1. Syncope is often related to cardiac causes in adults. Common cardiac causes include structural heart disease, arrhythmias, and obstructive lesions. 2. Long QT syndrome is an inherited condition that can cause syncope, seizures, or sudden cardiac death, especially with exercise or emotions. It is diagnosed by an elongated QT interval on ECG. 3. Congenital heart defects can cause left-to-right shunts, obstructive lesions, or valvular issues, each with their own pathophysiology that can potentially lead to syncope.

1. Paediatric Cardiology for
General Paediatricians
Dr Varsha Atul Shah

2. Essentials in looking at an ECG
Rhythm (sinus….nonsinus)
Rate, Atrial and ventricular rates.
QRS axis, T axis, QRS-T angle
Intervals: PR. QRS, and QT
P wave amplitude and duration
QRS amplitude and R/S ratio
Q wave
St- Segment and T wave abnormalities

3. ECG tips
 How do you determine Sinus rhythm?
 What is T axis?
 What is QRS/T angle?

4. Rhythm
 P before every QRS
 P axis (0-90). P inverted in aVR

5. P wave axis
 The location of the P-wave axis determines the origin of
an atrial-derived rhythm:
• 0 to 90 degrees = a high right (normal sinus rhythm)
• 90 to 180 degrees = a high left
• 180 to 270 degrees = a low left
• 270 to 0 degrees = a low right

6. T wave
 In most leads, the T wave is positive.
 A negative T wave is normal in lead aVR.
 Lead V1 may have a positive, negative, or biphasic T
wave. In addition
 It is not uncommon to have an isolated negative T wave
in lead III, aVL, or aVF.

7. Inverted (or negative) T waves can be a sign of
 Coronary ischemia
 Left ventricular hypertrophy

8. T axis
 Determined by the same methods as QRS
 0 to + 90 is normal
 T Axis out side the normal quadrant could suggest
conditions with Myocardial dysfunction.

9. QRS-T Angle
 Formed by the QRS axis and the T axis
 QRS-T angle >60 degrees is unusual but if > 90
degrees, it is abnormal.
 Abnormally wide angle, with T axis outside the normal
quadrant is seen in
- severe ventricular hypertrophy with starin
- Ventricular conduction disturbances
- Myocardial dysfunction of a metabolic or ischemic nature.

11. Top Tip For ECG
 Read more ECGs

12. Do not forget, nothing replaces good traditional
clinical examination and detailed history
teaching 1.asx

13. Syncope
 How often related to the heart?
 What are the related cardiac conditions?
 How do we approach it?

14. Definition
 Syncope is a transient loss of consciousness and muscle
tone.
 Near syncope:
premonitory signs and symptoms of imminent syncope
occur; dizziness with or without blackout, pallor,
diaphoresis, thready pulse and low BP

15. Cause
 Brain function depends on Oxygen and glucose.
 Circulatory, metabolic, or neuropsychiatric causes.
 Adults syncope mostly cardiac.
 Children’s mostly benign.

16. Causes of Syncope in Children
 Extra cardiac causes
 Vasovagal
 Orthostatic
 Failure of systemic venous return
 Cerebrovascular occlusive disease
 Hyperventilation
 Breath holding

17. 1- Vasovagal Syncope
Neurocardiogenic
Common Syncope
 Predrome for few seconds; dizziness, light-headedness,
pallor, palpitation, nausea, hyperventilation then Loss of
consciousness and muscle tone
 Falls without injury
 Lasts about a minute, awake gradually

18. Vasovagal Syncope
 Anxiety
 Fright
 Pain
 Blood
 Fasting
 Hot and humid conditions
 Crowded places
 Prolonged motionless standing

19. Vasovagal Syncope
Pathophysiology
 Standing posture without movement shifts blood to the
lower extremities
 Decrease venous return, stroke volume, BP
 Less stretching of vent muscle and mechanoreceptors
(mrcpts), decline in neural traffic form mrcpts, decreased
arterial pressure, increase sympathetic output with
 Higher HR, vasoconstriction (higher diastolic pressure)

20. Vasovagal Syncope Patients
 Decreased venous return produces large increase in
ventricular contraction force
 Activation of LV mechanoreceptors (normally only
responds to stretch)
 Increase neural traffic mimicking high BP condition

21.  Paradoxical withdrawal of sympathetic activity,
vasodilatation, hypotension and bradycardia
 Reduction of brain perfusion

22. Diagnoses
 ECG, Holter, EEG, glucose tolerance test all are
normally negative in V V E
 Tilt test

23. Management
 Supine +/- feet up
 Prevention
 Pseudoephedrine
 Metoprolol
 Fludrocortisone
 Disopyramide
 Scopolamine

24. 2- Orthostatic Hypotension
 What happen when we stand up?
HR, vasoconstriction
Absent or inadequate upright position response,
Hypotension without increased HR

25. Diagnoses
 BP and HR supine and standing up.
 BP drop after 5-10 minutes up still by 10-15 mmHG
 Positive tilt test without autonomic signs

26. Management
 Elastic stockings
 High salt diet
 Corticosteroids
 Slow upright position

27. Micturition Syncope
 Rare form of orthostatic
 Rapid bladder decompression associated with
degreased total peripheral vascular resistance.

28. 3- Failure of systemic venous return
 Increased intrathoracic pressure
 Decreased venous tone (drugs; nitroglycerin)
 Decreased volume (bleed…)

29. 4- Cerebrovascular occlusive disease
 Mainly adult

30. Cardiac causes of Syncope
 Structural heart disease
 Arrhythmia

31. Why Cardiac ?
 Syncope at rest
 Provoked by exercise
 Chest pain
 Heart disease
 FH of sudden death

32. What Cardiac
 Obstructive lesions
 Myocardial dysfunction
 Arrhythmias

33. Obstructive lesions
 AS, PS, HOCM, PHTX
 Precipitated by exercise, no increase in cardiac output to
accommodate increased demand.
Examination, CXR, ECG, Echo

34. Myocardial Dysfunction
 Ischemia, infarction secondary to CHD, Kawasaki’s..
 Myocarditis

35. Arrhythmia
Arrhythmia
Lack of output
(Fast or slow heart)
SVT, VT, SSS, CHB,
Abnormal Heart
Structure
Normal Ebstein's, MS, MR,
heart structure CCTGA
Long QT, WPW Post op, TOF, TGA
MVP VT
Cmpthy SVT, VT,
s brady

36. Long QT
 Syncope, seizures, palpitation during exercise or with
emotion
 ECG
 Ventricular arrhythmias (Tachy) with risk of sudden
death

37. Long QT
Defective ion
channels
Congenital
Over 50 mutations in
Acquired
4 sites
Drugs, illnesses,
Jarvell-lange-nielson
Autoimmune
Deafness AR
Neurological
Romano-ward
Nutritional
no deafness AD
Electrolytes
Sporadic no FH
no Deafness

38. clinically
 FH 60%
 Deafness 5%
 Presentation with Syncope 26%, seizure 10%, cardiac arrest 9%,
presyncope palpitation 6%
 Symptoms during exercise or emotion
 Normally symptoms related to ventricular arrhythmias, mostly end of
second decade of life.

39.  Syncope in adrenergic arousal, exercise (swimming is a
particular trigger)
 Abrupt noises (Alarm, doorbell, phone..)

40. Tests
 ECG with QTc >0.46 seconds
 Frequently finding abnormal T wave
 Bradycardia (20%)
 Exercise test, maximum prolongation after 2 minutes of
recovery, ventricular arrhythmia in 30% during exercise
 Holter monitoring may show longer QTc

41. Diagnoses Criteria
 Electrophysiological society
- QTc >0.44 with no other causes (0.46 sec)
- Positive family history plus unexplained syncope,
seizure or cardiac arrest proceeded by trigger such as
exercise, emotion

42. Treatment
 Discuss with cardiologist
 Avoid drugs associated with long QT
 Avoid swimming, competitive sports
 Beta blockers
 Demand cardiac pacing (Pacemaker and defib)
 Left cardiac sympathetic denervation

43. Prognoses
 Untreated 75-80% mortality
 Beta blockers reduce mortality to some extent
 The adjusted annual mortality rate on treatment is 4.5%
(10 year mortality of 50%)

44. Advise related to CHD
 If one child has CHD, what are the chances of the
second?
 One parent has CHD, can offspring be affected? What
are the chances?
See Handouts, statistical list of potential risks

45. Pathophysiology of congenital heart lesions

46. Pathophysiology of left to right shunt lesions ASD

47. Pathophysiology of left to right shunt
lesions VSD

48. Pathophysiology of left to right shunt
lesions PDA

49. Pathophysiology of left to right shunt
lesions AVSD

50. Pathophysiology of Obstructive and valvular
regurgitation lesions MR

51. Pathophysiology of Obstructive and valvular
regurgitation lesions AR

52. Pathophysiology of Obstructive and valvular
regurgitation lesions PR

53. Pathophysiology Cyanotic lesions
TGA with good mixing
65%
LA 90%
RV 80% LV 90%

54. Pathophysiology
TGA with poor mixing
30% 100%
45%
LA 92%
RV 45% LV 92%
45%

55. Pathophysiology
TGA with poor mixing
30% 100%
45%
LA 92%
RV 45% LV 92%
45%

56. Tips
 Read ECGs, easy to loose ECG skills.
 Ask for help
 As all specialties, it is only common sense.