How to take and read an ECG ECG Basics It is basically a recording of the depolarisation/repolarisation An upward (positive) deflection is indicative

tive of a electrical activity travelling towards the electode A downward deflection is indicative of electrical activity travelling away from the node N.B. that although the SA is the pacemaker of the heart, the rest of the tissue has an intrinsic pacemaker in case of failure SA Node: 60-100bpm AV node: 40-60pm Bundle of His: 40-60bpm Purkinje fibres: 15-40bpm
Help with the localisation of a myocardial infarct localisation Anterior MI Septal MI Lateral MI Inferior MI V1-V6 V1-V4, disappearance of septum Q in leads V5,V6 I, aVL, V5, V6 II, III, aVF ST elevation None none II,III, aVF I, aVL high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view) I, aVL PTa in I,II, or III Reciprocal ST depression coronary artery LAD LAD RCX or MO RCA (80%) or RCX (20%) RCX

Posterior MI Right Ventricle MI Atrial MI

V7, V8, V9

V1, V4R PTa in I,V5,V6

RCA RCA

 Remember patient comfort only chest exposed, warm room, etc Lying at 45 degrees Would shave if hairy, would alcohol wipe/abrade if greasy

1. Rate Either 300 number of big squares in the R-R interval Or 1500 number of small squares in the R-R interval In the case of irregular rhythm count the number of QRS complexes in the rhythm strip and x 6 2. Rhythm Regular/Irregular? If irregular is it regularly irregular or irregularly irregular? If in doubt get a piece of paper and mark QRS complexes and move it along, a difference of 0.12s (three small squares) is usually acceptable 3. Conduction PR interval from the start of P wave to the beginning of Q wave (or R if Q isnt present basically to the beginning of QRS complex) Normal is 0.12-0.2s (3-5 little squares) Remember to look at the rhythm strip instead of leads Long PR interval is seen in heart block 1st degree Heart block is when there is prolonged PR but every P wave is followed by a QRS complex Usually caused by AV nodal disease, but can also be due to scar tissue from previous cardiac trauma 2nd degree heart block ahs two types but is differentiated from 1st degree by the fact that there are dropped QRS complexes Mobitz I Wenckebach phenomenon.. Characterised by an increasing PR interval followed by a dropped QRS Mobitz II Constant PR interval followed by dropped QRS, described as a ratio of normal to dropped beats, e.g. 3:1 rd 3 degree or Complete heart block characterised by complete dissociation between the atrial and ventricular contraction so no concurrence between the P and QRS normal atrial contraction but no ventricular response QRS duration Should be 0.08s to 0.12s Possible causes of broad QRS LBBB (must be over 0.12s) RBBB (must be over 0.12s) Electrolyte disorders a. Hypercalcaemia b. Hyperkalaemia Paced rhythm QT interval Kind of a more specialised thing as people cant decide where about to place the QT lines.. However below 450ms for men and below 460ms for women The QT interval starts at the onset of the Q wave and ends where the tangent line for the steepest part of the T wave intersects with the baseline of the ECG pathological prolonged QT time, it takes longer than the normal amount of time for the myocardial cells to be ready for a new cycle. There is a possibility that some cells are not yet repolarized, but that a new cycle is already initiated. These cells are at risk for uncontrolled depolarization, induction of torsades de pointes or VF 4. Axis aVF aVL aVR III II

Calculated using leads I, II, III, aVR, aVL, aVF Choose the smallest and most equiphasic QRS complex and then use the opposing lead (from table on R) Use the value of the opposing lead (+ve or ve) as the axis Causes of RAD Causes of LAD Can be normal in kids/tall thin adults RV Hypertrophy Chronic lung disease (w/ or w/o pulmonary HTN) Anterolateral MI PE Wolff-Parkinson White ASD/VSD L posterior hemiblock 5. P-wave morphology The P wave morphology can reveal right or left atrial hypertrophy or atrial arrhythmias and is best determined in leads II and V1 during sinus rhythm The maximal height of the P wave is 2.5 mm (2-3 small squares) in leads II and / or III The P wave is positive in II and AVF, and biphasic in V1 The P wave duration is shorter than 0.12 seconds (3 small squares) Enlarged P wave = enlarged atria 6. QRS Morphology Are there any pathological Q waves? Are there any signs of hypertrophy? LVH V1+V5/6 is over 35mm (7 squares!) Often some ST depression can be seen in leads V5V6, which is in this setting is called a 'strain pattern' RVH R wave in V1 + S wave in V5 or V6 > 10.5 mm 7. ST Segment Localisation of ST event inferior II, III, aVF RCA, or RCX Anteroseptal V1-3 LAD Anterolateral V4-6, I and aVL ST elevation most common cause is acute ischaemia other causes include: Acute pericarditis ST elevation in all leads except aVR saddlebacking PE ST elevation in V1 and aVR Hypothermia ST elevation in V3-6, II, III and aVF Hypertrophic cardiomyopathy v3-v5 Hyperkalemia V1-V2 Cardiac aneurysm Cardiac contusion LVH Paced rhythms ST depression Indicative of subendocardial ischaemia Also can be post-MI Digoxin effect (look for backwards tick in the QRS-T segment) L anterior hemiblock Q waves of inferior MI Cardiac pacing Emphysema Hyperkalemia Tricuspid regurgitation

8. Compare with a previous ECG 9. Summarise One concise sentence!!!

Some classical pictures!

mall Q waves. A downward deflection immediately following a P wave that is wider than two small squares or gr

upright in every lead except aVR. T-wave inversion can represent current ischemia or previous infarction (see )

saw-tooth appearance. n funky baseline, irregularly irregular, can go up to 450 bpm bpm which is kinda classic

Remember WiLLiam MoRRow for bundle branch block tried to draw over it to show!