Interpretation of common ecg abnormalities

Examples of common ECG abnormalities

1. Dr LNR González Interpretation of commonECG abnormalities

2. Calibration 10 mm = 1 mV (amplitude) Paper speed = 25mm/s 1 mm = 0.04 s

3. Rate Number of QRS complexes multiplied by 6 If rhythm is regular, look at the R-R interval 300 divided by the number of large squares between R waves 60-100/min is generally regarded as normal

4. Abnormalities of Rate Bradycardia = heart rate <60/min Tachycardia = heart rate >100/min Rate & rhythm are inextricably linked, often an abnormality of rhythm causes an abnormal rate

5. Rhythm Identify the rhythm strip, usually lead II Regular vs irregular Bradycardia vs tachycardia Narrow complex vs broad complex Supraventricular vs ventricular

6. Sinus rhythm SA node acts as natural pacemaker Heart rate 60-100/min Every P wave followed by a QRS complex Every QRS complex preceded by a P wave

7. Sinus bradycardia As in sinus rhythm but rate <60/min Causes Athlete Drugs, eg . Digoxin, β -blockers, Ca -channel blockers IHD/MI Hypothyroidism Hypothermia Electrolyte abnormalities ↑ICP

8. Sinus tachycardia Sinus rhythm with heart rate 100-150/min Causes Physiological (anxiety, pain, fever, exercise) Drugs, eg . Adrenaline, atropine, caffeine, alcohol, salbutamol Anaemia Hyperthyroidism Hypovolaemia

9. Sinus arrhythmia Variation in heart rate with respiration Heart rate normally increases during respiration due to increased venous return

10. Paroxixmal Supraventricular Tachycardia Heart rate often >150/min P waves present but not always easily visible P waves abnormally-shaped due to ectopic focus

11. Atrial flutter Results from a re-entry circuit around the right atrium Atrial rate 250-350/min AV block occurs due to failure of AV node to conduct every impulse Usually regular block, ie . 2:1, 3:1, 4:1 Classic ‘ sawtooth ’ pattern of flutter waves with regular QRS complexes

12. Atrial fibrillation Rapid, chaotic depolarisation occurring throughout the atria arising from multiple foci

13. No P waves Fibrillating baseline ‘Irregularly irregular’ R-R interval due to erratic transmission through AV node May be Paroxysmal Persistent permanent

14. Junctional rhythms Impulse arises from the AV node Narrow complex P waves are absent or inverted with retrograde conduction Before QRS complexes After QRS complexes Life-threatening causes of a junctional rhythm AMI ↑ K + Digoxin toxicity

15. Usually 40-60/min Junctional tachycardia >100/min Accelerated junctional rhythm 60-100/min Junctional escape rhythm <40/min

16. Ventricular rhythms Broad QRS complexes Ventricular tachycardia >120/min Accelerated ventricular rhythm 40-120/min Idioventricular rhythm 30-40/min Ventricular escape rhythm <30/min

17. Ventricular tachycardia Defined as 3 or more successive ventricular beats at a rate exceeding 120/min Arises from either a re-entry circuit or a specific ventricular focus Episodes may be self-terminating, sustained, or may rapidly degenerate into VF When haemodynamic compromise is present, VT becomes a medical emergency – urgent DC cardioversion

18. Torsades de Pointes Polymorphic VT associated with a long QT interval May be precipitated by electrolyte abnormalities (Mg), anti-arrhythmic drugs, hereditary syndromes Characteristic undulating pattern on the ECG with ‘twisting of the points’ Risk of precipitating VF

19. Ventricular fibrillation Rapidly fatal arrhythmia Most commonly due to MI

20. Asystole Absence of electrical activity

21. P pulmonale Tall P waves >2.5mm Right atrial enlargement Pulmonary hypertension Pulmonary stenosis Tricuspid stenosis

22. P mitrale Wide P waves > 0.08 s Often bifid appearance Left atrial enlargement Often due to mitral valve disease

23. PR interval Measured from the start of the P wave to the start of the R wave Should be 0.12 – 0.2 s long Consistent in length

24. Short PR interval AV junctional rhythm Wolff-Parkinson-White syndrome Conduction through accessory pathway (bundle of Kent) between atria and ventricles Faster than through AV node Classic ‘delta’ wave

25. 1 st degree AV block Long but constant PR interval Each P wave followed by QRS complex Causes IHD ↑ K + Rheumatic heart disease Drugs, eg . digoxin, β -blockers, Ca -channel blockers

26. 2 nd degree AV block Mobitz type I Wenckebach phenomenon PR interval progressively lengthens P wave fails to be conducted PR interval then resets to normal

27. 2 nd degree heart block Mobitz type II Results from abnormal conduction in bundle of His Most P waves are followed by a QRS complex PR interval normal and constant Occasionally a P wave is not followed by a QRS complex May suddenly progress to complete heart block

28. 3 rd degree heart block P waves have no relationship to QRS complexes Broad QRS complexes – ventricular escape rhythm Urgent pacing required

29. Q waves Normal Q waves Small Result from septal depolarisation I, II, aVL , V5-V6 Pathological Q waves > 2mm deep > 25% of height of following R wave > 0.04 s wide Caused by MI LVH Bundle branch block

30. QRS complexes Should be < 0.12s in width R wave increases in height from V1-V6 R wave should be smaller than S wave in V1-V2 and bigger in V5-V6 Tallest R wave should not exceed 25mm Deepest S wave should not exceed 25mm

31. Tall complexes LVH RVH Posterior MI Wolff-Parkinson-White syndrome Thin chest wall

32. Small complexes Obesity Hyperinflated chest Pericardial effusion

33. Left bundle branch block Wide complex with W pattern in V1 and M pattern in V6 Always a sign of pathology May be presenting feature of MI Rest of ECG cannot be interpreted

34. LBBB

35. Right bundle branch block Wide complexes with M pattern in V1 and W pattern in V6 May be found in otherwise normal hearts Also could be a sign of underlying disease

36. RBBB

37. ST segment elevation Measured 0.04 s after the J point Significant > 1mm Causes STEMI Pericarditis LV aneurysm Prinzmetal angina LBBB Early repolarization

38. Pericarditis Saddle-shaped No Q wave No reciprocal changes Widespread over many leads

39. Myocardial injury Convex ‘camel-hump’ appearance Q waves Reciprocal changes Specific contiguous leads

40. ST depression Significant > 0.5mm Causes Myocardial ischaemia Myocardial strain Digoxin Hypokalaemia Reciprocal changes in MI

41. T wave Upright I, II, V3-V6 Inverted aVR Variable III, aVL , aVF

42. Tall T waves Hyperkalaemia Hypermagnesaemia Acute MI

43. Flattened T waves Hypokalaemia Pericardial effusion Hypothyroidism

44. T wave inversion Normal in aVR and V1 +V2 in younger people +V3 in black people MI Myocardial ischaemia Ventricular hypertrophy with strain pattern Digoxin toxicity Pericarditis Bundle branch block Hypokalaemia Anaemia Thyroid disease Beri-beri

45. Myocardial infarction Tall ‘ hyperacute ’ T waves St segment elevation Q wave formation ST segments return to normal T waves become inverted Q waves persist May also present with a new LBBB

46. Localisation of MIs Anterior V3-V4 Lateral I, aVL , V5-V6 Anterolateral I, aVL , V1-V6 Septal V1-V2 Inferior II, III, aVF

47. Right ventricle V4R, V5R, V6R same as normal praecordial leads but on the right side of the thorax instead Posterior Tall R waves in V1-V3 with ST depression. ST Segment elevation V7,V8,V9

48. Anterolateral MI

49. Inferior MI

50. Hypokalaemia Flattened T wave Prominent U wave ST depression T wave inversion

51. Hyperkalaemia Tall peaked T wave Flattened P wave Prolonged PR interval Smaller, broader QRS complexes Eventually VF

52. Hypothermia Irregular baseline Bradycardia J wave

53. Willem Einthoven’s Original Electrocardiograph