ECG Practicals.ppt for practical purpose
- 1. An Introduction to the 12 lead ECG
- 2. Reading 12-Lead ECGs The best way to read 12-lead ECGs is to develop a step-by-step approach (just as we did for analyzing a rhythm strip). In these modules we present a 6-step approach: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTION
- 3. The standard 12 Lead ECG 6 Limb Leads 6 Chest Leads (Precordial leads) avR, avL, avF, I, II, III V1, V2, V3, V4, V5 and V6 Rhythm Strip
- 4. Calculate Rate • Option 2 (cont) – Memorize the sequence: 300 - 150 - 100 - 75 - 60 - 50 Interpretation? 3 0 0 1 5 0 1 0 0 7 5 6 0 5 0 Approx. 1 box less than 100 = 95 bpm
- 5. Step 2: Determine regularity • Look at the R-R distances (using a caliper or markings on a pen or paper). • Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular R R
- 6. Step 3: Assess the P waves • Are there P waves? • Do the P waves all look alike? • Do the P waves occur at a regular rate? • Is there one P wave before each QRS? Interpretation? Normal P waves with 1 P wave for every QRS
- 7. Step 4: Determine PR interval • Normal: 0.12 - 0.20 seconds. (3 - 5 boxes) Interpretation? 0.12 seconds
- 8. Step 5: QRS duration • Normal: 0.04 - 0.12 seconds. (1 - 3 boxes) Interpretation? 0.08 seconds
- 9. NSR Parameters • Rate 60 - 100 bpm • Regularity regular • P waves normal • PR interval 0.12 - 0.20 s • QRS duration 0.04 - 0.12 s Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia
- 10. Arrhythmia Formation Arrhythmias can arise from problems in the: • Sinus node • Atrial cells • AV junction • Ventricular cells
- 11. Rate Rhythm Axis Intervals Hypertrophy Infarct • Causes of left axis deviation include: – Left ventricular hypertrophy – Inferior wall MI – Left bundle branch block – Left anterior fascicular block – Horizontal heart 0o -90o 90o 180o • Causes of right axis deviation include: – Right ventricular hypertrophy – Lateral wall MI – Right bundle branch block – Pulmonary hypertension – Vertical heart
- 13. Limb leads Chest Leads
- 14. Chest Leads 6 Unipolar leads Also known as precordial leads V1, V2, V3, V4, V5 and V6 - all positive
- 15. Think of the positive electrode as an ‘eye’… the position of the positive electrode on the body determines the area of the heart ‘seen’ by that lead.
- 16. Inferior II, III, AVF Antero-Septal V1,V2, V3,V4 Lateral I, AVL, V5, V6 Posterior V1, V2, V3 RIGHT LEFT
- 17. •The P wave represents atrial depolarisation •the PR interval is the time from onset of atrial activation to onset of ventricular activation •The QRS complex represents ventricular depolarisation •The S-T segment should be iso-electric, representing the ventricles before repolarisation •The T-wave represents ventricular repolarisation •The QT interval is the duration of ventricular activation and recovery.
- 18. Ischaemic Changes • S-T segment elevation • S-T segment depression • Hyper-acute T-waves • T-wave inversion • Pathological Q-waves • Left bundle branch block
- 19. ST Segment • The ST segment represents period between ventricular depolarisation and repolarisation. • The ventricles are unable to receive any further stimulation • The ST segment normally lies on the isoelectric line.
- 20. ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment.
- 21. ST Elevation Infarction ST depression, peaked T-waves, then T-wave inversion The ECG changes seen with a ST elevation infarction are: Before injury Normal ECG ST elevation & appearance of Q-waves ST segments and T-waves return to normal, but Q-waves persist Ischemia Infarction Fibrosis
- 22. ST Elevation Infarction Here’s a diagram depicting an evolving infarction: A. Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T- waves C. Infarction from ongoing ischemia results in marked ST elevation D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves
- 25. ST Segment Depression Can be characterised as:- • Downsloping • Upsloping • Horizontal
- 27. ST Segment Depression Downsloping ST segment depression:- • Can be caused by digoxin. Upward sloping ST segment depression:- • Normal during exercise.
- 28. T waves • The T wave represents ventricular repolarisation • Should be in the same direction as and smaller than the QRS complex • Hyperacute T waves occur with S-T segment elevation in acute MI • T wave inversion occurs during ischaemia and shortly after an MI
- 29. T waves Other causes of T wave inversion include: • Normal in some leads • Cardiomyopathy • Pericarditis • Bundle Branch Block (BBB) • Sub-arachnoid haemorrhage • Peaked T waves indicate hyperkalaemia
- 32. T wave inversion in an evolving MI
- 33. QRS Complex May be too broad ( more than 0.12 seconds) • A delay in the depolarisation of the ventricles because the conduction pathway is abnormal • A Left Bundle Branch Block can result from MI and may be a sign of an acute MI.
- 34. Wide QRS (LBBB)
- 35. QRS Complex • May be too tall. • This is caused by an increase in muscle mass in either ventricle. (Hypertrophy)
- 36. Q Waves Non Pathological Q waves Q waves of less than 2mm are normal Pathological Q waves Q waves of more than 2mm indicate full thickness myocardial damage from an infarct Late sign of MI (evolved)
- 38. The ECG in ST Elevation MI
- 40. Unstable Angina ECG during pain
- 41. A 55 year old man with 4 hours of “crushing” chest pain. Acute inferior myocardial infarction (with reciprocal changes) ST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads
- 42. A 63 Year Old woman with 10 hours of chest pain and sweating Can you guess her diagnosis? Acute anterior-lateral myocardial infarction ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression in the inferior leads
- 43. Rhythm #1 30 bpm • Rate? • Regularity? regular normal 0.10 s • P waves? • PR interval? 0.12 s • QRS duration? Interpretation? Sinus Bradycardia
- 44. Rhythm #2 130 bpm • Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.16 s • QRS duration? Interpretation? Sinus Tachycardia
- 45. Rhythm #3 70 bpm • Rate? • Regularity? occasionally irreg. 2/7 different contour 0.08 s • P waves? • PR interval? 0.14 s (except 2/7) • QRS duration? Interpretation?NSR with Premature Atrial Contractions
- 46. Rhythm #4 60 bpm • Rate? • Regularity? occasionally irreg. none for 7th QRS 0.08 s (7th wide) • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? Sinus Rhythm with 1 PVC
- 47. PVCs • Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.
- 48. Left Ventricular Hypertrophy Compare these two 12-lead ECGs. What stands out as different with the second one? Normal Left Ventricular Hypertrophy Answer: The QRS complexes are very tall (increased voltage)
- 49. Left Ventricular Hypertrophy • Criteria exists to diagnose LVH using a 12-lead ECG. – For example: • The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm. • However, for now, all you need to know is that the QRS voltage increases with LVH.
- 50. Right Bundle Branch Blocks What QRS morphology is characteristic? V1 For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2). “Rabbit Ears”
- 51. Left Bundle Branch Blocks What QRS morphology is characteristic? For LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2). Broad, deep S waves Normal
- 52. Rhythm #5 100 bpm • Rate? • Regularity? irregularly irregular none 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Fibrillation
- 53. Rhythm #6 70 bpm • Rate? • Regularity? regular flutter waves 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Flutter
- 54. PSVT • Deviation from NSR – The heart rate suddenly speeds up, often triggered by a PAC (not seen here) and the P waves are lost.
- 55. Rhythm #8 160 bpm • Rate? • Regularity? regular none wide (> 0.12 sec) • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Tachycardia
- 56. Rhythm #9 none • Rate? • Regularity? irregularly irreg. none wide, if recognizable • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Fibrillation
- 57. Rhythm #10 60 bpm • Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.36 s • QRS duration? Interpretation? 1st Degree AV Block
- 58. Rhythm #11 50 bpm • Rate? • Regularity? regularly irregular nl, but 4th no QRS 0.08 s • P waves? • PR interval? lengthens • QRS duration? Interpretation? 2nd Degree AV Block, Type I
- 59. 2nd Degree AV Block, Type I • Deviation from NSR – PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS).
- 60. Rhythm #12 40 bpm • Rate? • Regularity? regular nl, 2 of 3 no QRS 0.08 s • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? 2nd Degree AV Block, Type
- 61. Rhythm #13 40 bpm • Rate? • Regularity? regular no relation to QRS wide (> 0.12 s) • P waves? • PR interval? none • QRS duration? Interpretation? 3rd Degree AV Block