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 Block Mobitz Type I (Wenckebach)

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

40. 2nd Degree AV Block Mobitz 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 Block Mobitz 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
– 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

51. Atrial Fibrillation Pathophysiology Long-standing hypertension
Valvular heart disease (rheumatic)
LVH
CAD DM
AMI
CHF
Pulmonary embolism
Cardiomyopathy
Pericarditis
Hyperthyroidism
ETOH (holiday heart)
Postoperative revascularization
Use of illegal drugs, such as cocaine or amphetamine derivatives
Over-the-counter herbs (ephedra, ginseng)
Idiopathic or “Lone” AF

52. Atrial Fibrillation

53. Atrial Fibrillation

54. Atrial Fibrillation

55. Atrial Fibrillation with WPW

56. Atrial Flutter

57. Atrial Flutter Pathophysiology Long-standing hypertension
Valvular heart disease (rheumatic)
LVH
CAD with or without depressed left ventricular function DM
CHF
Pulmonary embolism
Pericarditis
Hyperthyroidism
Postoperative revascularization
Digitalis toxicity

58. Atrial Flutter

59. Atrial Flutter

60. AV Node (Junctional) Origin

61. Junctional Rhythm

62. Accelerated Junctional Rhythm

63. Ventricular Origins

64. Premature Ventricular Contraction

65. Interpolated PVC’s

66. Multifocal PVC’s

67. PVC Couplet

68. PVC Triplet

69. Ventricular Bigeminy

70. Ventricular Trigeminy

71. Ventricular Escape Rhythm

72. Accelerated Idioventricular Rhythm

73. Wide Complex Tachycardia
Ventricular - regular
Monomorphic ventricular tachycardia
Fascicular tachycardia
Right ventricular outflow tract tachycardia
Ventricular - irregular
Torsades de pointes tachycardia
Polymorphic ventricular tachycardia
Supraventricular
Bundle branch block with aberrant conduction
Atrial tachycardia with pre­excitation

74. Ventricular Tachycardia
VT rate normally 120­300 bpm
Rhythm is regular or almost regular ( < 40 ms beat to beat variation), unless disturbed by the presence of capture or fusion beats
If a monomorphic broad complex tachycardia has an obviously irregular rhythm the most likely diagnosis is atrial fibrillation with either aberrant conduction or pre­excitation

75. Frontal Plane Axis
QRS axis normally - 30° to + 90°, with the axis most commonly ~60°
With VT mean frontal plane axis changes and often bizarre
Axis shift > 40° left or right suggestive of VT
Lead aVR is situated in the frontal plane at -210°
aVR negative with normal cardiac axis
aVR positive extremely abnormal axis to the left or right
aVR positive originates close to the apex, with depolarization moving upwards towards base of the heart

76. Axis Shift Favoring VT

77. Direct Evidence of Independent Atrial Activity
With VT, sinus node continues to initiate atrial contraction
P waves are dissociated from the QRS complexes and are positive in leads I and II
Atrial rate usually slower than the ventricular rate
AV dissociation usually diagnostic for VT, lack of direct evidence of independent P wave activity does not exclude the diagnosis

78. AV Dissociation with VT

79. Indirect Evidence of Independent Atrial Activity
Capture beat
Occasionally an atrial impulse may cause ventricular depolarization via the normal conduction system
Resulting QRS complex occurs earlier than expected and is narrow
Shows that even at rapid rates the conduction system is able to conduct normally, thus making a diagnosis of SVT with aberrancy unlikely
Capture beats are uncommon and their absence does not exclude the diagnosis

80. Capture Beat

81. Indirect Evidence of Independent Atrial Activity
Fusion beats
Occurs when a sinus beat conducts to the ventricles via the AV node and fuses with a beat arising in the ventricles
Resulting QRS complex has an appearance intermediate between a normal beat and a tachycardia beat
Fusion beats are uncommon and their absence does not exclude the diagnosis

82. Fusion Beat

83. Fusion Beat

84. Indirect Evidence of Independent Atrial Activity
QRS concordance throughout the chest leads
QRS complexes in precordial leads are either predominantly positive or predominantly negative
Presence of concordance suggests that the tachycardia has a ventricular origin
Positive concordance probably indicates that the origin of the tachycardia lies on the posterior ventricular wall; the wave of depolarization moves towards all the chest leads and produces positive complexes
Similarly, negative concordance is thought to correlate with a tachycardia originating in the anterior ventricular wall

89. Answer: NSVT 28 yo female with palpitations and lightheadedness
Sinus rhythm (normal QTc) with non-sustained monomorphic VT (starting 2nd beat, rate 170 bpm)
Ventricular beats have a LBBB pattern and inferior / borderline rightward QRS axis raising consideration of monomorphic VT arising from the RVOT
Isolated PVCs and two ventricular couplets with the same morphology
Retrograde P waves
Patient had an idiopathic cardiomyopathy with global mild ventricular hypokinesis

91. Answer: Accelerated Idioventricular Rhythm
67 yo man with previous acute MI with normal QRS duration
Most consistent with AIVR, originating from the left ventricle and therefore accounting for the atypical RBBB morphology
ST elevations in the precordial leads are likely due to the injury current from underlying acute myocardial infarction
AIVR may be marker of reperfusion following acute MI
83 bpm too slow for VT and too fast for complete heart block

93. Answer: VT with Rate 170 bpm
RBBB morphology is atypical (monomorphic R, rather than rSR', in V1), and the R:S ratio is less than 1 in V6, both suggestive of ventricular tachycardia
Most common underlying diagnosis in adult patients with sustained monomorphic VT is coronary heart disease status post AMI
This patient had a non-ischemic cardiomyopathy
Morphology of the VT is suggestive of origin from the left side of the heart, near the base (RBBB with inferior/rightward axis)

95. Answer: VT with Underlying ST and AV Dissociation
77 yo with CAD
Wide complex tachycardia at 165 bpm and RBBB morphology
Underlying sinus tachycardia at 136 bpm and AV dissociation confirming the diagnosis of VT (Note the clear sinus P wave just after 5th QRS)
QRS morphology and axis are consistent with origin of the VT from the posterior septum
Patient had a prior large inferior-posterior MI

96. Torsades de pointes Tachycardia
Torsades de pointes (“twisting of points”) a polymorphic VT in which the cardiac axis rotates over a sequence of 5­20 beats
QRS amplitude varies similarly, such that the complexes appear to twist around the baseline
Usually associated with conditions that prolong QT interval
Usually not sustained
Recur unless the underlying cause is corrected
May be prolonged
May degenerate into ventricular fibrillation
Transient prolongation of the QT interval is often seen in AMI and may lead to torsades de pointes
Management different from the management of other VTs

97. Torsades de pointes

98. Torsades de pointes 62 yo woman on diuretics with syncope
Syncope recurred during this ECG recording
Serum potassium concentration was 2.3 mEq/L

101. Answer: Torsade de pointes
74 yo woman with syncope with life-threatening finding
Complex EKG showing
Underlying atrial fibrillation
Long QT(U)
Ventricular pacing with intermittent sensing failure
Run of torsade de pointes-type of polymorphic ventricular tachycardia

102. Pacemakers

103. Atrial Pacemaker

104. Ventricular Pacemaker

105. Pacemaker Failure to Sense

106. Pacemaker Failure to Capture

107. Pacemaker Output Failure

108. Pacemaker Fusion Beat

109. Last But Not Least

111. Ventricular Fibrillation
67 yo man at the onset of a cardiac arrest
Arrow indicates the early-occurring PVC that initiates the ventricular flutter that rapidly deteriorates into ventricular fibrillation

112. Ventricular Fibrillation

114. Answer: Ventricular Fibrillation / Ventricular Flutter
51 year male seen in the emergency department
Classic EKG obtained during a VF cardiac arrest
Findings typical of ventricular fibrillation with more organized ventricular electrical activity in the second half of the strip consistent with ventricular flutter
Characteristic systematic variation in QRS axis of torsade is not seen here (although torsade may degenerate terminally into ventricular fibrillation)

115. Asystole