ECG Interpretation

• 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)

ClinicalThe 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.

• 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

ClinicalSinus 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: IV atropine; transcutaneous pacing if atropine fails. In inferior MI, bradycardia is often vagally mediated and may respond to atropine. Consider reversible causes before pacing.

• 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

ClinicalSinus 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).

• 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

ClinicalEntirely 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.

• Rate Atrial ~350–600 bpm; ventricular variable
• Rhythm Irregularly irregular — no discernible pattern
• P waves Absent — replaced by chaotic fibrillatory baseline
• QRS Narrow (unless aberrant conduction or BBB)
• PR interval Not measurable
• Causes Hypertension, valve disease, heart failure, alcohol, thyrotoxicosis, ischaemia

ClinicalThe 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.

• 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

ClinicalA 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.

• 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

ClinicalPACs 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.

• 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

ClinicalSVT 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 (given as a rapid IV bolus, repeated 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.

• 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

ClinicalIsolated 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).

• 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

ClinicalAny 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). IV amiodarone is often the antiarrhythmic of choice in stable VT if cardioversion is not immediately available.

• Rate 200–300 bpm
• Rhythm Irregular
• QRS Wide, polymorphic — amplitude and axis twist around isoelectric line
• Association Prolonged QT interval (congenital or acquired)
• Treatment IV magnesium sulphate; correct electrolytes; withdraw offending drug
• Triggers Hypokalaemia, hypomagnesaemia, Class IA/III antiarrhythmics, macrolides, antipsychotics

ClinicalTorsades is polymorphic VT in the context of a prolonged QT interval. It may be self-terminating or degenerate into VF. IV magnesium sulphate is often 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.

• 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; IV adrenaline; amiodarone after the 3rd shock

ClinicalVF 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: IV adrenaline + IV amiodarone. Resume CPR immediately after each shock without checking rhythm.

• Rate Zero — no electrical activity
• Rhythm Flat line — confirm in ≥ 2 leads
• Pulse Absent — cardiac arrest
• Treatment CPR + adrenaline; identify and treat reversible causes
• Caution Fine VF may mimic asystole — check gain and multiple leads
• Pacemaker Small spikes may be visible in paced patients (failure to capture)

ClinicalAsystole 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).

• ECG Any organised electrical rhythm (may appear near-normal)
• Mechanism Electrical activity without sufficient mechanical contraction
• Pulse Absent — no palpable output despite electrical activity
• 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)

ClinicalPEA 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.

• PR interval > 0.20 s (> 5 small squares) — constant
• Rhythm Regular
• QRS Narrow (usually)
• P:QRS ratio 1:1 — every P wave followed by a QRS
• Causes High vagal tone, inferior MI, electrolyte imbalance, digoxin, beta-blockers, athletes

ClinicalGenerally 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.

• 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

ClinicalWenckebach 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.

• 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
• Causes Anterior MI, structural heart disease, cardiomyopathy
• Risk HIGH — can progress to complete heart block without warning

ClinicalMobitz 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.

• 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

ClinicalComplete 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.

• 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

ClinicalVentricular 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.

• Rate < 20 bpm — extremely slow
• QRS Very wide, bizarre, irregular — progressively deteriorating
• Morphology Complexes become broader and lower amplitude over time
• Pulse Usually absent or extremely weak
• Context Terminal rhythm — precedes asystole in the dying heart

ClinicalAn 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.