Explain me ecg changes of major heart diseases in emergency

Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Finding Sources
Finding Sources
Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Loading Image
Loading Image
Loading Image
I now have comprehensive data from Tintinalli's Emergency Medicine, Harrison's, Goldman-Cecil, and Rosen's Emergency Medicine. Let me compile the full answer:

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
This is a shared conversation. Sign in to Orris to start your own chat.