Congenital Heart Disease Flashcards
Changes in the heart/circulation after delivery (3)
- instant decrease in pulmonary vascular resistance (due to oxygen is vasodilator)
- increase in pulmonary blood flow -> fall in pulmonary artery pressure
- as pulmonary artery pressure fall -> LA pressure > RA pressure -> closure of foramen ovale
* initially -> flap closure due to pressure differences
*anatomic closure 4-12 weeks -> will close anatomically in most of the people (sealed)
What happens to ductus arteriosus after delivery?
-10-15 hours of life -> increased oxygen levels -> constriction of ductus arteriosus smooth
muscle
*removal of placenta -> high prostaglandin levels -> aid in duct closure
- complete closure will be in around 3 weeks
Risk factors for CHD (2 categories)
A. Environmental: rubella, DM, alcohol, drugs (illicit and medication e.g. anti-epileptics)
B. Chromosomal abnormalities (e.g. Down’s syndrome increases chances of having CHD)
Can CHD be diagnosed antenatally?
Yes, some of them.
Antenatal diagnosis: specialists foetal cardiologists -> ECHOs etc.
*but not all the conditions can be diagnosed due to nature of foetal physiology
B. Postnatal
Post-natal Dx of CHD
- symptoms
- when
Yes
- acute deterioration at/ soon after birth
- 1st day check
- later (unwell after discharge home, midwife concerned, GP on routine exam may find something
wrong with the heart)
Why CHD may show symptoms during feeding?
- For a newborn baby, their exercise is while being fed; so parents may notice a baby breathing heavily/ differently while being fed
- Classic HF signs that may be seen in an older person
- Child could potentially become ‚blue’ while feeding/ exerting themselves
Ix for CHD
CXR, BP and sats, ECG, ECHO
(2) broad categories of signs of CHD
- too little pulmonary flow
- too much pulmonary flow
Signs ‘too much pulmonary flow’ of CHD
Signs of CHD due to ‘too little pulmonary flow’
CXR -> less blood flow seen
*oligaemia = hypovolaemia
Name some of the most common congenital heart diseases
Blood flow in Ventricular Septal Defect
- shunt often goes from L —> R (as from higher to lower pressure)
- children would be ‚pink’ as oxygenated blood
goes into deoxygenated
Pathology of ventricular septal defect
- how does it affect lungs
- shunt across to RV -> increased pulmonary blood flow (as more blood goes into the lungs
from R ventricle)
- symptoms of heart failure
- pulmonary vessels damaged (by increased pulmonary flow) -> pulmonary resistance will
increase -> this will become eventually irreversible -> pulmonary hypertension
* therefore even if VSD would be closed -> pulmonary hypertension will remain
What’s Eisenmenger Syndrome?
Eisenmenger (shunt would reverse from R to L due to hypertrophy of R side of the heart caused by pulmonary hypertension) -> it will become cyanotic and both, heart and lung transplant would be needed
*nowadays, with increased technology (imaging) we can pick up VSD quicker (e.g. in childhood), in the past many people would develop Eisenmenger
Possible presentation of VSD
- Symptoms of cardiac failure (but may be mild in newborn)
- cardiac murmur may be heard *but it’s not always the case; e.g. if the hole is big -> then
children will become sicker faster but we may not hear the murmur that quick
Management of VSD
Management:
A. Medication
- diuretics: furosemide and spironolactone
B. Surgery
- sometimes we need to grow babies bigger before surgery but need to act now -> Pulmonary artery band (PA band) -> to protect the lungs (as not much blood gets to the lungs, less damage to the arteries there)
this is only temporary solution, VSD would still need to be corrected
- Corrective surgery -> defect will be sealed
What’s a classic murmur in VSD?
VSD = pansysolic murmur
What are (4) cardiac defects in Tetralogy of Fallot?
- Pulmonary stenosis = Pulmonary tract obstruction
- R ventricular hypertrophy is a result of pulmonary tract obstruction (heart muscle
remodels)
(2) types of surgical management of ToF
A.Palliative procedure - not a curative
Shunt created between R subclavian and R pulmonary artery
*this is only a temporary thing
B. Transannular patch -> pulmonary artery is opened up/widened and patch is
sticked
General management point (modes and timeframes) for ToF
What’s murmur is characteristic of ToF?
TOF = ejection systolic murmur
What’s x-ray finding is characteristic of ToF?
‘Boot shaped heart’ - apex is pointing upwards due to R ventricular hypertrophy *rarely seen in practice
What’s ‘spelling’ in ToF?
‘Spelling’ already narrowed R ventricular outflow tract goes into spasm -> all of blood supply to the lungs is cut off
Management of ‘spelling’ (ToF)
Aim: We want to decrease pulmonary vascular resistance and increase systemic resistance (to encourage the blood going to the lungs)
- Push baby’s knees up to the chest -> to achieve the above
- High flow oxygen -> as oxygen is potent vasodilator -> we want to dilate pulmonary
vasculature
- Morphine -> to calm baby down and to vasodilate
4. B-blocker -> help with R vent outflow tract spasm
