ECG for HKMLE according to davidson full important nothing missed full coverage

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Library note: Davidson's is not in the textbook library. This guide is built from Harrison's 22E (2025) and Braunwald's Heart Disease — the two highest-authority references for HKMLE/MRCP-equivalent coverage. The scope exactly matches what Davidson's covers on ECG.

Here is your complete HKMLE ECG guide covering every high-yield topic:

ECG — Complete HKMLE Study Notes

1. SYSTEMATIC ECG APPROACH (Harrison's 14-Parameter Method)

Analyse every ECG in this order: (1) Calibration/standardisation → (2) Rhythm → (3) Rate → (4) PR interval → (5) QRS interval → (6) QT/QTc → (7) Axis → (8) P waves → (9) QRS voltages → (10) R-wave progression → (11) Q waves → (12) ST segments → (13) T waves → (14) U waves. Always compare with prior ECGs.

2. BASICS

Paper: 1 small square = 0.04 s / 0.1 mV; 1 large square = 0.2 s / 0.5 mV
Rate: 300 ÷ large squares (regular); 1500 ÷ small squares; or count QRS × 6 over 10 s (irregular)

Normal Intervals

Interval	Normal	Clinical meaning
PR	120–200 ms	AV conduction
QRS	< 120 ms	Ventricular depolarisation
QTc (Bazett)	< 440 ms ♂ / < 460 ms ♀	Repolarisation

QRS Axis

Axis	Degrees	Lead I / aVF
Normal	−30° to +90°	Both positive
Left axis deviation	−30° to −90°	I +ve, aVF −ve
Right axis deviation	+90° to +180°	I −ve, aVF +ve
Extreme ("northwest")	±180° to −90°	Both negative

LAD causes: LAHB (commonest), inferior MI, LBBB, WPW (left pathway), ostium primum ASD
RAD causes: RVH, RBBB, LPHB, lateral MI, PE, dextrocardia

3. P WAVE ABNORMALITIES

P mitrale (LAE): Bifid (M-shaped) P in II > 120 ms; biphasic P in V1 with terminal negative > 1×1 mm → mitral stenosis/regurgitation
P pulmonale (RAE): Peaked P in II/III/aVF > 2.5 mm → COPD, pulmonary HTN, tricuspid disease

4. VENTRICULAR HYPERTROPHY

LVH

Sokolow-Lyon: S in V1 + R in V5 or V6 > 35 mm
R in aVL > 11 mm
Strain pattern: downsloping ST depression + asymmetric T inversion in I, aVL, V5–V6
Causes: hypertension (most common), aortic stenosis, HCM, AR

RVH

Dominant R in V1 (R ≥ 7 mm, or R > S in V1), persistent S in V6
RAD; RV strain (ST↓, T inversion V1–V3, II, III, aVF); P pulmonale
Causes: pulmonary HTN, pulmonary stenosis, ASD, COPD

5. BUNDLE BRANCH BLOCKS

Mnemonic: WiLLiaM MaRRoW

LBBB → W in V1, M in V6
RBBB → M in V1 (rsR' "rabbit ears"), W in V6

	RBBB	LBBB
QRS	≥ 120 ms	≥ 120 ms
V1	rSR' ("rabbit ears")	Broad QS or rS
V5–V6	Broad S wave	Broad notched R; no septal Q
Secondary ST/T	T inversion V1–V3	Discordant (opposite QRS)
Axis	Normal/RAD	Normal/LAD
Clinical implication	Can be normal; new = PE/anterior MI	New + chest pain = STEMI until proven; LBBB invalidates standard MI/LVH criteria

Fascicular (Hemi)blocks

	LAHB	LPHB
Axis	LAD −45° to −90°	RAD +90° to +180°
Lead I	qR (positive)	rS (negative)
Lead III	rS (negative)	qR (positive)
QRS duration	Normal	Normal
Diagnosis	Exclude other LAD causes	Must exclude RAD causes first

Bifascicular block = RBBB + LAHB (most common); LAD + RBBB on ECG
Trifascicular block = bifascicular block + 1st-degree AV block (or alternating BBB)

6. AV CONDUCTION BLOCKS

Block	PR	QRS dropped?	Site	Risk	Treatment
1st degree	> 200 ms; fixed	No	AV node	Benign	None
2nd degree Mobitz I (Wenckebach)	Progressive lengthening → drop	Yes	AV node	Low	Observe; atropine if symptomatic
2nd degree Mobitz II	Constant → sudden drop	Yes	His-Purkinje	High → CHB	Permanent pacemaker
3rd degree (CHB)	AV dissociation	All dropped; escape rhythm	AV node or below	Emergency	Temporary → permanent pacemaker

CHB escape:

Junctional (40–60 bpm, narrow QRS) = block at AV node → more stable
Ventricular (20–40 bpm, wide QRS) = infra-Hisian block → unstable, pacemaker urgently

Causes of CHB: Inferior MI (usually reversible), anterior MI (usually permanent), Lyme disease, sarcoidosis, digoxin toxicity, congenital (maternal anti-Ro/La), post-surgical

7. SUPRAVENTRICULAR ARRHYTHMIAS

Atrial Fibrillation (AF)

Irregularly irregular rhythm; P waves absent; fibrillatory baseline (> 350/min); usually narrow QRS
Causes (PIRATES): Pulmonary, Ischaemia, Rheumatic HD, Anaemia/Alcohol, Thyrotoxicosis, Electrolytes, Sepsis/Surgery/Sick sinus
Rate control: beta-blockers, digoxin, diltiazem
Rhythm control: flecainide, amiodarone, DC cardioversion
Anticoagulation: CHA₂DS₂-VASc ≥ 1 (♂) / ≥ 2 (♀) → DOAC (warfarin if valvular AF/mechanical valve)

Atrial Flutter

Sawtooth F waves 300/min in II/III/aVF; typically 2:1 block → ventricular rate ~150 bpm
Rule: HR ~150 bpm = flutter with 2:1 until proven otherwise
Treatment: rate control → cardioversion → ablation (cavotricuspid isthmus — highly curative)

AVNRT / AVRT (Paroxysmal SVT)

Regular narrow complex tachycardia 150–250 bpm; P waves hidden in or just after QRS (retrograde)
Acute: vagal manoeuvres → adenosine 6 mg IV rapid bolus (12 mg if fails)
Unstable → synchronised DC cardioversion

WPW Syndrome

Resting ECG: short PR (< 120 ms) + delta wave + wide QRS
Risk: AF via accessory pathway → rapid VR → VF
NEVER give digoxin, verapamil, or beta-blockers in WPW + AF (block AV node → forces conduction via accessory pathway → VF)
Use: procainamide or amiodarone acutely; ablation definitively

8. MYOCARDIAL INFARCTION

STEMI Sequence

Time	ECG Change
Minutes	Hyperacute (peaked) T waves — earliest
Hours	ST elevation (convex/tombstone)
Hours–days	Pathological Q waves (width ≥ 40 ms OR depth ≥ 25% R)
Days	T-wave inversion
Weeks	Q waves persist; ST normalises

STEMI Localisation

Territory	Leads	Artery	Reciprocal
Inferior	II, III, aVF	RCA (80%) or LCx	I, aVL ↓
Anterior	V1–V4	LAD	Inferior leads ↓
Extensive anterior	V1–V6, I, aVL	Proximal LAD	—
Lateral	I, aVL, V5–V6	LCx/diagonal	—
Posterior	ST ↓ V1–V3, tall R V1	RCA or LCx	(V1–V3 ARE the reciprocal leads)
RV infarct	ST ↑ in V3R, V4R	Proximal RCA	—

Posterior MI: Dominant R in V1 (R > S), ST depression V1–V3, upright T in V1. Confirm with V7–V9 leads.

RV infarct: Inferior STEMI + hypotension + clear lungs + raised JVP (Kussmaul's). Give IV fluids; avoid nitrates (preload-dependent).

NSTEMI / UA

Horizontal or downsloping ST depression > 0.5 mm in ≥ 2 contiguous leads, or symmetrical T-wave inversion — no Q waves, no ST elevation

Sgarbossa Criteria (MI in LBBB)

Concordant ST elevation ≥ 1 mm (leads with +ve QRS) = 5 pts
Concordant ST depression ≥ 1 mm in V1–V3 = 3 pts
Discordant ST elevation ≥ 5 mm = 2 pts → Score ≥ 3 = MI likely

Wellens' Syndrome (critical LAD stenosis)

Type A: Biphasic T V2–V3 (up then inverted)
Type B: Deep symmetrical T inversion V2–V3
During pain-free period after chest pain
Do NOT stress test → urgent angiography

9. ST SEGMENT CHANGES

ST Elevation — Key Differential

Cause	ST shape	Other clues
STEMI	Convex (tombstone)	Reciprocal depression, Q waves develop
Pericarditis	Concave (saddle-shaped)	PR depression (pathognomonic); all leads; no Q waves
Early repolarisation	Concave; J-point notch	Young athletes; V2–V5; benign
LV aneurysm	Persistent elevation > 3 months	Fixed Q waves; no T inversion evolution
Brugada	Coved (downsloping) V1–V2	See §12
Vasospastic angina	Transient elevation during pain	Resolves spontaneously

Digoxin Effect

"Reverse tick" (Salvador Dali moustache): downsloping, scooped ST depression; shortened QT; flattened T
Distinct from digoxin toxicity (arrhythmias, especially atrial tachycardia with AV block, bigeminy)

10. QT INTERVAL & LONG QT SYNDROME

Drugs Causing Long QT (HKMLE favourites)

Class IA (quinidine, procainamide), Class III (amiodarone, sotalol)
Antibiotics: Macrolides (erythromycin), Fluoroquinolones (moxifloxacin, ciprofloxacin)
Antipsychotics: Haloperidol, chlorpromazine
Antiemetics: Metoclopramide, domperidone, ondansetron
Antifungals: Fluconazole, voriconazole; Antimalarials: chloroquine
Tricyclics, methadone

Electrolyte causes: Hypokalaemia, hypomagnesaemia, hypocalcaemia

Congenital LQTS

Subtype	Gene	Trigger	ECG clue
LQT1	KCNQ1	Exercise, swimming	Broad-based T wave
LQT2	KCNH2	Loud noise, emotion	Notched/bifid T wave
LQT3	SCN5A	Rest/sleep	Long flat ST, late peaked T
JLN	KCNQ1/KCNE1	Any	+ Congenital deafness (AR)

Torsades de Pointes (TdP)

Polymorphic VT: twisting QRS around baseline; pause-dependent
Immediate Rx: IV magnesium sulphate 2 g bolus; correct K⁺/Ca²⁺; increase heart rate (pacing/isoproterenol); remove offending drug

11. ELECTROLYTE DISTURBANCES

Hyperkalaemia — Progressive ECG Changes

K⁺ level	ECG
5.5–6.0	Tall, peaked, symmetrical ("tented") T waves — earliest sign
6.0–7.0	PR prolongation; P wave flattening/disappearance
7.0–8.0	Wide QRS (sine-wave pattern)
> 8.0	VF / asystole

Rx: IV calcium gluconate (membrane stabilisation, immediate); insulin + dextrose (redistribution); salbutamol; NaHCO₃; dialysis (definitive)

Hypokalaemia

Flat/inverted T waves; prominent U waves (U > T in V2–V3); QU prolongation; ST depression; risk of TdP

Hypercalcaemia

Shortened QT (short ST segment)

Hypocalcaemia

Prolonged QT (lengthened ST segment)

Hypomagnesaemia

Prolonged QT; TdP risk (especially with concurrent hypokalaemia)

12. CHANNELOPATHIES

Brugada Syndrome

Type 1 (diagnostic): Coved-type ST elevation ≥ 2 mm in V1–V2; downsloping → inverted T
Type 2: Saddle-back ST elevation; not diagnostic alone
Gene: SCN5A (Na⁺ channel)
Demographics: Young Asian males (prevalent in SE Asia — "Brugada belt")
Triggers: Fever, Na⁺ channel blockers, alcohol, large meals
Risk: VF during sleep/rest
Rx: ICD; quinidine (for electrical storm); avoid Na channel blockers
Tip: Unmasked by fever — repeat ECG if febrile!

13. PERICARDITIS ECG (4 Stages)

Stage	Timing	ECG
1	Day 1–2	Diffuse concave (saddle) ST elevation all leads (except aVR/V1 which are depressed); PR depression (most specific finding)
2	Days 3–7	ST normalises; T flattening
3	Weeks	Diffuse T-wave inversion
4	Months	ECG returns to normal

Pericarditis vs STEMI:

Concave (saddle) vs convex ST; PR depression present; all leads vs territory; no Q waves; no reciprocal changes (except aVR/V1)

14. CARDIAC TAMPONADE (Classic ECG Triad — Harrison's)

Sinus tachycardia
Low voltage (QRS < 5 mm limb leads; < 10 mm chest leads)
Electrical alternans (alternating QRS amplitude — heart swinging in effusion)

15. PULMONARY EMBOLISM

Commonest ECG finding: Sinus tachycardia
Classic (uncommon, ~20%): S₁Q₃T₃ — S wave lead I, Q wave lead III, T inversion lead III
New RBBB, RAD, P pulmonale, T inversion V1–V4 (RV strain)

16. HYPOTHERMIA

Osborn (J) waves — positive deflection at J-point, best in V3–V6
Sinus bradycardia; AF common < 30°C; QT prolongation → VF/asystole

17. VENTRICULAR ARRHYTHMIAS

PVCs

Wide QRS (≥ 120 ms), no preceding P, full compensatory pause
R-on-T phenomenon → VF risk (acute MI, long QT)

VT vs SVT with Aberrancy

Feature	VT	SVT + aberrancy
AV dissociation	Yes	No
Fusion beats	Yes	No
Capture beats	Yes (narrow)	No
QRS	> 160 ms typically	120–140 ms
History	Structural heart disease	Young, no structural disease
Concordance	Positive or negative V1–V6	No

Management: Unstable → synchronised DC cardioversion; stable → amiodarone 300 mg IV; pulseless VT/VF → immediate defibrillation + CPR

AIVR (Accelerated Idioventricular Rhythm)

Rate 40–100 bpm; wide QRS; seen in post-MI reperfusion or digoxin toxicity
Benign; no treatment required

18. QUICK-REFERENCE TABLE

ECG Finding	Top Differential
Rate ~150 bpm regular	Atrial flutter 2:1 (until proven otherwise)
Irregularly irregular, no P waves	AF
Electrical alternans + low voltage	Cardiac tamponade
PR depression + saddle ST	Pericarditis
Coved ST V1–V2	Brugada syndrome
S₁Q₃T₃	Pulmonary embolism
Tented T waves	Hyperkalaemia
U waves prominent	Hypokalaemia
Short QT	Hypercalcaemia
Long QT	Hypocalcaemia, drugs, LQTS
Osborn (J) waves	Hypothermia
Deep Q V4–V6 + LVH	HCM
Giant T inversion V3–V6	Apical HCM (Yamaguchi)
Deep symmetric T inversion V2–V3	Wellens' syndrome (LAD stenosis)
Delta wave + short PR	WPW
Global QRS negativity in lead I	Dextrocardia
"Reverse tick" ST	Digoxin effect
Atrial tachycardia + AV block	Digoxin toxicity
Twisting QRS polymorphic VT	Torsades de Pointes

Sources: Harrison's Principles of Internal Medicine 22E (2025); Braunwald's Heart Disease; Goldman-Cecil Medicine — scope equivalent to Davidson's for HKMLE coverage.

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