How do you read an ECG systematically?
An electrocardiogram records the heart's electrical activity on paper moving at 25 mm/s. Each small square is 0.04 s and each large square is 0.2 s (five small squares); the machine is calibrated so that 1 mV moves the stylus 1 cm (10 small squares). Before reading the waves, confirm the speed and calibration — half-standard or double-speed tracings are a classic trap.
- Rate — regular rhythm: 300 ÷ large squares or 1500 ÷ small squares between two R waves; irregular rhythm: beats in a 10-second strip × 6.
- Rhythm — are P waves present and regular, is each P followed by a QRS, is the QRS narrow or wide, is the R–R interval regular?
- Axis — look at the QRS in lead I and aVF.
- Intervals — PR, QRS duration, QT/QTc.
- Morphology — P wave, Q waves, R-wave progression, ST segment, T wave and U wave.
- Compare with an old ECG and the clinical picture before concluding.
What are the normal ECG waves and intervals?
| Component | Represents | Normal value | Abnormal when |
|---|---|---|---|
| P wave | Atrial depolarisation (right atrium first, then left) | About 3 small squares wide and 2.5 small squares tall; upright in I and II, inverted in aVR | Abnormal shape or size suggests atrial enlargement |
| PR interval | Start of atrial depolarisation to start of ventricular depolarisation, including AV-node delay | 120–200 ms (3–5 small squares) | Over 200 ms = first-degree AV block; short in WPW and Lown-Ganong-Levine |
| QRS complex | Ventricular depolarisation | Under 120 ms, usually 60–100 ms | Wide in bundle branch block, hyperkalaemia, ventricular rhythms |
| Septal Q wave | Septal depolarisation (I, aVL, V5, V6) | Tiny, under 0.1 mV | Pathological if over 40 ms wide, over 1 mm deep or over 25% of the QRS |
| ST segment | End of depolarisation to start of repolarisation | Isoelectric, 80–120 ms | Elevation or depression of 1 mm or more at the J point |
| T wave | Ventricular repolarisation | Upright in leads with tall R waves; under 10 mm | Tall/peaked, flat, inverted or biphasic |
| QT interval | Whole ventricular depolarisation plus repolarisation | Under 400–440 ms; varies inversely with heart rate | QTc over 440 ms (men) or 460 ms (women) |
R waves get taller from V1 to V5 (R-wave progression) while S waves shrink from V1 to V6. Poor R-wave progression has several causes, including an old anteroseptal infarct, left ventricular hypertrophy and wrong lead placement.
QTc (Bazett) = QT ÷ √(RR interval in seconds)
Bazett is the correction formula most often asked; QT shortens as heart rate rises, so always correct before calling it prolonged.
How do you work out the cardiac axis?
The cardiac axis is the average direction of ventricular depolarisation in the frontal plane. StatPearls gives the normal range as −30° to +90°. The quickest method uses the net QRS direction in lead I and aVF.
| Lead I | aVF | Axis | Common causes |
|---|---|---|---|
| Positive | Positive | Normal | — |
| Positive | Negative | Left axis deviation (0° to −90°) | Old inferior MI, left ventricular hypertrophy, left bundle branch block |
| Negative | Positive | Right axis deviation (+90° to 180°) | Right ventricular hypertrophy, pulmonary hypertension, hyperkalaemia, WPW |
Ventricular hypertrophy. Right ventricular hypertrophy shows right axis deviation with R larger than S in V1 and S larger than R in V6. Left ventricular hypertrophy is suggested when S in V1 or V2 plus R in V5 or V6 exceeds 35 mm, or R in aVL exceeds 13 mm.
How do you localise a STEMI on the ECG?
STEMI criteria (StatPearls): new ST elevation at the J point in two contiguous leads of more than 0.1 mV (1 mm) in all leads except V2–V3. In V2–V3 the threshold is over 0.2 mV in men 40 or older, over 0.25 mV in men under 40 and over 0.15 mV in women. The ECG should be done and read within 10 minutes of first medical contact.
| Territory | Leads with ST elevation | Usual artery | Reciprocal change |
|---|---|---|---|
| Septal | V1–V2 | LAD (septal branches) | — |
| Anterior | V3–V4 | LAD | Inferior leads |
| Extensive anterior (proximal LAD) | V1–V6, I, aVL | Proximal LAD | Inferior leads; may show a new bundle branch block |
| Lateral | I, aVL, V5, V6 | Left circumflex or diagonal branch | III and aVF |
| Inferior | II, III, aVF | RCA (right-dominant circulation in 75–80%) or LCx | I and aVL |
| Posterior | No elevation on standard leads; horizontal ST depression V1–V3 with tall R and upright T | RCA or LCx | Confirm with V7–V9 |
| Right ventricle | V4R (right-sided leads) | Proximal RCA | Often with inferior MI |
LBBB and suspected MI (Sgarbossa). Concordant ST elevation of 1 mm or more, ST depression of 1 mm or more in V1–V3, and discordant ST elevation of 5 mm or more. The criteria are specific but not sensitive.
Pericarditis vs STEMI. Pericarditis gives diffuse ST elevation with PR depression (PR elevation in aVR); an infarct gives localised elevation, often with reciprocal depression. Early repolarisation, Prinzmetal angina, myocarditis, hyperkalaemia, pulmonary embolism, subarachnoid haemorrhage and Brugada syndrome can also raise the ST segment.
What ECG changes do hyperkalaemia and hypokalaemia cause?
| Serum K+ (mEq/L) | ECG change |
|---|---|
| 5.5–6.5 | Tall, peaked (tented) T waves |
| 6.5–7.5 | Flattening or loss of P waves |
| 7–8 | Widening of the QRS complex |
| 8–10 | Sine-wave pattern, severe arrhythmias, asystole |
Treating hyperkalaemia with ECG changes: give calcium first to stabilise the myocardium — it does not lower potassium. Calcium gluconate is preferred peripherally; calcium chloride has three times the elemental calcium but irritates veins. Then shift potassium into cells, for example 10 units of regular insulin with 50 mL of 50% dextrose, and remove potassium from the body.
Hypokalaemia produces, in order, T-wave flattening, ST depression, a prominent U wave and a prolonged QT (really a QU) interval. Hypomagnesaemia often coexists and the combination raises the risk of torsades de pointes.
How do you recognise atrial fibrillation and atrial flutter?
Atrial fibrillation is the most common sustained arrhythmia. The ECG shows an irregularly irregular ventricular rhythm with no discrete P waves and a wavy fibrillatory baseline. Thromboembolic risk is estimated with a validated score such as CHA₂DS₂-VASc; the 2023 ACC/AHA/ACCP/HRS guideline treats female sex as a risk modifier rather than an indication for anticoagulation on its own.
Atrial flutter is a macro-re-entrant circuit with an atrial rate of about 300/min. With the common 2:1 block the ventricular rate is about 150/min — a regular narrow-complex tachycardia at 150 should always make you look for flutter waves. Typical (counter-clockwise) flutter gives negative sawtooth waves in II, III and aVF.
| Feature | Atrial fibrillation | Atrial flutter |
|---|---|---|
| Atrial activity | Chaotic fibrillatory waves, no P waves | Regular sawtooth flutter waves, ~300/min |
| Ventricular rhythm | Irregularly irregular | Usually regular (2:1, 3:1, 4:1) or variable |
| Classic rate clue | Variable | About 150/min with 2:1 block |
| Best leads | V1 and rhythm strip | II, III, aVF (sawtooth) |
Multifocal atrial tachycardia (MAT) is the other irregular rhythm to separate from AF. It needs an atrial rate above 100/min with three or more different non-sinus P-wave shapes in the same lead, irregular PP intervals and an isoelectric baseline between P waves — so, unlike AF, discrete P waves are present. It is typically seen in elderly patients with COPD or acute respiratory failure, and with hypokalaemia, hypomagnesaemia or theophylline. A wandering atrial pacemaker looks the same but the rate is below 100/min. Treat the underlying cause and correct potassium and magnesium; if a drug is needed, a non-dihydropyridine calcium channel blocker (verapamil or diltiazem) is preferred in lung disease, while beta-blockers are first-line only without lung disease. Cardioversion, anticoagulation and antiarrhythmics have no role.
How do you tell first-, second- and third-degree heart block apart?
| Block | ECG | Level / significance | Usual management |
|---|---|---|---|
| First degree | PR over 200 ms; every P conducted | May be normal; drugs, myocarditis, hypokalaemia, rheumatic fever | Usually none |
| Mobitz I (Wenckebach) | PR lengthens progressively until a P wave is not conducted | Usually at the AV node; most patients asymptomatic | Observe; atropine or pacing only if unstable |
| Mobitz II | Sudden dropped QRS without progressive PR lengthening | Usually below the AV node (His bundle); can progress to complete block | Permanent pacemaker |
| Third degree (complete) | Complete AV dissociation; atria and ventricles beat at their own rates | Commonest cause is degenerative conduction disease; also MI and Lyme disease | Permanent pacemaker if irreversible |
Bundle branch blocks widen the QRS beyond 0.12 s. Right bundle branch block shows an RSR′ pattern in V1–V2; left bundle branch block shows broad or notched R waves in I, aVL, V5 and V6, usually with left axis deviation, and usually signals underlying heart disease.
What do WPW, Brugada syndrome and long QT look like?
Wolff-Parkinson-White. An accessory pathway bypasses the AV node, giving a short PR interval, a slurred upstroke of the QRS (delta wave) and a wide QRS in sinus rhythm. The term syndrome is used when this pattern coexists with tachyarrhythmia. In pre-excited atrial fibrillation, AV-nodal blockers are contraindicated because they can push conduction down the accessory pathway into ventricular fibrillation; procainamide or ibutilide are the drugs of choice, and accessory-pathway catheter ablation is the treatment of choice for symptomatic patients.
Brugada syndrome is an inherited (autosomal dominant) channelopathy; the first gene identified, SCN5A (cardiac sodium channel), accounts for about 15–30% of cases. It is 8–10 times more common in men. The diagnostic type 1 pattern is coved ST elevation of 2 mm or more in at least one of V1–V3 followed by a negative T wave. Fever can unmask it, and sodium-channel blockers (ajmaline, flecainide, procainamide) are used as a provocation test. An ICD prevents sudden death.
Long QT syndrome. QTc is prolonged when over 440 ms in men or 460 ms in women; over 500 ms carries a high risk of torsades de pointes. Congenital forms involve ion-channel genes — KCNQ1 (LQT1) is the commonest; syncope while swimming is relatively specific for LQT1, and Jervell and Lange-Nielsen syndrome adds congenital deafness. Acquired causes are commoner: hypokalaemia, hypocalcaemia, hypomagnesaemia and drugs that block the IKr (KCNH2) current, such as sotalol and amiodarone.
| Situation | First-line treatment |
|---|---|
| Torsades de pointes (stable) | IV magnesium sulfate, whatever the serum magnesium |
| Torsades, unstable | Non-synchronised defibrillation |
| Congenital long QT, long term | Beta-blocker; ICD after cardiac arrest or if beta-blockers fail |
| Pre-excited AF (WPW) | Procainamide or ibutilide; avoid AV-nodal blockers |
| Brugada with high risk | Implantable cardioverter-defibrillator |
What ECG traps come up most often in the exam?
- Regular narrow tachycardia at 150/min — atrial flutter with 2:1 block until proven otherwise.
- ST depression in V1–V3 with tall R waves — think posterior MI and ask for V7–V9, not just 'anterior ischaemia'.
- Hypotension after nitrates in an inferior MI — suspect right ventricular infarction; check V4R.
- Peaked T waves with a wide QRS — treat as hyperkalaemia and give calcium before waiting for the lab.
- Wide-complex irregular tachycardia in a young patient — pre-excited AF; do not give AV-nodal blockers.
- Saddleback ST elevation in V1–V2 — Brugada type 2 is not diagnostic unless it converts to type 1.
- Dropped beats with a constant PR — Mobitz II, which needs a pacemaker; Mobitz I usually does not.