ECG Interpretation Guide | GCC Nursing Platform

8-Step ECG Systematic Approach

Apply every step in order — never skip. Document findings before forming an interpretation.

1

Rate Normal 60–100 bpm
Regular rhythm: 300 ÷ large squares (5 mm) between R peaks. Precise: 1500 ÷ small squares (1 mm). Irregular rhythm: count complexes in a 10-second strip × 6 (or 6-second strip × 10).
2

Rhythm — Regular or Irregular?
Mark R-R intervals on paper. If all equal → regular. If chaotic → irregularly irregular (think AF). If a pattern → regularly irregular (e.g., Wenckebach). Confirm P wave precedes every QRS.
3

P Waves PR: 0.12–0.20 s (3–5 small sq)
Upright in I, II, aVF? Each followed by QRS? Morphology: peaked (RAE), notched/broad (LAE), biphasic (V1 in LAE). Absent P waves → AF, junctional, or VT. Sawtooth → flutter.
4

QRS Duration Normal < 0.12 s (3 small sq)
Narrow (<0.12 s): supraventricular origin. Wide (≥0.12 s): BBB, aberrant conduction, ventricular origin, hyperkalaemia, or sodium-channel blocking toxicity. Check WiLLiaM MaRRoW for BBB pattern.
5

QT Interval / QTc QTc >440 ms ♂ / >460 ms ♀
Measure from start of Q to end of T in the lead with longest visible QT. Correct for rate using Bazett formula: QTc = QT ÷ √RR (in seconds). Use the calculator below.
6

ST Segment Elevation ≥1 mm (limb) / ≥2 mm (precordial)
Assess relative to TP baseline. Elevation: STEMI, BER, pericarditis, Brugada. Depression: ischaemia, NSTEMI, digoxin (scooping), reciprocal. Note which leads are affected for territory localisation (Tab 3).
7

T Waves
Normal: upright in I, II, V3–V6; inverted in aVR. Peaked symmetrical T: hyperkalaemia, hyperacute STEMI. Inverted: ischaemia, PE (V1-V4), raised ICP, BBB. Flat/absent: hypokalaemia, hypothyroidism.
8

Overall Interpretation & Clinical Correlation
Synthesise all findings. State rate, rhythm, axis, intervals, and any ischaemic/structural changes. Correlate with symptoms, vitals, and history. Document findings per DHA/MOH standards and alert physician if red flags present.

Interactive QTc Calculator (Bazett)

Enter the measured QT interval and heart rate to calculate the corrected QT (QTc).

QT Interval (ms)

Heart Rate (bpm)

Patient Sex

Formula: QTc = QT(s) ÷ √(RR interval in s) | RR = 60 ÷ HR | Upper limit: >440 ms male, >460 ms female. >500 ms = high risk for torsades de pointes.

Quick Reference Intervals

PR Interval

0.12–0.20 s

3–5 small squares

QRS Duration

< 0.12 s

Up to 3 small squares

QTc Male

≤ 440 ms

>500 ms = critical

QTc Female

≤ 460 ms

>500 ms = critical

Normal Rate

60–100 bpm

Sinus node origin

Paper Speed

25 mm/s

1 small sq = 0.04 s

Voltage

10 mm/mV

Standard calibration

ST Elevation

≥1–2 mm

Limb / precordial

Rhythm Recognition — 15 Key Rhythms

TREAT= Requires immediate action WATCH= Monitor closely NORMAL= Physiologically expected

NORMAL

Normal Sinus Rhythm (NSR)

___/\___/\___/\___/\___

Baseline normal. Confirm calibration, patient ID, and clinical context before filing.

WATCH

Sinus Tachycardia

_/\_/\_/\_/\_/\_/\_/\_

Rate: >100 bpm | Regular | Normal P waves | Identify underlying cause: pain, fever, hypovolaemia, PE, thyrotoxicosis, anxiety, medications

Treat the cause. Rate >150 consider SVT. Do not treat tachycardia in septic/haemodynamically unstable patients with rate-lowering agents without physician order.

WATCH

Sinus Bradycardia

___/\______/\______/\_

Rate: <60 bpm | Regular | Normal P morphology | Causes: athletes, vagal, hypothyroidism, inferior MI, beta-blockers, digoxin

Treat only if symptomatic (hypotension, syncope, confusion). Atropine 0.5 mg IV if haemodynamically unstable. Escalate for transcutaneous pacing if refractory.

TREAT

Atrial Fibrillation (AF)

~~\/~~\/~\/~~\/~\/~~

Irregularly irregular | No distinct P waves | Fibrillatory baseline | Ventricular rate variable | QRS usually narrow unless BBB/WPW

Rate control (metoprolol, diltiazem) and/or rhythm control. Anticoagulation per CHA₂DS₂-VASc. Fast AF (>110 bpm) with haemodynamic compromise → cardioversion per ACLS. New onset <48 h: rate vs. rhythm decision.

TREAT

Atrial Flutter

/\/\/\/\___/\/\/\/\__

Sawtooth flutter waves ~300/min | Typically 2:1 block → ventricular rate ~150 bpm | Regular | Best seen in II, III, aVF, V1

Rate control. Cardioversion if haemodynamically unstable. Anticoagulate as for AF. Vagal manoeuvres/adenosine reveal flutter waves by slowing conduction.

TREAT

Supraventricular Tachycardia (SVT)

_/\/\/\/\/\/\/\/\/\_

Rate: 150–250 bpm | Regular | Narrow complex (unless aberrant) | P waves absent or retrograde (RP < PR) | Sudden onset/offset

Vagal manoeuvres first. Adenosine 6 mg rapid IV push if no response (12 mg repeat). If unstable → synchronised cardioversion. Identify re-entry mechanism: AVNRT most common.

WATCH

1st Degree Heart Block

__P___QRS__P___QRS__

PR interval >0.20 s | Every P followed by QRS | Regular | QRS usually normal | Causes: increased vagal tone, inferior MI, medications

Usually benign. Monitor for progression. Review contributing medications (digoxin, beta-blockers, calcium channel blockers, amiodarone).

WATCH

2nd Degree — Mobitz I (Wenckebach)

PR— PR—— PR——— drop

Progressively lengthening PR until a QRS drops | Grouped beating pattern | Usually narrow QRS | Benign if asymptomatic | AV node level

Monitor. Usually self-limiting. Associated with inferior MI. Atropine if symptomatic. Avoid agents that further slow AV conduction.

TREAT

2nd Degree — Mobitz II

Constant PR — sudden QRS drop | Wide QRS common | Infranodal block | Unpredictable progression

Fixed PR interval | Sudden non-conducted P wave | Bundle of His/bundle branch level | High risk of complete block

Requires cardiology review urgently. Transcutaneous pacing on standby. High risk of progression to complete heart block. Do NOT give atropine (may worsen).

TREAT

3rd Degree (Complete) Heart Block

P..P..P..P (QRS independent)

Complete AV dissociation | P rate > QRS rate | Regular P-P, regular R-R but unrelated | Escape rhythm: junctional (40–60, narrow) or ventricular (20–40, wide)

Emergency. Transcutaneous pacing immediately if haemodynamically unstable. Atropine unlikely to help if infranodal. Prepare for transvenous pacing. Code Blue criteria if no output.

WATCH

LBBB — Left Bundle Branch Block

V1: QS broad | V6: RR' broad

QRS ≥0.12 s | Broad notched R in V5-V6, I, aVL | Deep S in V1 | Secondary ST/T changes | Mnemonic: WiLLiam (W in V1, M in V6)

New LBBB with chest pain → treat as STEMI equivalent (Sgarbossa criteria). Old LBBB: confirm with previous ECG. Modifies ST analysis significantly.

WATCH

RBBB — Right Bundle Branch Block

V1: RSR' (bunny ears) | V6: wide S

QRS ≥0.12 s | RSR' in V1-V2 | Wide slurred S in I, V5-V6 | Mnemonic: MaRRoW (M in V1, W in V6) | T inversion V1-V3 expected

Isolated RBBB: monitor. New RBBB with anterior MI = bifascicular block risk. RBBB + left axis deviation = bifascicular block → higher CHB risk.

TREAT

Ventricular Tachycardia (VT)

/\/\/\/\/\ wide bizarre

Pulseless VT → CPR + defibrillation (unsynchronised). Pulsed VT with instability → synchronised cardioversion. Stable VT → amiodarone 150 mg IV. CALL CODE BLUE. Document time and rhythm.

TREAT

Ventricular Fibrillation (VF)

~~~~~\/~~~/\~~~\/~~~

Chaotic irregular deflections | No organised complexes | No identifiable P, QRS, or T | Coarse VF (large amplitude) vs fine VF (small)

CODE BLUE. Immediate defibrillation 200J biphasic. Continuous CPR with minimal interruptions. Adrenaline 1 mg IV every 3–5 min. Amiodarone after 3rd shock. Document per DHA resuscitation policy.

WATCH

PVCs (Premature Ventricular Complexes)

N N W-ide N N W-ide N

Isolated PVCs in structurally normal heart: benign. >6/min, multifocal, couplets, R-on-T → escalate. Identify trigger: hypokalaemia, hypomagnesia, ischaemia, digoxin toxicity, catecholamines.

NORMAL

Paced Rhythm

| LBBB-like QRS | spike

Pacing spike before QRS (ventricular) or P wave (atrial) | Wide LBBB-morphology QRS | 100% capture in demand mode | Rate set by programmer

Confirm capture (spike followed by appropriate deflection). Failure to pace or failure to capture requires urgent pacemaker check and cardiology notification.

WATCH

Junctional Rhythm

QRS narrow, no/retrograde P

Rate: 40–60 bpm | Narrow QRS | Absent, retrograde, or inverted P waves (II, III, aVF) | AV node is pacemaker | Accelerated junctional: 60–100 bpm

Associated with digitalis toxicity, inferior MI, post-cardiac surgery, sick sinus syndrome. Accelerated junctional tachycardia — consider digoxin toxicity. Monitor haemodynamics.

STEMI Territory Localisation

ST elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in ≥2 contiguous precordial leads is required for STEMI diagnosis.

Territory	Leads with ST Elevation	Reciprocal Changes	Culprit Artery	Clinical Notes
Anterior	V1V2V3V4	aVR (sometimes)	LAD (proximal)	Highest mortality. Risk of cardiogenic shock. Watch for LBBB, VT, complete heart block.
Inferior	IIIIIaVF	IaVL	RCA (80%), LCx (20%)	Always get right-sided leads (V4R). Risk of RV infarct. Avoid nitrates if RV involved. Bradycardia/heart block common.
Lateral	IaVLV5V6	IIIIIaVF	LCx	High lateral (I, aVL) → proximal LCx. Isolated lateral changes often subtle.
Posterior	ST depression + tall R in V1-V2 (mirror image)	V1V2	RCA / LCx	Use posterior leads V7-V9 to confirm. ST elevation in V7-V9 ≥0.5 mm diagnostic. Often accompanies inferior STEMI.
Right Ventricular	V4R (+ inferior leads)	Inferior STEMI pattern	Proximal RCA	STE ≥1 mm in V4R is diagnostic. AVOID nitrates (preload-dependent RV). IV fluids cautiously. High risk of haemodynamic collapse.
Anterolateral (Extensive)	IaVLV1–V6	IIIIIaVF	LAD proximal / LMCA	Left main occlusion. Haemodynamic collapse likely. Emergent PPCI required. Code Blue team alert.

Reciprocal Changes — Explained

Reciprocal changes are ST depressions in leads electrically opposite to the area of infarction. They confirm true STEMI (vs. non-ischaemic elevation) and help localise the territory:

Inferior STEMI → reciprocal ST depression in I and aVL
Anterior STEMI → reciprocal depression may appear in II, III, aVF (less consistent)
Posterior STEMI → ST depression + tall R wave in V1–V2 (mirror image of posterior elevation)
aVR elevation with widespread ST depression → LMCA or proximal LAD occlusion — highest risk pattern

STEMI Mimics — Do Not Miss, Do Not Over-Treat

Left Bundle Branch Block (LBBB)

New LBBB with symptoms: apply Sgarbossa criteria. STE ≥1 mm concordant with QRS, or ST depression ≥1 mm in V1-V3, or STE ≥5 mm discordant. Modified Sgarbossa uses ratio ST/S ≥0.25.

Benign Early Repolarisation (BER)

J-point elevation, concave ST morphology, often in young athletic males. Notching at J point, "fish-hook" pattern in V4. No reciprocal changes. Stable over time. Differentiate from anterior STEMI.

Pericarditis (Saddle-Shaped)

Diffuse concave (saddle-shaped) ST elevation in multiple leads (II, V5-V6). PR depression (almost pathognomonic). No reciprocal changes (except aVR). Pleuritic positional chest pain. Friction rub.

Left Ventricular Hypertrophy (LVH)

ST depression in lateral leads (I, aVL, V5-V6) — "strain pattern". May mimic lateral STEMI. Voltage criteria: Sokolow-Lyon (SV1 + RV5 or V6 ≥35 mm). No dynamic change.

Wellens Syndrome

Biphasic or deeply inverted T waves in V2-V3 during pain-free period. Indicates critical proximal LAD stenosis. Pattern A: biphasic T; Pattern B: deep symmetric inversion. HIGH risk for anterior STEMI. Do not stress test.

de Winter T-Waves

ST depression at J point with upsloping ST and tall symmetrical T waves in V1-V6. Represents LAD occlusion equivalent. No frank ST elevation. Must be treated as STEMI equivalent with emergent PPCI.

Brugada Pattern

Type 1 (coved): STE ≥2 mm with downsloping ST in V1-V2. Type 2/3 (saddle-back). Risk of VF in structurally normal heart. Provoked by sodium-channel blockers, fever. Implantable defibrillator considered.

NSTEMI vs Unstable Angina

Both: ST depression / T inversion, no STEMI criteria. NSTEMI: elevated troponin. UA: normal troponin. Both require dual antiplatelet, anticoagulation, and risk stratification (TIMI/GRACE score). Document symptom onset time.

Drug & Electrolyte ECG Effects

⚠ Digoxin Toxicity

Scooped "Salvador Dali moustache" ST depression (therapeutic, not toxic)
Bidirectional VT — hallmark of severe toxicity
Junctional rhythm, accelerated junctional tachycardia
AV block (1st, 2nd, 3rd degree)
Frequent PVCs, bigeminy
Shortened QT (therapeutic effect)
Any arrhythmia + bradycardia = digoxin toxicity until proven otherwise

▴ Hyperkalaemia Progression

K+ Level	ECG Changes
5.5–6.0	Tall, narrow, peaked (tent-like) T waves
6.0–7.0	PR prolongation, P wave flattening
7.0–8.0	Wide QRS, P waves disappear, sine wave pattern
>8.0	Sine wave → VF / asystole

Action: IV calcium gluconate (cardiac membrane stabilisation), sodium bicarbonate, salbutamol nebulisation, insulin/dextrose, dialysis if refractory. Do NOT give digoxin.

▼ Hypokalaemia

Prominent U waves (after T wave, same polarity)
Flat or inverted T waves
Prolonged QU interval (mimics QTc prolongation)
ST depression
Increased PVC frequency and risk of torsades
Replace K+ cautiously: max 10 mEq/h peripheral, 20 mEq/h central with cardiac monitoring

Calcium Disturbances

Hypercalcaemia: Short QT interval, short ST segment, J-waves, bradycardia, AV block, cardiac arrest
Hypocalcaemia: Prolonged QT (ST segment lengthens), torsades risk, may mimic STEMI
Check ionised calcium; total calcium corrected for albumin
IV calcium chloride or gluconate for symptomatic hypocalcaemia

💊 QT-Prolonging Drugs (GCC Common)

Haloperidol (psychiatric emergencies, anti-emetic) — significant risk
Metronidazole — often overlooked; dose-dependent
Azithromycin — commonly prescribed in GCC; avoid in cardiac patients
Ciprofloxacin — fluoroquinolone class effect
Amiodarone — intentional QT prolongation, monitor closely
Ondansetron >32 mg IV — risk at high doses
Tricyclic antidepressants — widened QRS + prolonged QT + tachycardia
Check crediblemeds.org for full risk classification

Amiodarone ECG Effects

Sinus bradycardia (most common)
Prolonged PR, QRS widening (dose-related)
QTc prolongation (monitor but rarely causes TdP at therapeutic levels)
U waves common
Corneal microdeposits, thyroid dysfunction, pulmonary toxicity (non-ECG)
Half-life 40–55 days — effects persist after stopping

Interactive Matching Quiz — Drug & Electrolyte ECG Changes

Drag each ECG description to the correct diagnosis. Click "Check Answers" when done.

ECG Descriptions (drag these)

Tall, narrow, peaked symmetric T waves; widening QRS; no visible P waves

Scooped ST depression, bidirectional VT, junctional tachycardia, bradycardia

Prolonged QT, flat T waves, prominent U waves, ST depression

Short QT interval, J-wave, bradycardia, AV block at very high levels

Diffuse concave ST elevation, PR depression, no reciprocal changes

Diagnoses (drop zones)

Drop the matching description here:

Hyperkalaemia

Digoxin Toxicity

Hypokalaemia

Hypercalcaemia

Pericarditis

10 ECG Practice Cases — GCC Clinical Context

How to Use

Read the clinical scenario and ECG description. Form your own interpretation before revealing the answer. Each case includes ACLS triggers, code blue criteria, and DHA/MOH documentation points.

65-year-old male, crushing chest pain radiating to jaw, diaphoresis, 40-minute history

BP 90/60 mmHg | HR 88 bpm | SpO2 93% | Onset in Accident & Emergency, Dubai

ECG FindingsST elevation 3–4 mm in leads II, III, aVF. Reciprocal ST depression in I and aVL. ST elevation 2 mm in V4R. Sinus rhythm, rate 88. No LBBB.

Inferior STEMI with Right Ventricular Involvement

ST elevation in II, III, aVF = RCA territory. Reciprocal changes in I/aVL confirm true STEMI. STE in V4R ≥1 mm = RV infarct — present here.

ACTIONS: Activate cath lab / PPCI team immediately. AVOID NITRATES (RV preload-dependent — may cause catastrophic hypotension). IV fluids (250–500 mL) if hypotensive. Aspirin 300 mg + Ticagrelor/Clopidogrel. ACLS: prepare for complete heart block. Document "STEMI with RV involvement" and time of first medical contact per DHA PPCI protocol. Target door-to-balloon <90 min.

72-year-old female, palpitations, mild shortness of breath, known hypertension

BP 148/92 mmHg | HR 130–160 bpm irregular | SpO2 97% | Abu Dhabi clinic referral

ECG FindingsIrregularly irregular rhythm. No distinct P waves — fibrillatory baseline in V1. Ventricular rate 130–160 bpm. Narrow QRS. No ST changes.

Atrial Fibrillation with Fast Ventricular Response

Irregularly irregular narrow complex tachycardia with fibrillatory baseline and absent P waves. Haemodynamically stable (BP maintained, no pulmonary oedema).

ACTIONS: Rate control goal HR <110 bpm. IV metoprolol 2.5–5 mg or IV diltiazem per protocol. Onset unknown or >48 h → anticoagulate before considering cardioversion. Calculate CHA₂DS₂-VASc (female = 1, HTN = 1, age 65–74 = 1 = total 3 → anticoagulate). Document rhythm, time of recognition, rate control response per DHA/MOH AF pathway. Cardiology referral.

58-year-old male post-CABG day 2, sudden loss of consciousness, unresponsive

BP unrecordable | HR 32 bpm per monitor | SpO2 unreadable | CSICU, Riyadh

ECG FindingsRegular P waves at 88/min. Regular wide QRS escape rhythm at 32/min. No consistent relationship between P waves and QRS complexes. QRS duration 0.16 s.

Complete (3rd Degree) Heart Block with Ventricular Escape

Complete AV dissociation: P rate (88) and QRS rate (32) are independent and unrelated. Wide QRS = ventricular escape (infranodal block). Post-CABG context = surgical trauma to conduction system.

ACTIONS: CODE BLUE. Transcutaneous pacing immediately — apply pads, set rate 70 bpm, increase output until capture. CPR if pulseless. Atropine generally ineffective for infranodal block. Prepare for transvenous pacing. Do NOT give atropine routinely. Document time, rhythm strip, interventions per MOH resuscitation policy. Cardiology/electrophysiology consult urgently.

45-year-old male with ESRD on haemodialysis, missed 2 sessions. Muscle weakness, confusion.

BP 160/100 mmHg | HR 58 bpm | SpO2 98% | K+ 7.2 mmol/L (lab result available)

ECG FindingsNarrow QRS 0.08 s. Tall, narrow, peaked symmetric T waves in precordial leads. P waves barely visible. Prolonged PR 0.24 s. No ST changes.

Hyperkalaemia (Moderate-Severe) — K+ 7.2 mmol/L

Classic hyperkalaemia: peaked symmetric T waves, PR prolongation, P wave flattening. QRS not yet widened (pre-sine wave stage). Correlates with lab K+ 7.2 mmol/L.

ACTIONS: IV Calcium Gluconate 10% 10 mL over 2–3 min IMMEDIATELY (membrane stabilisation — does not lower K+). Sodium bicarbonate 50 mEq IV if acidotic. Salbutamol 10–20 mg nebulised + Insulin 10 units with 50% dextrose 50 mL. Urgent haemodialysis. Cardiac monitor continuously. Repeat ECG after each intervention. Document per DHA critical value policy.

55-year-old male, pulseless, ongoing CPR by bedside nurse. Cardiac monitor attached.

Last seen well 4 minutes ago | ICU step-down unit | Doha, Qatar

ECG FindingsWide complex regular tachycardia at 180 bpm. QRS duration 0.18 s. No identifiable P waves. Monomorphic wide bizarre QRS complexes. Cannon A waves on jugular venous examination.

Pulseless Ventricular Tachycardia (VT)

Monomorphic wide complex tachycardia 180 bpm, no pulse = pulseless VT (shockable rhythm). AV dissociation evidenced by cannon A waves (clinical finding).

ACTIONS: CODE BLUE. Defibrillation 200J biphasic IMMEDIATELY — do not delay. Continue CPR with minimal interruption (<10 s pause for shock). Adrenaline 1 mg IV every 3–5 min. After 3rd shock: Amiodarone 300 mg IV bolus. Identify reversible causes (4H 4T). Document time of collapse, first rhythm, shocks delivered, drugs given per MOH/ACLS resuscitation sheet. Time-stamp all interventions.

28-year-old female, sudden onset palpitations, lightheadedness, no prior cardiac history

BP 110/70 mmHg | HR 186 bpm | SpO2 99% | Emergency Department

ECG FindingsRegular narrow complex tachycardia 186 bpm. P waves not visible or buried in QRS. Sudden onset. No delta waves. QRS 0.08 s.

Supraventricular Tachycardia (AVNRT most likely)

Regular narrow complex tachycardia with invisible or retrograde P waves = SVT. Haemodynamically stable. AVNRT is most common SVT in young females with no structural heart disease.

ACTIONS: Vagal manoeuvres — Valsalva (modified: supine, 40 mmHg pressure × 15 s then legs elevated), carotid sinus massage (if no carotid bruits). If unsuccessful: Adenosine 6 mg rapid IV push with saline flush (antecubital or larger vein). May repeat 12 mg × 2. If unstable at any point → synchronised cardioversion 50–100J. Document baseline ECG, interventions, and response per protocol.

80-year-old male on digoxin for AF, presenting with nausea, yellow-green visual disturbance, confusion

HR 48 bpm | BP 110/68 | Digoxin level: 3.2 nmol/L (therapeutic <2.6) | Renal impairment (eGFR 28)

ECG FindingsJunctional rhythm at 48 bpm. Frequent PVCs in bigeminy pattern. Scooped ST depression in lateral leads. Short QT. No P waves (underlying AF).

Digoxin Toxicity

Classic triad: bradyarrhythmia (junctional), PVCs/bigeminy, and scooped ST. Elevated digoxin level. Renal impairment reduces clearance. Visual and GI symptoms = systemic toxicity.

ACTIONS: STOP digoxin immediately. Continuous cardiac monitoring. Correct hypokalaemia and hypomagnesaemia (hypokalaemia potentiates toxicity). Digoxin-specific antibody fragments (Digibind/DigiFab) for severe toxicity (haemodynamic compromise, life-threatening arrhythmias, K+ >5 mmol/L). Do NOT use calcium, atropine (partial benefit only), or cardioversion (risk of refractory VF). Nephrology review. Document per pharmacovigilance and incident reporting (DHA/MOH).

50-year-old male, incidental finding on pre-op ECG. No symptoms. Planned for elective knee replacement.

BP 130/80 | HR 72 bpm | No known cardiac history | SpO2 99%

ECG FindingsRegular sinus rhythm 72 bpm. QRS 0.14 s. RSR' pattern in V1-V2 (M-shaped). Broad slurred S wave in I, V5, V6. T inversion V1-V3. No ST elevation or depression elsewhere.

Right Bundle Branch Block (RBBB) — Incidental

RSR' (bunny ears) in V1-V2, broad S in I/V5/V6, T inversion V1-V3 = classic RBBB. QRS 0.14 s confirms complete RBBB. No ischaemic changes. Isolated RBBB in asymptomatic patient = low risk.

ACTIONS: Compare with any previous ECG. If new RBBB with symptoms = investigate. Isolated incidental RBBB: no contraindication to elective surgery. Cardiology review if new or associated with symptoms. Document finding, annotate pre-op paperwork. Notify anaesthesiologist. No acute intervention required. Educate patient about the finding.

30-year-old male, sharp pleuritic chest pain, worse lying flat, improved leaning forward. Low-grade fever.

BP 118/76 | HR 96 bpm | SpO2 98% | Recent viral URTI 2 weeks ago | Troponin mildly elevated

ECG FindingsDiffuse concave (saddle-shaped) ST elevation in I, II, III, aVF, V3-V6. PR depression in II, V3-V6. PR elevation in aVR. No reciprocal ST depression. Rate 96, sinus rhythm.

Acute Pericarditis

Diffuse saddle-shaped ST elevation + PR depression across multiple leads without territorial pattern = pericarditis, not STEMI. PR elevation in aVR is specific. No reciprocal ST changes. Clinical picture (post-viral, positional pain, friction rub) confirms.

ACTIONS: NSAIDs (ibuprofen 600 mg TDS) + Colchicine 0.5 mg BD for 3 months (reduces recurrence). Restrict strenuous activity until symptoms resolve and CRP normalises. Monitor for pericardial effusion/tamponade (echo if clinically suspected). Avoid NSAIDs in post-MI pericarditis. Serial ECG and CRP monitoring. Do NOT administer thrombolytics. Document ECG changes, troponin trend, and management per DHA cardiology pathway.

22-year-old male athlete, palpitations and pre-syncope during exercise, family history of sudden cardiac death

BP 118/72 | HR 112 bpm | SpO2 100% | Arrived by ambulance after episode on football pitch

ECG FindingsSinus tachycardia 112 bpm. Short PR interval 0.10 s. Delta waves visible as slurred upstroke of QRS in multiple leads. Wide QRS 0.13 s. Pseudo-LBBB pattern in V1-V3.

Wolff-Parkinson-White (WPW) Syndrome

Short PR + delta wave + wide QRS = WPW preexcitation. The accessory pathway (Bundle of Kent) bypasses the AV node causing early ventricular activation. Risk of rapid AF conducting at 300+ bpm → VF in athletes.

ACTIONS: DO NOT use adenosine, verapamil, diltiazem, or digoxin (block AV node, may accelerate accessory pathway → VF). If haemodynamically unstable → synchronised cardioversion. If stable → procainamide or amiodarone. Urgent cardiology/electrophysiology referral for risk stratification. Radiofrequency catheter ablation is curative (>95% success). Restrict from competitive sport until evaluated. Document per DHA sudden cardiac death prevention pathway. Family screening recommended.