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Ecg interpretation
This document provides an overview of systematic ECG interpretation. It discusses the key components that should be analyzed in an ECG including rate, rhythm, axis, P wave, PR interval, QRS complex, QT interval, ST segment, and other waves. For each component, the document outlines what should be assessed such as amplitude, duration, and abnormalities. It also reviews conditions that can cause abnormalities in various ECG components, such as left ventricular hypertrophy, right ventricular hypertrophy, bundle branch blocks, and long QT syndrome. The document emphasizes a systematic approach to ECG interpretation and provides guidance on evaluating rhythms, pediatric considerations, and differentiating ventricular arrhythmias from supraventricular arrhythmias with aberran
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Ecg interpretation
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- 2. Components of ECG Rate Rhythm Axis P PR QRS QT ST Other waves Delta Epsilon Osborne U
- 4. Rate Small square0.04 Big square 0.2 Slow 300/big square Fast 1500/small square Irregular – count complexes on rhythm strip x 6 gives average rate Big squares rate 2 150 2.5 120 3 100 3.5 86 4 75 4.5 66 5 60 5.5 54 6 50 6.5 46 7 42
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- 6. Axis differentials Left-30 to -90 LBBB LAFB LVH Inferior MI Paced rhythm Right +90 to +180 RVH LPFB Lateral MI Lung disease – acute/chronic Hyperkalemia Na channel blockade Dextrocardia NORMAL IN INFANTS and skinny adults
- 7. P WAVE PRinterval 120 – 200 msec Long – any heart block Short – WPW, pre- excitation Elevation/depression - pericarditis Width < 120 msec Amplitude <2.5mm in limb leads <1.5mm in precordial leads V1 biphasic Avf inverted
- 9. QRS Amplitude Duration Q wave R wave Hypertrophy Bundle branch block J point
- 11. Q wave Pathologicalif >40 ms wide >2mm deep >0.25% QRS Present in leads v1-v3 > 2mm Can be normal in leads III /avR
- 12. R wave inV1 RVH - PE Posterior MI RBBB HOCM WPW Dextrocardia Normal in Kids
- 13. R Wave R wavein AVR Na channel blockade VT Dextrocardia Limb lead reversal R wave progression R wave <3mm in V3 Signifies anteroseptal MI LVH
- 14. Left Ventricular hypertrophy Voltage+ non voltage Muscle wall thickens Leading to increased S wave amplitude in right sided leads Increased R wave amplitude in left sided leads Prolonged depolarisation Repolarisation abnormalities in lateral leads Causes HTN AR/AS MR HOCM
- 15. LVH voltage S inV1 + R in V5/V6 > 35mm AVL R wave 11mm Non voltage ST depression/T wave inversion in lateral leads Increased R wave peak time > 50msec in V5 V6
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- 17. RVH Right axis Dominant R in V1 > 7mm or RS ratio >1 Dominant S in V6 > 7mm or RS ratio <1 RV strain – ST depression in V1-4 and inferiorly
- 18. Causes PE Chroniclung disease Pulmonary HTN Mitral stenosis Congenital heart disease Arrythmogenic RV cardiomyopathy
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- 23. J point Notching -BER Osborne wave - hypothermia
- 27. QT Ventricular depolarisationand repolarisation Calculate in lead 2 or V5 V6 Include U waves 440 msec for women 450msec for men Prolongs at slower HR QT> 500 increased risk of toursades Bezetts formula accurate over HR 60-100 HR nomogram for toxicology for risk of toursades
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- 30. T waves Invertedin V1 and AVR Can be – flat, biphasic, inverted, camel humped or hyperacute Dynamic change most important Don’t miss Wellens syndrome
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- 34. Rhythm Regular, irregular,regularly irregular Heart block Atrial , AVNRT, Accessory pathways Junctional rhythm Ventricular rhythms Distinguish VT from SVT with BBB
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- 39. VT or SVTwith abberancy If >35 or Hx of IHD – likely VT Look for Width > 160msec QRS VT likely Concordance Fusion beats Capture beats Right/left axis AV dissociation – p waves notching the QRS First rabbit ear taller RSR1
- 43. Children Right sideddominance as infants Should be normal by age 3-4 Rate age dependent Inverted T waves V1-4 can be normal Infant QT 490 https://www.starship.org.nz/for-health- professionals/starship-clinical- guidelines/e/electrocardiograph-ecg/
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