Explain me ecg changes of major heart diseases in emergency

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ECG Changes in Major Cardiac Emergencies

Sources: Tintinalli's Emergency Medicine, Harrison's Principles of Internal Medicine 22E, Goldman-Cecil Medicine, Rosen's Emergency Medicine, Braunwald's Heart Disease

Pathophysiology of ST Changes (The Foundation)

Ischemia exerts complex time-dependent effects on myocardial cells. Severe acute ischemia lowers the resting membrane potential, creating a voltage gradient between normal and ischemic zones — "currents of injury" — visible as ST deviation. The direction of the ST vector determines whether you see elevation or depression:
Subendocardial vs transmural ischemia ST vectors
A = Subendocardial ischemia → ST depression in overlying leads. B = Transmural (epicardial) ischemia → ST elevation in overlying leads.

1. STEMI — ST-Elevation Myocardial Infarction

Diagnostic Criteria (per Tintinalli's)

New ST elevation at the J-point:
  • ≥1 mm in all leads except V₂–V₃
  • ≥2 mm in V₂–V₃ (men ≥40 y), ≥2.5 mm (men <40 y), ≥1.5 mm (women)

Localisation by Territory

TerritoryLeads with ST ElevationInfarct-Related Artery
AnteroseptalV₁, V₂ (±V₃)Proximal LAD
AnteriorV₁–V₄LAD
AnterolateralV₁–V₆, I, aVLProximal LAD / LCx
LateralI, aVLLCx or diagonal
InferiorII, III, aVFRCA (most common) or LCx
InferolateralII, III, aVF + V₅, V₆RCA or dominant LCx
True posteriorTall R in V₁–V₂, R/S ≥1, ST depression V₁–V₃LCx / RCA
Right ventricular (RV)II, III, aVF + ST elevation in V₃R–V₆RProximal RCA
Inferior STEMI ECG (RCA occlusion):
Inferior STEMI — ST elevation in II, III, aVF with reciprocal depression in I and aVL
ST elevation in III > II, ST depression in I and aVL — 100% RCA occlusion confirmed at catheterisation.
Anterior STEMI ECG (LAD occlusion):
Anterior STEMI — ST elevation in I, V1–V3 from distal LAD occlusion
ST elevation in I, V₁–V₃ with absence of depression in II/III/aVF — distal LAD.

Evolutionary ECG Sequence

TimeECG Finding
Minutes (hyperacute)Tall, broad, peaked hyperacute T waves
HoursST elevation — convex ("tombstone") or concave
Hours–daysT-wave inversion begins in same leads
Hours–daysPathological Q waves develop (>40 ms wide, >25% of R height)
Days–weeksST normalises; T waves may remain inverted
Months–yearsQ waves persist (marker of old infarct)

Key Points

  • Reciprocal ST depression in leads opposite the infarct zone indicates larger injury, more severe CAD, worse prognosis
  • New LBBB with chest pain was historically a STEMI equivalent, but <10% actually have AMI — use Sgarbossa criteria
  • RV infarction: always obtain right-sided leads (V₄R) in inferior STEMI; ST elevation ≥1 mm in V₄R is highly suggestive

2. NSTEMI / Unstable Angina

ECG Findings

  • ST depression ≥0.5 mm in ≥2 contiguous leads (subendocardial ischemia pattern)
  • T-wave inversions — symmetric, deep
  • ST elevation in aVR with diffuse ST depression elsewhere → suggests left main or proximal LAD occlusion (or severe 3-vessel disease)
  • Normal ECG in 1–6% of confirmed NSTEMI — does not exclude the diagnosis

Wellens' Syndrome (Critical LAD Stenosis)

A warning pattern indicating critical proximal LAD stenosis — often pain-free at time of ECG:
  • Type A (25%): Biphasic T waves in V₂–V₃
  • Type B (75%): Deeply symmetric T-wave inversions in V₂–V₃ (may extend to V₄–V₆)
  • T-wave changes normalise when pain returns, reappear when pain subsides — dynamic pattern

3. Acute Pericarditis

Stages of ECG Change

StageTimingECG
Stage IAcute (days)Diffuse concave ("saddle-shaped") ST elevation in nearly all leads (I, II, III, aVF, V₂–V₆); PR depression (most specific); ST elevation in aVR with PR elevation
Stage II1–2 weeksST and PR normalise
Stage IIIWeeksDiffuse T-wave inversions
Stage IVMonthsECG returns to normal

Distinguishing from STEMI

FeaturePericarditisSTEMI
ST distributionDiffuse (all leads)Regional (territory)
ST shapeConcave (saddle)Convex (tombstone)
Reciprocal changesAbsent (except aVR)Present
PR depressionYesNo
Q wavesNoYes (evolving)
ST:T ratio in V₆>0.25 → pericarditis<0.25

4. Cardiac Tamponade

ECG Findings

  • Sinus tachycardia — almost universal
  • Low voltage (QRS amplitude <5 mm in limb leads, <10 mm precordial) — from pericardial fluid insulating electrical activity
  • Electrical alternans — beat-to-beat alternation in QRS amplitude/morphology as the heart swings within fluid; pathognomonic when present
"The cardiac position will alternate, with the heart returning to its original position with every other beat, thus electrical alternans may be seen." — Rosen's Emergency Medicine
  • Electrical alternans is highly specific but seen in only ~20% of tamponade; its absence does not exclude tamponade

5. Pulmonary Embolism (PE)

The ECG in PE is often non-specific or normal in minor PE. In massive PE with right heart strain:

Classic Pattern — S₁Q₃T₃

  • S wave in lead I (right axis deviation)
  • Q wave in lead III
  • T-wave inversion in lead III

Other RV Strain Patterns

  • Sinus tachycardia — most common finding
  • New RBBB (complete or incomplete) — indicates severe RV strain/hypertension
  • T-wave inversions in V₁–V₄ — RV strain
  • Right axis deviation
  • P pulmonale (peaked P in II >2.5 mm) — right atrial enlargement
  • Atrial fibrillation/flutter
  • ST elevation in V₁ ± aVR
"A new right bundle branch block suggests right ventricular strain and severe pulmonary hypertension." — Goldman-Cecil Medicine
The S₁Q₃T₃ is specific but present in only ~20% of PE cases; sinus tachycardia + anterior T-wave inversions is more commonly seen with large PE.

6. Hyperkalemia

ECG changes progress in a predictable sequence with rising K⁺:
K⁺ LevelECG Change
5.5–6.5 mEq/LTall, peaked (tent-shaped) T waves, narrow base, shortened QT
6.5–7.5 mEq/LLoss of P waves, PR prolongation, widening QRS
7.0–8.0 mEq/LWide QRS, ST changes (depression), bundle branch blocks
>8.0–9.0 mEq/LSine wave pattern (QRS merges with T wave) → imminent cardiac arrest, VF
The sine wave is a medical emergency requiring immediate IV calcium.

7. Wolff-Parkinson-White (WPW)

ECG Triad During Sinus Rhythm

  1. Short PR interval (<120 ms) — rapid conduction via accessory pathway bypasses AV node delay
  2. Delta wave — slurred upstroke of initial QRS (pre-excitation of ventricle)
  3. Widened QRS complex — fusion of normal and accessory pathway depolarisation
  4. Secondary ST-T changes — discordant to QRS direction

Tachyarrhythmias in WPW (Emergency)

TypeECGRateDanger
Orthodromic AVRT (65%)Narrow QRS, regular, no delta wave160–220 bpmModerate
Antidromic AVRT (5–10%)Wide QRS, regular, can mimic VT160–220 bpmHigh
AF with pre-excitation (25%)Wide, bizarre, irregular QRS, delta waves, rate often >200 bpm>200 bpmImmediately life-threatening
Critical Warning: In WPW + AF, avoid AV-nodal blocking agents (adenosine, verapamil, digoxin, beta-blockers) — they block the normal pathway, forcing all conduction down the accessory pathway, potentially triggering VF.

8. Ventricular Tachycardia (VT) vs. SVT with Aberrancy

VT Features on ECG (Favour VT)

  • AV dissociation (P waves independent of QRS) — most specific sign
  • QRS width >160 ms
  • Concordance in precordial leads (all positive or all negative)
  • Fusion beats and capture beats
  • Extreme axis (Northwest axis, −90° to ±180°)
  • Brugada criteria / Josephson's sign (notching near S-wave nadir)

SVT with Aberrancy

  • QRS usually <160 ms
  • Typical RBBB or LBBB morphology
  • Responds to vagal manoeuvres or adenosine

9. Aortic Dissection

ECG is usually non-specific, but important to obtain urgently to exclude MI (since thrombolytics given for MI are fatal in dissection):
  • Most common: normal ECG or non-specific ST-T changes
  • ST elevation in inferior leads — if dissection involves the RCA ostium (Type A with coronary involvement)
  • LVH pattern — from underlying hypertension (common predisposing factor)
  • Pericardial effusion changes (low voltage, electrical alternans) — from haemopericardium in Type A

10. Brugada Syndrome

A channelopathy causing sudden cardiac death in structurally normal hearts:
  • Type 1 (diagnostic): Coved ST elevation ≥2 mm in V₁–V₂ with T-wave inversion — "coved pattern"
  • Type 2: Saddle-back ST elevation ≥2 mm in V₁–V₂ (high takeoff) — not diagnostic alone
  • Pattern can be concealed and unmasked by fever, sodium channel blockers, class IC antiarrhythmics

11. Long QT Syndrome / Torsades de Pointes

  • QTc >440 ms (men), >460 ms (women) — prolonged
  • QTc >500 ms — high risk for Torsades de Pointes (TdP)
  • Torsades: Polymorphic VT with rotating axis ("twisting of the points") around baseline — characteristically self-terminates but can degenerate to VF
  • Triggers: hypomagnesaemia, hypokalaemia, QT-prolonging drugs (class IA/III antiarrhythmics, antipsychotics, antiemetics)
  • Treatment: IV magnesium 2g, correct electrolytes, consider overdrive pacing

Quick Reference Summary Table

EmergencyKey ECG FindingDo Not Miss
Anterior STEMIST elevation V₁–V₄Check for aVR elevation (LM/proximal LAD)
Inferior STEMIST elevation II, III, aVFGet right-sided leads → RV infarction
Posterior MITall R + ST depression V₁–V₃Mirror image: posterior leads show elevation
NSTEMI/UAST depression, T inversionNormal ECG does not exclude
Wellens' syndromeBiphasic/deep T in V₂–V₃ (pain free)Do NOT stress test — proximal LAD critical stenosis
PericarditisDiffuse concave ST elevation + PR depressionDifferentiate from STEMI
TamponadeLow voltage + electrical alternansTreat clinically + echo, not ECG alone
PE (massive)Sinus tachy, S₁Q₃T₃, new RBBB, T inversion V₁–V₄Normal ECG does not exclude PE
HyperkalemiaPeaked T → loss of P → wide QRS → sine waveSine wave = give IV calcium STAT
WPW + AFWide irregular QRS >200 bpmNO AV blockers — can cause VF
VTWide QRS + AV dissociationTreat as VT until proven otherwise
BrugadaCoved ST in V₁–V₂Fever can unmask; high SCD risk
Long QT / TdPQTc >500 ms, polymorphic VTIV Mg 2g + correct K⁺/Mg²⁺

Sources: Tintinalli's Emergency Medicine (9e), Harrison's Principles of Internal Medicine 22E (2025), Goldman-Cecil Medicine, Rosen's Emergency Medicine, Braunwald's Heart Disease
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