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Year 5 - Paediatrics > Paeds CARDIO > Flashcards

Paeds CARDIO Flashcards

1
Q

Recall 2 differentials for a right atrium anomaly in children

A

Tricuspid atresia: requires ASD + VSD to remain patent to allow shunt
Ebstein’s anomaly: less severe as not reliant on shunting

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2
Q

Recall 3 differentials for a right ventricle anomaly in children

A

Pulmonary stenosis
Pulmonary atresia
Tetralogy of Fallot

(This is what it says in Ludley’s notes - bit confused about how pulmonary valve abnormalities are ventricular issues rather than atrial)

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3
Q

What is the tetralogy of fallot?

A

A cyanotic heart defect that is characterised by four features:
VSD
Overarching aorta
Right outflow tract obstruction
RV hypertrophy

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4
Q

Recall 2 differentials for a left atrium anomaly in children

A

Mitral stenosis
Mitral atresia

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5
Q

Recall 4 differentials for a left ventricle anomaly in children

A

Hypoplastic left heart
Coarctation of aorta
Interrupted arch
Aortic stenosis

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6
Q

What is ToGA?

A

Transposition of the Great Arteries - a congenital heart defect in which the aorta leaves the right ventricle and the pulmonary trunk leaves the left ventricle, resulting in the complete separation of the systemic and pulmonary circulations

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7
Q

When does ToGA present?

A

When ductus arteriosus closes at 2-4 days old

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8
Q

How can ToGA be managed?

A

Give prostaglandin infusion to keep DA open
Need urgent surgical readjustment

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9
Q

How quickly after birth does AVSD present?

A

First few hours of life

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10
Q

Where is the ductus arteriosus?

A

Between the aorta and pulmonary artery

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11
Q

When do aortic problems (coarctation or stenosis) present?

A

First few weeks of life (but not within days)

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12
Q

What test is used to diagnose heart disease in a cyanosed neonate, and how is it done?

A

Nitrogen washout test
Give 100% oxygen for 10 mins
Measure right radial artery blood gas oxygen
If it stays low (<15kPa) = positive for CHD

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13
Q

What is a ‘blue baby’ presentation a red flag for?

A

R-L shunt

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14
Q

What is a ‘breathless baby’ presentation indicative of?

A

L-R shunt

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15
Q

Recall the 3 types of L-R shunt

A

VSD, ASD, PDA

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16
Q

What are the differentials for cardiac outflow obstruction and how can you clinically differentiate between them

A

If child is otherwise well: P or A stenosis
If child is also in CV collapse + shock: coarctation

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17
Q

What does ‘cyanotic heart disease’ refer to?

A

Right to left shunt

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18
Q

What are the types of ASD and which is more common?

A

Secundum (more common): defect in atrial septum (failure of closure of foramen ovale)
Partial (AVSD): defect of AV septum

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19
Q

What are the signs and symptoms of ASD?

A

Asymptomatic
May have recurrent chest infections/ wheeze

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20
Q

What murmur is associated with ASD?

A

Ejection systolic murmum at ULSE
Fixed wide splitting of S2

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21
Q

How will the different types of ASD appear on ECG?

A

Secundum: RBBB + RAD
Partial: superior QRS axis

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22
Q

How should the different types of ASD be managed?

A

Secundum: cardiac catheterisation + insertion of occlusive device
Partial: surgical correction

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23
Q

What investigation is diagnostic of ASD?

A

Echo

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24
Q

How are VSDs classified?

A

By size:
small <3mm
large >3mm

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25
Q

What are the signs and symptoms of VSD?

A

Small: May be asymptomatic, may have breathless 3m old with normal sats, poor feeding with tiredness, LOUD murmur

Large: Heart failure, SOB, recurrent chest infections, hepatomgaly

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26
Q

Describe the murmur in VSD?

A

Small: LOUD, Pan-systolic, LLSE

Large: SOFT pan-systolic murmur

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27
Q

How shouls small VSDs be managed?

A

Self-limiting: they close over time

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28
Q

What does a small VSD increase the risk of?

A

Endocarditis

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29
Q

What does large VSD increase the risk of?

A

Eisenmenger syndrome - “the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect causes pulmonary HTN + eventual reversal of the shunt into a cyanotic right-to-left shunt”

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30
Q

How should a large VSD be managed?

A

CDC
Calories (additional calorie input)
Diuretics
Captopril

Surgery is usually performed at 3-6 months to prevent permanent lung damage from pulmonary HTN + high blood flow

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31
Q

By what time should the DA usually close?

A

1 month postpartum

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32
Q

Describe the murmur in PDA

A

Continuous ‘machine-like’ at ULSE

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33
Q

What would be found OE in PDA?

A

Left sub-clavicular thrill
Heaving apex beat
Wide pulse pressure
Bounding, collapsing pulses
Resp symptoms from increased work

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34
Q

Recall the medical and surgical management of PDA

A

Medical: Indomethacin (NSAID): to prompt duct closure
Surgical: at 1 year

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35
Q

How can cyanosis be tested for?

A

Hyperoxia nitrogen washout test

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36
Q

How should cyanosis be immediately managed?

A

ABCs
Prostaglandin infusion (to maintain PDA patency)

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37
Q

Recall the timeline of presentation of the different types of cyanotic heart disease after birth

A

<10 mins: Tricuspid atresia

Few hours: ToGA

Up to 3 weeks: AVSD

Any age (at a few days, often): ToF

10-15 years: Eisenmenger

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38
Q

Which 2 types of cyanotic HD produce an ESM at the left sternal edge?

A

ToGA + ToF

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39
Q

What is Ebstein’s abnormality?

A

Malformation of tricuspid valve leading to severe tricuspid regurgitation

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40
Q

What maternal medication is associated with Ebstein’s abnormality?

A

Lithium

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41
Q

What would be heard on auscultation in Ebstein’s abnormality?

A

split 1st + 2nd heart sounds

42
Q

How should Ebstein’s be managed?

A

Prostaglandin - cone repair of tricuspid valve

43
Q

What is tricuspid atresia?

A

Complete absence of tricuspid valve: so LV is the only effective ventricle (right too small)

44
Q

Describe the presentation of tricuspid atresia

A

Cyanosis + SOB within first 10 mins of life

45
Q

What is the murmur in tricuspid atresia?

A

ESM at LSE due to VSD

46
Q

Recall in detail the management of tricuspid atresia

A

1st need to maintain a secure supply of blood to the lungs

Option 1 is a Blalock-Taussig shunt insertion

Option 2 is pulmonary banding operation to reduce pulmonary blood flow

COMPLETE CORRECTIVE SURGERY NOT POSSIBLE IN MOST CASES

47
Q

Why is ToGA not instantly fatal?

A

Usually found alongside ASDs/ VSDs/PDAs etc which aid mixing

48
Q

What is heard upon auscultation in ToGA?

A

Loud S2 but no murmur

49
Q

What investigations should be done in suspected ToGA?

A

CXR - cardiomegaly, ‘egg-on-a-string’ appearance
Echo - diagnostic

50
Q

What would a CXR show in ToGA??

A

Narrow upper mediastinum (‘egg on side’)

51
Q

Recall the management of ToGA

A

Immediate prostaglandin infusion to maintain PDA patency
Balloon atrial septostomy (this tears atrial septum down to allow mixing)
Arterial surgery to switch the vessels

52
Q

What is the most common association with AVSD?

A

Down’s syndrome

53
Q

How does AVSD present?

A

Cyanosis at 2-3w of life

54
Q

How should AVSD be managed?

A

Treat heart failure medically + surgery at 3 months

55
Q

What are the 4 characteristics of the tetralogy of fallot?

A

VSD
Overriding aorta (compression of PA –> )
Pulmonary stenosis (back pressure –> )
RVH

56
Q

What would be heard on auscultation in tetralogy of fallot?

A

Murmur from pulmonary stenosis = loud ESM at left lower sternal border

57
Q

What investigations should be done in suspected tetralogy of fallot?

A

CXR
Echo

58
Q

What does CXR show in tetralogy of fallot?

A

Boot-shaped, small heart due to RVH

59
Q

How is tetralogy of fallot managed?

A

1st medical, then surgery at 6 months old

Medical: PG/ alprostadil to maintain PDA + reverse severe cyanosis

Severe/ prolonged cyanosis should be managed using a BT shunt from subclavian-pulmonary artery or balloon dilatation of RV outflow

60
Q

What is Eisenmenger syndrome?

A

Irreversibly raised pulmonary vascular resistance from chronically raised pulmonary arterial pressure + flow (ie from a large VSD or chronic PDA) which leads to formation of a right to left shunt

61
Q

Recall the pathophysiology of Eisenmenger syndrome

A

High pulmonary flow from large L-to-R shunt untreated
Artery wall thickens
Resistance increases
Eventually shunt decreases + child becomes less symptomatic
At 10-15y the shunt reverses as a teenager + they become blue + cyanotic

62
Q

How should Eisenmenger be managed?

A

Early intervention for pulmonary blood flow
Heart transplantation not easy but can be done

63
Q

What is the cause of congenital aortic/ pulmonary stenosis?

A

Partial fusion of valve leaflets

64
Q

What are the most likely co-existent conditions with aortic/pulmonary stenosis?

A

Coarctation of aorta + mitral valve stenosis

65
Q

What are the signs and symptoms of aortic/pulmonary stenosis?

A

NO CYANOSIS
AS: carotid thrill (ESM)
PS: no carotid thrill, harsh heart murmur at LSE (ESM)

66
Q

How should a/p stenosis be managed?

A

Transcatheter balloon dilatation

67
Q

When does coarctation of the aorta present?

A

3 days - a few weeks of life

68
Q

Recall some signs and symptoms of coarctation of the aorta

A

Sx: asymptomatic
Signs:
1. ESM
2. High BP in arms, low BP in legs

69
Q

How should coarctation be managed?

A

If sick infant: follow ABC + PG infusion guidelines

If well child –> surgical repair OR balloon angioplasty + stenting

70
Q

Recall the signs and symptoms of hypoplastic left heart syndrome

A

Often the sickest of all the left-outflow presentations
Will be cyanotic

71
Q

How should hypoplastic left heart syndrome be managed?

A

1st = ABCs + PG

2nd = Blalock-Taussig (BK) shunt or Norwood Stage 1

3rd = BK shunt removal –> Glenn/ hemi-Fontan –> Fontan/ Total Cavo-Pulmonary Connection

72
Q

What is a BK shunt?

A

Arterficial ductus arteriosus

73
Q

What HR is expected in SVT?

A

250-300bpm

74
Q

Recall the main symptom of SVT in neonates

A

Hydrops fetalis

75
Q

What would be seen on an ECG in SVT?

A

Narrow complex tachycardia + T wave inversion due to ischaemia

76
Q

How should SVT be managed?

A
  1. Circulatory + respiratory support (correct any tissue acidosis)
  2. Vagal stimulating manoevres - 80% success
  3. IV adenosine
  4. Electrical cardioversion with synchronised DC shock if adenosine fails
77
Q

What is the common cause of rheumatic fever?

A

Group A beta-haemolytic strep

78
Q

What age child can get rheumatic fever?

A

5-15 y/o

79
Q

What is the long term risk of rheumatic fever?

A

Mitral stenosis

80
Q

Describe the typical presentation of rheumatic fever

A

Latent interval of 2-6w after pharyngeal infection: polyarthritis
Pericarditis
Erythema marginatum (map-like outlines)

81
Q

What are the diagnostic criteria for rheumatic fever?

A

Jones criteria
2 majors / 1 major + 2 minors
Major = CASES
Carditis, Arthritis, SC nodules, Erythema marginatum, Sydenham’s chorea

Minor = FRAPP: fever, raised ESR/CRP, Arthralgia, Prolonged PR, Previous RF

82
Q

How should rheumatic fever be managed?

A

Anti-inflammatories
High dose aspirin (suppresses inflammatory responses in heart + joints)
Abx (if evidence of present infection)
Corticosteroids (if not resolved rapidly)

83
Q

What should be done following resolution of rheumatic fever?

A

Prophylatic monthly injections of benzyl penicillin until age 21
May need surgical valve repair

84
Q

Recall the signs and symptoms of infective endocarditis in a child

A

Necrotic skin lesions: from infected emboli
Splinter haemorrhages
Changing cardiac signs
Fever, aneamia, pallor
Splenomegaly
Arthritis/ arthralgia
Clubbing

85
Q

How is infective endocarditis diagnosed in children?

A

Multiple blood cultures (before ABx) + echocardiography to identify vegetations

86
Q

What is the most common pathogen implicated in paediatric IE?

A

Streptococcus viridians

87
Q

How should infective endocarditis be managed in children?

A

6 weeks IV Abx
Strep viridians (native/prosthetic valve) = amoxicillin + gentamicin/vancomycin

Staph aureus (native valve): Amoxicillin/ vancomycin/ daptomycin

Staph aureus (prosthetic valve): nafcillin/ oxacillin

88
Q

How is the liver affected by cardiac failure?

A

May see hepatomegaly

89
Q

How is the respiratory system affected by cardiac failure?

A

Increased RR
Recurrent chest infections

90
Q

What basic investigations are necessary in cardiac failure?

A

O2 sats
BP
FBC
U+Es
calcium
BNP/ANP

91
Q

Recall systematically the management of paediatric cardiac failure

A

Decrease preload: diuretics (furosemide)/ GTN

Enhance contractility: eg digoxin, dopamine, dobutamine

Reduce afterload: ACE inhibitors

Improve oxygen delivery: B-blockers (eg carvedilol)

92
Q

How should cyanosis be managed?

A

Prostaglandin infusion

93
Q

How would tetralogy of fallot present?

A

Cyanosis – possibly at rest depending on severity
Dyspnoea on feeding / crying / exertion
Failure to thrive
Murmur – usually harsh, and at the left sternal edge, grade 3-6.
- Due to pulmonary outflow obstruction rather than VSD
- Systolic thrill may also be present

94
Q

What is the most common congenital heart defect?

A

Tetralogy of Fallot

95
Q

What is a ‘tet spell’?

A
  • Sudden onset dyspnoea / cyanosis
  • Typically triggered by an event that slightly reduces O2 concentration (e.g. crying, defecating, feeding, distress)
  • Can be a vicious cycle, as the tet spell can make the child more distressed
  • Sometimes preceded by rapid, deep breathing
  • This increases venous return to the right ventricle, whose output is mainly via the aorta – and thus this is part of the vicious cycle

Severe spells can lead to death.

96
Q

Who do tet spells tend to affect?

A

Babies aged between 2 and 4 months old

97
Q

How may a toddler react to a tet spell?

A

Some toddlers may adopt a squatting position – which reduces venous return to the heart, and may help increase blood O2

98
Q

What are some risk factors for ToGA?

A

Maternal diabetes
Maternal smoking
Advanced maternal age

99
Q

Why is ToGA a ‘shunt-dependent’ defect?

A

Because infants survive only if a shunt between the two circulations exist to mix oxygenated blood into the systemic circulation such as:
- Patent ductus arteriosus (PDA)
- Ventricular septal defect (VSD)
- Atrial septal defect (ASD)
- Patent foramen ovale (PFO)

100
Q

What the normal HR ranges for a) under 1, b) 1-2, c) 2-5, d) 5-12 and e) >12?

A

<1: 110-160
1-2: 100-150
2-5: 95-140
5-12: 80-120
>12: 60-100 (normal adult range)

101
Q

What the normal RR ranges for a) under 1, b) 1-2, c) 2-5, d) 5-12 and e) >12?

A

<1: 30-40
1-2: 25-35
2-5: 25-30
5-12: 20-25
>12: 15-20

Year 5 - Paediatrics (15 decks)

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