ECG and arrhythmias
ECG, Arrhythmias and Heart Block: FCPS Part 1 Physiology Guide
ECG waves and intervals, rate, axis, heart block levels, re-entry, flutter, VF, long QT, Brugada, electrolytes and MI territories for FCPS Part 1. Explains why Mobitz II needs pacing, why torsades needs magnesium and what pericarditis and PE look like.
What the ECG records
- The ECG records current flowing between regions of myocardium that are at different electrical states: waves appear only while a wave of depolarisation or repolarisation is moving. When the ventricles are fully depolarised (ST segment) or fully repolarised (TP segment), the trace is isoelectric.
- The SA node, AV node and His bundle are too small to register; their activity is inferred. Atrial repolarisation is normally hidden in the QRS; it becomes visible (Ta wave) when P waves are not followed by QRS, as in complete heart block.
| Feature | Represents | Normal |
|---|---|---|
| P wave | Atrial depolarisation | Under 0.12 s |
| PR interval | Atrial depolarisation plus AV nodal delay (allows ventricular filling) | 0.12–0.20 s |
| QRS | Ventricular depolarisation | Under 0.12 s |
| ST segment | Ventricles fully depolarised (plateau) | Isoelectric |
| T wave | Ventricular repolarisation | |
| QT interval | Whole ventricular depolarisation and repolarisation: the electrical counterpart of ventricular systole | QTc under about 0.44–0.46 s |
| U wave | Late repolarisation (Purkinje or papillary muscle); prominent in hypokalaemia |
- Conduction velocity is fastest in the Purkinje fibres (about 4 m/s) and slowest in the AV node (about 0.05 m/s).
- A β-blocker prolongs the PR interval by slowing AV nodal conduction (less cAMP, smaller calcium current).
Rate and axis
- At 25 mm/s, a small square is 0.04 s and a large square 0.2 s. Rate = 300 ÷ large squares between R waves, or 1,500 ÷ small squares, or 60 ÷ RR interval in seconds.
- RR of 4 large squares: 300 ÷ 4 = 75/min. RR of 0.55 s: 60 ÷ 0.55 = about 109/min. For irregular rhythms, count QRS complexes in 6 seconds and multiply by 10.
| Lead I | aVF | Axis |
|---|---|---|
| Positive | Positive | Normal |
| Positive | Negative | Left axis deviation (left anterior hemiblock, inferior MI) |
| Negative | Positive | Right axis deviation (RVH, PE, tall thin people) |
Heart block: the level decides the danger
| Type | ECG | Site | Management |
|---|---|---|---|
| First degree | PR over 0.20 s, all conducted | AV node | Benign |
| Mobitz I (Wenckebach) | PR lengthens until a beat drops | Within the AV node | Usually benign; physiological at night in athletes (vagal); do not pace if asymptomatic |
| Mobitz II | Constant PR with sudden dropped beats, often broad QRS | His–Purkinje system (infranodal) | Permanent pacemaker; can progress to complete block |
| 2:1 block | Two P waves per QRS | Either; broad QRS suggests infranodal | Judge by QRS width and symptoms |
| Complete (third degree) | P and QRS independent | Node or below | Escape: narrow junctional 40–60/min, or broad ventricular 20–40/min; pacing; cannon a waves |
- Atropine speeds conduction only through the vagally innervated AV node. In infranodal block it does not help and can worsen it by raising the atrial rate.
- Absent P waves with normal narrow QRS: the pacemaker is in the AV junction (40–60/min).
- Inferior MI causes AV block because the right coronary artery usually supplies the AV node.
Exam trap A constant PR with dropped beats and a broad QRS in a syncopal patient means infranodal block: pace, do not rely on atropine.
Re-entry and tachyarrhythmias
- Re-entry needs two conditions: unidirectional (one-way) block in one limb of a circuit and slow enough conduction around the circuit that tissue at the block has recovered when the impulse returns. Adenosine breaks circuits that pass through the AV node.
| Rhythm | Mechanism | ECG |
|---|---|---|
| Atrial flutter | Macro-re-entry around the right atrium (cavotricuspid isthmus) | Saw-tooth waves at 300/min in II, III, aVF; 2:1 block gives 150/min; 3:1 gives 100/min; adenosine unmasks waves but does not cure |
| Atrial fibrillation | Multiple wavelets, pulmonary vein triggers | No P waves (fibrillatory baseline), irregularly irregular QRS |
| AVNRT, AVRT | Re-entry through or around the AV node | Regular narrow complex; adenosine terminates |
| WPW | Accessory pathway (Kent bundle) | Short PR, delta wave; ablation; avoid AV-node blockers in pre-excited AF |
| VT | Ventricular re-entry around scar | Broad regular complexes |
| Ventricular fibrillation | Multiple chaotic re-entrant wavelets in the ventricles, often within 48 hours of MI | Irregular low-amplitude waves, no QRS; no pulse; defibrillate |
| Torsades de pointes | Early afterdepolarisations on a long QT | Polymorphic VT twisting around the baseline |
- Torsades: a patient on clarithromycin and ondansetron with diarrhoea (low K+ and Mg2+) develops torsades with QTc 560 ms. Give IV magnesium sulphate to prevent recurrence, correct potassium, stop QT drugs. Amiodarone and sotalol are wrong: they prolong QT further.
Inherited channelopathies
- Congenital long QT syndrome (potassium or sodium channel mutations): syncope triggered by sudden noise (alarm clock), exercise or swimming, QTc around 500 ms or more; unexplained drowning. Treat with β-blockers; screen relatives.
- Brugada syndrome (sodium channel loss): coved ST elevation with T inversion in V1–V2, unmasked by fever or sodium channel blockers; family history of sudden death in sleep. Treat fever promptly; ICD for high risk.
ECG patterns to recognise
| Condition | ECG |
|---|---|
| Hyperkalaemia (renal failure, multiple transfusions) | Tall peaked T, flat P, long PR, wide QRS, sine wave |
| Hypokalaemia (furosemide) | Flat T, prominent U waves, ST depression, long QU |
| Hypercalcaemia, hypocalcaemia | Short QT, long QT |
| Hypothermia | Bradycardia, J (Osborn) waves |
| Digoxin effect | Sagging reverse tick ST depression at therapeutic levels: effect, not toxicity |
| Acute pericarditis | Widespread concave ST elevation with PR depression, ST depression in aVR, normal troponin; do not thrombolyse |
| Large pericardial effusion | Low-voltage QRS with electrical alternans (heart swinging in fluid) |
| Pulmonary embolism | Sinus tachycardia, S1Q3T3, right bundle branch block, right axis: acute right ventricular strain; a normal ECG does not exclude PE |
| Acute MI | Hyperacute T waves, then ST elevation, then Q waves |
| Location of ST elevation | Territory and artery |
| V1–V4 | Anterior: left anterior descending |
| I, aVL, V5–V6 | Lateral: circumflex |
| II, III, aVF | Inferior: right coronary |
| ST depression V1–V3 with tall R | Posterior |
Remember PR is the AV node, QT is systole, U is low potassium, peaked T is high potassium.
How FCPS asks about this
- Lengthening PR then a dropped beat: Mobitz I, block within the AV node.
- Constant PR, dropped beats, broad QRS: His–Purkinje block; permanent pacemaker.
- Torsades with long QTc: IV magnesium sulphate.
- Rate from 4 large squares or RR 0.55 s: 75/min; about 109/min.
- Fastest conduction: Purkinje fibres; the PR interval reflects AV nodal delay.
- Two conditions for re-entry: one-way block plus slow conduction; flutter is right atrial macro-re-entry.
- Low voltage with electrical alternans: large pericardial effusion.
Test yourself on this topic
5 of the 45 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 66-year-old man has palpitations with a regular narrow-complex tachycardia at 150/min. IV adenosine briefly slows the ventricular rate, revealing regular saw-tooth atrial waves at 300/min in leads II, III and aVF; the rate returns to 150/min afterwards. Which of the following is the mechanism of this atrial rhythm?
Answer: Right atrial macro-re-entry
Typical atrial flutter is a single large re-entrant circuit in the right atrium, running counter-clockwise around the tricuspid annulus and through the narrow cavotricuspid isthmus. This produces regular atrial activity at about 300/min, seen as negative saw-tooth waves in the inferior leads. The AV node usually conducts every second wave, giving a ventricular rate of about 150/min. Adenosine increases AV block without stopping the circuit, unmasking the flutter waves, and ablation of the isthmus cures it.
Atrial flutter
- Macro-re-entry in right atrium
- Around the tricuspid annulus
- Atria 300/min, ventricles often 150/min
- Cured by isthmus ablation
Remember Regular 150 in an older adult: think flutter with 2:1 block.
Exam trap Adenosine is diagnostic, not curative, in flutter; it only unmasks the waves.
Why the other options are wrong
- Re-entry within the AV node AV nodal re-entry would usually terminate with adenosine.
- Re-entry via an accessory pathway Accessory pathway re-entry uses the AV node and usually stops with adenosine.
- Multiple random atrial wavelets This describes atrial fibrillation, which is irregular.
- Enhanced automaticity of the SA node Sinus tachycardia does not reach 300/min with saw-tooth waves.
Which ECG change is characteristic of hypokalaemia?
Answer: U waves, flat T waves
Hypokalaemia (K⁺ below 3.5 mmol/L) causes flattened or inverted T waves, prominent U waves, ST depression and apparent QT (QU) prolongation, with a risk of arrhythmias, especially with digoxin. Clinical features: muscle weakness, cramps, ileus, constipation and polyuria. Causes: diuretics, vomiting, diarrhoea, hyperaldosteronism, insulin or β2 agonists. Replace orally if mild; IV at no more than 10 mmol/hour via a peripheral line. Also check magnesium, which is needed for potassium correction.
Hypokalaemia
- ECG: U waves, flat T, ST depression
- Weakness, ileus, polyuria
- Causes: diuretics, vomiting, aldosterone excess
- Correct magnesium too; IV ≤ 10 mmol/h
Remember Low potassium: U waves show up.
Why the other options are wrong
- Tall peaked T waves Hyperkalaemia.
- Shortened QT interval Hypercalcaemia.
- Wide QRS, sine-wave pattern Severe hyperkalaemia.
- Delta waves Wolff-Parkinson-White syndrome.
A fit 20-year-old athlete's night-time ECG shows PR intervals lengthening beat by beat until one P wave is not conducted. Which of the following is the site of the block?
Answer: Within the AV node
Progressive PR prolongation before a dropped beat is Mobitz type I (Wenckebach) block. AV nodal cells depend on slow calcium-mediated action potentials and show decremental conduction: each impulse arrives earlier in the recovery period, conducts more slowly, until one fails. It is common at night and in athletes with high vagal tone, and usually needs no treatment. Infranodal block gives a fixed PR with sudden dropped beats.
Wenckebach block
- PR lengthens then a beat drops
- Site: AV node
- Decremental conduction
- Benign with high vagal tone
Remember Longer, longer, drop: the AV node.
Exam trap Do not pace an asymptomatic athlete with nocturnal Wenckebach; it is physiological.
Why the other options are wrong
- Bundle of His His bundle block gives a fixed PR with dropped beats.
- Bundle branches Bundle branch disease gives a fixed PR and broad QRS.
- SA node exit SA exit block drops the P wave as well.
- Purkinje fibres Purkinje disease gives broad complexes, not progressive PR.
An ECG shows ST elevation in leads V1–V4. Which artery is most likely occluded?
Answer: Left anterior descending artery
ECG territories: anterior (V1–V4 or V3–V4) and anteroseptal—LAD (anterior wall of LV, anterior two-thirds of septum, apex); lateral (I, aVL, V5–V6)—left circumflex or diagonal branches; inferior (II, III, aVF)—usually RCA (right dominant); posterior (ST depression V1–V3 with tall R waves)—PDA or circumflex. Proximal LAD occlusion ('widow-maker') causes extensive anterior infarction with risk of heart failure and VSD.
ECG territories
- V1–V4: LAD (anterior/septal)
- I, aVL, V5–6: circumflex (lateral)
- II, III, aVF: RCA (inferior)
- V1–V3 depression: posterior
Remember Leads point to the artery.
Why the other options are wrong
- Right coronary artery Inferior leads II, III, aVF.
- Left circumflex artery Lateral leads I, aVL, V5–V6.
- Posterior descending artery Posterior changes.
- Marginal branch of the right coronary artery Right ventricular infarction (V4R).
A woman on digoxin for AF has no nausea or visual symptoms, and her serum digoxin level is within the therapeutic range. Her ECG shows sagging, 'reverse tick' ST depression in the lateral leads. What does this indicate?
Answer: Digoxin effect, not toxicity
Digoxin commonly produces a characteristic downsloping ('reverse tick') ST depression, shortened QT and sometimes T-wave flattening at therapeutic levels. This digoxin effect does not mean toxicity. Toxicity causes symptoms (nausea, confusion, yellow vision) and arrhythmias such as frequent ectopics, bigeminy, atrial tachycardia with block or bradycardia, often with low potassium.
Digoxin on the ECG
- Reverse tick ST depression
- Short QT
- Effect ≠ toxicity
- Toxicity: arrhythmias, symptoms
Remember Reverse tick: digoxin is on board.
Exam trap Low potassium increases digoxin toxicity.
Why the other options are wrong
- Acute myocardial infarction No symptoms and a typical pattern.
- Digoxin toxicity needing antibody No features of toxicity.
- Hyperkalaemia Would cause peaked T waves.
- Pericarditis Widespread saddle-shaped ST elevation.
Where this sits in the CPSP syllabus
- Paper 1: Cardiovascular system, ECG and arrhythmias; heart block
- Surgery & Allied, Paper 2: Cardiovascular system, ECG and arrhythmias; heart block
- Medicine & Allied, Paper 2: Cardiovascular system, ECG and arrhythmias; heart block
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