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Yr 4 - Paediatrics > Cardiology - VSD & AVSD > Flashcards

Cardiology - VSD & AVSD Flashcards

1
Q

What is the most common congenital heart defect (CHD)?

A

Ventricular septal defect (VSD)

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2
Q

What is VSD?

A

Condition where there is a hole in the septum separating the left and right ventricles.

This can vary in size from tiny to the entire septum, forming one large ventricle.

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3
Q

VSDs can occur in isolation, however there is often an underlying genetic condition.

What 2 conditions are they often associated with?

A

1) Down’s syndrome

2) Turner’s syndrome

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4
Q

VSDs can occur in isolation, or can occur alongside other CHDs.

VSD occurs in approximately what % of all children with a CHD?

What % in isolation?

A

50% of all children with a CHD.

20% as isolated lesion.

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5
Q

What is the most common type of VSD?

A

Peri-membranous defects (70%) –> these occur in the upper, membranous portion of the ventricular septum, near the valves.

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6
Q

Pathophysiology of VSD?

A

1) Due to the increased pressure in the left ventricle compared to the right, blood typically flows from left the right through the hole.

2) Blood is still flowing around the lungs before entering the rest of the body, therefore they remain acyanotic (not cyanotic) because their blood is properly oxygenated.

3) A left to right shunt leads to right sided overload, right heart failure and increased flow into the pulmonary vessels.

4) The extra blood flowing through the right ventricle increases the pressure in the pulmonary vessels over time, causing pulmonary hypertension.

5) If this continues, the pressure in the right side of the heart may become greater than the left, resulting in the blood being shunted from right to left and avoiding the lungs.

6) When this happens the patient will become cyanotic because blood is bypassing the lungs –> Eisenmenger Syndrome.

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7
Q

What is the main determinant of t he haemodynamic consequences of the VSD?

A

The size of the defect

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8
Q

What are very small VSDs also called?

A

Restrictive VSD.

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9
Q

What happens in a very small/restrictive VSD?

A

The flow of blood through the VSD is minimal, so there is no significant increase in pulmonary blood flow. These patients tend to be asymptomatic.

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10
Q

What happens in a moderate sized VSD?

Is the patient symptomatic?

A

1) The flow of blood through the VSD is great enough to cause a significant increase in blood flow through the pulmonary circulation.

2) As the shunt is happening in systole, the extra volume of blood is pumped directly to the pulmonary circulation, so there is no initial effect on the right ventricle.

3) The left side of the heart though, is receiving a greater volume of blood, which can cause dilatation of the left atrium and ventricle.

Symptoms:

  • These patients are at risk of developing congestive heart failure and arrhythmias.
  • Patients can progressively develop. pulmonary hypertension and the wall of the right ventricle can hypertrophy as it pumps against higher pulmonary pressures.
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11
Q

What does pulmonary HTN result in?

A

Hypertrophy of the RV –> can result in right HF.

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12
Q

What happens in large VSDs?

Is the patient symptomatic?

A

1) A significant amount of blood is passing from the left to the right ventricle.

2) These patients develop early heart failure and severe pulmonary hypertension.

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13
Q

When do symptoms of cardiac failure appear in VSD?

A

Evident after the first weeks of life.

This occurs because the initially high pulmonary artery pressures drop, allowing more blood to shunt through the defect and into the lungs and thus creating pulmonary plethora.

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14
Q

What is Eisenmenger’s Syndrome?

A

A condition where the pressure in the right ventricle exceeds that of the left ventricle and is caused by a significant gradual increase in the pulmonary vascular resistance.

It results in a shunt reversal, with deoxygenated blood flowing from the right ventricle into the left ventricle and entering the systemic circulation.

This causes decreased systemic oxygen saturation and these patients become cyanotic.

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15
Q

Risk factors for VSD?

A

1) Maternal diabetes mellitus

2) Maternal rubella infection

3) Alcohol (foetal alcohol syndrome)

4) Uncontrolled maternal phenylketonuria (PKU) during pregnancy

5) FH of VSD

6) Congenital conditions:
- Down’s syndrome
- Trisomy 18 (Edwards syndrome)
- Trisomy 13 (Patau syndrome)
- Holt-Oram Syndrome
- Turner’s syndrome

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16
Q

Presentation of a moderate VSD?

A

Often VSDs are initially symptomless and patients can present as late as adulthood.

  • Excessive sweating
  • Easily fatigued
  • Tachypnoea
    This may be especially notable when feeding.
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17
Q

How are VSDs often picked up?

A
  • Can present as late as adulthood
  • May be picked up on antenatal scans
  • May be picked up when a murmur is heard during the newborn baby check
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18
Q

Symptoms of a large VSD?

A
  • Dyspnoea
  • Tachypnoea
  • Failure to thrive (height & weight)
  • Poor feeding
  • Frequent chest infections
  • Can progress to Eisenmenger’s Syndrome (cyanosis)

In severe cases, symptoms similar to cardiac failure:

  • Intolerance to exercise
  • Dizziness
  • Chest pain
  • Ankle swelling
  • A bluish complexion
  • Clubbing of the fingers and toes
  • Haemoptysis (severe)
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19
Q

What murmur is typically heard in VSD?

A

Pansystolic mumur, more prominently heard at the left lower sternal border in the third and fourth intercostal spaces.

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20
Q

What are the 3 causes of a pan systolic murmur?

A

1) VSD

2) Mitral regurgitation

3) Tricuscpid regurgitation

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21
Q

Possible examination findings in VSD (‘inspection’)?

A

1) Undernourished: due to fatigue during feeding.

2) Sweat on forehead: A sign of increased sympathetic activity as a compensatory mechanism for decreased cardiac output.

3) Increased work of breathing attributed to pulmonary congestion.

4) May develop cyanosis: check lipds, tongue, nail beds & conjunctiva.

5) Chromosomal disorders e.g. Down’s Syndrome, Holt Oram Syndrome

6) Clubbing

7) Tachypnoea

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22
Q

What causes clubbing in VSD?

A

Clubbing of the fingernails and toenails can be a sign of long standing arterial desaturation that may be too mild to cause a bluish complexion.

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23
Q

Possible examination findings in VSD (‘palpation’)?

A

1) HR: raised in congestive heart failure

2) Precordial palpation: The area above the heart where the heartbeat is normally felt is moving too much (hyperactive precordium – caused by a volume overload in the left side of the heart)

3) Thrills: A thrill of maximal intensity in the lower left sternal border would be expected.

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24
Q

Where is thrill felt in VSD?

A

A systolic thrill of maximal intensity in the lower left sternal border would be expected.

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25
Q

Location & quality of murmur in VSD?

A

Location –> lower left sternal border in the third and fourth intercostal spaces.

Quality –> a uniform, high pitched sound, often described as a ‘blowing’ sound.

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26
Q

How does size of VSD affect volume of murmur?

A

pan-systolic murmur is LOUDER in SMALLER defects

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27
Q

What investigation is required to differentiate between VSD and mitral regurgitation?

A

Echo

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28
Q

What may an ECG show in VSD?

A

May show signs of Left Ventricular Hypertrophy or Bilateral Ventricular Hypertrophy

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29
Q

Gold standard investigation for diagnosis of VSD?

A

Echo

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30
Q

Complications of VSD if left untreated?

A

May cause significant morbidity and mortality:

1) Congestive heart failure

2) Growth failure

3) Aortic valve regurgitation due to prolapse of a valve leaflet through the defect

4) Pulmonary HTN that in severe cases can lead to Eisenmenger’s Syndrome

5) Frequent chest infections

6) Infective Endocarditis

7) Arrhythmias

8) Sudden death

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31
Q

What is contraindicated in pulmonary HTN?

A

Pregnancy !!!

Pregnancy in women with pulmonary hypertension carries a 30-50% risk of mortality.

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32
Q

What % of VSDs close spontaneously?

A

50%

33
Q

How can the risk of infective endocarditis be reduced in patients with VSD?

A
  • Good oral hygiene
  • Avoid non-medical procedures, such as piercings and tattoos.
34
Q

Management of a small, asymptomatic VSD?

A

No management required - watch and wait.

35
Q

What can assist in enduring adequate weight gain in babies with VSD?

A

Increased calorific density of feedings.

Oral feeds may need to be supplemented with nasogastric tube feedings.

36
Q

Medical management options in VSD?

A

1) Diuretics –> to relieve pulmonary congestion

2) ACEi –> reduce the left to right shunt

3) Digoxin –> used to treat congestive heart failure (controversial)

37
Q

Which diuretics are typically given in VSD?

A

Furosemide & spironolactone can be added to minimise potassium loss.

38
Q

How do ACEi reduce left to right shunt in ASD?

A

Reducing mainly the systemic arterial pressures (afterload reduction) and allowing more blood to flow through the aortic valve and less through the VSD.

39
Q

What should you be cautious about in patients with VSD on diuretics & ACEi?

A

ACEi can increase serum potassium levels, in which case Spironolactone should be discontinued.

40
Q

Is there need for exercise restriction in VSD?

A

Usually no

41
Q

When is the surgical closure of a VSD indicated?

A

When there is a Qp/Qs (pulmonary-to-systemic blood flow ratio) of 2.0 or more.

42
Q

What are 3 surgical options in VSD?

A

1) Surgical repair: open heart surgery.

2) Catheter procedure (less common): catheter inserted into femoral artery and mesh device used to close hole.

3) Hybrid approach

43
Q

What is a palliative surgery option in VSD?

A

Pulmonary artery banding.

A band is wrapped around the pulmonary artery and tightened to decrease its diameter and decrease pulmonary blood flow in order to minimise the damage to the pulmonary vessels. Full surgical repair is usually performed in a later stage.

44
Q

What are atrioventricular septal defects (AVSD)?

A

This covers a spectrum of congenital cardiac malformations that share a defect of atrioventricular septum and abnormalities of the AV valves (mitral and tricuspid valve).

45
Q

What 2 groups can AVSDs be classified into?

A

1) Partial AVSD

2) Complete AVSD

46
Q

What condition do AVSDs have a strong association with?

A

Down Syndrome (Trisomy 21).

About 40-45% of children with Down syndrome have congenital heart defects and among these approximately 45% have an AVSD.

47
Q

Aetiology of AVSDs?

A

1) In normal development, the primitive AV canal connects the atria to the ventricles. At 4-5 weeks of gestation, the superior and inferior endocardial cushions of the common AV canal fuse and contribute to formation of AV valves (mitral and tricuspid) and the AV septum.

2) Defects arise due to failure of endocardial cushions to fuse correctly leading to apical displacement of AV valves and causing the inlet portion of ventricular septum to be scooped out.

48
Q

What does complete failure of superior and inferior endocardial cushions to fuse cause?

A

Causes an ASD (primum atrial septal defect) and VSD (ventricular septal defect) and a single common atrio ventricular valve.

49
Q

What does incomplete fusion between the superior and inferior endocardial cushions result in?

A

Partial AV canal defects with a primum ASD, a common valvular annulus with two separate AV valve orifices, and a cleft in anterior mitral leaflet.

50
Q

What does the pathophysiology of AVSDs depend on?

A

Depends on the magnitude of blood flow through the septal defect and the amount of atrioventricular valve regurgitation.

51
Q

What occurs in complete AVSD?

A

There is increased shunting of blood from left to right side of the heart which occurs at both atrial and ventricular levels.

In most cases, the pulmonary vascular resistance decreases normally over the first 6 weeks of life, and the patient develops a large left-to-right shunt through both the atrial and ventricular defects.

This in turn causes excessive pulmonary blood flow leading to heart failure and eventually elevated pulmonary vascular resistance. The atrioventricular valves are usually abnormal and incompetent resulting in regurgitation.

52
Q

What occurs in partial AVSD?

A

Partial defects have left to right shunting at the level of atrial septal defect (primum ASD).

This causes volume overload of both right atrium and right ventricle and pulmonary over circulation, but the pulmonary artery pressures are usually normal to mildly elevated –> symptoms may be minimal until adulthood or may present in late childhood.

The cleft in the anterior mitral valve leaflet causes regurgitation from left ventricle to left atrium. However, this can also occur from left ventricle to right atrium through the defect, resulting in LV to RA shunt and right sided volume overload.

53
Q

Level of left to right shunting in complete vs partial AVSDs?

A

Complete –> shunting of blood from left to right side of the heart occurs at both atrial and ventricular levels.

Partial –> shunting at the level of atrial septal defect (primum ASD).

54
Q

How does AVSD affect the left ventricular outflow tract (LVOT)?

A

The structural changes lead to an increased distance between the aorta and the apex of the heart.

This results in an elongation of LVOT and abnormal position of the aortic valve which is displaced anterosuperior rather than being wedged between right and left AV valves.

55
Q

What anatomical change is seen on an ECHO in AVSD?

A

“Goose neck deformity” - elongation of the LVOT.

56
Q

Symptoms of AVSD?

A

1) Tachypnoea

2) Tachycardia

3) Poor feeding

4) Sweating

5) Failure to thrive (due to excessive metabolic cardiovascular requirements and poor caloric intake) – which in turn is due to tachypnoea.

57
Q

When do symptoms in COMPLETE AVSD present?

A

Virtually all patients with complete AVSD have symptoms by 1 year of age.

58
Q

Examination findings in AVSD (‘inspection’)?

A

1) Undernourished

2) May have signs of Down’s syndrome: flat nasal bridge, up slanting palpebral fissures, prominent inner epicanthal folds, single palmar crease and fifth finger clinodactyly.

3) Signs of congestive heart failure: hepatomegaly, gallop rhythm, generalized oedema and crackles may be present.

4) Pallor

5) Harrison grooves in slightly older children

59
Q

What are Harrison grooves?

A

horizontal depression along lower border of chest at diaphragm insertion site due to chronic tachypnoea.

60
Q

Examination findings in AVSD (‘palpation’)?

A

1) A hyperactive precordium

2) Prominent systolic heave along the left sternal border (as a consequence of the volume and pressure overload on the right ventricle)

3) Palpable apical thrill (may result due to regurgitation of the atrioventricular valve).

61
Q

What causes a prominent systolic heave along the left sternal border in AVSD?

A

A consequence of the volume and pressure overload on the right ventricle

62
Q

What causes a palpable apical thrill in AVSD?

A

May result due to regurgitation of the atrioventricular valve.

63
Q

Auscultation findings in complete AVSD?

A

1) An accentuated S1

2) Loud pulmonary component of S2

3) Ejection-systolic murmur

4) Mid-diastolic murmur

5) Pansystolic murmur

64
Q

What causes the loud pulmonary component of S2 in complete AVSD?

A

In complete AVSD, the second heart sound narrowly splits and P2 increases in intensity (due to elevated pulmonary artery pressure).

65
Q

What causes the ejection systolic murmur in AVSD?

A

due to increased blood flow through a normal pulmonary valve.

66
Q

Where is the ejection systolic murmur in AVSD best heard?

A

Along the left upper sternal border (pulmonary area).

67
Q

Where is the mid diastolic murmur in AVSD best heard?

A

Best auscultated along left lower sternal border and apex

68
Q

What causes the mid diastolic murmur in AVSD?

A

Due to the increased flow across the common atrioventricular valve.

69
Q

Where is the pansystolic murmur in AVSD best heard?

A

Best auscultated along Left lower sternal border and at cardiac apex

70
Q

What causes the pansystolic murmur in AVSD?

A

Heard if left atrioventricular valve regurgitation is present.

71
Q

Auscultation findings in partial AVSD?

A

1) Wide and fixed splitting of S2: the character of S2 does not change with inspiration

2) Ejection systolic murmur: best auscultated at Left upper sternal border due to turbulent blood flow across the pulmonary valve – may radiate to the lung fields.

3) Mid-diastolic murmur: best auscultated at Left lower sternal border. Usually low pitched and represents significant left AV valve regurgitation.

4) Pansystolic murmur: may be heard at the apex due to regurgitation through anterior mitral cleft

72
Q

What investigation should be done in AVSD due to the strong association with Down syndrome?

A

Karyotyping.

73
Q

What is the characteristic ECG finding in complete AVSD?

A

Superior QRS axis with the QRS axis between -40 to -150 degrees

74
Q

What is the primary diagnostic tool for evaluation of complete AVSD?

A

Echo

75
Q

When do infants with complete AVSD develop heart failure?

A

Within first few months of life.

76
Q

Management of AVSD?

A

Medical (focused on symptomatic relief of heart failure):
- Diuretics
- ACEi
- Adequate caloric intake

Surgical:
- Palliative surgery: pulmonary artery banding
- Corrective surgery: carried out via median sternotomy under cardiopulmonary bypass.

77
Q

Complications of AVSD?

A
  • Failure to thrive
  • Recurrent lower respiratory tract infections
  • Congestive heart failure
  • Pulmonary vascular disease
  • Eisenmenger’s syndrome
78
Q
A

Yr 4 - Paediatrics (78 decks)

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