Discussion of syncope and sudden cardiac death syndromes.

1. “He done fell out. . .”
Malachi Winters
MICT I/C CCEMTP

2. Called for a fainting spell. . .

3. Syncope Rule of 15%
• Subarachnoid Bleed
• Acute Coronary Syndrome (AMI)
• Thoracic Aortic Dissection
• Pulmonary Embolism
• AAA Rupture/Leak
• Ruptured Ectopic Pregnancy

4. Causes of sudden cardiac death
• Brugada Syndrome
• Hypertrophic Cardiomyopathy (HCM)
• Long QT Syndrome
• Wolff Parkinson White Syndrome
• Life threatening electrolyte abnormalities

5. Brugada Syndrome

6. Brugada Syndrome
• Discovered by the Brugada brothers in 1992.
• Inherited defect of sodium channels (SCN5A
gene).
• Epicardial area of the RV has repolarization
abnormality.
• Prone to spontaneous Ventricular Arrhythmias.

7. Brugada = Sailboat of DEATH in
V1-V3.

9. Post cardiac arrest 41 y/o

10. Post cardiac arrest 41 y/o

11. Brugada Syndrome

12. Brugada Syndrome

13. Brugada Syndrome

14. Brugada Syndrome

15. Brugada Syndrome

16. Brugada Syndrome

17. Brugada Syndrome

18. Brugada Syndrome

19. Brugada Syndrome leads to
ventricular arrhythmias.

21. When a patient begins showing
signs of Brugada Syndrome
(syncope), mortality increases by
10% for every year Brugada is
untreated.

22. Ddon’t give Brugada patients Na+
Channel Blockers!
• TCAs
• Flecinide
• Procainamide
• Bupivicaine
• Lidocaine (recommended)
• Amiodarone (recommended)

23. Hypertrophic Cardiomyopathy
(HCM)

24. Hypertrophic Cardiomyopathy
• A leading cause of
sudden cardiac death in
young athletes.
• Can be familial or a
spontaneous mutation.
• Risk for sudden
ventricular arrhythmias.

27. Hypertrophic Cardiomyopathy
• True diagnosis requires more than an ECG
• Huge QRS in V leads (caused by left
ventricular hypertrophy).
• Pathological Q waves (caused by septal
hypertrophy).

28. Hypertrophic Cardiomyopathy

29. Hypertrophic Cardiomyopathy

30. Hypertrophic Cardiomyopathy

31. Hypertrophic Cardiomyopathy

32. Long QT Syndromes

33. Inherited Long QT Syndromes
• Jervell and Lange-Nielsen Syndrome
– Congenital defect affecting K+ channels in heart and ears.
– Results in congenital deafness and sudden cardiac death
• Romano Ward Syndrome
– Group of at least six genetic defects.
– Only symptoms are syncope and sudden cardiac death.

34. QT Segment

35. A prolonged QT segment increases
risk of R on T and thus SCD.

36. QT Segment varies with HR

37. QTc measurement corrects the QT
interval for rate.
• Bazzett’s Formula
• QT interval/√(RR Interval)

39. QTc should not exceed 0.450s
(or 450 ms)

40. For rates between 60-100, the QT interval
should NOT exceed ½ the RR interval.

41. Prolonged QT interval

42. Patient with a seizure

43. Patient with a seizure

44. Psych patient in triage “needs to be
medically cleared”.
• Patient is somnolent, suicidal.
• Not forthcoming with history.
• Triage note: “Patient is faking syncope”.
• Records indicate that patient is taking
antipsychotics.

45. ECG from psych patient.

46. Lovely Torsades De Pointes

47. 55 year old man taking methadone and
complaining of syncope.
QTc is 551 ms

48. A few minutes later. . .

49. Wolff Parkinson White
Syndrome

50. Wolff-Parkinson-White Syndrome
(WPW)

51. Wolff Parkinson White Syndrome

52. Bundle of Kent.
• In WPW, an accessory pathway (called a bundle of Kent)
allows for the atrial activity to stimulate the ventricles without
slowing at the AV node.

53. WPW conduction

54. EKG changes in WPW
• Characterized by a short PR interval and a delta wave.

55. EKG changes in WPW
• Delta wave is caused by early aberrant depolarization of the
ventricles starting at the Kent bundle.
• Soon the normal conduction via the Ventricular Conduction
system depolarizes the rest of the ventricles.
• This causes a widening of the QRS at the beginning of the
QRS. Last part of the QRS is normal.

59. Significance of WPW
• While WPW is generally benign on a day to
day basis, two major problems may arise.
• 1) A reentrant circuit may form with the AV
node and the bundle of Kent, leading to SVT.
• 2) In the pressence of atrial fibrillation or
flutter, there is a very fast uncontrolled
ventricular response.

60. WPW reentry circuit
• Reentrant circuit leads
to SVT.
• Because electrical
activity is passing
retrogradely through
Kent bundle, Delta
wave may not be seen.

61. Orthodromic AVRT

62. Antidromic AVRT

64. WPW with A-fib/A-flutter
• Very frequent electrical
impulses are passed
through Kent bundle
without pause like in the
AV node.
• Results in a VERY
FAST ventricular
response.

65. WPW with A-fib

68. Treatment WPW a-fib/a-flutter with
WPW
• Avoid calcium channel blockers!
• Calcium channel blockers decrease conduction
through AV node, not through Kent bundle.
By giving calcium channel blockers, you can
actually increase the conduction through the
Kent bundle and increase ventricular response.
• The same applies with Adenosine.

69. Treatment WPW a-fib/a-flutter with
WPW
• Recommended first line treatment is
cardioversion.
• If cardioversion is unsuccessful, Procainamide
and Amiodarone may be used.
• Ultimate treatment is eblasion to get rid of the
Kent bundle.

70. Potassium changes

71. Potassium Changes

72. Hyperkalemia

73. Potassium 7.5

74. Severe Hyperkalemia
• After potassium levels
exceed 7.5, some very
drastic changes begin to
occur.
• The QRS and T wave
meld together into one
monophasic wave that is
called a sine wave.
• AV blocks, V-tach, and
V-fib soon follow.

77. Hypokalemia

78. Hypokalemia

79. Severe Hypokalemia
• AV blocks, bradycardias and asystole are common
with severe hypokalemia.

82. Hypokalemia prolongs the QT interval and
increases PVC frequency.

84. Summary
• Take syncope seriously!
• Screen for:
– Brugada
– HCM
– Prolonged QT
– WPW
– Hyper/Hypokalemia

85. wintersm@cowley.edu
Malachi Winters