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# Cardiology for g psaediatrics[1]

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### Cardiology for g psaediatrics[1]

1. 1. Paediatric Cardiology for General Paediatricians Dr Varsha Atul Shah
2. 2. Essentials in looking at an ECGRhythm (sinus….nonsinus)Rate, Atrial and ventricular rates.QRS axis, T axis, QRS-T angleIntervals: PR. QRS, and QTP wave amplitude and durationQRS amplitude and R/S ratioQ waveSt- Segment and T wave abnormalities
3. 3. ECG tips How do you determine Sinus rhythm? What is T axis? What is QRS/T angle?
4. 4. Rhythm P before every QRS P axis (0-90). P inverted in aVR
5. 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. 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. 7. Inverted (or negative) T waves can be a sign of Coronary ischemia Left ventricular hypertrophy
8. 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. 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.
10. 10. Top Tip For ECG Read more ECGs
11. 11. Do not forget, nothing replaces good traditional clinical examination and detailed history teaching 1.asx
12. 12. Syncope How often related to the heart? What are the related cardiac conditions? How do we approach it?
13. 13. 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
14. 14. Cause Brain function depends on Oxygen and glucose. Circulatory, metabolic, or neuropsychiatric causes. Adults syncope mostly cardiac. Children’s mostly benign.
15. 15. Causes of Syncope in Children Extra cardiac causes  Vasovagal  Orthostatic  Failure of systemic venous return  Cerebrovascular occlusive disease  Hyperventilation  Breath holding
16. 16. 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
17. 17. Vasovagal Syncope Anxiety Fright Pain Blood Fasting Hot and humid conditions Crowded places Prolonged motionless standing
18. 18. 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)
19. 19. 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
20. 20.  Paradoxical withdrawal of sympathetic activity, vasodilatation, hypotension and bradycardia Reduction of brain perfusion
21. 21. Diagnoses ECG, Holter, EEG, glucose tolerance test all are normally negative in V V E Tilt test
22. 22. Management Supine +/- feet up Prevention  Pseudoephedrine  Metoprolol  Fludrocortisone  Disopyramide  Scopolamine
23. 23. 2- Orthostatic Hypotension What happen when we stand up? HR, vasoconstriction Absent or inadequate upright position response, Hypotension without increased HR
24. 24. 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
25. 25. Management Elastic stockings High salt diet Corticosteroids Slow upright position
26. 26. Micturition Syncope Rare form of orthostatic Rapid bladder decompression associated with degreased total peripheral vascular resistance.
27. 27. 3- Failure of systemic venous return Increased intrathoracic pressure Decreased venous tone (drugs; nitroglycerin) Decreased volume (bleed…)
28. 28. 4- Cerebrovascular occlusive disease Mainly adult
29. 29. Cardiac causes of Syncope Structural heart disease Arrhythmia
30. 30. Why Cardiac ? Syncope at rest Provoked by exercise Chest pain Heart disease FH of sudden death
31. 31. What Cardiac Obstructive lesions Myocardial dysfunction Arrhythmias
32. 32. Obstructive lesions AS, PS, HOCM, PHTX Precipitated by exercise, no increase in cardiac output to accommodate increased demand. Examination, CXR, ECG, Echo
33. 33. Myocardial Dysfunction Ischemia, infarction secondary to CHD, Kawasaki’s.. Myocarditis
34. 34. Arrhythmia Arrhythmia Lack of output (Fast or slow heart) SVT, VT, SSS, CHB, Abnormal Heart Structure Normal Ebsteins, MS, MR, heart structure CCTGALong QT, WPW Post op, TOF, TGA MVP VT Cmpthy SVT, VT, s brady
35. 35. Long QT Syncope, seizures, palpitation during exercise or with emotion ECG Ventricular arrhythmias (Tachy) with risk of sudden death
36. 36. Long QT Defective ion channels CongenitalOver 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
37. 37. 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.
38. 38.  Syncope in adrenergic arousal, exercise (swimming is a particular trigger) Abrupt noises (Alarm, doorbell, phone..)
39. 39. 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
40. 40. 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
41. 41. 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
42. 42. 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%)
43. 43. 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
44. 44. Pathophysiology of congenital heart lesions
45. 45. Pathophysiology of left to right shunt lesions ASD
46. 46. Pathophysiology of left to right shunt lesions VSD
47. 47. Pathophysiology of left to right shunt lesions PDA
48. 48. Pathophysiology of left to right shunt lesions AVSD
49. 49. Pathophysiology of Obstructive and valvular regurgitation lesions MR
50. 50. Pathophysiology of Obstructive and valvular regurgitation lesions AR
51. 51. Pathophysiology of Obstructive and valvular regurgitation lesions PR
52. 52. Pathophysiology Cyanotic lesions TGA with good mixing 65% LA 90% RV 80% LV 90%
53. 53. PathophysiologyTGA with poor mixing 30% 100%45% LA 92% RV 45% LV 92% 45%
54. 54. PathophysiologyTGA with poor mixing 30% 100%45% LA 92% RV 45% LV 92% 45%
55. 55. Tips Read ECGs, easy to loose ECG skills. Ask for help As all specialties, it is only common sense.
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