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Congenital heart disease and other anomalies Flashcards

1
Q

Describe the development of the heart in utero until day 28.

A

clusters of angiogenic cells form mesodermal cardiogenic plate (arise from L+R endocardial tubes)
lateral foldings bring the tubes together
this forms the primitive heart tube (occurs at day 21)
the heart is beating by day 23
tube lengthens and folds further into the bulboventricular loop
by day 28 there is septation of the atria, ventricles and outflow tract

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2
Q

What is the difference between early and late CHD?

A

early CHD = AVSD from endocardial cushion

late CHD = simple ASD or VSD

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3
Q

What foetal structure in the heart allows blood to bypass the pulmonary circulation?

A

Foramen ovale

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4
Q

In utero, what keeps the ductus arteriosus open?

A

Prostaglandin E1

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5
Q

What is the primary stimulus for the closure of the ductus arteriosus?

A

Increase in neonatal blood oxygen

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6
Q

What is the primary stimulus for the closure of the foramen ovale?

A

reduced pressure in the pulmonary circulation/right side of the heart
therefore blood shunts left to right rather than right to left and this closes the foramen

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7
Q

What is the primary stimulus for the closure of the ductus venosus?

A

Reduced blood flow in the IVC

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8
Q

Why can persistent pulmonary hypertension of the newborn result in death?

A

There is an increase in pressure in the pulmonary artery
This keeps the foramen ovale open
Deoxygenated blood is shunted into the systemic circulation
Cells in the body have no oxygen = death of cells = death

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9
Q

Define cyanosis.

A

Deoxygenated blood >50 g/L in capillaries or >34 g/L in arterial blood

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10
Q

What are the differences between cyanosis in CHD and cyanosis in lung disease?

A

CHD:

  • normal alveolar gas exchange
  • no dyspnoea
  • normal pulmonary venous saturation
  • results form shunting of deoxygenated blood from R to L

Lung disease:

  • impaired alveolar gas exchange (increase CO2)
  • tachypnoea and recession
  • reduced pulmonary venous saturation
  • results from O2 diffusion problems or ventilation: perfusion mismatch within the lung
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11
Q

Describe what transposition of great vessels is and how it affects the baby.

A

Aorta connected to RV and pulmonary artery to LV
This forms 2 separate circulations
Baby remains alive because there is mixing of blood in the foramen ovale and ductus arteriosus

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12
Q

What 4 abnormalities occur in tetralogy of fallot?

A
  1. ventricular septal defect
  2. overriding aorta
  3. RV hypertrophy
  4. pulmonary stenosis
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13
Q

Give other examples of cyanotic CHD.

A

Tricuspid atresia (complete valve closure)
Pulmonary valve atresia
Critical pulmonary stensois
Truncus arteriosus (single artery from heart; large ventricular septal defect below valve of trunk)
Total anomalous pulmonary venous drainage (pulmonary veins not connected to LA but to one of the veins draining back to right atrium)

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14
Q

What are the two main causes of acyanotic CHD?

A
  1. L to R shunts (increased pulmonary blood flow - leads to pulmonary oedema and hypertension)
  2. Left heart outflow tract obstruction (pulmonary oedema/impaired tissue perfusion/ lactic acidosis)
    - also increased back pressure on pulmonary veins back into pulmonary circulation
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15
Q

What is an Eisenmenger shunt?

A

Long standing L to R shunt causes pulmonary hypertension and eventually reverses into a R to L cyanotic shunt

**when cyanosis is a secondary feature of an acyanotic lesion

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16
Q

How can ventricular septal defect lead to pulmonary hypertension?

A

The pressure in the left ventricle is much higher than the pressure in the right
This leads to blood leaking into the right ventricle
Right ventricular pressure and volume increases
Causes pulmonary hypertension

17
Q

What is a common complication of preductal coarctation of the aorta?

A

Can cause pulmonary oedema as there is increased pulmonary pressure
(pre ductal = before ductus arteriosus)

18
Q

Give other examples of acyanotic CHD.

A

Atrial Septal Defect
Atrioventricular Septal Defect
Critical aortic stenosis
Patent ductus arteriosus

19
Q

How does a baby with a hypoplastic left heart survive?

A

hypoplastic left heart = no blood flowing through the LV to the aorta due to underdevelopment of both structures
Relies on foetal circulation
Blood from LA shunts to RA through foramen ovale
Allows mix of oxygenated and deoxygenated blood
PDA allows the mixed blood to flow into the aorta and into the systemic circulation

20
Q

What is a double outlet right ventricle?

A

The aorta connects to the right ventricle instead of the left

21
Q

Why might a PDA or foramen ovale be missed initially?

A
  1. Bypass obstruction
    - tetralogy of fallot
    - pulmonary atresia
    - coarctation
    hypoplastic left heart
  2. Allow mixing
    - transposition

may only cause mild cyanosis which is easily missed - symptoms are only obvious once the duct/foramen closes

22
Q

What methods are there to keep the DA/FO open?

A

ductus arteriosus: prostaglandin E

foramen ovale: enlarging foramen (balloon septostomy transposition)

23
Q

How does spina bifida occulta arise? What is the most serious form?

A

Failure of the 1st vertebrae in the spine to form properly

Myelomeningocoele is the most serious form (neural tube is exposed)

24
Q

What is meningocoele?

A

Meninges protruding from spinal column

25
Q

What is encephalocoele?

A

protrusion of the neural tissue (brain) from the head

26
Q

What is anencephaly?

A

absence of major portion of brain, skull + scalp

27
Q

What treatment options are there for myelomeningocoele?

A

Closure will reduce risk of infection but will not restore normal neural function
Closure may also lead to hydrocephalus

*Hydrocephalus treated with a plastic catheter that is put through the ventricle and runs under the skin into the peritoneal cavity (ventricular peritoneal shunt)

28
Q

What are the neuro-consequences of myelomeningocoele?

A

Mixed sensory, motor and autonomic problems
Depends on level of lesions and degree of neural disruption
Loss of bladder control. faecal incontinence and loss of sensation in legs

29
Q

What is gastrochisis?

A

defect in the abdominal wall lateral to the umbilicus
bowel is free within the abdominal cavity

surgical closure is possible
bowel may take 1-3 months to start functioning normally

30
Q

What is cleft lip?

A

common defect where the maxilla fails to fuse with the frontonasal process

complete surgical correction is possible

31
Q

What is cleft palate?

A

failure of the secondary plate (MPS) to fuse
may occur because the tongue is too large and stops the plates from turning horizontally
or can be due to general failure of rotation

(can affect eustachian tube function - risk fo conductive hearing loss)

HD (26 decks)

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