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MRCPCH > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Failure of the palatine processes and the nasal septum to fuse

A

cleft palate

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2
Q

Failure of the aorticopulmonary septum to spiral during septation

A

transposition of the great arteries

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3
Q

Acyanotic congenital heart disease causes?

A

ventricular septal defects (VSD) - most common ~30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis

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4
Q

Causes of cyanotic congenital heart disease?

A

tetralogy of Fallot transposition of the great arteries (TGA) tricuspid atresia

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5
Q

Soft systolic murmur, musical/vibrating tone, best heard at LLSE, may disappear on standing

A

Still’s murmur (innocent)

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6
Q

Pansystolic murmur at LLSE, may be associated with a thrill, split or loud single S2

A

Ventricular septal defect

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7
Q

Systolic ejection murmur best heard at ULSE, wide split fixed S2, sometimes associated diastolic flow rumble at LLSE

A

Atrial septal defect

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8
Q

Continuous machinery murmur at the ULSE, often associated with a thrill

A

Patent ductus arteriosus

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9
Q

Systolic ejection murmur heard at ULSE and LLSE, thrill palpable at the ULSE, single S2

A

Tetralogy of Fallot

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10
Q

Pansystolic murmur at LLSE or midsternal border, may have a mid-diastolic murmur at the apex, single S2

A

Tricuspid atresia

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11
Q

Systolic ejection murmur at LSE, hyperdynamic precordium, single S2

A

Hypoplastic left heart syndrome

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12
Q

Low-pitched, quiet mid-systolic ejection murmur in axilla or back

A

Peripheral pulmonary stenosis (innocent)

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13
Q

Systolic ejection murmur at the ULSE with radiation to back, axilla, infraclavicular area, sometimes a “click” is heard, loud S1

A

Pulmonary stenosis

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14
Q

Systolic ejection murmur at URSE with radiation to carotid arteries, left ventricular heave, and possible thrill

A

Aortic stenosis

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15
Q

Systolic murmur at LLSE and mid-diastolic murmur at apex, single S2

A

Transposition of the great arteries

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16
Q

Systolic ejection murmur at ULSE, mid-diastolic flow rumble at LLSE, wide split fixed S2

A

Total Anomalous Pulmonary Venous Drainage

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17
Q

Systolic murmur, mid-diastolic rumble

A

Truncus arteriosus

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18
Q

Most common cardiovascular abnormality in William’s syndrome?

A

Supravalvular aortic stenosis 2nd most common: pulmonary artery stenosis other; Mitral valve regurgitation and prolapse

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19
Q

2nd most common cardiovasc abnormality in William’s syndrome?

A

Pulmonary artery stenosis 1st most common: Supravalvular aortic stenosis Other: Mitral valve regurgitation and prolapse

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20
Q

CATCH 22?

A

Cardiac defects Abnormal facial features Thymic aplasia/hypoplasia Cleft palate Hypocalcemia/Hypoparathyroidism 22- Due to 22q11 deletion

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21
Q

ECG changes of hypercalcaemia?

A

Tall T waves, Reduced QT, Prolonged and depressed ST, Arrhythmia

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22
Q

ECG changes of hyperK?

A

Tall T waves ST- changes Reduced QT interval Increased PR interval Smaller or absent P waves Widened QRS, broadening to VF

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23
Q

ECG changes of hypoK?

A

Flat T waves ST depression U wave Atrial and ventricular ectopics VF and VT

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24
Q

ECG changes of hypoCa?

A

Prolonged QT Prolonged ST Flat or absent T waves U waves

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25
Q

Differences in ECG in children under age 3/4 compared to teenagers?

A

In neonates, the RV is thicker than the left and the L becomes dominant age 3/4: right ventricular hypertrophy changes include: R axis deviation T-wave inversions in V1, V2, and V3 Dominant R wave in V1

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26
Q

ECG findings in transposition of great arteries?

A

R axis deviation

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27
Q

CXR findings in transposition of great arteries?

A

Cardiomegaly, increased pulmonary markings

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28
Q

Definitive treatment of transposition of great arteries?

A

atrial switch operation (Rastelli procedure)

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29
Q

Mx of transposition of great arteries?

A

Interim balloon atrial septostomy Definitive: atrial switch operation (Rastelli procedure)

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30
Q

what does ghrelin do?

A

ghrelin stimulates hunger. It is produced mainly by the P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels increase before meals and decrease after meals

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31
Q

what does leptin do?

A

leptin decreases appetite. It is produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite. More adipose tissue -> high leptin levels. Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)

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32
Q

Most common underlying cause of infective endocarditis in children?

A

VSD, followed by tetralogy of fallot

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33
Q

Most common IE causative organism in children?

A

Staphylococcus aureus, followed by Streptococcus viridans

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34
Q

what are Osler’s nodes?

A

immune complex deposits painful, red, nodes found on hands and feet immunologic signs are 1 /6 minor criteria for Duke’s

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35
Q

What are Janeway lesions?

A

micro-abscesses: small, non-tender nodes or macules on the palms vascular signs are 1/6 minor criteria for Dukes

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36
Q

Examples of vascular signs of infective endocarditis?

A
  • Major arterial emboli - Septic pulmonary infarct - Mycotic aneurysm - Intracranial haemorrhage - Conjunctival haemorrhage - Janeway lesions
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37
Q

Examples of immunologic signs of infective endocarditis?

A
  • Glomerulonephritis - Osler’s nodes - Roth spots - Rheumatoid factor
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38
Q

Echo findings that constitute major criteria in Duke’s for infective endocarditis?

A
  • Abscess - New partial dehiscence of prosthetic valve - New valvular regurgitation - Oscillating intracardiac mass on valve or supporting structures
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39
Q

Duke’s criteria for IE: major criteria

A

Characteristic positive blood culture for typical infective endocarditis organisms Characteristic ECHO findings*

40
Q

Duke’s criteria for IE: minor criteria

A
  • Underlying heart condition - Temp > 38.0° C - Vascular signs** - Immunological signs *** - Positive blood cultures not meeting major criteria - ECHO findings not meeting major criteria
41
Q

Duke’s criteria for IE: what is diagnostic?

A

2 major criteria is diagnostic 1 major criteria and 3 minor criteria is diagnostic 5 minor criteria is diagnostic

42
Q

normal range of HR for a newborn?

A

110-150

43
Q

normal range of HR in 2 yo?

A

85-125

44
Q

normal range of HR in 4yo?

A

75 - 115

45
Q

normal range of HR in >6yo?

A

60-100

46
Q

What is the Fontan procedure?

A

used in children with univentricular hearts. involves diverting the venous blood from the IVC and SVC to the pulmonary arteries without passing through the RV.

47
Q

most common organism for IE in patients with indwelling lines/ following prosthetic valve surgery?

A

Staphylococcus epidermidis

48
Q

what organism for IE is linked with poor dental hygiene or following a dental procedure?

A

Streptococcus viridans: ie. Streptococcus mitis and Streptococcus sanguinis.

49
Q

what organism for IE is associated with colorectal cancer?

A

Strep bovis

50
Q

Associations of Wolff Parkinson white?

A

HOCM mitral valve prolapse Ebstein’s anomaly thyrotoxicosis secundum ASD

51
Q

Management of WPW?

A

definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide avoid sotalol if co-existing AF.

52
Q

Failure of the _______ to develop properly will result in a ventricular septal defect.

A

endocardial cushions

53
Q

Starlings law?

A
  • Increase in end diastolic volume will produce larger stroke volume. This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.
54
Q

Laplace’s law in cardiac physiology?

A

explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function.

55
Q

Bainbridge reflex?

A

Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors - normally Increased blood volume will cause increased parasympathetic activity

56
Q

Who is offered screening by a fetal cardiologist in the antenatal period?

A

if:

  • abnormal four-chamber view on routine/ anomaly scan
  • increased nuchal translucency (also increases risk of Down’s)
  • Previous child/ FHx of CHD
  • Maternal risk: e.g. Phenylketonuria, DM
  • Suspected Down’s/ other syndrome
57
Q

Echodensity on anterior mitral valve papillary muscle found on fetal echocardiogram?

A
  • ie ‘golf valls’

thought to be calcification during development

no importance for CHD

assoc w Down’s Syndrome

no need for echo after delivery

58
Q

Arrhythmias in fetus in antenatal period:

what investigations are required?

A

Echo required

  • to confirm normal anatomy
  • to confirm type of arrhythmia
  • fetal ECG is not yet routine
  • presence of hydrops is a poor prognostic sign
59
Q

Arrhythmias in fetus in antenatal period: management of multiple atrial ectopics?

A

Usually not treated

60
Q

Arrhythmias in fetus in antenatal period: management of SVT?

A

Usually with maternal digoxin or flecainide

61
Q

Arrhythmias in fetus in antenatal period: management of Heart Block?

A

maternal isoprenaline or salbutamol

62
Q

Most common Congenital heart defects?

A

VSD - 30%

Persistent arterial duct - 12%

ASD - 7%

Pulmonary Stenosis - 7%

63
Q

Which family history increases risk of Congenital heart disease the most?

A

Mother with CHD

64
Q

Risk factors of congenital heart disease?

A

Family history: mother/ father w CHD, siblings with CHD

Presence of other anomaly/ syndrome

Parents w abnormal genotype

Maternal lithium use (ebstein anomaly)

3rd trimester enterovius/ Coxsackievirus -> myocarditis, dilated cardiomyopathy

Maternal SLE (anti-ro/la abs -> complete heart block)

65
Q

cardiac symptoms to ask in a history?

A
  • heart failure: breathelessness, poor feeding, faltering growth, cold hands/feet
  • cyanosis
  • neonatal collapse
66
Q

apart from symptoms of the child, what are important questions in a cardiac history?

A
  • was child born preterm?
  • asymptomatic heart murmur found on routine exam?
  • syndrome ie. Downs?
  • family history of CHD
  • did mother have any illnesses/ take any medication during pregnancy?
67
Q

Examination of child for congenital heart disease:

bedside signs?

A

dysmorphism

obvious cyanosis or scars

68
Q

Examination of child for congenital heart disease:

what are some findings suggestive of heart failure?

A
  • thin, malnourished child (faltering growth)
  • excessive sweating around the forehead
  • tachycardia
  • SOB ± subcostal/ intercostal recession
  • Poor peripheral perfusion w cold hands/ feet
  • large liver
69
Q

Finding of heart failure in a neonate in up to 7 days of life suggests ?

A

an emergency

implies a duct dependent lesion

e.g. Hypoplastic left heart/ coarctation

70
Q

What is the second heart sound composed of?

A

closure of first the aortic and then the pulmonary valves

71
Q

What causes fixed splitting of second heart sound?

*Listen at mid-left sternal edge in expiration

A

ASD

RBBB

72
Q

What causes a single second heart sound?

A

Transposition of Great arteries

Pulmonary atresia

Hypoplastic Left Heart Syndrome

73
Q

What causes a quiet second heart sound?

A

Pulmonary valve stenosis

Pulmonary artery band

74
Q

Ejection systolic murmur at ULSE?

A

Pulmonary stenosis

or

ASD

75
Q

Ejection systolic murmur at mid/ lower left sternal edge?

A

possible innocent murmur

76
Q

Long harsh systolic murmur + cyanosis?

A

Tetralogy of Fallot

77
Q

Ejection systolic murmur at URSE?

A

Aortic stenosis (with carotid thrill)

78
Q

Pansystolic murmur at lower left sternal edge +/- thrill?

A

VSD

79
Q

Continous murmur at any other site (ie lungs, shoulder, head, hind-quarter)?

A

AV fistula

80
Q

Continuous murmur infraclavicular + cyanosis + lateral thoracotomy?

A

BT (Blalock-Taussig Shunt)

  • surgical procedure to increase blood flow to lungs ie. shunt from branch of subclavian/ carotid artery to pulmonary art.
  • typically to relieve cyanosis while infant is waiting for corrective/ definitive surgery
81
Q

Median sternotomy + diastolic murmur +/- Pulmonary stenosis murmur

A

Tetralogy of Fallot, repaired

82
Q

features of an innocent murmur?

A

soft (no thrill)

systolic

short (never pansystolic)

asymptomatic

left sternal edge

may change w posture

diastolic murmurs are not innocent

83
Q

what happens to pulmonary vascular and pulmonary arterial pressure after fetal life?

A
  • pulmonary vascular resistance falls rapidly in the first few breaths, continues until 3 months of age
  • pulmonary arterial pressure falls
84
Q

from fetal life to normal child: what closes?

A
85
Q

causes of small arterial pulse volume?

A

cardiac failure

hypovolaemia

vasoconstriction

86
Q

causes of large arterial pulse volume?

A

vasodilation

pyrexia

anaemia

aortic regurg

hyperthyroid

CO2 retention

87
Q

Pulsus paradoxus?

A

exaggeration of normal rise and fall of BP with respiration, seen in airway obstruction, such as asthma

88
Q

Management of SVT in child?

in infants: rate usually >220 bpm

A

If haemodynamically stable:

vagal manoeuvre + IV adenosine

if shock / difficult access:

repeated synchronous DC shocks without delay if vagal manoeuvre is unsuccessful

89
Q

Secundum ASD vs Primum ASD (partial AVSD)

A

Secundum ASD:

middle

  • defect in the centre of the atrial septum involving the fossa ovalis

Primum ASD:

lower

  • a defect in the lower atrial septum, involving the left AV valve which has three leaflets and tends to leak
90
Q

Clinical features of ASD:

A

asymptomatic

80% ASD = secundum, 10% are primum

soft systolic murmur at LSE

Fixed split S2 (difficult to hear)

In primum: apical pansystolic murmur (AV valve regurgitation)

91
Q

ECG findings in ASD?

A

Partial RBBB

RVH

In primum: superior axis

92
Q

CXR findings in ASD?

A

Increased pulmonary vascular markings

93
Q

Management of ASD?

secundum vs primum

A
  • Closure at 3-5 years (ideally)
  • Secundum: 90% undergo device closure in cath lab

10% undergo surgical closure (too large/ personal preference)

  • Primum: all require surgical closure (bc need to repair valve)
94
Q

A defect at the upper end of the atrial septum, such that the SVC overrides the atrial septum. The right pulmonary veins are usually anomalous and drain directly into the SVC or right atrium adding to the L->R shunt.

A

Sinus Venosus ASD

95
Q

Management of Sinus venosus ASD?

A

Closure at 1- 5 years

All require surgical closure and repair to anomalous pulmonary veins.

5% of ASDs

96
Q
A

MRCPCH (27 decks)

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