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Y4 Paediatrics > Cardio > Flashcards

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1
Q

Describe the foetal circulation.

A
  • oxygenated bloods from placenta is carried via umbilical vein into IVC
  • oxygenated blood arrives at RA and flows through foramen ovale into LA then to LV –> aorta and body
  • portion of blood makes it to RV and is pumped to pulmonary artery which moves to aorta via ductus arteriosus (high pressure in collapsed lung)
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2
Q

what could go wrong to cause congenital heart defects?

A
  • Genes like trisomy 21, cardiomyopathy genes
  • Environment factors such as teratogens like alcohol, smoking, warfarin and lithium
  • Maternal disorders like rubella
  • Maternal diabetes
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3
Q

what are the foetal shunts available?

A
  • Foramen ovale : from foetally higher pressure RA to LA via atrial septum with intention of bypassing the lungs
  • Ductus arteriosus : shunt from pulmonary artery into aorta to bypass lungs in systole
  • Ductus venosus : umbilical vein into IVC (bypassing liver?)
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4
Q

what cause the foetal shunts to close?

A
  • with initial breaths and increase in volume of blood to lungs and resistance in pulmonary circulation the LA pressure rises
  • RA pressure falls due to exclusion of placental circulation and this change in pressure causes foramen ovale flap to shut - septum primum against septum secundum
  • ductus arteriosus closes within first few hours to days
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5
Q

what might be the initial presentation of a congenital heart defect?

A
  • antenatal cardiac USS detects 50-60%
  • cyanosis at birth
  • detection of murmur
  • HF
  • shock when foramen ovale shuts causing obstruction
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6
Q

how do you differentiate between an innocent murmur and a pathological one?

A
  • aSymptomatic
  • Soft blowing murmur
  • Systolic murmur only
  • left Sternal edge
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7
Q

how does HF present in a baby?

A
  • breathlessness
  • sweating
  • poor feeding
  • recurrent chest infections
  • poor weight gain, tachypnoea, tachycardia, murmur etc
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7
Q

what are some examples of acyanotic heart defects?

A
  • VSD
  • ASD
  • PDA
  • coarctation of aorta
  • aortic valve stenosis
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8
Q

what are some classic features of an acyanotic heart lesion?

A
  • L -> R shunting with mixing
  • increased pulmonary blood flow risking pulmonary HTN and Eisenmenger
  • lesions above nipple ejection systolic murmur
  • lesions below nipple pan systolic murmur
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9
Q

What are some examples of cyanotic congenital heart disease?

A
  • TOF
  • TGA
  • tricuspid atresia
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10
Q

what is an ASD?

A

left to right shunt from LA into RA down pressure gradient
- acyanotic
- may lead to right sided strain and Eisenmenger
- types: ostium secondum, primum and patent foramen ovale

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11
Q

what might you find on examination for ASD?

A
  • Ejection systolic murmur heard loudest at the upper-left sternal border
  • Widely fixed splitting of the second heart sound
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12
Q

how might ASD present?

A

*asymptomatic, recurrent infections
- may present at 4-5y
- 40+ with arrhythmias and dyspnoea

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13
Q

how might you investigate acyanotic congenital heart defects?

A
  • pulse oximetry
  • Echo
  • CXR: cardiomegaly and pulmonary oedema?
  • ECG: may show hypertrophy
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14
Q

how is an ASD managed?

A
  • 7-8mm may spontaneously close so w&w
  • large defects require percutaneous catheter closure via femoral vein
  • tx at about 3-5y to prevent RHF and arrhythmias
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15
Q

what is a VSD?

A

VSD means left to right shunt from LV into RV down pressure gradient through a defect in septum
*most common CHD
*associated with Down’s and Turner’s

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16
Q

how might VSD present?

A

Small – may be asymptomatic, normal growth
Moderate – poor feeding, failure to thrive (FTT), short of breath (SOB)
Large – poor feeding, FTT (falls below centiles), SOB, sweaty and pale with feeds

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17
Q

what might you find on examination for VSD?

A

Pan-systolic murmur heard loudest at the lower left sternal border (LLSB)
- may palpate systolic thrill
- loud P2 shows pulmonary HTN

18
Q

how is VSD managed?

A
  • <5mm may close spontanously
  • moderate: diuretic therapy with (furosemide+spironolactone) and high caloric feeds (infantrini)
  • large: moderate mx, optimise weight gain, surgery before 12m to present PPHN –> transvenous catheter closure
19
Q

how might a PDA present on examination?

A

Symptoms usually present 3-5 days after birth when the duct begins to close
- bounding pulses and wide pulse pressure
- continuous machinery murmur at upper-left sternal border and thrill

20
Q

how is PDA managed?

A
  • preterm may close spontaneously
  • medical: indomethacin, ibuprofen to neonate
  • surgical: catheter closure or PDA ligation when weight 5kg
21
Q

why might it be not so wise to close a PDA in certain situations?

A

if associated with another heart defect amenable to surgery then prostaglandin E1 given to keep duct open until after repair - alprostadil

*to prevent obstruction

22
Q

what are the 4 abnormalities found in a patient with a TOF?

A
  • large VSD
  • pulmonary stenosis
  • hypertrophy of RV
  • overriding aorta (over VSD not LV)
23
Q

what are some RF for TOF?

A

Males
1degree family history of CHD
Teratogens like Alcohol (fetal alcohol syndrome)
Warfarin (fetal warfarin syndrome)
Trimethadione
genetics

24
when would TOF present?
mild: asymptomatic, continues to progress to cyanosis moderate: first few weeks (post PDA closure), prone to recurrent chest infections, failure to thrive extreme: may have pulmonary atresia, hence PDA dependent
25
How would TOF present?
- cyanotic spells due to RV outflow tract obstruction - murmur caused by pulmonary stenosis: crescendo-decrescendo with harsh ejection systolic over L sternal edge - cyanosis, poor feeding, sweating during feeds - tet spells: neonate going blue when feeding - CHF signs
26
how might you investigate TOF?
ECG: RVH, R axis deviation bloods for genetic syndromes CXR: boot shaped heart for RVH, reduced lung markings ECHO: gold standard cardiac catheter? delineate lesion
27
How is TOF managed?
- severe cyanosis: prostaglandin infusion to maintain patency of PDA until correction - tet spells management - HF: digoxin, loop diuretics - endocarditis prophylaxis - surgical: Blalock-Taussig shunt to mimic PDA, *lifelong followup with exercise tolerance, ECG etc
28
how are tet spells managed?
*Knee to chest position to increase systemic vascular resistance and promote blood flow into the pulmonary circulation Oxygen Morphine B-blockers
29
what is transposition of the great arteries?
aorta arises from the RV and pulmonary artery from the LV, resulting in deoxygenated blood from the RV being circulated around the body RF: diabetic mothers
29
how does TGA present?
*when PDA closes at day 3-5 - signs of CCF like tachypnoea, tachycardia, failure to gain weight - cyanosis - poor feeding - murmur: systolic murmur if VSD, loud single S2
30
How is TGA managed?
- emergency: prostaglandin infusion, correct metabolic acidosis, atrial balloon septostomy - definitive: atrial switch by age 4w *pregnancy complications for patients later
31
how does aortic stenosis present?
*born with narrow aortic valve which restricts blood from LV into aorta - ejection systolic murmur loudest in aortic area, crescendo-decrescendo radiating to carotids - slow rising pulse and narrow pulse pressure
32
how is aortic stenosis managed?
- precutaneous balloon aortic valvoplasty - surgical aortic valvotomy - valve replacement
33
what is pulmonary stenosis and what is it associated with?
usually consists of 3 leaflets that open and close and let blood out into pulmonary artery and prevent back flow into RV when leaflets abnormally fuse or thicken there is a narrowing between the RV and PA causing a restricted exit of blood - associated with TOF, Williams syndrome, Noonan syndrome and congenital rubella
34
how might pulmonary stenosis present?
- ejection systolic murmur loudest at pulmonary area - palpable thrill over pulmonary area - RV heave due to RVH - raised JVP
35
how is pulmonary stenosis managed?
- mild may not require intervention hence watch and wait - symptomatic or significantly stenosed - balloon valvuloplasty via venous catheter
36
what is hypoplastic left heart?
- abnormal development of left sided cardiac structures which results in obstruction to blood flow from LV - mitral valve, left ventricle, aortic valve, the ascending aorta, and aortic arch - survival depends on two key factors - patent ductus arteriosus - non-restrictive atrial septal defect to ensure adequate mixing
37
how does a hypoplastic left heart present?
- initially healthy until duct closes - with PDA closing systemic perfusion decreases - hypoxaemia, acidosis, shock - cardiogenic shock if duct restricted from birth - due to ischaemia to myocardium
38
how is hypoplastic left heart managed?
- initial - prostaglandin infusion, diuretics, intubation and ventilation, urgent balloon atrial septostomy to ensure mixing - definitive - surgical - norwood procedure, glenn, fontan
39
what is coarctation of the aorta?
congenital narrowing narrowing of aortic arch, usually around the ductus arteriosus *when duct closes aorta also constricts causing obstruction to LV outflow *associated with Turner's
40
how might you detect coarctation of aorta?
- weak femoral pulses : four limb blood pressure to reveal high BP in limbs supplied from arteries that come before narrowing and lower BP after - ejection systolic murmur - grey floppy baby - underdeveloped L arm?
41
how is coarctation managed?
- mild may be symptom free until adulthood without requiring surgical input - urgent - prostaglandin E to keep DA open while waiting for surgery, allows some flow into systemic distal to co-arctation - surgery - correct narrowing and ligate DA

Y4 Paediatrics (16 decks)

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