ECG Interpretation
Educational use only. This content is derived from paramedicine study notes and is intended as a study and revision aid. Always follow your service's current clinical practice guidelines and defer to senior clinicians in practice.
Interactive ECG Waveform — click a component to learn more
Click a button above or a waveform component to see its definition and normal values.
Grid: 1 small square = 0.04 s / 0.1 mV | 1 large square = 0.2 s / 0.5 mV (standard 25 mm/s, 10 mm/mV)
Normal Values & Measurements
| Component | Normal Duration | Normal Amplitude | Clinical Significance |
|---|---|---|---|
| P wave | < 0.12 s (< 3 small sq) | < 2.5 mm | Atrial depolarisation; absence suggests AF or atrial standstill |
| PR interval | 0.12–0.20 s (3–5 sq) | — | AV conduction time; prolonged = 1° AV block; short = pre-excitation |
| QRS complex | < 0.12 s (< 3 sq) | Varies by lead | Ventricular depolarisation; wide ≥ 0.12 s = BBB, aberrant, or ventricular origin |
| ST segment | 0.08–0.12 s | Isoelectric (± 1 mm) | Ventricular repolarisation plateau; elevation/depression = ischaemia |
| T wave | 0.10–0.25 s | Same direction as QRS | Ventricular repolarisation; inversion may indicate ischaemia |
| QT interval | < 0.44 s (M) / < 0.46 s (F) | — | Total ventricular activity; prolonged QT = risk of Torsades de Pointes |
| U wave | — | Small, follows T | Prominent U waves may indicate hypokalaemia |
Heart Rate Calculation Methods
300 Method
Count large squares between two R waves. Divide 300 by this number. Best for regular rhythms.
300 ÷ large squares = rate
1500 Method
Count small squares between two R waves. Divide 1500 by this number. More accurate for regular rhythms.
1500 ÷ small squares = rate
6-Second Strip
Count QRS complexes in 6 seconds (30 large squares). Multiply by 10. Best for irregular rhythms (e.g. AF).
QRS count × 10 = rate
Normal Sinus RhythmNSR
- Rate 60–100 bpm
- Rhythm Regular — consistent R-R intervals
- P waves Present, upright in II, one before every QRS
- PR interval 0.12–0.20 s, normal and constant
- QRS Narrow (< 0.12 s)
Rate 60–100
Regular
P before every QRS
Sinus BradycardiaSB
- Rate < 60 bpm
- Rhythm Regular
- P waves Normal morphology, one before every QRS
- PR interval Normal (0.12–0.20 s)
- QRS Narrow — all other features identical to NSR
- Causes Athletes, high vagal tone, beta-blockers, hypothyroidism, inferior MI, raised ICP
Rate <60
Regular
Normal morphology
Sinus TachycardiaST
- Rate > 100 bpm (usually 100–160)
- Rhythm Regular
- P waves Normal, may merge into T at high rates
- PR interval Normal or slightly shortened
- QRS Narrow
- Causes Pain, fear, hypovolaemia, hypoxia, fever, anaemia, PE, sepsis, thyrotoxicosis
Rate >100
Regular
Normal P waves
Sinus ArrhythmiaSA
- Rate 60–100 bpm (varies with respiration)
- Rhythm Irregular — R-R intervals vary > 0.12 s
- P waves Normal morphology throughout
- PR interval Normal and constant
- Mechanism Vagal tone variation — HR increases on inspiration, decreases on expiration
Irregular R-R
Normal P waves
Normal morphology
Normal Sinus Rhythm — Clinical Note
The gold standard of cardiac rhythms. All criteria must be met simultaneously. Any single deviation from these parameters defines a specific arrhythmia. NSR does not exclude structural heart disease or significant pathology.
Sinus Bradycardia — Clinical Note
Sinus bradycardia is normal in well-trained athletes (rates as low as 35–40 bpm at rest). Only treat if haemodynamically compromised. In the acute setting: atropine 0.5–1 mg IV (repeat to 3 mg max); transcutaneous pacing if atropine fails. In inferior MI, bradycardia is often vagally mediated and may respond to atropine. Consider reversible causes before pacing.
Sinus Tachycardia — Clinical Note
Sinus tachycardia is almost always secondary — a physiological response to an underlying stressor. Treat the cause, not the rate. Cardioversion is not indicated. Failing to identify and treat the underlying cause (e.g. hypovolaemia, sepsis, PE) is dangerous. A rate persistently above 150 bpm warrants evaluation for an alternative arrhythmia (consider atrial flutter 2:1).
Sinus Arrhythmia — Clinical Note
Entirely benign. Very common in children, young adults, and athletes. The P-P interval varies but P wave morphology remains constant — this distinguishes it from a wandering atrial pacemaker (where P morphology changes). No treatment required.
Atrial FibrillationAF
- Rate Atrial ~350–600 bpm; ventricular variable
- Rhythm Irregularly irregular — no discernible pattern
- P waves Absent — replaced by chaotic fibrillatory baseline
- PR interval Not measurable
- QRS Narrow (unless aberrant conduction or BBB)
- Causes Hypertension, valve disease, heart failure, alcohol, thyrotoxicosis, ischaemia
Irregularly Irregular
No P waves
Narrow QRS
Atrial FlutterAFL
- Rate Atrial ~300 bpm; ventricular depends on ratio
- Rhythm Regular with fixed block; irregular with variable block
- Flutter waves Classic sawtooth — negative in II, III, aVF
- QRS Narrow
- Conduction ratio Usually 2:1 (ventricular ~150 bpm); may be 3:1 or 4:1
Atrial ~300 bpm
Sawtooth F waves
~150 bpm at 2:1
Premature Atrial ComplexPAC
- Timing Premature — before the next expected sinus beat
- P wave (P') Different morphology from sinus P — ectopic focus
- PR interval May vary depending on origin
- QRS Narrow (usually); wide if aberrantly conducted
- Pause Incomplete compensatory pause follows
- Causes Caffeine, stress, electrolyte imbalance, alcohol, atrial stretch
Early beat
Abnormal P'
Narrow QRS
SVTSupraventricular Tachycardia
- Rate 150–250 bpm — abrupt onset and termination
- Rhythm Regular
- P waves Hidden in QRS or T wave; often inverted (retrograde)
- QRS Narrow (< 0.12 s) unless aberrant conduction
- Mechanism Re-entry via AV node (AVNRT) or accessory pathway (AVRT)
- Treatment Vagal manoeuvres → adenosine → DC cardioversion if unstable
Rate 150–250
Regular
Narrow QRS
P hidden/inverted
Atrial Fibrillation — Clinical Note
The most common sustained arrhythmia. Hallmarks: no P waves, fibrillatory baseline, and an irregularly irregular ventricular response. AF carries a significant thromboembolic risk — the left atrial appendage pools blood during AF and clot formation can lead to stroke. Management goals: rate control (digoxin, diltiazem, beta-blockers) or rhythm control (cardioversion); anticoagulation if indicated. In the prehospital setting, haemodynamically unstable AF with rapid ventricular rate warrants urgent cardioversion.
Atrial Flutter — Clinical Note
A rate of exactly 150 bpm should always raise suspicion for 2:1 atrial flutter. Carotid sinus massage or adenosine can temporarily slow the ventricular rate, revealing the underlying flutter waves. Atrial flutter is often unstable and may convert to AF or revert to sinus rhythm. Cardioversion is highly effective (lower energy required than AF). Ablation is the long-term curative option.
Premature Atrial Complex — Clinical Note
PACs are common and generally benign in isolation. Key differentiator from PVCs: narrow QRS and an abnormal (but present) P' wave. Frequent PACs may trigger AF or atrial flutter in susceptible patients. An incomplete compensatory pause follows because the ectopic P' resets the SA node. Treatment is rarely required.
SVT — Clinical Note
SVT is an umbrella term for any tachycardia originating above the bundle of His (excluding sinus tachycardia and AFL/AF). AVNRT accounts for approximately 60% of cases. Adenosine (6 mg IV rapid bolus, repeat 12 mg if no effect) is both diagnostic and therapeutic — it blocks the AV node re-entry and terminates most SVTs. Warn the patient of transient flushing, chest discomfort, and dyspnoea. Adenosine is contraindicated in asthma — use diltiazem or verapamil instead.
Premature Ventricular ComplexPVC
- Timing Premature — before next expected beat
- P wave Absent — ectopic origin in ventricle
- QRS Wide (> 0.12 s), bizarre morphology with T wave discordance
- Pause Full compensatory pause (P-P around PVC = 2 × sinus cycle)
- Monomorphic All PVCs identical = same focus
- Polymorphic Varying PVC morphology = multiple foci
- R-on-T PVC on T wave → may trigger VF or Torsades
Wide & bizarre
Early
Full comp pause
No P wave
Ventricular TachycardiaVT
- Rate > 100 bpm (classically 120–200)
- Rhythm Regular (monomorphic VT)
- QRS Wide (≥ 0.12 s), broad and uniform (monomorphic)
- P waves Dissociated — independent of QRS (AV dissociation)
- Fusion beats Narrow beats during VT = pathognomonic
- Capture beats SA node transiently captures ventricle
- Duration Sustained ≥ 30 s; non-sustained < 30 s
Rate >100
Wide QRS
Regular
AV dissociation
Torsades de PointesPolymorphic VT
- Rate 200–300 bpm
- Rhythm Irregular
- QRS Wide, polymorphic — amplitude and axis twist around isoelectric line
- Association Prolonged QT interval (congenital or acquired)
- Triggers Hypokalaemia, hypomagnesaemia, Class IA/III antiarrhythmics, macrolides, antipsychotics
- Treatment IV magnesium sulphate 2 g; correct electrolytes; withdraw offending drug
Polymorphic
Twisting axis
Long QT assoc.
Ventricular FibrillationVF
- Rate Unmeasurable — no organised rhythm
- Rhythm Completely chaotic
- Waveform Irregular disorganised fibrillatory waveforms of variable amplitude
- Pulse Absent — cardiac arrest
- Treatment Immediate CPR + unsynchronised defibrillation; adrenaline 1 mg IV; amiodarone 300 mg after 3rd shock
CARDIAC ARREST
No QRS
Shockable
AsystoleFlatline
- Rate Zero — no electrical activity
- Rhythm Flat line — confirm in ≥ 2 leads
- Caution Fine VF may mimic asystole — check gain and multiple leads
- Pacemaker Small spikes may be visible in paced patients (failure to capture)
- Pulse Absent — cardiac arrest
- Treatment CPR + adrenaline 1 mg every 3–5 min; identify and treat reversible causes
CARDIAC ARREST
No QRS
Non-shockable
Pulseless Electrical ActivityPEA
- ECG Any organised electrical rhythm (may appear near-normal)
- Pulse Absent — no palpable output despite electrical activity
- Mechanism Electrical activity without sufficient mechanical contraction
- Treatment CPR + adrenaline; aggressively identify and treat reversible causes
- 4 Hs Hypoxia, Hypovolaemia, Hyper/Hypokalaemia, Hypothermia
- 4 Ts Tension pneumothorax, Tamponade, Toxins, Thrombosis (PE/coronary)
CARDIAC ARREST
Organised ECG
No mechanical output
PVCs — Clinical Note
Isolated PVCs are common and often benign. Higher concern features: >10,000 PVCs/24h, runs of ≥ 3 consecutive PVCs (= VT), polymorphic PVCs, R-on-T phenomenon, and PVCs in the context of acute MI. Bigeminy = PVC every other beat; Trigeminy = every third beat. Full compensatory pause distinguishes PVCs from PACs (PACs have an incomplete pause).
Ventricular Tachycardia — Clinical Note
Any wide complex tachycardia should be treated as VT until proven otherwise. AV dissociation, fusion beats, and capture beats confirm VT. If haemodynamically unstable → synchronised DC cardioversion. If pulseless → treat as VF (unsynchronised defibrillation + CPR). Amiodarone 300 mg IV is the antiarrhythmic of choice in stable VT if cardioversion is not immediately available.
Torsades de Pointes — Clinical Note
Torsades is polymorphic VT in the context of a prolonged QT interval. It may be self-terminating or degenerate into VF. IV magnesium sulphate (2 g over 10 min) is the treatment of choice even if serum Mg is normal. Identify and withdraw any QT-prolonging drugs. Correct hypokalaemia and hypomagnesaemia. Overdrive pacing or isoprenaline may be used to increase heart rate and shorten the QT interval.
Ventricular Fibrillation — Clinical Note
VF is a shockable cardiac arrest rhythm. Defibrillation as early as possible is the definitive treatment — every minute without shock reduces survival by 7–10%. Deliver shocks at 200 J (biphasic); continue CPR while the defibrillator charges. After 3 shocks: adrenaline 1 mg IV + amiodarone 300 mg IV. Resume CPR immediately after each shock without checking rhythm.
Asystole — Clinical Note
Asystole is a non-shockable arrest rhythm. Always confirm in multiple leads and increase gain to exclude fine VF before diagnosing asystole. Prognosis is generally poor without an identified and correctable reversible cause. Atropine is no longer recommended in asystole. Focus is on high-quality CPR and treating reversible causes (4 Hs and 4 Ts).
PEA — Clinical Note
PEA requires aggressive identification and reversal of the underlying cause. Point-of-care ultrasound is invaluable in PEA — cardiac standstill on echo suggests a grim prognosis; tamponade, massive PE, or severe hypovolaemia may be immediately reversible. The ECG may look almost normal (fine PEA) or may show a broad, slow agonal-type rhythm (coarse PEA). Rate is not prognostically useful in PEA.
R-on-T Phenomenon
A PVC that falls on the T wave of the preceding beat (during the vulnerable period of repolarisation) can trigger Ventricular Fibrillation or Torsades de Pointes. The T wave represents the relative refractory period — stimulation during this window is most likely to produce re-entry arrhythmias.
1st Degree AV BlockProlonged PR
- PR interval > 0.20 s (> 5 small squares) — constant
- P:QRS ratio 1:1 — every P wave followed by a QRS
- QRS Narrow (usually)
- Rhythm Regular
- Causes High vagal tone, inferior MI, electrolyte imbalance, digoxin, beta-blockers, athletes
PR >0.20s
Every P→QRS
Constant PR
2nd Degree — Mobitz IWenckebach
- PR interval Progressively lengthens each beat until one QRS is dropped
- Pattern Cyclical — resets after the dropped beat
- QRS Narrow — block is at AV nodal level
- P:QRS ratio More P waves than QRS (e.g. 3:2, 4:3)
- Causes Inferior MI, increased vagal tone, digoxin toxicity, myocarditis
PR lengthens
Dropped QRS
Cyclical
2nd Degree — Mobitz IIBelow His bundle
- PR interval Constant — does not change before the dropped beat
- Dropped QRS Sudden and unpredictable — no warning
- QRS Often wide — block is at or below the His bundle (infranodal)
- P:QRS ratio Fixed ratio (2:1, 3:1) — but with sudden drops
- Risk HIGH — can progress to complete heart block without warning
- Causes Anterior MI, structural heart disease, cardiomyopathy
Constant PR
Sudden drop
HIGH RISK
3rd Degree — Complete Heart BlockCHB
- AV relationship Complete dissociation — no P→QRS relationship
- P waves Regular at sinus rate, completely independent of QRS
- QRS Escape rhythm — wide if ventricular (20–40 bpm), narrow if junctional (40–60 bpm)
- Rhythm P-P regular and R-R regular, but independently
- Causes Inferior MI (transient), anterior MI (permanent), congenital, Lyme disease, degenerative
AV dissociation
P & QRS independent
Escape rate 20–40
1st Degree AV Block — Clinical Note
Generally benign and requires no treatment. Represents delayed but complete conduction through the AV node. Monitor for progression to higher degree block, particularly in the context of acute inferior MI or new drug introduction. Isolated 1° AV block in an otherwise healthy young person may be a normal variant.
Mobitz I (Wenckebach) — Clinical Note
Wenckebach is considered the more benign of the 2nd degree blocks. It is often associated with inferior MI (high vagal tone, RCA territory) and may be transient. The hallmark is that R-R intervals get progressively shorter before the dropped beat (because PR lengthens by smaller increments each cycle), then reset. Rarely requires pacing unless symptomatic with haemodynamic compromise.
Mobitz II — Clinical Note
Mobitz II is a high-risk, unstable rhythm. It can progress suddenly to complete heart block without warning. Transcutaneous pacing should be prepared immediately. Do NOT give atropine — Mobitz II is an infranodal block and atropine may paradoxically worsen it by increasing the atrial rate (more P waves competing for the blocked conduction system). Transvenous pacing is the definitive treatment.
Complete Heart Block — Clinical Note
Complete heart block requires urgent pacing. In inferior MI, CHB is usually transient and vagally mediated — atropine may be effective. In anterior MI, CHB reflects extensive septal infarction and requires permanent pacemaker implantation. Never use lignocaine or other drugs that suppress ventricular automaticity in CHB — they may abolish the escape rhythm, causing asystole. The narrower and faster the escape rhythm, the higher the block and the more stable the patient.
AV Block Comparison
| Degree | Name | PR Interval | Dropped QRS? | P:QRS Ratio | Risk |
|---|---|---|---|---|---|
| 1° | First Degree | Prolonged (>0.20s), constant | No — every P has QRS | 1:1 | Low |
| 2° I | Wenckebach / Mobitz I | Progressively lengthens | Yes — periodically | Variable, cyclical | Moderate |
| 2° II | Mobitz II | Constant, then suddenly drops | Yes — unpredictably | Fixed ratio (2:1, 3:1) | High |
| 3° | Complete Heart Block | No relationship | No QRS follows P (dissociated) | Independent | Critical |
V1 pattern — RBBB
WiLLiaM
RBBB shows a W in V1 and an M in V6 (RSR' pattern)
V1 pattern — LBBB
MoRRoW
LBBB shows an M in V1 and a W in V6 (QS / rS in V1, broad R in V6)
Right Bundle Branch BlockRBBB
- QRS duration ≥ 0.12 s (≥ 3 small squares)
- V1 morphology RSR' pattern — "rabbit ears" or M-shape
- V6 morphology Wide, slurred terminal S wave
- Mnemonic WiLLiaM — W in V1, M in V6
- T waves Discordant in V1 (opposite direction to last QRS deflection)
- Causes Right heart strain (PE, pulmonary HTN), RV infarction, congenital — or normal variant
QRS ≥0.12s
RSR' in V1
W in V1, M in V6
Left Bundle Branch BlockLBBB
- QRS duration ≥ 0.12 s
- V1 morphology Dominant S wave (QS or rS) — deep and broad, W-shape
- V5/V6 morphology Broad, notched R wave — no septal Q wave
- Mnemonic MoRRoW — M in V1, W in V6
- Secondary changes ST elevation in V1–V3 and depression in V5–V6 are EXPECTED secondary changes in LBBB
- STEMI recognition Use Sgarbossa Criteria — concordant ST changes are abnormal
- Causes Hypertension, cardiomyopathy, anterior MI, aortic valve disease — rarely a normal variant
QRS ≥0.12s
rS/QS in V1
Broad R in V5/V6
RBBB — Clinical Note
RBBB does not significantly interfere with STEMI identification in most leads. Isolated RBBB in a healthy person can be a normal variant — prevalence increases with age. New RBBB with chest pain warrants investigation, particularly for anterior or right ventricular involvement. RBBB can also be seen in massive PE (along with sinus tachycardia, S1Q3T3 pattern, and right axis deviation).
LBBB — Clinical Note
New LBBB (or presumed new) with ischaemic chest pain should be treated as a STEMI equivalent. LBBB has inherent secondary ST/T changes — only concordant (same direction as QRS) ST changes are truly abnormal. LBBB is rarely a normal variant and usually implies significant underlying cardiac pathology. New LBBB should prompt urgent investigation.
Sgarbossa Criteria — STEMI in LBBB
LBBB makes standard STEMI recognition difficult. The Sgarbossa Criteria identify true STEMI: (1) Concordant ST elevation ≥1 mm in a lead with a positive QRS — highest specificity; (2) Concordant ST depression ≥1 mm in V1–V3; (3) Excessively discordant ST elevation ≥5 mm. New LBBB with ischaemic symptoms should be treated as a STEMI equivalent until proven otherwise.
Ventricular Paced RhythmVP
- Pacemaker spike Vertical deflection immediately before QRS — the defining feature
- QRS morphology Wide (LBBB-like) — RV apex stimulation
- Rate Set by pacemaker (typically 60 bpm lower limit)
- P waves May or may not be present (VVI vs DDD pacemaker)
- STEMI Very difficult to identify — use Sgarbossa Criteria as for LBBB
Pacemaker spikes
Wide QRS
Regular
Accelerated Idioventricular RhythmAIVR
- Rate 40–100 bpm — faster than escape (>40) but not tachycardia (<100)
- QRS Wide (> 0.12 s) — ventricular origin
- P waves May be absent or dissociated
- Rhythm Regular
- Context Commonly seen post-ROSC or as reperfusion arrhythmia after MI/thrombolysis
Rate 40–100
Wide QRS
Often benign
Ventricular Escape RhythmVER
- Rate 20–40 bpm — intrinsic ventricular automaticity
- QRS Wide, bizarre morphology — ventricular origin
- P waves May be inverted (retrograde) or absent; may be hidden after QRS
- Mechanism Safety mechanism — fires when SA and AV nodes both fail
- Context Complete heart block, severe SA node dysfunction
Rate 20–40
Wide QRS
Inverted/hidden P
Agonal RhythmPre-asystole
- Rate < 20 bpm — extremely slow
- QRS Very wide, bizarre, irregular — progressively deteriorating
- Morphology Complexes become broader and lower amplitude over time
- Context Terminal rhythm — precedes asystole in the dying heart
- Pulse Usually absent or extremely weak
Rate <20
Very wide
Terminal
Paced Rhythm — Clinical Note
Pacemaker spikes are the key identifier — a vertical deflection immediately before each paced beat. Ventricular pacing produces an LBBB-like morphology as the RV apex is stimulated first. DDD pacemakers may show both atrial and ventricular spikes. Failure to capture (spike not followed by complex) or failure to sense (pacing when intrinsic beat present) are pacemaker emergencies. STEMI identification requires Sgarbossa Criteria as with LBBB.
AIVR — Clinical Note
AIVR is essentially a slow VT — it occupies the rate range between an idioventricular escape rhythm and VT. It is most commonly seen as a reperfusion arrhythmia after successful thrombolysis or PCI — its appearance can indicate successful vessel re-opening. It is often benign and self-limiting. Treatment is rarely required unless there is haemodynamic compromise; suppressing AIVR may paradoxically cause a slower escape rhythm to emerge.
Ventricular Escape Rhythm — Clinical Note
Ventricular escape rhythm is a safety net — it activates when all higher pacemakers fail. While it maintains cardiac output, it is slow and haemodynamically inefficient. Treatment targets the underlying cause (e.g. complete heart block) plus pacing, rather than suppressing the escape rhythm, which would cause asystole. Do not administer antiarrhythmics to suppress this rhythm.
Agonal Rhythm — Clinical Note
An agonal rhythm represents the last gasps of dying cardiac tissue. It indicates severely compromised cardiac function and typically precedes asystole within minutes if untreated. Prognosis is extremely poor unless a reversible cause is rapidly identified and corrected. CPR and resuscitation are indicated. Without a reversible cause, survival is rare.
ST Segment Changes
ST Elevation — STEMI
- →Measured at the J point (junction of QRS and ST segment)
- →Significant: ≥ 1 mm in limb leads; ≥ 2 mm in precordial leads (V1–V4)
- →Must be present in ≥ 2 contiguous leads to localise the territory
- →New LBBB with ischaemic chest pain = STEMI equivalent
- →Reciprocal ST depression in opposite leads supports true STEMI
ST Depression / T Wave Changes — NSTEMI / ACS
- →ST depression ≥ 0.5 mm in ≥ 2 contiguous leads = subendocardial ischaemia
- →T wave inversion may indicate ischaemia, PE, LVH strain pattern, or Wellens' syndrome
- →Hyperacute T waves (tall, peaked, symmetric) = very early ischaemia
- →Always correlate with symptoms, troponin, and clinical picture
STEMI Lead Localisation — Click a Territory
Coronary territory mapping — click a region to see culprit artery and clinical considerations
Anterior Wall
V1V2V3V4
Left Anterior Descending (LAD) artery
Inferior Wall
IIIIIaVF
Right Coronary Artery (RCA) — most common
Lateral Wall
IaVLV5V6
Left Circumflex (LCx) artery
Posterior Wall
V7V8V9
ST depression in V1–V3 (reciprocal) — posterior leads needed
Right Ventricular
V3RV4R
Right-sided leads — consider in all inferior STEMIs
Territory Details
Select a territory to see the culprit artery, reciprocal changes, and key clinical considerations.
Special ST Patterns
Pericarditis
- →Diffuse ST elevation — saddle-shaped (concave upward) across most leads
- →PR depression — key differentiating feature from STEMI
- →No reciprocal ST depression (except aVR which may show ST elevation)
- →Can closely mimic STEMI — always correlate with clinical symptoms
Benign Early Repolarisation
- →Common in young, healthy patients (especially athletes)
- →ST elevation with notching or slurring at the J point
- →Predominantly in mid-precordial leads (V2–V5)
- →Concave ST morphology; no reciprocal changes; stable over time
- →Diagnosis of exclusion — still requires clinical correlation
Left Ventricular Hypertrophy (LVH) — Voltage Criteria
Sokolow-Lyon Criteria
S (V1) + R (V5 or V6) ≥ 35 mm
The deepest S wave in V1 added to the tallest R wave in V5 or V6. A sum ≥ 35 mm (3.5 mV) is diagnostic. Left axis deviation and a lateral strain pattern are common additional findings.
- →Associated with hypertension, aortic stenosis, HCM
- →Lateral strain pattern (ST depression + T inversion) can mimic ischaemia
- →Tall R waves in V5/V6 and deep S waves in V1/V2
- →Left axis deviation commonly seen
| Rhythm | Rate | Regular? | P Wave | QRS | Key Feature |
|---|---|---|---|---|---|
| Normal Sinus | 60–100 | Yes | Upright, before each QRS | Narrow <0.12s | Normal in every way |
| Sinus Brady | <60 | Yes | Normal | Narrow | Same as NSR, just slow |
| Sinus Tachy | >100 | Yes | Normal | Narrow | Same as NSR, just fast |
| Sinus Arrhythmia | 60–100 | Irregular | Normal | Narrow | Varying R-R with respiration |
| AF | Variable | Irreg. Irreg. | Absent — fibrillatory | Narrow | No P waves, chaotic baseline |
| Atrial Flutter | ~150 (2:1) | Yes | Sawtooth F waves ~300 | Narrow | Classic sawtooth pattern |
| PAC | Underlying rate | Irregular | Early, different P' | Narrow | Premature beat with incomplete pause |
| SVT | 150–250 | Yes | Hidden/inverted | Narrow | Abrupt onset/offset, very fast |
| PVC | Underlying rate | Irregular | Absent | Wide >0.12s bizarre | Early, full compensatory pause |
| VT (Monomorphic) | >100 | Yes | Dissociated | Wide, uniform | Regular wide complex tachycardia |
| Torsades de Pointes | 200–300 | Irregular | Dissociated | Wide, varying | Twisting axis — long QT association |
| VF | — | Chaotic | None | None | Arrest — shockable |
| Asystole | 0 | — | None | None | Arrest — non-shockable |
| PEA | Variable | Variable | May be present | Organised | Arrest — ECG activity, no pulse |
| 1° AV Block | Normal | Yes | Normal | Narrow | PR >0.20s, constant |
| 2° Mobitz I | Normal | Cyclic | Normal | Narrow | Progressive PR → dropped QRS |
| 2° Mobitz II | Slow | Irregular | Normal | May be wide | Constant PR, sudden drop — HIGH RISK |
| 3° CHB | 20–40 | P&QRS indep. | Independent of QRS | Wide (escape) | Complete AV dissociation |
| RBBB | Normal | Yes | Normal | Wide — RSR' V1 | WiLLiaM: W in V1, M in V6 |
| LBBB | Normal | Yes | Normal | Wide — rS V1 | MoRRoW: M in V1, W in V6 |
Normal Interval Values
PR Interval
0.12–0.20 s
3–5 small squares
QRS Duration
< 0.12 s
< 3 small squares
QT Interval
<0.44s (M) / <0.46s (F)
Rate-dependent — use QTc