Practical Electrocardiography - Rate and Rhythm -

1. Practical Electrocardiography- Rate and Rhythm - Scott E. Ewing DO Interventional Cardiology Fellow Lecture #2

2. Review • Electrophysiology • Anatomy • Depolarization • EKG Paper • Lead Placement • Normal EKG • Waves / Intervals / Segments

3. Cardiac Action Potential • SA node, AV, Purkinje cells display pacemaker activity (phase 4 depolarization) • Body surface manifestation of the depolarization and repolarization waves • P wave is generated by atrial depolarization • QRS by ventricular muscle depolarization • T wave by ventricular repolarization • PR interval is a measure of conduction time from atrium to ventricle • QRS duration indicates the time required for all of the ventricular cells to be activated (i.e., the intraventricular conduction time) • QT interval reflects the duration of the ventricular action potential

5. Depolarization

6. EKG Frontal Plane

7. Normal EKG

8. QRS Complex

9. Waveform Review

10. 8-Step Method EKG Interpretation • Rate • Rhythm • Axis • P wave • PR interval • QRS complex • QT interval • ST segment and T wave

11. Rate Determination

13. Rate

14. Rate?

15. Rate?

16. Rate?

17. Rate?

18. Rate?

19. Rhythm • Atrial • Junctional • Ventricular • Pacemaker • Last but not least

20. Normal Sinus Rhythm

21. Normal Sinus Rhythm

22. Sinus Bradycardia

23. Sinus Bradycardia • Pathophysiology • Increased vagal tone in athletes • Inferior wall myocardial infarction • Digitalis glycosides, β-blockers, CCB agents, class I antiarrhythmic agents, amiodarone • Other drugs, toxins, environmental exposure (lithium, paclitaxel, toluene, dimethyl sulfoxide, topical ophthalmic acetylcholine, fentanyl, reserpine, clonidine) • Electrolyte disorders • Infection (diphtheria, rheumatic fever, viral myocarditis) • Sleep apnea • Hypoglycemia • Hypothyroidism • Hypothermia • Increased intracranial pressure

24. Sinus Bradycardia

25. Sinus Tachycardia

26. Sinus Tachycardia • Pathophysiology • Hypoxia • Hypovolemia / Sepsis • Pain • Fever • Anxiety • Hyperthyroidism • PE • Exercise • Drugs (nicotine, caffeine, atropine, pseudoephedrine, cocaine, methamphetamines, ecstasy)

27. Sinus Tachycardia

28. Sinus Arrhythmia

29. Sinus Pause

30. Wandering Atrial Pacemaker

31. Atrial Tachycardia

32. PAC’s

33. Nonconducted PAC

34. Atrial Bigeminy

35. 1st Degree AV Block

36. 1st Degree AV Block • Pathophysiology • PR interval represents time needed for electrical impulse from sinoatrial node to conduct through the atria, AV node, bundle of His, bundle branches, and Purkinje fibers • PR interval prolongation due to conduction delay within the right atrium, the AV node, or the His-Purkinje system • AV nodal dysfunction accounts for the majority of cases • 1st degree AV block caused by conduction delay in the His-Purkinje system often is associated with BBB

37. 1st Degree AV Block

38. 2nd Degree AV BlockMobitz Type I (Wenckebach)

39. Karel Frederik Wenckebach(1864 – 1940) • 1988 – Doctorate University of Utrecht, Netherlands • 1901-1910 – professor of IM Groningen, Netherlands • 1911-1914 – professor of IM Strasbourg , France • 1915-1929 – professor of IM Vienna, Austria, retired from his chair 1929 • Early work concerned embryology, later pathology of heart and circulatory diseases • 1903-1904 – first description of the beneficial effects of quinine alkaloids on arrhythmias and mainly in patients with auricular fibrillation of recent onset • 1905-1906 – 2nd degree AV block independently discovered by English physician John Hay and Wenckebach • 1934 – monograph on beriberi

40. 2nd Degree AV BlockMobitz Type I (Wenckebach) • Pathophysiology • Conduction disturbance in the AV node • Rarely secondary to AV nodal structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present • May be vagally mediated (well-trained athletes, digoxin excess, neurally mediated syncopal syndromes) • Vagally mediated AV block improves with exercise and may occur more commonly during sleep when parasympathetic tone dominates • Cardioactive drugs (digoxin, β-blockers, CCBs, certain antiarrhythmic drugs) • Various inflammatory, infiltrative, metabolic, endocrine, collagen vascular disorders

41. 2nd Degree AV Block Mobitz Type I

42. 2nd Degree AV Block Mobitz Type I

43. 2nd Degree AV BlockMobitz Type II (Hay) • Intermittent failure of conduction of P waves • PR interval is constant (may be normal or prolonged) • May include wide QRS • May progress to complete 3rd degree AV block

44. 2nd Degree AV Block Mobitz Type II

45. Woldemar Mobitz(1889 – 1951) • Born May 31, 1889 St. Petersburg, Russia, the son of a prominent surgeon • 1908 – gymnasium Meiningen, Saxony • 1914 – doctorate University of Munich • Internship, hospital service, and assistant years in the surgical clinics in Berlin and Halle, and medical clinics Munich and Freiburg • 1924 – first classified 2nd degree AV block into Type I and II • 1928-1943 – professor extraordinary at University of Freiburg in Breisgau • Remained in Magdeburg until it was occupied by the Russian army in 1945 • Suffered from laryngeal tuberculosis until his death April 11, 1951 • Primary interest in cardiovascular circulation and arrhythmias

46. 3rd Degree Heart Block

47. 3rd Degree Heart Block • Pathophysiology • Class Ia antiarrhythmics (quinidine, procainamide) • Class Ic antiarrhythmics (flecainide, propafenone) • Class II antiarrhythmics (β-blockers) • Class III antiarrhythmics (amiodarone, sotalol, dofetilide, ibutilide) • Class IV antiarrhythmics (CCBs) • Digoxin or other cardiac glycosides • Infection • Profound hypervagotonicity • Anterior wall MI • Cardiomyopathy, eg, Lyme carditis and acute rheumatic fever • Metabolic disturbances, eg, severe hyperkalemia

48. 3rd Degree Heart Block

49. 3rd Degree Heart Block

50. Atrial Fibrillation