ELECTROCARDIOGRAMs (ECGs)

1. Cardiac Wellness Institute of Calgary ELECTROCARDIOGRAMs (ECGs) Updated May 2010

2. Material to be Covered • ACSM’s Resource Manual for Guidelines for Exercise Testing and Prescription (6th ed.) • Chapter 27 • Rapid Interpretation of EKG’s (6th ed.)

3. LEAD PLACEMENT Standard 12-lead ECG: • Limb Leads - 6 in all - I, II, III, aVL, aVR, aVF • Chest leads - 6 in all -V1,V2,V3,V4,V5,V6

4. Bipolar Augmented - - aVR aVL + + - + I + + III II + aVF LIMB LEADS

5. CHEST LEADS Along the horizontal plane: • V1 and V2 - Right side of the heart • V3 and V4 - Intraventricular septum • V5 and V6 - Left side of the heart

6. PROCESS SA Node - Heart pacemaker; located in the RA; initiates next step

7. PROCESS P Wave - Atrial depolarization and contraction

8. PROCESS AV Node - Slows the depolarization of the atria;connects atria and ventricles electrically

9. PROCESS QRS complex - ventricular depolarization; begins inBundle of His

10. PROCESS

11. VENTRICULAR DEPOLARIZATION His Bundle Left Bundle Branch & Right Bundle Branch Purkinje Fibers

12. VENTRICULAR DEPOLARIZATION • Q Wave - 1st downward wave of the complex • R Wave - 1st upward wave of the complex • S Wave - downward wave preceded by an upward wave

13. PROCESS ST Segment - Initial plateau phase ofventricular repolarization

14. PROCESS T wave - Rapid phase of ventricular repolarization

15. NORMAL ECG

16. RHYTHM • Normal sinus rhythm: • Each P wave is followed by a QRS • Regular or irregular

17. RATE • P wave rate 60 - 100 bpm with <10% variation - Normal • Rate < 60 bpm = Sinus Bradycardia - Results from: • - Excessive vagal stimulation - SA nodal ischemia (Inferior MI) • Rate > 100 bpm = Sinus Tachycardia - Results from: • - Pain / anxiety - CHF - Volume depletion - Pericarditis - Chronotropic Drugs (Dopamine)

18. RATE • Methods: • Method 1 = 1500/ # of small boxes between RR • Method 2

19. P WAVE • Normal: • Height < 2.5 mm in lead II • Width < 0.11 s in lead II

20. P WAVE ABNORMALITY

21. P WAVE ABNORMALITIES • Right atrial hypertrophy: • A P wave in lead II taller then 2.5 mm (2.5 small squares) • The P wave is usually pointed

23. P WAVE ABNORMALITIES • Left atrial abnormality (dilatation or hypertrophy): • M shaped P wave in lead II • Prominent terminal negative component to P wave in lead V1

24. P WAVE ABNORMALITIES • Premature Atrial Complex (PAC): • An abnormal P wave (arrowed in figure below) • As P waves are small and rather shapeless, the difference in a PAC is usually subtle; the one shown here is a clear example • Occurs earlier than expected • Followed by a compensatory pause - but not a full compensatory pause

25. P WAVE ABNORMALITIES • Hyperkalemia: • The following changes may be seen in hyperkalemia - Small or absent P waves - Atrial fibrillation - Wide QRS - Shortened or absent ST segment - Wide, tall and tented T waves - Ventricular fibrillation

26. P WAVE ABNORMALITIES • Arrhythmias (will cover later): • Premature atrial complex (PAC) • Atrial flutter • Atrial fibrillation • Paroxysmal reentrant tachycardia (SVT) • Multifocal atrial tachycardia

27. PR INTERVAL • Normal PR interval: • 0.12 to 0.20 s (3 - 5 small squares)

28. PR INTERVAL ABNORMALITIES Shorter PR interval: • Wolf-Parkinson-White syndrome • - Short PR interval, less than 3 small squares (120 ms) • - Slurred upstroke to the QRS indicating pre-excitation (delta wave) • - Broad QRS • - Secondary ST and T wave changes

29. PR INTERVAL ABNORMALITIES • Long PR interval (will cover later): • AV blocks

30. QRS COMPLEX • QRS Axis • Normal duration of complex is < 0.12 s (3 small squares) • NO pathological Q waves • NO left or right ventricular hypertrophy

31. AXIS • Using leads I and aVF, the axis can be assigned to one of the four quadrants at a glance

32. AXIS - NORMAL • Both I and aVF +ve = NORMAL AXIS • Lead I +ve and aVF -ve -If the axis is in the "left" quadrant take your second glance at lead II. - Lead II +ve = NORMAL AXIS - Lead II -ve = LEFT AXIS DEVIATION

33. AXIS - LEFT AXIS DEVIATION • Left anterior hemiblock • Left ventricular hypertrophy • Q waves of inferior myocardial infarction • Artificial cardiac pacing • Emphysema • Hyperkalemia • Wolff-Parkinson-White syndrome - right sided accessory pathway • Tricuspid atresia • Ostium primum ASD • Injection of contrast into left coronary artery

34. AXIS - NORTHWEST TERRITORY • Both I and aVF -ve = axis in the NORTHWEST TERRITORY • Causes of “No man’s land” • - Emphysema • - Hyperkalemia • - Lead transposition • - Artificial cardiac pacing • - Ventricular tachycardia

35. AXIS - RIGHT AXIS DEVIATION • Lead I -ve and aVF +ve = RIGHT AXIS DEVIATION • Causes: • - Normal finding in children and tall thin adults - Right ventricular hypertrophy - Chronic lung disease even without pulmonary hypertension - Anterolateral myocardial infarction - Left posterior hemiblock - Pulmonary embolus - Wolff-Parkinson-White syndrome - left sided accessory pathway - Atrial septal defect - Ventricular septal defect

36. WIDE QRS COMPLEX • Right Bundle Branch Block: • Wide QRS, more than 120 ms (3 small squares) • Secondary R wave in lead V1 (RSR) • Other features include slurred S wave in lateral leads and T wave changes in the septal leads

37. WIDE QRS COMPLEX

38. WIDE QRS COMPLEX • Left Bundle Branch Block: • Wide QRS, more than 120 ms (3 small squares) • M shape QRS , R’R’

39. WIDE QRS COMPLEX

40. WIDE QRS • Hyperkalemia: • Changes that can be seen: - Small or absent P waves - Atrial fibrillation - Wide QRS - Shortened or absent ST segment - Wide, tall and tented T waves - Ventricular fibrillation

41. WIDE QRS Ventricular rhythm (will cover later):

42. PATHOLOGICAL Q WAVES • Q waves > 1mm • Their depth > 25% of the height of the QRS • Q waves in V6 and aVL (not pathological…small) • Look for anatomical site, ignore aVR

43. PATHOLOGICAL Q WAVES

44. NON Q WAVE MI • Not all MIs develop Q waves (up to 1/3 never do or they develop and resolve) • WHY? • Infarct was not complete (transmural) • Infarct occurred in a electrically “silent” area of the heart, where an EKG cannot record the injury • Acute Infarct (Q waves will eventually appear)

45. RIGHT VENTRICULAR HYPERTROPHY (RVH) • Right axis deviation • Deep S waves in the lateral leads • A dominant R wave in lead V1

46. LEFT VENTRICULAR HYPERTROPHY (LVH) • Sokolow + Lyon (Am Heart J, 1949;37:161) • S in V1+ R in V5 or V6 > 35 mm • Cornell criteria (Circulation, 1987;3: 565-72) • S in V3 + R in aVL > 28 mm in men • S in V3 + R in aVL > 20 mm in women • Framingham criteria (Circulation,1990; 81:815-820) • R in aVL > 11mm, R in V4-6 > 25mm • S in V1-3 > 25 mm, • S in V1 or V2 + R in V5 or V6 > 35 mm, • R in I + S in III > 25 mm

47. LVH • Increased amplitude in height and depth

48. QT INTERVAL • Calculate the corrected QT interval - QTc = QT / RR = 0.42 - Normal = 0.42 s

49. LONG QT INTERVAL • Causes: • Myocardial infarction, myocarditis, diffuse myocardial disease • Hypocalcemia, Hypercalcemia (Short QT), hypothyrodism • Subarachnoid hemorrhage, intracerebral hemorrhage • Drugs (e.g. Sotalol, Amiodarone) • Heredity

50. ST SEGMENT • Normal ST segment: • No elevation or depression