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Y3 Lecture week III > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

1
Q

Changes in the heart/circulation after delivery (3)

A
  • 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)

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2
Q

What happens to ductus arteriosus after delivery?

A

-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
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3
Q

Risk factors for CHD (2 categories)

A

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)

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4
Q

Can CHD be diagnosed antenatally?

A

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

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5
Q

Post-natal Dx of CHD

  • symptoms
  • when
A

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)

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6
Q

Why CHD may show symptoms during feeding?

A
  • 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
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7
Q

Ix for CHD

A

CXR, BP and sats, ECG, ECHO

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8
Q

(2) broad categories of signs of CHD

A
  • too little pulmonary flow
  • too much pulmonary flow
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9
Q

Signs ‘too much pulmonary flow’ of CHD

A
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10
Q

Signs of CHD due to ‘too little pulmonary flow’

A

CXR -> less blood flow seen

*oligaemia = hypovolaemia

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11
Q

Name some of the most common congenital heart diseases

A
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12
Q

Blood flow in Ventricular Septal Defect

A
  • shunt often goes from L —> R (as from higher to lower pressure)
  • children would be ‚pink’ as oxygenated blood

goes into deoxygenated

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13
Q

Pathology of ventricular septal defect

  • how does it affect lungs
A
  • 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

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14
Q

What’s Eisenmenger Syndrome?

A

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

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15
Q

Possible presentation of VSD

A
  • 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

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16
Q

Management of VSD

A

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
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17
Q

What’s a classic murmur in VSD?

A

VSD = pansysolic murmur

18
Q

What are (4) cardiac defects in Tetralogy of Fallot?

A
  • Pulmonary stenosis = Pulmonary tract obstruction
  • R ventricular hypertrophy is a result of pulmonary tract obstruction (heart muscle

remodels)

19
Q

(2) types of surgical management of ToF

A

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

20
Q

General management point (modes and timeframes) for ToF

A
21
Q

What’s murmur is characteristic of ToF?

A

TOF = ejection systolic murmur

22
Q

What’s x-ray finding is characteristic of ToF?

A

‘Boot shaped heart’ - apex is pointing upwards due to R ventricular hypertrophy *rarely seen in practice

23
Q

What’s ‘spelling’ in ToF?

A

‘Spelling’ already narrowed R ventricular outflow tract goes into spasm -> all of blood supply to the lungs is cut off

24
Q

Management of ‘spelling’ (ToF)

A

Aim: We want to decrease pulmonary vascular resistance and increase systemic resistance (to encourage the blood going to the lungs)

  1. Push baby’s knees up to the chest -> to achieve the above
  2. High flow oxygen -> as oxygen is potent vasodilator -> we want to dilate pulmonary

vasculature

  1. Morphine -> to calm baby down and to vasodilate

4. B-blocker -> help with R vent outflow tract spasm

25
Q

Patent ductus arteriosus

  • patophysiology (simple)
  • symptoms
  • management
A
26
Q

Arterial Septal Defect (ASD)

  • symptoms
  • management
A
27
Q

What’s AVSD?

A
28
Q

How does AVSD look like? (picture)

A
29
Q

Pathology of Transposition of Great Arteries

A

Pathology: blood vessels connected to wrong ventricles -> ventricles are in correct

arrangement but great arteries are not

  • Aorta comes of R ventricle
  • pulmonary arteries from L

Result: in uterus it is fine, as we have got shunting, so blood mixes together; but when

we are born, shunts close down -> serious issue

30
Q

Surgery for transposition of great arteries

A

‘Arterial switch’ -> arteries are chopped off and plugged to the other sides

problem is:

coronary arteries are connected to aorta -> therefore if someone had that operation may show sign of myocardial ischaemia (due to damage to coronary artery)

31
Q

Classical x ray finding in transposition of great arteries

A

‘Egged shaped heart’ - it does not really look like -> narrow mediastinum due to different

arrangement of vessels

32
Q

Criteria for a diagnosis of Kawasaki disease

A
33
Q

Management of Kawasaki disease

A

A. Immunoglobulins

B. Aspirin (although normally contraindicated in children (Reyes) -> here it will be needed

anyway

34
Q

Pathophysiology of hypertrophic cardiomyopathy

A

Hypertrophic: cause smaller than normal ventricular cavities -> filling of the heart is impaired

+ contractile function enhanced

*often cause of sudden death in young athletes (when the point is reached that cardiac muscle is so big and aorta is pressing on it and obstructing; on exertion it may just not eject properly)

  • is 50% AD condition
  • L ventricle hypertrophied
35
Q

Symptoms of hypertrophic cardiomyopathy

A

angina pain, lightheaded, syncope, arrhythmia

36
Q

Dilated cardiomyopathy

  • what happens
  • symptoms
A

Dilated: contractile function is decreased + dilation

  • most common cardiac myopathy
  • majority idiopathic

Symptoms: fatigue, weakness, previous viral infection

37
Q

What happens in restrictive cardiomyopathy (structural changes)

A

Restrictive: restricted diastolic filling (stiff heart), marked atrial dilatation

38
Q

Organisms that commonly cause bacterial endocarditis in:

A. neonates

B. children

A
39
Q

Risk factors (3) for bacterial endocarditis

A

May happen in both, structurally normal and abnormal hearts

  • often it is a complication of central venous lines in NICU/PICU
  • pressure gradients and turbulent blood flow that is created in CHD will predispose the valve to get damaged and therefore be colonised by bacteria
40
Q

Possible causes of myocarditis (paediatrics)

A
41
Q

Possible presentation of myocarditis in neonate

A

Neonate -> sudden onset:

  • anorexia/vomiting/lethargy
  • HF signs
  • Cardiomegaly on CXR

*mortality in neonates is 75%

42
Q

Advice for adult patient with cyanotic CHD

A
  • more likely to develop thrombo-embolism -> contraception needed
  • advice not to get pregnant if pulmonary HTN
  • risk of endocarditis: oral hygiene, better not to get piercing or tattoos etc.
  • in some cardiac conditions, e.g. TOF, although treated there is a risk of malignant arrhythmias-> therefore advice the patient that if something like that develops (e.g. palpitations) it requires

urgent medical attention

Y3 Lecture week III (11 decks)

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