ECG change with their image and treatment

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ECG changes ST elevation MI STEMI

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ECG atrial fibrillation LBBB heart block Wolff-Parkinson-White

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ECG ventricular tachycardia ventricular fibrillation heart block complete

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ECG hyperkalemia hypokalemia QT prolongation electrolyte changes

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normal sinus rhythm ECG P wave QRS T wave labeled diagram

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ECG pericarditis saddle shaped ST elevation diffuse PR depression

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ECG Changes: Patterns, Images & Treatment

🫀 Normal Sinus Rhythm (Reference)

Normal Sinus Rhythm – 12-lead ECG with normal P waves, QRS complexes, and isoelectric ST segments

ECG features: Regular P before every QRS, PR interval 120–200 ms, QRS < 120 ms, isoelectric ST segments, upright T waves in I, II, V4–V6.

1. STEMI — Inferior Wall (RCA territory)

Inferior STEMI: ST elevation in II, III, aVF with reciprocal depression in I and aVL

ECG features:

ST elevation ≥1 mm in leads II, III, aVF
Reciprocal ST depression in I and aVL
May show early hyperacute T waves

Treatment:

Primary PCI within 90 minutes of first medical contact (door-to-balloon < 90 min)
Antiplatelet: Aspirin 325 mg loading + P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel)
Anticoagulation: UFH, bivalirudin, or enoxaparin
If PCI unavailable within 120 min: fibrinolysis (tenecteplase/alteplase)
Beta-blocker (within 24 h if hemodynamically stable), ACE inhibitor, high-intensity statin
Monitor for RV infarction (right-sided leads; avoid nitrates if RV involvement)

2. STEMI — Anterior Wall (LAD territory)

Anterior STEMI: tombstoning ST elevation V1–V4 with reciprocal inferior changes

ECG features:

ST elevation in V1–V4 (convex/"tombstone" morphology)
Hyperacute T waves in V2–V4
Reciprocal ST depression in II, III, aVF
Loss of R-wave progression → pathological Q waves (later)

Treatment: Same STEMI protocol as above. Proximal LAD occlusion carries highest mortality risk; early PCI is critical. ACE inhibitor mandatory for anterior MI + reduced EF.

3. Anterolateral STEMI

Anterolateral STEMI: ST elevation V1–V6, I and aVL with inferior reciprocal changes

ECG features:

ST elevation across V1–V6, I, and aVL
Hyperacute peaked T waves V2–V4
Reciprocal depression in II, III, aVF
Often proximal LAD occlusion

Treatment: Urgent PCI; consider intra-aortic balloon pump or mechanical support if cardiogenic shock develops.

4. NSTEMI / UA (Non-ST Elevation ACS)

NSTEMI: T-wave inversions in inferior and lateral leads without ST elevation

ECG features:

ST depression (horizontal or downsloping) ± T-wave inversion
No ST elevation, no new LBBB
Symmetric deep T inversions in V1–V4 = Wellens' pattern (critical LAD stenosis)

Treatment:

Risk stratify with GRACE/TIMI score
Dual antiplatelet + anticoagulation
Early invasive strategy (angiography < 24–72 h) for high-risk features
Troponin-positive → treat as NSTEMI; admit, IV heparin, beta-blocker, statin

5. Atrial Fibrillation (AF)

Atrial Fibrillation with LBBB: irregularly irregular rhythm, absent P waves, wide QRS

ECG features:

Irregularly irregular RR intervals
No discernible P waves — replaced by fibrillatory (f) waves
Narrow QRS unless aberrant conduction or accessory pathway

Treatment:

Rate control: beta-blockers (metoprolol), non-DHP CCBs (diltiazem, verapamil), digoxin in HFrEF
Rhythm control: electrical cardioversion (if < 48 h onset or anticoagulated ≥ 3 weeks), flecainide/propafenone (no structural disease), amiodarone (structural disease), ablation
Anticoagulation: CHA₂DS₂-VASc ≥ 2 (men) or ≥ 3 (women) → DOAC (apixaban, rivaroxaban, dabigatran preferred over warfarin)
Treat precipitating causes (thyrotoxicosis, infection, alcohol)

6. Wolff-Parkinson-White (WPW) Syndrome

Pre-excited AF in WPW: irregular wide-complex tachycardia with varying QRS morphology

ECG features (sinus rhythm):

Short PR < 120 ms
Delta wave (slurred QRS upstroke)
Widened QRS

Pre-excited AF (shown above): Very rapid (>200 bpm), irregularly irregular, wide bizarre QRS — life-threatening emergency.

Treatment:

Pre-excited AF (WPW + AF): AVOID AV-nodal blockers (adenosine, digoxin, verapamil, diltiazem — may accelerate conduction → VF)
Drug of choice: Procainamide IV or electrical cardioversion
Definitive: Radiofrequency catheter ablation of accessory pathway (curative)

7. Complete (3rd-Degree) AV Block

Complete AV block: AV dissociation with slow junctional escape rhythm

ECG features:

Complete AV dissociation — P waves and QRS complexes march through independently
Slow escape rhythm (ventricular: 20–40 bpm; junctional: 40–60 bpm)
Wide QRS if ventricular escape; narrow if junctional (Hisian)

Treatment:

Atropine 0.5–1 mg IV (temporary, mainly for junctional escape)
Transcutaneous pacing (emergency bridge)
Transvenous temporary pacing → definitive permanent pacemaker implantation
If caused by inferior MI (usually RCA): may be transient; monitor; pace if symptomatic

8. Ventricular Tachycardia (VT) vs. Normal Sinus Rhythm

VT vs NSR: wide-complex regular tachycardia with absent P waves vs normal baseline

Complete AV block → Torsades de Pointes: QT prolongation progressing to TdP

ECG features of VT:

Wide QRS (> 120 ms), rate 100–250 bpm, regular
AV dissociation, fusion beats, capture beats
Monomorphic = uniform QRS; Polymorphic = varying QRS (including Torsades de Pointes)

Treatment:

Stable VT: Amiodarone 150 mg IV bolus; lidocaine as alternative
Unstable VT / pulseless VT: Immediate unsynchronized DC shock (200 J biphasic)
Torsades de Pointes: IV Magnesium sulfate 2 g bolus; correct hypokalemia; stop QT-prolonging drugs; temporary overdrive pacing
Underlying cause: treat ischemia, electrolytes, drug toxicity
Long-term: ICD if structural heart disease + EF < 35%

9. Acute Pericarditis

Acute pericarditis: diffuse saddle-shaped ST elevation with PR depression in multiple leads

ECG features:

Diffuse concave ("saddle-shaped") ST elevation in multiple leads (I, II, aVF, V2–V6)
PR-segment depression (most visible in lead II) — pathognomonic
Reciprocal ST depression and PR elevation in aVR
Spodick's sign: downsloping TP segment
No reciprocal changes matching a single coronary territory (distinguishes from STEMI)

Treatment:

First-line: NSAIDs (ibuprofen 600 mg TID or aspirin 750–1000 mg TID) + Colchicine 0.5 mg BD × 3 months (reduces recurrence by ~50%)
Restrict physical activity until symptom-free + CRP normalized
Avoid glucocorticoids (first-line) — increase recurrence
Steroids reserved for: autoimmune pericarditis, contraindication to NSAIDs, refractory cases

10. Electrolyte Disturbances

Hyperkalemia & Hypokalemia — All Stages

Electrolyte ECG changes: hypokalemia (U waves, flat T), hyperkalemia (peaked T), hypocalcemia (long ST), hypercalcemia (short QT)

Electrolyte	ECG Change	Treatment
Hyperkalemia	Peaked ("tented") T waves → wide QRS → sine wave → VF	Calcium gluconate (membrane stabilize), insulin + dextrose, salbutamol, kayexalate, dialysis
Hypokalemia	Flat/inverted T waves, U waves, prolonged QU, ST depression	Oral/IV potassium replacement; correct hypomagnesemia
Hypocalcemia	Prolonged ST segment → long QT	IV calcium gluconate; correct vitamin D deficiency
Hypercalcemia	Shortened QT interval, short ST segment	IV saline hydration, furosemide, bisphosphonates, treat underlying cause

Quick Reference Summary

ECG Pattern	Key Finding	Urgent Action
Inferior STEMI	STE II, III, aVF	Primary PCI < 90 min
Anterior STEMI	STE V1–V4	Primary PCI < 90 min
NSTEMI/UA	ST depression, T inversion	Risk stratify; early angiography
AF	Irregularly irregular, no P waves	Rate/rhythm control; anticoagulate
WPW pre-excited AF	Very rapid irregular wide QRS	Procainamide; NO AV nodal blockers
Complete AV block	AV dissociation, escape rhythm	Pacemaker
VT	Wide regular tachycardia	Amiodarone or DC shock
Torsades de Pointes	Twisting polymorphic VT	Mg²⁺ sulfate IV
Pericarditis	Diffuse saddle ST, PR depression	NSAIDs + colchicine
Hyperkalemia	Peaked T → sine wave	CaCl₂ + insulin/dextrose
Hypokalemia	U waves, flat T	KCl replacement

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