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Year 4 - Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the role of the placenta in utero?

A

Blood passes via the placenta to collect oxygen and nutrients, and to dispose of waste products such as carbon dioxide and lactate.

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2
Q

What are the three fetal shunts?

A
  1. Ductus venosus - connects the umbilical vein and inferior vena cava, allowing blood to bypass the liver.
  2. Foramen ovale - connects the right atrium and the left atrium, allowing blood to bypass the right ventricle and pulmonary circulation.
  3. Ductus arteriosus - connects the pulmonary artery and the aorta, allowing blood to bypass the pulmonary circulation.
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3
Q

Explain how foramen ovale closes following birth.

A

Baby’s first breaths expand the alveoli, reducing pulmonary vascular resistance.

Pressure in the right atrium falls below the the left atrial pressure, closing the foramen ovale.

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4
Q

Explain how ductus venosus closes following birth.

A

Immediately after birth ductus venosus stops functioning because the umbilical cord is clamped, meaning no blood can pass through umbilical veins.

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5
Q

Explain how ductus arteriosus closes following birth.

A

Prostaglandins are required to keep the ductus arteriosus open.

Increased blood oxygenation following birth causes a drop in circulating prostaglandins, resulting in closure of ductus arteriosus.

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6
Q

What are innocent murmurs?

A

Common flow murmurs in children that have typical features:
- Soft
- Short
- Systolic
- Symptomless
- Situational

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7
Q

When do murmurs warrant referral to a paediatric cardiologist?

A

When you are not reassured they are innocent murmurs:
- murmur louder than 2/6
- diastolic murmur
- louder on standing
- other symptoms (e.g. failure to thrive, feeding difficulty, cyanosis, shortness of breath)

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8
Q

How are paediatric murmurs investigated?

A
  • ECG
  • echocardiogram
  • CXR
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9
Q

What are the differentials of a pan-systolic murmur?

How can they be differentiated?

A

Mitral regurgitation: heard in 5th ICS MCL.

Tricuspid regurgitation: heard in 5th ICS LSB.

Ventricular septal defect: heard in lower LSB.

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10
Q

What are the differentials of an ejection systolic murmur?

How can they be differentiated?

A

Aortic stenosis: heard in 2nd ICS RSB.

Pulmonary stenosis: heard in 2nd ICS LSB.

Hypertrophic obstructive cardiomyopathy: heard in 4th ICS LSB.

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11
Q

What causes splitting of the second heart sound?

A

During inspiration, contraction of the chest wall and diaphragm causes negative intrathoracic pressure.

This causes the right side of the heart to fill faster as it pulls in blood from the venous system.

The increased volume in the right ventricle means it takes longer to empty during systole, delaying the closure of the pulmonary valve.

When the pulmonary valve closes slightly later than the aortic valve, this causes a ‘split’ second heart sound.

NB: Split second heart sound heard in held expiration is NOT normal.

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12
Q

Risk factors for patent ductus arteriosus.

A
  • genetic
  • rubella infection
  • prematurity
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13
Q

Pathophysiology of a patent ductus arteriosus.

A
  1. Pressure of aorta > pressure of pulmonary vessels.
  2. Blood moves down its pressure gradient, from the aorta to the pulmonary vessels (L>R shunt).
  3. Pulmonary hypertension occurs, increasing the afterload for the right ventricle.
  4. Right ventricular hypertrophy compensates for increased afterload, increasing preload for left ventricle.
  5. Eventual left ventricular hypertrophy.
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14
Q

Presentation of patent ductus arteriosus.

A
  • murmur
  • shortness of breath
  • difficulty feeding
  • poor weight gain
  • lower respiratory tract infections
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15
Q

Murmur heard in patent ductus arteriosus.

A

Normal first heart sound with a continuous crescendo-decrescendo machinery murmur, making the second heart sound difficult to hear.

A small patent ductus arteriosus may not have any abnormal heart sounds, and may be asymptomatic.

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16
Q

How is patent ductus arteriosus diagnosed?

A

Confirmed by echocardiogram.

The use of doppler flow studies can assess the size and characteristics of the left to right shunt.

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17
Q

Management of patent ductus arteriosus.

A

Monitor until 1 year of age using echocardiograms, with expectant closure of PDA unless there is evidence of heart failure.

After 1 year of age it’s unlikely the PDA will close spontaneously:
- trans-catheter closure
- surgical closure

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18
Q

Pathophysiology of atrial septal defects.

A
  1. Pressure of left atrium > Pressure of right atrium.
  2. Blood moves down its pressure gradient, from the left atrium to the right atrium (L>R shunt).
  3. Increased flow to the right side of the heart leads to right sided overload, and right heart strain.
  4. Right-sided overload can lead to right heart failure and pulmonary hypertension.
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19
Q

Complications of atrial septal defects.

A
  • stroke
  • atrial fibrillation / flutter
  • pulmonary hypertension
  • right sided heart failure
  • Eisenmenger syndrome
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20
Q

While a patient is being treated for DVT, they develop a large stroke.

What is the likely underlying pathology?

A

Lifelong asymptomatic atrial septal defect.

The thrombus has embolised to the right side of the heart, through the septal defect, and into the left side of the heart. From here, it travels via the systemic circulation to the brain.

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21
Q

Presentation of atrial septal defect.

A
  • murmur
  • antenatal scan detection
  • shortness of breath
  • difficulty feeding
  • poor weight gain
  • lower respiratory tract infections

It may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure or stroke.

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22
Q

Murmur in atrial septal defects.

A

Mid-systolic, crescendo decrescendo murmur loudest at upper LSB.

Fixed split second heart sound, because blood flows from the left atrium across the ASD, increasing the volume of blood the right ventricle has to empty. This causes a delay in the closure of the pulmonary valve, irrespective of respiration.

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23
Q

Management of atrial septal defects.

A

Surgical correction using a transvenous catheter closure, or open heart surgery.

Anticoagulants can be used to reduce the risk of clots and stroke in adults.

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24
Q

Risk factors for ventricular septal defects.

A
  • Down’s syndrome
  • Turner’s syndrome
  • genetic
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25
Q

Pathophysiology of ventricular septal defects.

A
  1. Pressure in left ventricle > Pressure in right ventricle.
  2. Blood moves down its pressure gradient, from the left to right ventricle (L>R shunt).
  3. Right side of the heart becomes overloaded
  4. Increased pressure in the pulmonary vessels over time, causing pulmonary hypertension.
  5. Eventual strain and right sided heart failure.
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26
Q

Presentation of ventricular septal defects.

A
  • murmur
  • antenatal scan
  • poor feeding
  • dyspnoea
  • tachypnoea
  • failure to thrive
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27
Q

Murmur in ventricular septal defects.

A

Pan-systolic murmur, heard at the lower LSB at 3rd ICS.

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28
Q

Treatment of ventricular septal defects.

A

Small VSDs often close spontaneously so require no treatment.

VSDs can be corrected surgically:
- transvenous catheter closure
- open heart surgery

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29
Q

Risks associated with VSDs.

A

Increased risk of infective endocarditis, therefore prophylactic abx should be considered during surgical procedures to reduce the risk.

30
Q

What lesions are associated with Eisenmenger’s syndrome?

A
  • atrial septal defects
  • ventricular septal defects
  • patent ductus arteriosus
31
Q

Pathophysiology of Eisenmenger syndrome.

A

PDA, VSD and ASD causes overload of the right heart, increasing pressure in the pulmonary vessels and causing pulmonary hypertension.

When the pulmonary pressure exceeds the systemic pressure, blood begins to flow from the right side of the heart to the left (R>L shunt). This causes deoxygenated blood to bypass the lungs and enter the body, resulting in cyanosis.

The bone marrow responds to hypoxaemia by producing more erythrocytes and haemoglobin, resulting in polcythaemia. This increases the viscocity of blood, making patients more prone to developing blood clots.

32
Q

Examination findings associated with pulmonary hypertension.

A
  • right ventricular heave: the right ventricle contracts forcefully against increased pressure in the lungs.
  • loud P2: forceful shutting of the pulmonary valve.
  • raised JVP: increased afterload for systemic circulation.
  • peripheral oedema: increased afterload for systemic circulation.
33
Q

Examination findings related to Eisenmenger’s syndrome.

A
  • cyanosis
  • clubbing
  • dyspnoea
  • plethoric complexion (red complexion related to polycythaemia)
34
Q

Prognosis of Eisenmenger syndrome.

A

Reduces life expectancy by around 20 years:
- heart failure
- infection
- thromboembolism
- haemorrhage

The mortality raises to 50% in pregnancy, therefore close monitoring by cardiology in pregnancy is required.

35
Q

Management of Eisenmenger syndrome.

A

Underlying defect should be managed optimally or corrected surgically to prevent the development of Eisenmenger syndrome.

The only definitive treatment is a heart-lung transplant, however this has a high mortality.

Medical management may include:
- supplementary oxygen
- treatment of arrhythmias
- venesection for polycythaemia
- anticoagulation to prevent thrombosis
- prophylactic abx to prevent infective endocarditis

36
Q

Pathophysiology of coarctation of the aorta.

A

Congenital narrowing on the aortic arch, reducing the pressure of the blood flowing to the arteries that are distal to the narrowing.

In arteries proximal to the narrowing, such as the heart and first three branches of the aorta, pressure is increased.

37
Q

Presentation of coarctation of the aorta.

A
  • weak femoral pulses
  • murmur
  • tachypnoea
  • poor feeding
  • grey and floppy baby
  • left ventricular heave
  • underdeveloped left arm
  • underdevelopment of the legs
38
Q

Murmur in coarctation of the aorta.

A

Systolic murmur heard below the left clavicle, and below the left scapula.

39
Q

Management of coarctation of the aorta.

A

Prostaglandin E used to keep ductus arteriosus open while awaiting for surgical correction.

40
Q

Pathophysiology of congenital aortic valve stenosis.

A

Patients are born with a narrow aortic valve, restricting blood flow from the left ventricle into the aorta.

Patients with aortic stenosis may have a bicuspid valve.

41
Q

Presentation of aortic stenosis.

A
  • asymptomatic
  • fatigue
  • shortness of breath
  • dizziness
  • fainting
  • worse on exertion
42
Q

Signs of aortic stenosis.

A

Ejection systolic murmur heard loudest in the aortic area, which is the second intercostal space, right sternal border.

Crescendo-decrescendo character, radiating to the carotids.

43
Q

Management of aortic stenosis.

A

Diagnosed using echocardiogram.

Patients with significant stenosis need:
- percutaneous balloon aortic valvoplasty
- surgical aortic valvotomy
- valve replacement

44
Q

Complications of aortic stenosis.

A
  • left ventricular outflow tract obstruction
  • heart failure
  • ventricular arrhythmia
  • bacterial endocarditis
  • sudden death on exertion
45
Q

Pathophysiology of congenital pulmonary valve stenosis.

A

Congenital abnormality causing the pulmonary valve to become thickened or fused.

This results in a narrow opening between the right ventricle and pulmonary artery.

46
Q

Associations of congenital pulmonary valve stenosis.

A
  • Tetralogy of Fallot
  • William syndrome
  • Noonan syndrome
  • Congenital rubella syndrome
47
Q

Presentation of pulmonary valve stenosis.

A

Mostly asymptomatic and a routine finding of routine baby checks.

Significant stenosis can present with:
- fatigue on exertion
- shortness of breath
- dizziness
- fainting

48
Q

Signs of pulmonary valve stenosis.

A
  • ejection systolic mumur heard loudest in 2nd ICS, LSB
  • palpable thrill
  • right ventricular heave
  • raised JVP
49
Q

Management of pulmonary valve stenosis.

A

Diagnose with echocardiogram.

In symptomatic patients, surgical options is balloon valvuloplasty via a venous catheter into the femoral vein.

50
Q

Features of Tetralogy of Fallot.

A
  • ventricular septal defect
  • overriding aorta
  • pulmonary valve stenosis
  • right ventricular hypertrophy
51
Q

Risk factors for Tetralogy of Fallot.

A
  • Rubella infection
  • increased age of mother
  • alcohol consumption during pregnancy
  • diabetic mother
52
Q

How does Tetralogy of Fallot cause cyanosis?

A

The VSD allows blood to flow between the ventricles. The term “overriding aorta” refers to the fact that the entrance to the aorta (the aortic valve) is placed further to the right than normal, above the VSD. This means that when the right ventricle contracts and sends blood upwards, the aorta is in the direction of travel of that blood, therefore a greater proportion of deoxygenated blood enters the aorta from the right side of the heart.

Stenosis of the pulmonary valve provides greater resistance against the flow of blood from the right ventricle. This encourages blood to flow through the VSD and into the aorta rather than taking the normal route into the pulmonary vessels. Therefore, the overriding aorta and pulmonary stenosis encourage blood to be shunted from the right heart to the left, causing cyanosis.

The increased strain on the muscular wall of the right ventricle as it attempts to pump blood against the resistance of the left ventricle and pulmonary stenosis causes right ventricular hypertrophy, with thickening of the heart muscle.

These cardiac abnormalities cause a right to left cardiac shunt. This means blood bypasses the child’s lungs. Blood bypassing the lungs does not become oxygenated. Deoxygenated blood entering the systemic circulation causes cyanosis. The degree to which this happens is related mostly to the severity of the patients pulmonary stenosis.

53
Q

Investigating Tetralogy of Fallot.

A

Echocardiogram with doppler flow studies, to assess the severity of the abnormality and shunt.

54
Q

CXR findings of Tetralogy of Fallot.

A

“Boot shaped” heart due to right ventricular thicckening.

55
Q

Presentation of Tetralogy of Fallot.

A

Most cases diagnosed antenatally.

Ejection systolic murmur may be heard on newborn baby check.

Severe cases will present with heart failure before one year of age.

56
Q

Signs and symptoms of Tetralogy of Fallot.

A
  • cyanosis
  • clubbing
  • poor feeding
  • poor weight gain
  • ejection systolic murmur
  • Tet spells
57
Q

What are Tet spells?

A

Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode.

This occurs when the pulmonary vascular resistance increases, or the systemic resistance decreases.

Episodes may be precipitated by waking, physical exertion or crying. This causes them to generate carbon dioxide, leading to systemic vasodilation. This reduces systemic vascular resistance and blood will favourably bypass the lungs.

58
Q

Tet Spell treatment options.

A

Position child with knees to chest to increase systemic vascular resistance.

Any medical management should involve an experienced paediatrician, as they can be potentially life threatening:
- supplementary oxygen
- beta blockers (relax right ventricle and improve flow to the pulmonary vessels)
- IV fluids (increase pre-load, increasing the volume of blood flowing to the pulmonary vessels)
- morphine (decrease respiratory drive, increasing breathing efficacy)
- sodium bicarbonate (buffer metabolic acidosis)
- phenylephrine infusion (increase systemic vascular resistance)

59
Q

Management of Tetralogy of Fallot.

A

Prostaglandin infusion in neonates to maintain the ductus arteriosus.

Total surgical repair by an open heart surgery is definitive.

60
Q

Prognosis of Tetralogy of Fallot.

A

5% mortality for surgical correction.

Prognosis poor without treatment; around 90% with treatment.

61
Q

What is Ebstein’s anomaly?

A

A congenital heart condition where the tricuspid valve is set lower in the right side of the heart, causing a bigger right atrium and a smaller right ventricle.

This leads to poor flow to the pulmonary vessels.

It is associated with a right to left shunt across an atrial septal defect, allowing blood to bypass the lungs and resulting in cyanosis.

62
Q

Associations of Ebstein’s anomaly.

A
  • maternal lithium use
  • Wolff-Parkinson-White syndrome
63
Q

Presentation of Ebstein’s anomaly.

A
  • evidence of heart failure
  • Gallop rhythm (S1, S2, S3, S4)
  • cyanosis
  • shortness of breath
  • tachypnoea
  • poor feeding
  • collapse or cardiac arrest
64
Q

Why does Ebstein’s anomaly usually present days after birth, rather than immediately?

A

Prostaglandins keep ductus arteriosus open, allowing blood to flow from the aorta to the pulmonary vessels to get oxygenated. This minimises the cyanosis.

After a few days, prostaglandins fall and ductus arteriosus closes, meaning cyanosis worsens.

65
Q

Diagnosis of Ebsteins anomaly.

A

Echocardiogram used to diagnose and assess severity.

66
Q

Management of Ebstein’s anomaly.

A

Medical management includes treating arrhythmias and heart failure.

Prophylactic antibiotics used to prevent infective endocarditis.

Definitive management is by surgical correction of the underlying defect.

67
Q

What is transposition of the great arteries?

A

Condition where the attachments of the aorta and the pulmonary trunk are swapped.

This means the right ventricle pumps blood into the aorta, and the left ventricle pumps blood into the pulmonary vessels. This means there are two separate circulations athat don’t mix.

68
Q

Associations of transposition of the great arteries.

A
  • ventricular septal defect
  • coarctation of the aorta
  • pulmonary stenosis
69
Q

Presentation of transposition of the great arteries.

A

Diagnosed during pregnancy with antenatal ultrasound scans.

When a defect is not detected during pregnancy, it will present with cyanosis at or within a few days of birth. It is immediately life threatening.

70
Q

How may a baby born with transposition of the great arteries survive a few days?

A

A patent ductus arteriosus or ventricular septal defect can initially compensate by allowing a right to left shunt.

Within a few days or weeks, they will develop respiratory distress, tachycardia, poor feeding, growth failure and sweating.

71
Q

Management of transposition of the great arteries.

A

Prostaglandin infusion to maintain the ductus arteriosus.

Open heart surgery is the definitive management.

Year 4 - Paediatrics (17 decks)

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