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Year 4 - 3. Paediatrics > Paediatric Cardiology > Flashcards

Paediatric Cardiology Flashcards

1
Q

State and describe the 3 types of foetal shunts

A
  1. Foramen ovale - links right atrium to left atrium (bypass right ventricles and pulmonary circuit)
  2. Ductus arteriosus - links pulmonary artery to aorta (bypass pulmonary circuit)
  3. Ductus venous - links umbilical vein to inferior vena cava (bypass liver)
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2
Q

For the 3 types of foetal shunts, describe how they are closed

A
  1. Foramen ovale
    - First breaths of life expand the alveoli, decreasing pressure in pulmonary circuit and subsequent fall in right atrial pressure
    - This causes the LA pressure > RA pressure, squashing the atrial septum
    - Structurally closes some weeks later to become the fossa ovalis
  2. Ductus arteriosus
    - When the baby takes it’s full breath, the blood becomes more oxygenated
    - This causes prostaglandin levels to drop (prostaglandins are needed to keep ductus arteriosus to remain open)
    - Drop in prostaglandin level causes closes of the ductus arteriosus, which becomes the ligamentum arteriosum
  3. Ductus venosus
    - Immediately after birth, umbilical cord is clamped
    - There is no flow in the umbilical veins, therefore the ductus venosus stops functioning
    - Ductus venosus becomes the ligamentum venosum a few days later
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3
Q

State some ‘S’s of innocent / flow murmurs in children

A
  • Short
  • Soft
  • Systolic
    +
  • Symptomless
  • Situation dependent e.g. quieter with standing, or only present when child is ill
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4
Q

State when incidental innocent / flow murmurs should be investigated in children and suggest some investigations

A

Indications for investigation:
May not need any if clear innocent murmur with no concerning features
- Additional symptoms e.g. failure to thrive, cyanosis, SOB, feeding difficulties
- Diastolic murmur
- Murmur louder than 2/6

Investigations:
- ECG
- Echocardiogram
- Chest x-ray

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5
Q

Suggest some cardiac abnormalities which could cause a pan-systolic murmur

A
  • Mitral regurgitation (loudest mitral area)
  • Tricuspid regurgitation (loudest tricuspid area)
  • Ventricular septal defect (left lower sternum)
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6
Q

Suggest some cardiac abnormalities which could cause an ejection-systolic murmur

A
  • Aortic stenosis
  • Pulmonary stenosis
  • Hypertrophic obstructive myopathy
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7
Q

State the murmur heard in atrial septal defects

A

Mid-systolic, crescendo-decrescendo
Loudest at upper left sternal border, fixed split secondary heart sound

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8
Q

State the murmur heard in patent ductus arteriosus

A

May not cause any abnormal heart sounds
Continuous crescendo-decrescendo ‘machinery’ murmur (can make second heart sound hard to hear)

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9
Q

State the murmur heard in Tetralogy of Fallot

A

Ejection systolic murmur
Loudest in pulmonary area, left 2nd ICS at sternal border

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10
Q

Categorise which congenital heart defects cause
1. Left-to-right shunt (acyanotic heart disease)
2. Right-to-left shunt (cyanotic heart disease)

A
  1. Left-to-right shunt (acyanotic heart disease)
    - Atrial septal defect (ASD)
    - Ventricular septal defect (VSD)
    - Patent ductus arteriosus (PDA)
    - Obstructive lesions e.g. coarctation of the aorta, aortic / pulomnary / mitral stenosis
  2. Right-to-left shunt (cyanotic heart disease)
    - Tetralogy of Fallot
    - Transposition of the great arteries
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11
Q

Why aren’t patients with atrial septal defects, ventricular septal defects or patent ductus arteriosus always cyanotic

A

Because the pressure on the LEFT side of the heart is greater than the right, therefore blood still flows from the LEFT to the right

However if pulmonary pressure increases, then blood flows from RIGHT to left causing cyanosis = Eisenmenger Syndrome

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12
Q

Patent ductus arteriosus - state the following:
- Normal situation (non-patent)
- Pathophysiology
- Presentation
- Murmur heard
- Diagnosis
- Management

A

Normal situation (non-patent):
- At birth, corticosteroid production drops which causes a closure of the ductus arteriosus
- By 2-3 weeks, this has structurally closed

Pathophysiology:
- Patent ductus arteriosus occurs due to a failure of the ductus arteriosus to close
- Unclear why, but linked to prematurity, genetics or maternal infections e.g. Rubella
- Shunt of blood from LA to RA
- Overtime this leads to right sided overload and right heart strain
- Small PDAs may be asymptomatic and close spontaneously, or may not close and cause adult heart failure

Presentation:
Can be picked up on newborn examination
- Heart murmur
- SOB
- Recurrent LRTIs
- Poor weight gain
- Difficulty feeding

Murmur heard:
- Continuous ‘machinery’ crescendo-decrescendo murmur

Diagnosis:
- Echocardiogram
- Doppler flow studies

Management:
- Referral to paediatric cardiologist
- Monitored until 1 year, with echos (after 1 year, unlikely to close spontaneously)
- Trans-catheter or open surgical closure

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13
Q

Atrial septal defect - state the following:
- Normal situation (non-patent)
- Pathophysiology
- Presentation
- Murmur heard
- Diagnosis
- Management

A

Normal situation (non-patent)
- First breaths of life decreases the pressure in pulmonary circuit
- This causes the LA pressure > RA pressure, squashing the atrial septum
- Structurally closes some weeks later to become the fossa ovalis

Pathophysiology:
- Failure of the foramen ovale to close
- Shunt of blood from LA to RA
- Overtime this leads to right sided overload and right heart strain
- Eventually pulmonary hypertension can lead to Eisenmenger syndrome and cyanosis

Presentation:
Can be picked up on newborn examination
- Heart murmur
- SOB
- Tachypnoea
- Recurrent LRTIs
- Poor weight gain
- Difficulty feeding

Murmur heard:
- Mid-systolic crescendo-decrescendo
- Loudest at upper left sternal border
- Fixed split second heart sound

Diagnosis:
- Echocardiogram
- Cardiac MRI and CT

Management:
- Referral to paediatric cardiologist
- If small and asymptomatic, watch and wait
- Trans-catheter or open surgical closure
- Anticoagulation to reduce risk of strokes in adults

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14
Q

List 3 types of atrial septal defect (from most common to least common)

A
  1. Ostium secondum - septum secondum fails to completely close, leaving a hole in the wall
  2. Patent foramen ovale - foramen ovale fails to fully close
  3. Ostium primum - septum primum fails to completely close, leaving a hole in the wall
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15
Q

State some potential complications of atrial septal defects

A
  • Stroke from DVT
  • Atrial fibrillation
  • Right sided heart failure and pulmonary HTN
  • Eisenmenger syndrome
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16
Q

State some risk factors for development of atrial septal defects

A
  • Diabetes
  • Rubella
  • Maternal smoking in 1st trimester
  • Maternal drug use e.g. cocaine & alcohol
  • Treacher-Collins syndrome
  • Thrombocytopenia-absent radii syndrome (TAR syndrome)
17
Q

Name 2 genetic conditions that are associated with ventricular septal defects

A
  1. Down’s syndrome
  2. Turner’s syndrome
18
Q

Ventricular septal defects - state the following:
- Pathophysiology
- Presentation
- Murmur heard
- Management

A

Pathophysiology:
- Hole in the septum separating the ventricles
- Can be either a partial or entire septal defect

Presentation:
Can be picked up on newborn examination
Often initially asymptomatic and can present in adulthood
- Heart murmur
- SOB
- Tachypnoea
- Poor weight gain
- Difficulty feeding

Murmur heard:
- Pan-systolic murmur
- Left lower sternal border, 3rd and 4th ICS
- May be systolic thrill on palpation

Management:
- Referral to paediatric cardiologist
- If small and asymptomatic, watch and wait
- Trans-catheter or open surgical closure
Higher risk of infective endocarditis - will need prophalactic antibiotics during surgery
- May use diuretics e.g. Furosemide or ACEi

19
Q

State 3 differentials for a pan-systolic murmur

A
  • Ventricular septal defect
  • Mitral regurgitation
  • Tricuspid regurgitation
20
Q

State some risk factors for developing a ventricular septal defect

A
  • Diabetes
  • Rubella
  • Maternal alcohol use
  • Family history of VSD
  • Chromosomal trisomys (Down’s syndrome, Patau syndrome and Edwards syndrome)
21
Q

Briefly describe Eisenmenger’s Syndrome and at what age it can occur

A

Condition where the pressure in the right ventricle exceeds that of the left ventricle
- Caused by a gradual increase in the pulmonary vascular resistance (pressure in pulmonary circuit)
- The change in pressure reverses the shunt (from LV to RV) to RV to LV
- This causes deoxygenated blood from the right ventricle to enter the systemic circulation

= Cyanosis

Can occur after 1-2 years with a significant shunt
Can occur in adulthood if the shunt is small

22
Q

List 3 defects that can lead to Eisenmenger’s Syndrome

A
  1. Atrial septal defect (ASD)
  2. Ventricular septal defect (VSD)
  3. Patent ductus arteriosus (PDA)
23
Q

List examination findings for patients with pulmonary hypertension and if they’ve had chronic hypoxia (R to L shunt)

A
  • Raised JVP
  • Peripheral oedema
  • Right ventricle heave
  • Loud second heart sound
  • Heart murmur associated with underlying septal defect

If chronic hypoxia (R to L shunt):
- Cyanosis
- Clubbing
- SOB
- Red complexion (related to polycythaemia)

24
Q

Outline some complications of Eisenmenger syndrome and how having the condition impacts on life expectancy

A
  • VTE / thromboembolism
  • Heart failure
  • Infection
  • Haemorrhage

Reduces life expectancy by ~20 years :(

25
Q

Outline some management steps for Eisenmenger syndrome

A

Ideally, steps need to be taken to prevent the development by correcting underlying defect

Only definitive management: heart-lung transplant (high mortality!)

Other options:
- Oxygen (symptomatic relief)
- Anticoagulation (thrombosis)
- Prophylactic antibiotics (infective endocarditis)
- Sildenafil (for pulmonary HTN)
- Venesection (polycythaemia)

26
Q

Coarctation of the aorta - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Narrowing of the arch of the aorta, commonly around the area of the ductus arteriosus
- Reduces the pressure distal to the narrowing, but decreases the pressure proximal to the narrowing
- Severity of the narrowing can vary
- Associated with Turner’s syndrome in particular

Presentation:
- Weakness of femoral pulses
- May have systolic murmur
- Tachypnoea
- Poor feeding
- Grey/floppy baby
Over time, may have underdevelopment of legs and left arm

Management:
Depends on severity!
- Mild = may be asymptomatic until adulthood
- Severe = may require emergency surgery after birth (give prostaglandin E)

27
Q

Aortic valve stenosis - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management

A

Pathophysiology:
- Narrow aortic valve, restrict blood from left ventricle to aorta

Presentation:
May be asymptomatic if mild
- Ejection systolic murmur, radiating to carotids (loudest in aortic area)
- SOB
- Fatigue
- Dizziness
- Fainting
Symptoms are typically worse on exertion

Diagnosis:
- Echocardiogram

Management:
- Referral to paediatric cardiologist
- Regular follow ups with ECGs, exercise testing and echocardiograms
- Percutaneous balloon valvoplasty
- Surgical aortic valvotomy / valve replacement

28
Q

Pulmonary valve stenosis - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management

A

Pathophysiology:
- Narrow aortic valve, restrict blood from right ventricle to pulmonary artery
- Occurs if the normal 3 leaflet valve develops abnormally (thickened or fused)

Presentation:
Often completely asymptomatic, found on routine baby checks
- Ejection systolic murmur (loudest in pulmonary area)
- Palpable thrill (in pulmonary area)
- Right ventricle heave
- Raised JVP
- SOB
- Fatigue
- Dizziness
- Fainting

Diagnosis:
- Echocardiogram

Management:
- Referral to paediatric cardiologist
- If mild, generally don’t need intervention, can take watch and wait approach
- If significant or symptomatic, percutaneous balloon valvoplasty (open surgery if fails)

29
Q

State some complications of aortic valve stenosis

A
  • Left ventricular outflow tract obstruction
  • Heart failure
  • Ventricular arrhythmias
  • Infective endocarditis
  • Sudden death
30
Q

State some conditions that are associated with pulmonary valve stenosis

A
  • Rubella
  • Tetralogy of Fallot
  • William syndrome
  • Noonan syndrome
31
Q

Tetralogy of Fallot - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management

A

Pathophysiology:
Congenital condition with 4 concurrent issues
1. Ventricular septal defect
2. Overarching aorta
3. Pulmonary valve stenosis
4. Right ventricular hypertrophy
- Causes a right to left shunt and cyanosis (level depends on severity of TOF)

Presentation:
- Ejection systolic murmur (loudest in pulmonary area)
- Cyanosis
- Clubbing
- Poor feeding
- Poor weight gain
- ‘Tet’ spells

Diagnosis:
- Echocardiogram
- Doppler flow study

Management:
- Referral to paediatric cardiologist
- In neonates, use prostaglandin infusion to maintain the ductus arteriosus
- Open heart surgery to repair at around 6 months

32
Q

State some potential risk factors for developing Tetralogy of Fallot

A
  • Rubella
  • Diabetes
  • Maternal age > 40
  • Alcohol during pregnancy
33
Q

Describe what change might be seen on chest x-ray in Tetralogy of Fallot

A

Boot shaped heart (due to right ventricle thickening)

34
Q

Describe what a ‘tet’ spell is in Tetralogy of Fallot, how it presents and how it can be managed in the acute phase

A

Periods where a Tetralogy of Fallot patient becomes temporarily symptomatic, caused by the right-to-left shunt worsening = cyanotic episode

Precipitating episodes:
- Crying
- Physical exercise
- Waking

Caused by either an increase in the pulmonary resistance or a fall in the systemic resistance, causes more blood to be pumped to the aorta (rather than the pulmonary artery)

Presentation:
- Cyanosis
- SOB
- Irritable
In severe cases: reduced consciousness, seizures, death

Management = aim to increase systemic pressure:
- Squat / bring knees to chest
- Supplementary O2
- Beta blockers
- IV fluids
- Morphine (reduced respiratory rate)
- Sodium bicarbonate
- Phenylephrine infusion

35
Q

State some potential complications of Tetralogy of Fallot if left untreated

A
  • Infective endocarditis
  • Congestive cardiac failure
  • Stroke
  • Polycythaemia
  • Cerebral abscess

Death (up to 25% in the 1st year of life)

35
Q

Transposition of the great arteries - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management

A

Pathophysiology
- Condition where the right ventricle connects to the aorta attaches and the left ventricle connects to the pulmonary artery
- This creates 2 separate circuits, one is a systemic circuit (right ventricle) and the other is a pulmonary circuit (left ventricle)

Presentation:
Often picked up during antenatal scans during pregnancy
If not, babies will develop the following a few days after birth
- Cyanosis
- Respiratory distress
- Tachycardia
- Poor feeding
- Sweating

Management:
- Prostaglandin infusion
- Emergency balloon septostomy (creates atrial septal defect)
- Definitive management = open heart surgery, arterial switch operation

36
Q

State some rough potential causes of a blue baby

A
  • Congenital heart problems (most commonly Tetralogy of Fallot or also transposition of the great arteries)
  • Respiratory distress from lung disease e.g. asthma or foreign body

Year 4 - 3. Paediatrics (16 decks)

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