ECG interpretation is largely a matter of experience and systematic analysis. This is most easily performed by answering number of questions in logical sequence about P, QRS and T waves, segments and intervals in turn, A simple system is presented in the following sequence Usually ImV 1. Standardization Fciuced wi eae Should be registered on the ECG paper to avoid misinterpretation Increased to 2 mV —J ‘Usually 25 mm/sec. 2. Paper speed ubled to.SO'mmisec! 7] sy ould Be registered on the ECG aia : Paper to avoid misinterpretation Halved to 12,5 mm/sec, — ‘Normally 60 — 100 beats‘min 3. Heart rate Bradycardia less than. 60 beats/min. Tachycardia more than 100 teats'min. 4. Rhythm Sinus rhythm (See chapter 4) Arthythmiastrial fibrillation Sinus arrest or SA block “AV junctional rhythm Hyperkalemia Electrode misplacement Inverted P wave P P-QRS-T all are inverted 5. P wave Dextrocardia ‘end | and aVL. Retrograde atrial depolarization (i.¢., the atria are activated from down up) Tall P wave > 2.5mm — —PRight atrial enlargement (p pulmonale) Wide P wave > 3 mm—p Left atrial enlargement (p mitrale) Absent P wave Different morphology. qe ectopic so nen sts/min Rat > 3 different P onary anente tachyeardia Rate < 100 beats/min ‘Wandering atrial pacemaker May be normal WPW syndrome Short AY Junctional rhythm: LGL syndrome 6. PR interval Long —p/itst-degree heart block . ‘Can be measured —p Second-degree AV block Variable — Cannot be measured ee Thin degree AV block AV dissociation Depressed — Pericarditis Elevated — Atrial infarctionLeft axis deviation —p Abnormal axis € ight axis deviation Extreme axis deviation Indeterminate axis deviation Incomplete bundle branch block 7. ORS —_p eet morphology with normal duratios Fasticular block WPW syndrome Hyperkalaemia Bundle branch block (complete) Ventricular arrhythmias Electronic ventricular pacemaker Low Voltage NalFanel ECG ealib Half usual ECG calibration Voltage < SESE effusion High Voltage Myxedema ‘Cardiomyopathies including dilated type Normal variant Double usual ECG calibration LVH (tall R in Vs, Ve, deep $ in Vi, V3) RVH (tall R in Vj), Vs, deep S in Vs, Vs) Posterior MI(R in V,) Leabnormal duration and morphology 'WPW syndrome type A(R in V)) Dextrocardia (R in Vi) Vertical heart position Normal variant . = Horizontal heart position 8. Owave Physiological (septal q waves) I, aVL, Vs and Vi Pathological (> 25 % of the R wave amplitude, and more than one small box duration) i Posie intaictioa Myocardial infarction Hypertrophic obstructive Ventricular hypertrophy cardiomyopathy WPW syndrome Left bundle branch block Pulmonary embolism QS varianta Angina Myocardial ischemia" Non ST elevation MI .eciprocal changes of MI Drugs (digoxin, Quinidine) Depression ‘Ventricular hypertrophy with "strain" 9. ST segment . Hypokalemia Elevation. Acute MI Pericarditis Ventricular aneurysm Benign early repolarization (normal variant) Prinzmetal angina Hyperkalemia (V,, V3) Hyperkalemia Peaked ai Acute MI 10. T wave Hypokalemia Flat = il Hypothyroidism Inverted Normal (aVR, V\) Juvenile T wave inversion (V;, V2, V3) Myocardial ischemia and infarction Ventricular hypertrophy (with strain) Bundle branch block Secondary = WPW syndrome Ventricular paced beats Primary Nesisnedfe Digoxin toxicity Subarachnoid hemorrhage ‘Cerebrovascular accident ‘Mitral valve prolapse Pulmonary embolism Hyperventilation, cholecystitis Paroxysmal tachycardia (rate dependant) Idiopathic global T wave inversionHypercalcaemia Short Digoxin effect 11. OT interval Hyperthermia ypocalcaemia Long - Acute myocarditis The Jervell-Lange-Neilsen syndrome Hereditary syndrome QT dispersion Romano-Ward syndrome (the difference between the longest and Acute myocardial infarction the shortest QT interval in same ECG) Hypertrophic cardiomyopathy Hypothermia Drugs (quinidin, phenothiazine) Cerebrovascular accident (CVA) Hypokalemia Hypercalcaemia rominent Hyperthyroidism 12. U wave < Cerebrovascular accident (CVA) Inverted ————p Usually accompanies T wave inversion (see inverted T wave above)