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Yr 4 - Paediatrics > Cardiology - PDA & ASD > Flashcards

Cardiology - PDA & ASD Flashcards

1
Q

When does the ductus arteriosus usually stop functioning?

When does it close completely?

A

Within 1-3 days of birth.

Closes completely within the first 2-3 weeks of life.

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2
Q

What is a patent ductus arteriosus (PDA)?

A

When the ductus arteriosus fails to close.

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3
Q

What is a key risk factor for PDA?

A

Prematurity

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4
Q

A small PDA can be asymptomatic, cause no functional problems and close spontaneously.

Occasionally patients can remain asymptomatic throughout childhood and present in adulthood with signs of heart failure.

What is the pathophysiology behind PDA causing heart failure?

A

1) The pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery.

2) This creates a left to right shunt where blood from the left side of the heart crosses to the circulation from the right side.

3) This increases the pressure in the pulmonary vessels causing pulmonary hypertension, leading to right sided heart strain as the right ventricle struggles to contract against the increased resistance.

4) Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy.

5) The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy.

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5
Q

Presentation of PDA?

A

1) Can be picked up during the newborn examination if a murmur is heard

2) SOB

3) Difficulty feeding

4) Poor weight gain

5) Lower respiratory tract infections

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6
Q

How is a diagnosis of PDA made?

A

Echocardiogram:

  • The use of doppler flow studies during the echo can assess the size and characteristics of the left to right shunt.
  • An echo is also useful for assessing the effects of the PDA on the heart, for example demonstrating hypertrophy of the right ventricle, left ventricle or both.
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7
Q

Management of a PDA?

A

1) Patients are typically monitored until 1 year of age using echocardiograms.

2) After 1 year of age it is highly unlikely that the PDA will close spontaneously and trans-catheter or surgical closure can be performed.

3) Symptomatic patient or those with evidence of heart failure as a result of PDA are treated earlier.

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8
Q

After what age is a PDA unloikely to close spontaneously (and trans-catheter or surgical closure can be performed?)?

A

After 1 year of age

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9
Q

Is PDA classed as cyanotic or acyanotic?

A

Generally classed as acyanotic.

However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis.

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10
Q

What is there a connection between in PDA?

A

Pulmonary trunk and descending aorta.

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11
Q

When does the ductus arteriosus usually close?

A

Usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance

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12
Q

Risk factors for PDA?

A

1) Premature babies
2) Born at high altitude
3) Maternal rubella infection in 1st trimester

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13
Q

Potential examination findings in PDA?

A

1) left subclavicular thrill

2) continuous ‘machinery’ murmur

3) large volume, bounding, collapsing pulse

4) wide pulse pressure

5) heaving apex beat

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14
Q

Describe the murmur in PDA

A

A continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear.

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15
Q

What can be given to neonates to assist closure of ductus arteriosus?

A

Indomethacin or ibuprofen (NSAIDs).

These inhibit prostaglandin synthesis and cause closure in the majority of cases.

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16
Q

What is the most likely congenital heart defect to be found in adulthood?

A

Atrial septal defect (ASD)

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17
Q

What is ASD?

A

An atrial septal defect is a defect (a hole) in the septum (the wall) between the two atria.

This connects the right and left atria allowing blood to flow between them.

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18
Q

Is ASD cyanotic or acyanotic?

A

Acyanotic

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19
Q

Why is ASD acyanotic?

A

Due to the pressure in left atrium (LA) being greater oxygenated blood from the LA is being forced through the ASD into the right atrium (RA).

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20
Q

How does an ASD develop?

A

1) During the development of the fetus the left and right atria are connected. Two walls grow downwards from the top of the heart, then fuse together with the endocardial cushion in the middle of the heart to separate the atria. These two walls are called the septum primum and septum secondum.

2) Defects this these two walls lead to atrial septal defects, a hole connecting the left and right atria.

3) There is a small hole in the septum secondum called the foramen ovale. The foramen ovale normally closes at birth.

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21
Q

Defects in what structures leads to ASD?

A

Defects in the two walls that grown downwards from the top of the heart to separate the atria –> the septum primum and septum secondum.

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22
Q

How are the atria separated in a fetus?

A

1) During the development of the fetus the left and right atria are connected.

2) Two walls grow downwards from the top of the heart, then fuse together with the endocardial cushion in the middle of the heart to separate the atria.

3) These two walls are called the septum primum and septum secondum.

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23
Q

What do the septum primum and septum secondum fuse with to separate the atria?

A

Endocardial cushion.

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24
Q

In a fetus, there is a small hole in the septum secondum?

What is this called?

A

Foramen ovale

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25
Q

What happens to the foramen ovale at birth?

A

It closes shortly after birth when vascular resistance changes: systemic BP increases with decreasing pulmonary pressure, with a decrease in right atrium pressure.

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26
Q

Pathophysiology of an ASD?

A

1) An ASD leads to a shunt, with blood moving between the two atria.

2) Blood moves from the left atrium to the right atrium because the pressure in the left atrium is higher than the pressure in the right atrium.

3) This means blood continues to flow to the pulmonary vessels and lungs to get oxygenated and the patient does not become cyanotic

4) However, the increased flow to the right side of the heart leads to right sided overload and right heart strain.

5) This right sided overload can lead to right heart failure and pulmonary hypertension.

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27
Q

How can ASD lead to Eisenmenger syndrome?

A

Eventually pulmonary hypertension can lead to Eisenmenger syndrome.

This is where the pulmonary pressure is greater than the systemic pressure, the shunt reverses and forms a right to left shunt across the ASD, blood bypasses the lungs and the patient becomes cyanotic.

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28
Q

What is the most common type of ASD?

A

Ostium secundum defect.

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29
Q

What are the 5 types of ASD, from commonest to least common?

A

1) Ostium secundum defect

2) Patent foramen ovale

3) Ostium primum defect

4) Sinus venosus defect

5) Coronary sinus defect

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30
Q

What happens in an ostium secundum defect?

A

Where the septum secondum fails to fully close, leaving a hole in the wall between the atria.

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31
Q

What occurs in a patent foramen ovale?

A

The foramen ovale fails to close (although this not strictly classified as an ASD).

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32
Q

What occurs in an ostium primum defect?

A

The septum primum fails to fully close and fuse with the endocardial cushions, leaving a hole in the wall (allowing blood to travel from left to right atrium).

This tends to lead to atrioventricular valve defects making it an atrioventricular septal defect.

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33
Q

What are the 2 types of ostium primum defects?

A

1) Complete AVSD

2) Partial AVSD

(will explain more later)

34
Q

What can sinus venosus defects be split into?

A

1) Superior defect (more common)

2) Inferior defect

35
Q

What happens in a superior sinus venosus defect?

A

1) When superior vena cava (SVC) opening runs on top of oval fossa (foramen ovale remnant) of atrial septum.

2) This stops SVC draining blood from both LA and RA.

Usually co-exists with abnormal communication between SVC and right superior pulmonary vein5.

36
Q

What happens in an inferior sinus venosus defect?

A

Occurs when IVC orifice overrides LA & RA.

Can co-exist with abnormal communication between IVC and right inferior pulmonary vein.

37
Q

What is a coronary sinus defect?

A

Unroofed coronary sinus defect is an absence in the roof of the coronary sinus. This can be partial or focal, allowing transmission between coronary sinus and left atrium.

38
Q

Risk factors for ASDs?

A

1) Maternal smoking in 1st trimester

2) Maternal diabetes

3) Maternal rubella

4) Maternal drug use e.g. cocaine, alcohol

5) FH of ASD

6) Congenital syndromes –> Ostium secundum ASD is associated with:
- Treacher-Collins syndrome
- Thrombocytopenia-absent radii syndrome (TAR syndrome)

39
Q

What 2 congenital syndromes is ostium secundum ASD associated with?

A

1) Treacher-Collins syndrome

2) Thrombocytopenia-absent radii syndrome (TAR syndrome)

40
Q

Symptoms of an ASD in paediatrics?

A

It is important to remember that vast majority of ASD are asymptomatic.

Symptoms of large ASD in paediatrics:

1) Tachypnoea (SOB)
2) Poor weight gain
3) Recurrent chest infections
4) Difficulty feeding

41
Q

When are most ASDs and PFO diagnosed?

A

Following stroke/TIA assessments in adulthood.

42
Q

Symptoms of untreated large ASDs in adults?

A

1) Exercise intolerance

2) Palpitations

3) Recurrent chest infections

4) Fatigue

5) Syncope

43
Q

Cardiac auscultation findings in ASD?

A

1) Murmur: soft, systolic ejection murmur, best heard over pulmonary valve region.

2) Wide, fixed split S2

3) Diastolic rumble in lower left sternal edge in patients with large ASD

44
Q

Describe the murmur in ASD

A

Soft, systolic ejection murmur, best heard over pulmonary valve region.

Fixed splitting of S2.

45
Q

What does splitting of the second heart sound mean?

A

Where you hear the closure of the aortic and pulmonary valves at slightly different times.

46
Q

What causes a fixed split of S2 in ASD?

A

This occurs in an atrial septal defect because blood is flowing from the left atrium into the right atrium across the atrial septal defect, increasing the volume of blood that the right ventricle has to empty before the pulmonary valve can close.

This doesn’t vary with respiration.

47
Q

Differentials for ASD?

A

1) Atrioventricular septal defect

2) Ventricular septal defect (VSD)

3) Innocent murmur: usually soft and musical

4) Pulmonary stenosis murmur: more turbulent

48
Q

What are some possible ECG findings in large ASD?

A
  • Tall P wave (right atrial enlargement)
  • Right bundle branch block (incomplete)
  • Right axis deviation

In adults, atrial fibrillation (AF) or atrial flutter may be seen.

49
Q

What is the gold standard for diagnosing ASD?

A

Transthoracic echocardiogram.

This provides information regarding both the size of ASD, and direction of blood flowing through the defect (using Doppler). It is also able to approximate the pulmonary artery pressure.

50
Q

Why isn’t CT imaging used for diagnosis of ASD?

A

Due to radiation risk

51
Q

Management of ASD?

A

1) Refer to paediatric cardiologist for ongoing management.

2) If small and asymptomatic, can watch and wait.

3) Can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery.

4) Anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke in adults.

52
Q

What size ASD should spontaneously close?

A

<5mm should spontaneously close within 12 months of birth.

53
Q

If ASD is found in adults, what is management?

A

If patient presenting with no signs of right heart failure and a small defect –> monitor every 2-3 years with echo.

If presenting with arrhythmia –> control rhythm with drugs & anticoagulated before definitive surgical treatment.

54
Q

Definitive management of ASD?

A

Surgical closure: percutaneously (transcatheter) or open chest (central stenotomy) using cardiopulmonary bypass.

55
Q

What size ASD is typically managed surgically?

A

> 1cm (10mm)

56
Q

What are the 2 options for surgical management of ASD?

A

1) percutaneously (transcatheter)

2) open chest (central stenotomy) using cardiopulmonary bypass.

57
Q

Who is surgical closure of ASD NOT recommended in?

A

Not recommended in patients where pulmonary hypertension is present (mean pulmonary pressure of 30mmHg), as this can induce RV failure if the ASD is closed up.

58
Q

Why is surgical management of ASD not recommended in pulmonary HTN?

A

As this can induce RV failure if the ASD is closed up.

59
Q

What pulmonary pressure defines pulmonary HTN?

A

Pulmonary pressure of 30mmHg

60
Q

Complications of percutaneous closure of ASD?

A

1) Arrhythmias

2) Atrioventricular block

3) Thromboembolism (VTE aspirin)

61
Q

Complications of untreated large ASDs?

A

1) Arrhythmias e.g. AF or atrial flutter (caused by atrial stretch leading to abnormal foci development)

2) Pulmonary hypertension and right sided heart failure

3) Eisenmenger syndrome (presenting with: chronic cyanosis, exertional dyspnoea, syncope, increased risk of infections, increased pulmonary vascular resistance)

4) Cyanosis (only if Eisenmenger)

5) Peripheral oedema (if eventually leading to heart failure)

6) TIA / stroke in the context of VTE

62
Q

How can a DVT cause a stroke in patients with ASD?

A

1) Normally when patients have a DVT and this becomes an embolus, the clot travels to the right side of the heart, enters the lungs and becomes a pulmonary embolism.

2) In patients with an ASD the clot is able to travel from the right atrium to the left atrium across the ASD.

3) This means the clot can travel to the left ventricle, aorta and up to the brain, causing a large stroke.

An exam question may feature a patient with a DVT that develops a large stroke and the challenge is to identify that they have had a lifelong asymptomatic ASD.

63
Q

What congenital heart defect is Holt–Oram syndrome associated with?

A

Ostium secundum

64
Q

What is Holt-Oram syndrome?

A

The characteristic hand malformation is digitalisation of a triphalangeal thumb so that the thumb is attached in the same plane as other fingers.

65
Q

What is Eisenmenger syndrome?

A

This occurs when blood flows from the RIGHT side of the heart to the LEFT, across a structural heart lesion, bypassing the lungs.

66
Q

What are the three underlying lesions that can result in Eisenmenger syndrome?

A

1) Atrial septal defect

2) Ventricular septal defect

3) Patent ductus arteriosus

67
Q

Pathophysiology in Eisenmenger syndrome

A

1) Normally when there is a septal defect blood will flow from the left side of the heart to the right (as pressure in the left side is greater than in the right).

2) A left to right shunt means blood still travels to the lungs and gets oxygenated, so the patient does not become cyanotic.

3) Over time the extra blood flowing into the right side of the heart and the lungs increases the pressure in the pulmonary vessels –> pulmonary HTN.

4) When the pulmonary pressure exceeds the systemic pressure, blood begins to flow from the right side of the heart to the left across the septal defect (right to left shunt).

5) This causes deoxygenated blood to bypass the lungs and enter the body –> cyanosis.

68
Q

What is cyanosis?

A

Cyanosis refers to the blue discolouration of skin relating to a low level of oxygen saturation in the blood.

69
Q

How does cyanosis lead to an increased risk of clots?

A

1) Bone marrow responds to low O2 sats by producing more RBCs and Hb

2) This leads to polycythaemia ( a high concentration of haemoglobin in the blood)

3) High conc of RBCs and Hb makes blood more viscous –> more prone to developing blood clots.

70
Q

How can polycythaemia affect complexion?

A

Can cause plethoric complexion.

71
Q

Examination findings in pulmonary HTN?

A

1) Right ventricular heave: the right ventricle contracts forcefully against increased pressure in the lungs

2) Loud P2: loud second heart sound due to forceful shutting of the pulmonary valve

3) Raised JVP

4) Peripheral oedema

72
Q

Describe the murmur heard in the following septal defects:

1) ASD
2) VSD
3) Patent ductus arteriosus

A

1) mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border

2) pan-systolic murmur loudest at the left lower sternal border

3) continuous crescendo-decrescendo “machinery” murmur

73
Q

What exam findings may be seen in Eisenmenger syndrome that are related to the right to left shunt and chronic hypoxia?

A

1) cyanosis
2) clubbing
3) dyspnoea
4) plethoric complexion (a red complexion related to polycythaemia)

74
Q

Prognosis of Eisenmenger syndrome?

A

Eisenmenger syndrome reduces life expectancy by around 20 years compared with healthy individuals.

75
Q

What are the main causes of death in Eisenmenger syndrome?

A

1) HF
2) Infection
3) VTE
4) Haemorrhage
5) Pregnancy (mortality can be up to 50% in pregnancy)

76
Q

When does it become medically impossible to reverse Eisenmenger syndrome?

A

Once the pulmonary pressure is high enough to cause the syndrome, it is not possible to medically reverse the condition.

77
Q

What is the only definitive treatment for Eisenmenger syndrome?

A

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

78
Q

What medicine can be used in the management of pulmonary HTN?

A

Sildenafil (PDE-5 inhibitor)

79
Q

Treatment of polycythaemia?

A

Vensection

80
Q

Management options in Eisenmenger syndrome:

A

1) Oxygen can help manage symptoms but does not affect overall outcomes

2) Treatment of pulmonary hypertension, for example using sildenafil

3) Treatment of arrhythmias

4) Treatment of polycythaemia with venesection

5) Prevention and treatment of thrombosis with anticoagulation

6) Prevention of infective endocarditis using prophylactic antibiotics

81
Q

What infection in the 1st trimester can lead to PDA in the neonate?

A

Maternal rubella infection

82
Q
A

Yr 4 - Paediatrics (78 decks)

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