1. What is the QRS axis? Is it normal or abnormal?

2. Is the QRS axis normal or abnormal. Bonus: What is the rhythm
Is the QRS axis normal or abnormal? Bonus: What is the rhythm? (hint: the axis might help you decide )

3. Rate and Rhythm?

4. Rate and Rhythm?

5. Rate and Rhythm?

6. Rate and Rhythm?

7. Rate and Rhythm?

8. Rate and Rhythm?

9. Rate and Rhythm?

10. Scott E. Ewing DO Lecture #4
ECG Rhythm II -
Scott E. Ewing DO
Lecture #4

11. 8-Step Method ECG Interpretation
Rate
Rhythm
Axis
P wave
PR interval
QRS complex
QT interval
ST segment and T wave

12. Rhythm
Atrial
Junctional
Ventricular
Pacemaker
Last but not least

13. Premature Ventricular Contraction

14. Interpolated PVC’s

15. Multifocal PVC’s

16. PVC Couplet

17. PVC Triplet

18. Ventricular Bigeminy

19. Ventricular Trigeminy

20. Ventricular Escape Rhythm

21. Accelerated Idioventricular Rhythm

22. 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

23. 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

24. 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

25. Axis Shift Favoring VT

26. 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

27. AV Dissociation with VT

28. 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

29. Capture Beat

30. 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

31. Fusion Beat

32. Fusion Beat

33. 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

38. 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

40. 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

42. 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)

44. 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

45. 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

46. Torsades de pointes

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

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

51. Pacemakers

52. Atrial Pacemaker

53. Ventricular Pacemaker

54. Pacemaker Failure to Sense

55. Pacemaker Failure to Capture

56. Pacemaker Output Failure

57. Pacemaker Fusion Beat

58. Last But Not Least

60. 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

61. Ventricular Fibrillation

63. Answer: Ventricular Fibrillation / Ventricular Flutter
51 year male seen in the emergency department
Classic ECG 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)

64. Asystole