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ECG interpretation Sara RamachandranElectrical pathwayECG basics 0.04 secs As with any data interpretation: Check 1 small box = 0.04 seconds Name 1 large box = 0.2 seconds DOB Address/hospital number 0.2 secs Type of investigation Date and time of investigation Check speed 1 small box = 0.1 mV • Default usually 25mm/sec • Calculations based on this 1 large box = 0.5mV speed 0.5mV 0.1mVRate If regular: 0.04 secs 300 ÷ (large boxes between R waves) 1 small box = 0.04 seconds OR 1500 ÷ (small boxes between R waves) 1 large box = 0.2 seconds 0.2 secs Large boxes Small boxes Rate 5 25 60 5 boxes = 60bpm 4 20 75 3 15 100 4 boxes = 75bpm 2 10 150 1 5 300 3 boxes = 100bpm If irregular (or regular): 2 boxes = 150bpm Number of R waves in rhythm strip × 6 1 boxes = 300bpm Normal rate in adults: 60-100bpmRhythm Determination of normal sinus rhythm • P wave in-front each QRS complex • Regular P-R and R-R intervalsRhythm RegularRhythm Irregular Regularly irregular: Irregular R-R interval but, regular pattern to irregularity Irregularly irregular: Irregular R-R interval, no pattern to irregularityNormal axis I Positive ↑ AVF Positive ↑Left axis deviation “Leaving” I Positive ↑ AVF Negative ↓ • Normal variant with increased age • LBBB, anterior fascicular block • Ventricular pacing (single/dual chambers) • Inferior MI • Left ventricular hypertrophyRight axis deviation “Returning” I Negative ↓ AVF Positive ↑ • Normal variant in neonates • RBBB, left posterior fascicular block • Right ventricular hypertrophy • Anterolateral MI • Right heart strain (i.e., PE, COPD, pulmonary stenosis)Extreme axis deviation I Negative ↓ AVF Negative ↓ Very weird… • SEVERE right ventricular hypertrophy • Arrythmias arising from inferior ventricle (i.e., VT from lateral MI)P waves • Atrial depolarization • <0.12secs (3 small), <0.25mV (1/2 large box) • Lead II/AVF P pulmonale P mitrale • Tall P waves >0.25mV • Bifid P waves • R heart strain 🡪 hypertrophy • L heart strain 🡪 hypertrophy • COPD, pulmonary hypertension, • Mitral stenosis (i.e., rhematic heart disease), tricuspid stenosisP-R interval • Measures atrial depolarization reaching up to AVN + contraction • Beginning of P wave to beginning of QRS complex • Normal: 0.12secs-0.2secs (3-5 small boxes) • Each P wave followed by a QRS complex st Short PR – pre-excitation, i.e., Prolonged PR - 1 degree heart WPW blockP-R interval Each P wave followed by a QRS complex Mobitz type I (Wenkebach pnenomenon) Mobitz type II R R R R R P P P P P P P P Complete heart block (junctional escape rhythm)QRS complex Depolarisation of ventricles Q: • 1 –ve, septal L 🡪 R (esp Bundle of His) • <0.2mV (2 small boxes) • Pathological in V1-V3/ >0.2mV in other leads R: • +ve, Left ventricular depolarization S: nd • 2 –ve, up Purkinje fibres • S1Q3T3 in PEQRS complex - Width Narrow •<120ms (3 small boxes) •supraventricular •NSR, SVT (AF, flutter, AVRT, AVNRT), 1 /2 nd degree HB, CHB (junctional escape rhythm)QRS complex – Width Broad • >120ms (3 small boxes) • Ventricular • VT, VF, CHB (ventricular escape rhythm), bundle branch blocks, SVT with aberrancyQRS complex – Width Left bundle branch block V6 V1 V2 V3 V4 V5 • Broad QRS • “WiLLiaM” - W in V1/2, M in V5/6 • Loss of q waves in lateral leads *new LBBB + angina – should • prominent S wave in V1, notched/monophasic R wave in V5/6 be considered as STEMI • Left axis deviation equivalent* • Appropriate discordance • Almost always pathological – MI, IHD, DCM, AS, LVH, post TAVI, PPM • Hyperkalaemia, digoxin toxQRS complex – Width Right bundle branch block V6 V5 V1 V2 V3 V4 • Broad QRS • “MaRRoW” - M in V1/2, W in V5/6 Bifascicular block • Wide slurred S wave in V5/6 • RBBB + left axis deviation = anterior fascicle • prominent S wave in V1, notched/monophasic R wave in V5/6 • RBBB + right axis deviation = posterior fascicle • Normal axis deviation (LV larger) Pseudo-RBBB – Brugada • Appropriate discordance – ST depression/T waves inversion (V1-3• ‘M’ in V1 • RVH, PE, cor pulmonale, MI (OM1) • V1/2 🡪 ST elevation + T wave inversion/biphasic • Congenital heart defects 🡪 RVH (i.e., ASD/VST/TOF)QRS complex - Amplitude Normal progression in precordial leads: • R wave ‘rises’, S waves ‘sets’ High amplitude • LVH – S wave in V1/2 + R wave in V5/6 > 3.5mV (7 big boxes) – can be normal in the young • RVH – R wave in V1/2 + S wave in V5/6 > 1.05mV (around 2 big boxes) Alternating • Electrical alternans – alternating high/low voltage QRS complexes – pericardial effusion/tamponade ST segment Isoelectric region between ventricular depolarisation and repolarisation • From J point (end of S wave) to beginning of T wave ST segment Depression Elevation J point Limb leads ≥0.1mV (1 small box) V2/3 ≥ 0.5mV (0.5 small box Precordial leads ≥ 0.2mV (2 small All others ≥0.1mV (1 small Positive deflection boxes) box) Brugada STEMI ≥2contiguous leads Down-sloping Up-sloping Sagging Other Hypothermia LBBB, Brugada, Prinzmetal angina NSTEMI Tachycardia Digoxin Hypokalaemia Hypercalcaemia Pericarditis, Perimyocarditis Reciprocal change Some NSTEMIs RBBB/LBBB (saddle) RVH/LVH Takatsubo PE, raised ICPST segment Big Lie, little lie, as as and ALL Lateral – Circumflex artery Inferior – Right coronary artery Anterior/anterior septal – Left anterior descending T waves Represents ventricular repolarisation, polarity concordant to QRS complex T wave Inversion Flattened Peaked biphasic NSTEMI ≥2contiguous leads Hypokalaemia Hyperkalaemia Initial positive Normal in III, AVR, V1, Wellens children Brugada PE (S1Q3T3) Initial negative LBBB/RBBB Hypokalaemia Digoxin Raised ICPQT interval From the beginning of the QRS complex to the end of the T wave Prolonged if >440 in men, >460 in women Affected by rate - calculate corrected cT hypothermiahypokalaemia, hypomagnesemia, hypocalcaemia, Congenital long QT : Romano-Ward, Jervell-Lange-Neilsen, LQT1, LQT2, LQT3 Drugs: anti’s – antidepressants, antipsychotics, antihistamines, antibioticsSummary Say what you see, say what you think Summarise your findings in a systematic way: Rate, rhythm, axis, waves and segments Always offer differentials at the end of your interpretation. Familiarise yourself with theachycardia, bradycardia and cardiac arrest guidelines/pathways Name: Charlotte Lucus/1/25 Hosp No: H276482e: 9:27 Case 1 Mrs Lucus is a 27-year-old woman, pregnant, G1P0, 20weeks gestation, who has come in for her 20-week scan. Her observations: heart rate of 180bpm and BP of 107/68, otherwise well. Alert and responsive. She is moved to a bed and has an A-E assessment and a 12 lead ECG. Can you interpret her ECG: 21/07/1997ttTime: 9:47/25 Case 1 H276482 She is now on a cardiac monitor. As vagal manouvers were unsuccessful, She was given 6mg of IV adenosine. Her rhythm on the monitor appears different so you obtain another 12 lead ECG. She is still awake but feels ‘funny’ and looks drowsy. Interpret her ECG Name: Gary Date: 27/1/25 Case 2 DOB: 4/3/19Time: 14:15 Hosp No: J746294 Mr Collins is an 86-year-old gentleman with a background of HTN and AF, on Ramipril 5mg, Bisoprolol 5mg OD. He has medicationsakifor overhes5 years. He presented to A&E with 3 episodes of TLOC over the last month. ECG:se interpret his 12 lead Case 3 Name: Jess HeDate: 27/1/25 Hosp No: X492937e: 14:15 Mrs Hertz is a 76-year-old gentleman who presented with shortness of breath, palpitations, jaw ache and feeling very dizzy and sweaty. He has vomited twice in the last hour. Please interpret his 12 lead ECG: Case 4 Mr Long is a DOB: 18/6/1959hDate: 27/1/25 Hosp No: X492937ime: 14:15 65-year-old gentleman with a background of previous anterior STEMI (July, 2024) and liver cirrhosis (NAFLD), who has been started on Sotalol for haemodynamically stable recurrent VT. She has a routine 12 lead ECG the following morning. Please interpret this ECG:Thank you!