1. Electrical and Mechanical properties of the heart [Part 3] Clinical Electrocardiography

2. At the end of the lecture, students should be able to:At the end of the lecture, students should be able to: Explain the term arrhythmia and heart block and types. Describe the physiologic basis of changes in ECG observed in arrhythmias: sinus arrhythmia; first degree, second degree and complete heart block; atrial fibrillation, paroxysmal supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation; acute myocardial infarction; Describe the principal ECG changes associated with each of the following electrolyte abnormalities: hyperkalemia, hypokalemia, hypocalcemia. Learning Outcomes…

3. Arrhythmia and Heart block

4. Arrhythmia an abnormality in the heart's rhythm, or heartbeat pattern. can be too slow, too fast, extra beats, skip a beat, or beat irregularly. Known causes of arrhythmias include heart disease, stress, caffeine, tobacco, alcohol, diet pills, and decongestants in cough and cold medicines. Due to origin of impulse other than the sinus node, producing an abnormal rate or rhythm or conduction "block" prevents the electrical signal traveling through the normal pathway.

6. Origin of Arrhythmia Arrhythmias can arise from problems in the: Sinus node Atrial cells AV junction Ventricular cells

7. SA Node Problems The SA Node can: fire too slow fire too fast Sinus Bradycardia Sinus Tachycardia Sinus Tachycardia may be an appropriate response to stress.

8. Atrial Cell Problems Atrial cells can: fire occasionally from a focus fire continuously due to a looping re-entrant circuit Premature Atrial Contractions (PACs) Atrial Flutter

9. Atrial Cell Problems Atrial cells can also: fire continuously from multiple foci or fire continuously due to multiple micro re-entrant “wavelets” Atrial Fibrillation

10. Multiple micro re- entrant “wavelets” refers to wandering small areas of activation which generate fine chaotic impulses. Colliding wavelets can, in turn, generate new foci of activation. Atrial tissue re-entrant pathway

12. AV Junctional Problems The AV junction can: fire continuously due to a looping re-entrant circuit block impulses coming from the SA Node Paroxysmal Supraventricular Tachycardia AV Junctional Blocks

13. Ventricular Cell Problems Ventricular cells can: fire occasionally from 1 or more foci fire continuously from multiple foci fire continuously due to a looping re-entrant circuit Premature Ventricular Contractions (PVCs) Ventricular Fibrillation Ventricular Tachycardia

14. Arrhythmias; Types Sinus Rhythms Premature Beats Supraventricular Arrhythmias Ventricular Arrhythmias AV Junctional Blocks

15. Sinus Rhythms Sinus Bradycardia Sinus Tachycardia

16. Example #1 ~33 bpm Rate? Regularity? regular normal 0.10 s P waves? PR interval? 0.12 s QRS duration? Interpretation? Sinus Bradycardia

17. Deviation from NSR - Rate~33 bpm

18. Sinus Bradycardia Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

19. Example #2 130 bpm Rate? Regularity? regular normal 0.08 s P waves? PR interval? 0.16 s QRS duration? Interpretation? Sinus Tachycardia

20. Deviation from NSR - Rate> 100 bpm

21. Sinus Tachycardia Etiology: SA node is depolarizing faster than normal, impulse is conducted normally. Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

22. Premature Beats Premature Atrial Contractions (PACs) Premature Ventricular Contractions (PVCs)

23. Example #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

24. Premature Atrial Contractions Deviation from NSR –These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.

25. Premature Atrial Contractions Etiology: Excitation of an atrial cell forms an impulse that is then conducted normally through the AV node and ventricles.

26. Mechanism When an impulse originates anywhere in the atria (SA node, atrial cells, AV node, Bundle of His) and then is conducted normally through the ventricles, the QRS will be narrow (0.04 - 0.12 s).

27. Example #4 60 bpm Rate? Regularity? occasionally irreg. none for 7 th QRS 0.08 s (7th wide) P waves? PR interval? 0.14 s QRS duration? Interpretation? Sinus Rhythm with 1 PVC

28. PVCs Deviation from NSR –Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes. –When there are more than 1 premature beats and look alike, they are called “uniform”. When they look different, they are called “multiform”.

29. PVCs Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.

30. Mechanism When an impulse originates in a ventricle, conduction through the ventricles will be inefficient and the QRS will be wide and bizarre.

31. Example #5 100 bpm Rate? Regularity? irregularly irregular none 0.06 s P waves? PR interval? none QRS duration? Interpretation? Atrial Fibrillation

32. Deviation from NSR –No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node). –Atrial activity is chaotic (resulting in an irregularly irregular rate). –Common, affects 2-4%, up to 5-10% if > 80 years old

33. Atrial Fibrillation Etiology: is due to multiple re-entrant wavelets conducted between the R & L atria. Either way, impulses are formed in a totally unpredictable fashion. The AV node allows some of the impulses to pass through at variable intervals (so rhythm is irregularly irregular).

34. Example #6 70 bpm Rate? Regularity? regular flutter waves 0.06 s P waves? PR interval? none QRS duration? Interpretation? Atrial Flutter

35. Deviation from NSR –No P waves. Instead flutter waves (note “sawtooth” pattern) are formed at a rate of 250 - 350 bpm. –Only some impulses conduct through the AV node (usually every other impulse).

36. Atrial Flutter Etiology: Reentrant pathway in the right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in the AV node as the node repolarizes).

37. Ventricular Conduction Normal Signal moves rapidly through the ventricles Abnormal Signal moves slowly through the ventricles

38. Example #7 74  148 bpm Rate? Regularity? Regular  regular Normal  none 0.08 s P waves? PR interval? 0.16 s  none QRS duration? Interpretation? Paroxysmal Supraventricular Tachycardia (PSVT)

39. PSVT Deviation from NSR –The heart rate suddenly speeds up, often triggered by a PAC (not seen here) and the P waves are lost.

40. PSVT Etiology: There are several types of PSVT but all originate above the ventricles (therefore the QRS is narrow). Most common: abnormal conduction in the AV node (reentrant circuit looping in the AV node).

41. Ventricular Arrhythmias Ventricular Tachycardia Ventricular Fibrillation

42. Example #8 160 bpm Rate? Regularity? regular none wide (> 0.12 sec) P waves? PR interval? none QRS duration? Interpretation? Ventricular Tachycardia

43. Deviation from NSR –Impulse is originating in the ventricles (no P waves, wide QRS).

44. Ventricular Tachycardia Etiology: There is a re-entrant pathway looping in a ventricle (most common cause). Ventricular tachycardia can sometimes generate enough cardiac output to produce a pulse; at other times no pulse can be felt.

45. Example #9 none Rate? Regularity? irregularly irreg. none wide, if recognizable P waves? PR interval? none QRS duration? Interpretation? Ventricular Fibrillation

46. Deviation from NSR –Completely abnormal.

47. Ventricular Fibrillation Etiology: The ventricular cells are excitable and depolarizing randomly. Rapid drop in cardiac output and death occurs if not quickly reversed

48. Heart Blocks Refers to a delay in the normal flow of electrical impulses that cause the heart to beat. classified as –first- degree block, –second- degree block, –third- degree block.

49. first-degree heart block signal is just slowed down a little as it travels along the defective part of the conduction system so that it arrives late traveling from the atrium to the ventricle. 1st Degree AV Block

50. Second -degree heart block every impulse does not reach to its destination. The block may affect every other beat, every second or third beat, or be very rare. If the blockage is frequent, it results in an overall slowing of the heart called bradycardia. 2nd Degree Block Type 1 (Wenckebach)

51. Third-degree block also called complete heart block, no signals can travel through the AV node, the heart uses its backup impulse generator in the lower portion of the heart. it is too slow to be an effective pump. Complete heart block

52. AV Nodal Blocks 1st Degree AV Block 2nd Degree AV Block, Type I 2nd Degree AV Block, Type II 3rd Degree AV Block

53. Example #10 60 bpm Rate? Regularity? regular normal 0.08 s P waves? PR interval? 0.36 s QRS duration? Interpretation? 1st Degree AV Block

54. Deviation from NSR –PR Interval> 0.20 s

55. 1st Degree AV Block Etiology: Prolonged conduction delay in the AV node or Bundle of His.

56. 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

57. Deviation from NSR –PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS).

58. 2nd Degree AV Block, Type I Etiology: Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually the 3rd or 4th) fails to make it through the AV node.

59. Example #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 II

60. Deviation from NSR –Occasional P waves are completely blocked (P wave not followed by QRS).

61. 2nd Degree AV Block, Type II Etiology: Conduction is all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His.

62. Example #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

63. Deviation from NSR –The P waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction.

64. 3rd Degree AV Block Etiology: There is complete block of conduction in the AV junction, so the atria and ventricles form impulses independently of each other. Without impulses from the atria, the ventricles own intrinsic pacemaker kicks in at around 30 - 45 beats/minute.

65. Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. Rhythm Strip 12-Lead ECG

66. The 12-Lead ECG The 12-Lead ECG sees the heart from 12 different views. Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart. The rhythm strip is only 1 of these 12 views.

67. ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment.

68. ST Elevation (cont) Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

69. Anterior View of the Heart The anterior portion of the heart is best viewed using leads V 1 - V 4.

70. Anterior Myocardial Infarction If you see changes in leads V 1 - V 4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

71. Putting it all Together Do you think this person is having a myocardial infarction. If so, where?

72. Interpretation Yes, this person is having an acute anterior wall myocardial infarction.

73. Other MI Locations Now that you know where to look for an anterior wall myocardial infarction let’s look at how you would determine if the MI involves the lateral wall or the inferior wall of the heart.

74. Putting it all Together Now, where do you think this person is having a myocardial infarction?

75. Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.

76. Putting it all Together How about now?

77. Anterolateral MI This person’s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6, I, and aVL)!

78. ECG Changes in Hyperkalemia Appearance of tall, pointed, narrow T waves. Decreased P wave amplitude, decreased R wave height, widening of QRS complexes, ST segment changes (elevation/depression), 1st degree heart block. Absent P waves, very broad, bizarre QRS complexes, AV block, VT, VF or ventricular asystole.

79. Effects of hyperkalemia: 1. increased excitability due to decreased resting membrane potential (less negative potential, so closer to the threshold value) 2. decreased amplitude of action potential (amplitude is measured from the resting value to the spike value, and with hyperkalemia the resting value is decreased and so as the amplitude) 3. the main effect is: due to decreased potassium concentration gradient, repolarization is prolonged (refractory period is prolonged) so the frequency of action potentials is decreased

80. Hypokalaemia ST segment depression, decreased T wave amplitude, increased U wave height Cardiac arrhythmias Prolongation of the QRS duration, increased P wave amplitude and duration Various types of arrhythmias may occur in hypokalaemia. These may include atrial and ventricular ectopics, atrial tachycardia, heart blocks, VT and VF.

81. Hypercalcaemia The main change is reduction in the Q-T interval on the ECG. The T wave duration is unaffected but the ST segment duration is shortened. Patients with hypercalcaemia have an increased sensitivity to digitalis and may present with a variety of arrhythmias.

82. Hypocalcaemia The main ECG change is prolongation of the Q-T interval. There is no increase in T wave duration but the ST segment is prolonged.