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1 of 30
 up to 1 month 160.
 1 year 120.
 Above 100.
The normal Heart Rate
 Heart rate >100 beats/min
 Rightward QRS axis > +90°
 T wave inversions in V1-3 (“juvenile T-wave
pattern”)
 Dominant R wave in V1
 RSR’ pattern in V1
 Marked sinus arrhythmia
 Short PR interval (< 120ms) and QRS duration
(<80ms)
 Slightly peaked P waves
 Q waves in the inferior and left precordial leads.
ECGs in children
 Parameters vary through age
 Right ventricular dominance owing to high
pulmonary pressures, normalize at 6 months
 T waves; usually upright in most leads for first
7/7, then downwards in most leads until
adolescence.
Upright T waves in childhood may reflect RVH.
The normal ECG
Heart rate
Age Bradycardia Tachycardia
< 1 y < 80 min-1 > 180 min-1
> 1 y < 60 min-1 > 160 min-1
 Mostly related to complete 3rd degree heart block
 Mum may have history of Lupus
 Anti-La or anti-Ro antibodies
 Incidence: 1:15000-20000
 Picked up in antenatal (hydrops) or postnatal
period (CCF or well with low heart rate)
 Heart rate: <70 Regular or Irregular
 Temporary Pacemaker: HR <45, Pauses: >3 sec
 Almost always need permanent pacemaker in the
long run
Bradycardia in infancy
 Bradyarrythmias rare in structurally normal hearts
 Usually pre-terminal following hypoxia and ischaemia
 Vagal stimulation
 Raised ICP
 Poisoning with digoxin/ beta-blockers
 Congenital CHB seen in infants of mothers with anti
ro and la antibodies
Bradycardia - causes
 Oxygenation
 Adrenaline – 10mcg/kg
• Atropine - Consider when vagal stimulation e.g. airway
instrumentation – 20mcg/kg
 Pacing (rarely required)
Bradycardia Treatment
Electrical Heart Diseases
Tachyarrhythmia
0-5 years
Serious
Non- Specific Symptoms
Maternal History
5- 10 years
Significant
Specific Symptoms
Maternal and Patient History
10-16 years
Significant and Interesting
Specific Symptoms
Patient History
History is the
Tachycardia
Narrow QRS complex Broad QRS complex
ST VT or SVT
SVT Treat as VT
Sinus Tachycardia
ST – Treat the cause
 Physiological response:
Crying
Exercise
Anxiety/fear
Pain
 Compensatory
mechanism for:
Respiratory failure
Hypovolaemia
Sepsis
Anaemia
Supraventricular tachycardia
SVT
 Most common primary cardiac arrhythmia in
children, can be asymptomatic.
 Paroxysmal, regular, narrow QRS complexes
 Caused by re-entry mechanism through an
accessory pathway or AV conduction system
 HR > 220 bpm in infants or > 180 bpm in
children.
 Chronic SVTs can lead to poor LV function.
Supraventricular Tachycardia
ST or SVT
SVT
Infants and Toddlers
Unaware
Funny Turn
Pallor, Poor feeding
Older children
Palpitation (common)
Dizziness (common)
SOB ,nausea
Syncope
Chest pain, fatigue
Diaphoresis
Clinical manifestations
 Majority has a structurally normal heart.
 Short lived SVTs are not life threatening.
 ECG: absence or abnormal P wave.
 Baseline ECG: May reveal predisposing features
 24 hour ECG
 Event recorder
Diagnosis
 Valsalva maneuver
 IV Adenosine
100 mcg/kg
200 mcg/kg
maximum 1st dose 6mg, 2nd dose 12mg
 Amiodarone in refractory SVT
 DC cardioversion – for decompensated children
SVT - Management
 No treatment
 Vagal manoeuvres
 Drugs
 Beta Blockade: Propranolol, Atenolol
 Flecanide, Amiodarone
 Radiofrequency Catheter Ablation
SVT
Long term treatment
Atrial Myxoma
Most common 1° Heart tumour (40-50%)
90% solitarty and pedunculated
 Multiple tumours occur in 50% of familial case
10% familial ( autosomal dominant)
75-85% occur in LA ~25% RA
Attach to fossa ovalis
Symptomatic ~ 70g 140g
Background
 Myxoma-
 polypoid, round, oval in
shape
 Smooth / lobulated
surface
 White/ yellow/ brown
 Produce numberus
growth factors and
cytokines e.g.
interleukin-6
 lipidic cells embedded in a vascular myxoid stroma
 In a series of 37 cases,
 74% of tumors showed immunohistochemical
expression of interleukin-6 while
 17% had abnormal DNA content
Histology
 US ~ 75 case / million autopsies
 75% sporadic – Female
 Mean age – 56
 15% present as sudden death
 tumour embolism, HF, mechanical obstruction
Epidemiology
Asymptomatic (20%) symptomatic sudden death (15%)
Mechanical interference with cardiac fx embolization
LHF RHF systematic (L) Pulmonary (R)
Exertional SOB fatigue infarct / haemorrhage PE
Orthopnea peripheral edema of viscera Pul infarction
PND ascites e.g. CVA Pul HT
Pul edema visual loss
Postural dizziness
Constitutional symptoms : fever, Wt loss, arthralgias, Raynaud ~ 50% of patient due to
interleukin-6 overporduction
History
 ↑JVP
 Loud S1 ( delay mitral valve closure)
 Early diastolic sound (Tumor plop) tumor hit
against the endocardial wall
 Diastolic atrial rumble ( obstruction in MV)
 MR/ TR ( valvar damage/ prolapse)
Physical Examination
 Mitral Regurgitation
 Mitral Stenosis
 Pul Embolism
 Pul HT , primary
 Tricuspid Regurgitation
 Tricuspid Stenosis
DDX
 Lab: ESR, CRP, CBC, serum interleukin-6
 CXR
 ECHO
 need to differentiate thrombus from myxoma
 Thrombus ( in posterior portion, in layers)
 Myxoma ( presence of stalk and mobility)
 MRI (point of attachment )
 CT scan
Investigations
 Medical treatment for CHF and arrhythmia
 Surgical excision is the definitive tx
 Safe and curative
 Recurrence is possible if incomplete excision
Treatment
Thank you

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arrythmias and cardiac tumorsCone excision of the major ducts (subareolar resection). When the duct of origin of nipple bleeding is uncertain or when there is bleeding or discharge from multiple ducts, the entire major duct system

  • 1.
  • 2.  up to 1 month 160.  1 year 120.  Above 100. The normal Heart Rate
  • 3.  Heart rate >100 beats/min  Rightward QRS axis > +90°  T wave inversions in V1-3 (“juvenile T-wave pattern”)  Dominant R wave in V1  RSR’ pattern in V1  Marked sinus arrhythmia  Short PR interval (< 120ms) and QRS duration (<80ms)  Slightly peaked P waves  Q waves in the inferior and left precordial leads. ECGs in children
  • 4.  Parameters vary through age  Right ventricular dominance owing to high pulmonary pressures, normalize at 6 months  T waves; usually upright in most leads for first 7/7, then downwards in most leads until adolescence. Upright T waves in childhood may reflect RVH. The normal ECG
  • 5. Heart rate Age Bradycardia Tachycardia < 1 y < 80 min-1 > 180 min-1 > 1 y < 60 min-1 > 160 min-1
  • 6.  Mostly related to complete 3rd degree heart block  Mum may have history of Lupus  Anti-La or anti-Ro antibodies  Incidence: 1:15000-20000  Picked up in antenatal (hydrops) or postnatal period (CCF or well with low heart rate)  Heart rate: <70 Regular or Irregular  Temporary Pacemaker: HR <45, Pauses: >3 sec  Almost always need permanent pacemaker in the long run Bradycardia in infancy
  • 7.  Bradyarrythmias rare in structurally normal hearts  Usually pre-terminal following hypoxia and ischaemia  Vagal stimulation  Raised ICP  Poisoning with digoxin/ beta-blockers  Congenital CHB seen in infants of mothers with anti ro and la antibodies Bradycardia - causes
  • 8.  Oxygenation  Adrenaline – 10mcg/kg • Atropine - Consider when vagal stimulation e.g. airway instrumentation – 20mcg/kg  Pacing (rarely required) Bradycardia Treatment
  • 9. Electrical Heart Diseases Tachyarrhythmia 0-5 years Serious Non- Specific Symptoms Maternal History 5- 10 years Significant Specific Symptoms Maternal and Patient History 10-16 years Significant and Interesting Specific Symptoms Patient History History is the
  • 10. Tachycardia Narrow QRS complex Broad QRS complex ST VT or SVT SVT Treat as VT
  • 12. ST – Treat the cause  Physiological response: Crying Exercise Anxiety/fear Pain  Compensatory mechanism for: Respiratory failure Hypovolaemia Sepsis Anaemia
  • 14.  Most common primary cardiac arrhythmia in children, can be asymptomatic.  Paroxysmal, regular, narrow QRS complexes  Caused by re-entry mechanism through an accessory pathway or AV conduction system  HR > 220 bpm in infants or > 180 bpm in children.  Chronic SVTs can lead to poor LV function. Supraventricular Tachycardia
  • 16. SVT Infants and Toddlers Unaware Funny Turn Pallor, Poor feeding Older children Palpitation (common) Dizziness (common) SOB ,nausea Syncope Chest pain, fatigue Diaphoresis Clinical manifestations
  • 17.  Majority has a structurally normal heart.  Short lived SVTs are not life threatening.  ECG: absence or abnormal P wave.  Baseline ECG: May reveal predisposing features  24 hour ECG  Event recorder Diagnosis
  • 18.  Valsalva maneuver  IV Adenosine 100 mcg/kg 200 mcg/kg maximum 1st dose 6mg, 2nd dose 12mg  Amiodarone in refractory SVT  DC cardioversion – for decompensated children SVT - Management
  • 19.  No treatment  Vagal manoeuvres  Drugs  Beta Blockade: Propranolol, Atenolol  Flecanide, Amiodarone  Radiofrequency Catheter Ablation SVT Long term treatment
  • 21. Most common 1° Heart tumour (40-50%) 90% solitarty and pedunculated  Multiple tumours occur in 50% of familial case 10% familial ( autosomal dominant) 75-85% occur in LA ~25% RA Attach to fossa ovalis Symptomatic ~ 70g 140g Background
  • 22.  Myxoma-  polypoid, round, oval in shape  Smooth / lobulated surface  White/ yellow/ brown  Produce numberus growth factors and cytokines e.g. interleukin-6
  • 23.  lipidic cells embedded in a vascular myxoid stroma  In a series of 37 cases,  74% of tumors showed immunohistochemical expression of interleukin-6 while  17% had abnormal DNA content Histology
  • 24.  US ~ 75 case / million autopsies  75% sporadic – Female  Mean age – 56  15% present as sudden death  tumour embolism, HF, mechanical obstruction Epidemiology
  • 25. Asymptomatic (20%) symptomatic sudden death (15%) Mechanical interference with cardiac fx embolization LHF RHF systematic (L) Pulmonary (R) Exertional SOB fatigue infarct / haemorrhage PE Orthopnea peripheral edema of viscera Pul infarction PND ascites e.g. CVA Pul HT Pul edema visual loss Postural dizziness Constitutional symptoms : fever, Wt loss, arthralgias, Raynaud ~ 50% of patient due to interleukin-6 overporduction History
  • 26.  ↑JVP  Loud S1 ( delay mitral valve closure)  Early diastolic sound (Tumor plop) tumor hit against the endocardial wall  Diastolic atrial rumble ( obstruction in MV)  MR/ TR ( valvar damage/ prolapse) Physical Examination
  • 27.  Mitral Regurgitation  Mitral Stenosis  Pul Embolism  Pul HT , primary  Tricuspid Regurgitation  Tricuspid Stenosis DDX
  • 28.  Lab: ESR, CRP, CBC, serum interleukin-6  CXR  ECHO  need to differentiate thrombus from myxoma  Thrombus ( in posterior portion, in layers)  Myxoma ( presence of stalk and mobility)  MRI (point of attachment )  CT scan Investigations
  • 29.  Medical treatment for CHF and arrhythmia  Surgical excision is the definitive tx  Safe and curative  Recurrence is possible if incomplete excision Treatment