewarming (mild) / Active rewarming (severe)
• VF in hypothermia: defibrillate (may need multiple attempts as temp rises)
• Warm IV fluids, warm humidified O2
• ECMO for refractory hypothermic cardiac arrest

---

CASE 38 — Brugada Syndrome

ECG Findings:

• Type 1 (diagnostic): Coved ST elevation ≥2mm in V1–V2, followed by negative T wave — "shark fin" pattern
• Type 2: "Saddle-back" ST elevation in V1–V2
• Type 3: <1mm ST elevation
• RBBB-like pattern

Brugada vs Normal RBBB:

Normal RBBB: rsR' in V1 with descending ST
Brugada: rsR' with elevated ST going up then coved (like a shark fin/dome shape)

Treatment:

• ICD (only proven effective treatment)
• Avoid sodium channel blockers (flecainide, procainamide, ajmaline — can unmask)
• Quinidine (adjunct)
• Avoid fever (worsens Brugada pattern — paracetamol for fever)

---

CASE 39 — Long QT Syndrome (Congenital)

ECG Findings:

• QTc >440ms (men), >460ms (women) = prolonged
• QTc >500ms = high risk
• Abnormal T-wave morphology: bifid T, broad T, notched T

QT Calculation:

QTc = QT ÷ √R-R interval (Bazett formula)
Quick tip: At 60 bpm, QT should be <440ms; at 100 bpm, <380ms

Causes:

• Congenital: LQT1 (K channel, exercise-triggered), LQT2 (K channel, emotional/auditory trigger), LQT3 (Na channel, sleep/rest-triggered)
• Acquired: Drugs, electrolytes (see Case 9)

Treatment:

• Beta-blocker (especially LQT1, LQT2)
• ICD if high risk, prior cardiac arrest
• Avoid QT-prolonging drugs
• Mexiletine for LQT3
• Genetic counseling, family screening

---

CASE 40 — Normal Sinus Rhythm (Reference)

ECG Findings — Normal Values:

---

📊 QUICK REFERENCE SUMMARY TABLE

---

🧠 ECG DEKHNE KA SHORTCUT (Bedside Mnemonic)

"RRAPQRST"

• Rate — fast/slow/normal?
• Rhythm — regular/irregular?
• Axis — normal/left/right deviation?
• P waves — present? morphology? PR interval?
• QRS — width? pathological Q?
• R wave — progression V1→V6?
• ST segment — elevation/depression?
• T waves — upright/inverted? peaked?

---

Note: All ECG images are from peer-reviewed clinical literature. Always correlate ECG findings with clinical history, examination, and laboratory values. This guide is for educational purposes; management should follow current institutional and international guidelines (ACC/AHA/ESC).