This document provides an overview of how to interpret common ECG abnormalities through 3 sentences or less summaries: 1) It outlines how to measure rate, rhythm, intervals, complexes, and waves on an ECG and identifies what is considered normal. 2) Key abnormal rhythms, rates, intervals, and waves are defined along with their potential causes, such as sinus bradycardia, atrial fibrillation, various heart blocks, ventricular tachycardia, ST segment changes, T wave inversions, bundle branch blocks, and more. 3) Methods for localizing myocardial infarctions and abnormalities seen in conditions like hyperkalemia and hypothermia are also summarized.

1. D R L N R G O N Z Á L E Z
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

8. 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

9. 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

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

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

12. 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

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

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

15. 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

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

17. 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

18. 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

19. 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

20. Ventricular fibrillation
 Rapidly fatal arrhythmia
 Most commonly due to MI

21. Asystole
 Absence of electrical activity

22. P pulmonale
 Tall P waves >2.5mm
 Right atrial enlargement
 Pulmonary hypertension
 Pulmonary stenosis
 Tricuspid stenosis

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

24. 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

25. 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

26. 1st 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

27. 2nd degree AV block
 Mobitz type I
 Wenckebach phenomenon
 PR interval progressively lengthens
 P wave fails to be conducted
 PR interval then resets to normal

28. 2nd 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

29. 3rd degree heart block
 P waves have no relationship to QRS complexes
 Broad QRS complexes – ventricular escape rhythm
 Urgent pacing required

30. 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

31. 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

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

33. Small complexes
 Obesity
 Hyperinflated chest
 Pericardial effusion

34. 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

35. LBBB

36. 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

37. RBBB

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

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

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

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

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

43. Tall T waves
 Hyperkalaemia
 Hypermagnesaemia
 Acute MI

44. Flattened T waves
 Hypokalaemia
 Pericardial effusion
 Hypothyroidism

45. 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

46. 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

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

49.  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

50. Anterolateral MI

51. Inferior MI

52. Hypokalaemia
 Flattened T wave
 Prominent U wave
 ST depression
 T wave inversion

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

54. Hypothermia
 Irregular baseline
 Bradycardia
 J wave

55. Willem Einthoven’s Original Electrocardiograph