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Pediatrics > Congenital heart disease > Flashcards

Congenital heart disease Flashcards

1
Q

Most common congenital malformation and incidence

A

Congenital heart disease 7-8/1000

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2
Q

Anomaly with fetal lithium exposure

A

Ebstein’s anomaly

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3
Q

CHD that typically presents in the newborn period (4)

A

Coarctation of the aorta Transposition of the great arteries Tetralogy of fallot Patent ductus arteriosus

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4
Q

Defects causing left to right shunt (2)

A

VSD ASD

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5
Q

Obstructive lesions (2)

A

Aortic stenosis Pulmonary stenosis

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6
Q

CHD presenting with shock, %,, murmur

A

VSD AVSD PDA

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7
Q

CHD presenting with a murmur, %, murmur

A

Pulmonary valve stenosis Atrial septal defect

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8
Q

Presenting with cyanosis

A

Tetralogy of fallot Transposition of the great arteries

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9
Q

Paediatric circulation from placenta

A

oxygenated blood from placenta–> umbilical vein–> ductus venosus–> IVC–> R atrium–> shunted through foramen ovale–> L atrium–> L ventricle–> aorta–> brain/myocardium/ upper extremities

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10
Q

Paediatric circulation from deoxygenated blood returning via SVC

A

deoxygenated blood returns via SVC to R atrium–> 1/3 of blood entering R atrium does not flow through foramen ovale and flows to the R ventricle–> pulmonary arteries–> ductus arteriosus–> aorta–> systemic circulation placenta for reoxygenation

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11
Q

Most critical time for fetal heart development

A

Critical stage at 3-8 weeks

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12
Q

What is the shunt for deoxygenated blood

A

Ductus arteriosus

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13
Q

What are the shunts for oxygenated blood (2)

A

Foramen ovale Ductus venosous

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14
Q

What does the ductus venosous connect

A

Umbilical vein and IVC->bypassing the liver

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15
Q

Changes in circulation at birth

A
  1. First breath->lung open-> -ve pulmonary resistance= +pulmonic blood flow 2. Separation of low resistance placenta->systemic circulation becomes high resistance system -> ductus venosus closure 3. Increased pulmonic flow -> +left atrial pressure->foramen ovale closure 4. +oxygen concentration in blood after first breath= -ve prostaglandins-> ductus arteriosus closure 5. Closure of fetal shunts and changes in vascular resistance->infant circulation assumes normal adult adult flow
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16
Q

Epidemiology, common presentations, most common lesio

A

Number of live briths: 8/1000 Heart murmur Heart failure Cyanosis VSD most common

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17
Q

Investigations

A

Echo ECG CXR

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18
Q

At what concentration of deoxy Hb does cyanosis occur

A

At least 3g/dL

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19
Q

Pathogenesis of acyanotic

A

acyanotic heart disease: (i.e. L to R shunt, obstruction occurring beyond lungs) blood passes through pulmonic circulation g oxygenation takes place –> low levels of deoxygenated blood in systemic circulation –> no cyanosis

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20
Q

Division of acyanotic HD

A
  1. Left to right shunt: ASD, VSD, PDA, AVSD 2. Obstructive->CA, AS, PS
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21
Q

Division of cyanotic

A
  1. R->L shunt: TOF, ebstein’s anomaly 2. Other: TGA, total anomalous pulmonary venous drainage, tricuspid atresia
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22
Q

Complications/progression of L to R shunt

A

Pulmonary vascular disease Left ventricular dilatation and dysfunction RV hypertension and hypertrophy R to L shunts

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23
Q

Types of ASD

A

ostium primum (common in Down syndrome), ostium secundum (most common type, 50-70%), sinus venosus (defect located at entry of superior vena cava into right atrium

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24
Q

How common are ASD

A

Responsible for 5% CHD

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25
Q

Spontaneous closure rate of ASD

A

Spontaneous closure in 80-100% when

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26
Q

History of ASD

A

Asymptomatic common in childhood May present with HF / pulmonary hypertension later in adulthood

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27
Q

Physical examination in ASD: palpation, auscultation

A

Palpation: Normal, may have RV+ Auscultation: +flow to right, low pitch diastolic, TR, pulmonary ejection murmur Fixed splitting P2 No direct murmur

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28
Q

Investigations in ASD

A

Echo CXR ECG

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29
Q

Management of ASD

A

left-to-right shunt 1st line: observation adjunct: corrective closure adjunct: prophylactic antibiotics->after closure for 6 months (amoxicillin) right-to-left shunt reversible 1st line: corrective closure plus: prophylactic antibiotics irreversible (Eisenmenger’s syndrome) 1st line: supportive medical therapy with pulmonary vasodilators->bosentan plus: monitoring and treatment of hyperviscosity plus: prophylactic antibiotics 2nd line: heart-lung transplantation

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30
Q

Why do patients with eisenmenger’s develop a hyperviscocity

A

To cope with the hypoxemia

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31
Q

Most common CHD

A

Ventricular septal defect

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32
Q

Causes of VSD

A

Congenital Alcoholism MI

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33
Q

Most common location of VSD

A

Interventricular septum

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34
Q

Presentation if small VSD

A

Asymptomatic, normal growth and development Early/holosystolic murmur, LLSB

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35
Q

Investigations in VSD when small and management

A

CXR and echo are normal Most will close spontaneously

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36
Q

Moderate to large VSD: CHF presentation, clinical history, PE findings

A

CHF by 2 monthsd Pulmonary hypertension Clinically can have delayed growth, -ve exercise tolerance, recurrent URTI/asthma episodes PE: Holosystolic LLSB S3, S4 +on expiration, Loudness ++when small RV heave

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37
Q

Investigation findings when moderate VSD

A

CXR: +pulmonary vasculature, ECG: biventricular hypertrophy Cardiomegaly, CHF

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38
Q

Management of moderate VSD

A

Treat CHF and surgical closure by 1 year old

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39
Q

Complications of VSD

A
  1. Endocarditis 2. Progressive aortic regurgitation 3. CHF 4. Pulmonary hypertension and refersal
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40
Q

Management of VSD

A

congenital: small 1st line: observation adjunct: prophylactic antibiotics congenital: medium or large asymptomatic 1st line: corrective closure adjunct: prophylactic antibiotics symptomatic with left-to-right shunt 1st line: preoperative medical therapy plus: corrective closure adjunct: prophylactic antibiotics symptomatic with right-to-left shunt (Eisenmenger’s syndrome) 1st line: supportive medical therapy with pulmonary vasodilators plus: prophylactic antibiotics adjunct: monitoring and treatment of hyper-viscosity 2nd line: heart-lung transplantation

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41
Q

Functional and anatomical closure of PDA

A

Functional closure at 15 hours, anatomical closure within first few days

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42
Q

When is closure delayed, and is this different to PDA in term

A

Delayed in prematurity, different to term

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43
Q

When is spontaneous closure more common

A

Premature infants

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44
Q

Clinical presentations

A

If small may be asymptomatic TacyP Failure to thrive SOB +respiratory symptoms of URTI

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45
Q

Risk factors

A

Prematurity Maternal rubella Female

46
Q

Clinical examination findings

A

TacyP Bounding pulse Wide pulse pressure Hyperdynamic praecordium Systolic thrill Continous machinery murmur

47
Q

Investigations and findings

A

ECG: deep Q, tall R waves in 2,3,aVF, V5, V6. May have widened P wave suggesting LAE, LVH, RVH CXR: cardiomegaly, +pulmonary vascular markings Echo: Two-dimensional and/or colour Doppler evidence of a PDA. Diastolic forward flow in the pulmonary artery. Left ventricular and/or left atrial enlargement. Diastolic flow reversal in the distal aortic arch

48
Q

When is surgery contraindicated in PDA

A

When pulmonary disease, right to left shunt

49
Q

Management of PDA: premature, term/children, smptomatic and too small

A

Premature: Indomethacin (or ibuprofen) in premature Surgery->ligation Term and children: Percutaneous catheter closure Frusemide->if not large enough for surgery just yet and are symptomatic- can give time for them to grow Term/symptomatic and too small for percutaneous device closure: surgical ligation

50
Q

When is surgery for PDA generally indicated

A

When medical therapy has failed

51
Q

Is indomethacin ever given prophylactically

A

Yes, in the very low birth weight infants to avoid the hemodynamic challenges

52
Q

What is used if the DA needs to be kept open and in what situation may this be required

A

Prostaglandin E Transposition of the great arteries

53
Q

How do infants with obstructive lesions present

A

Pallor Cool extremities Fatigue Reduced urine output Cardiogenic shock

54
Q

Coarctation of the aorta general features

A

Narrowing of aorta- most commonly at division of left subclavian/ligamentum arteriosa

55
Q

Clinical features

A
  1. HTN in upper extremities with hypotension in lower extremities 2. Well-developed upper body with underdeveloped lower half 3. Midsystolic murmur heard best over the back 4. Symptoms include headache, cold extremities, claudication with exercise, and leg fatigue. 5. Delayed femoral pulses when compared to radial pulses 6. Prevalence of coarctation of the aorta is increased in patients with Turner’s syndrome
56
Q

Risk factors for COA

A

Strong male gender young age Turner’s syndrome DiGeorge’s syndrome Cardiac defects include tetralogy of Fallot, interruption of aortic arch, aortic coarctation, truncus arteriosus, and ventricular septal defects. hypoplastic left heart syndrome Shone’s complex PHACE syndrome

57
Q

Features of PHACE syndrome

A

A rare syndrome in which the association: 1. Posterior fossa malformations, 2. Haemangioma, 3. Arterial anomalies, 4. Cardiovascular anomalies 5. Eye abnormalities

58
Q

CHD seen in Digeorge

A

Tetralogy of Fallot, interruption of aortic arch, aortic coarctation, truncus arteriosus, and ventricular septal defects.

59
Q

Investigations and findings in COA

A
  1. ECG shows LVH. 2. CXR a. Notching of the ribs b. “Figure 3” appearance due to indentation of the aorta at site of coarctation, with dilation before and after the stenosis 3. Echo: discrete narrowing in the thoracic aorta; pressure gradient across narrowing
60
Q

Complications of COA

A

Severe treatment resistant hypertension Rupture of cerebral aneurysms Infective endocarditis Aortic dissection/aneurysm

61
Q

Management: critical in neonates, non critical 1y, recurrent

A

Critical: alprostadil + surgical repair Non critical: 1y: surgical repair or percutaneous angioplasty with or without stent implantation Recurrent: percutaneous angioplasty

62
Q

Types of aortic stenosis

A
  1. valvular (75%) 2. subvalvular (20%), 3. supravalvular 4. idiopathic hypertrophic subaortic stenosis (IHSS) (5%)
63
Q

Clinical presentation of AS

A

presence of risk factors dyspnoea chest pain syncope

64
Q

Risk factors for AS

A

Strong age >60 years congenitally bicuspid aortic valve rheumatic heart disease chronic kidney disease->calcification

65
Q

Examination findings AS

A

systolic murmur ≥3/6, with a diamond-shaped crescendo-decrescendo pattern that peaks in mid-systole and radiates to the carotid arteries. RUSB A2 prolonged Expiration, the pulmonic sound (P2) is heard before A2 in severe

66
Q

Can people with AS bleed more

A

Yes, can develop an acquired vWD

67
Q

Grading of murmurs

A

Murmurs are generally graded on a scale of 1 to 6: Grade 1: murmur is faint and heard only with effort Grade 2: murmur is faint but easily detected Grade 3: murmur is loud Grade 4: murmur is very loud and associated with a palpable thrill Grade 5: murmur is so loud that it can be heard with only the edge of the stethoscope Grade 6: murmur is extremely loud and heard even when the stethoscope is no longer in contact with the patient.

68
Q

Severity of AS classification

A

Mild: Jet velocity 1.5 cm^2 Moderate: Jet velocity 3.0 to 4.0 m/second Mean pressure gradient 25 to 40 mmHg Valve area 1.0 to 1.5 cm^2 Severe: Jet velocity >4.0 m/second Mean pressure gradient >40 mmHg Valve area

69
Q

Investigations and findings in AS

A

Transthoracic echo: elevated aortic pressure gradient; measurement of valve area and left ventricular ejection function ECG: may demonstrate left ventricular hypertrophy and absent Q waves, AV block, hemiblock, or bundle branch block

70
Q

Management overview AS

A
  1. Surgical valve replacement 2. Anticoagulation 3. Endocarditis prophylaxis
71
Q

General characteristics of TOF

A

Overriding aorta Pulmonary steonsis VSD Right ventricular hypertrophy

72
Q

Clinical features in TOF

A

Cyanosis Tachypnoea Tet spells Murmur is typically crescendo–decrescendo in nature and heard best at the left upper sterna border. Parasternal impulse, heave

73
Q

What are Tet spells and what is their purpose

A

Patient with TOF will squat following exertion (exercise, crying)->+SVR->able to shunt blood to the lungs rather than the aorta

74
Q

Investigations and findings in TOF

A

Pulse oximetry: low oxygenation CXR: boot shaped Echo: overriding aorta, RVH, pulmonary stenosis, VSD ECG: RVH with a rightwards axis, R in V1 and S in V6 above age-appropriate normals

75
Q

Management of hypercyanotic spells

A

Manouevres to +venous return->knees to chest Supportive: fluids, morphine to calm, oxygen (but try not to ++activity) 2nd line: beta blockers 3rd line: phenylephrine

76
Q

How are beta blockers thought to help during hypercyanotic spells

A

helps to decrease the infundibular obstruction by decreasing the heart rate, prolonging diastolic filling, and decreasing contractility

77
Q

How does phenylephrine work to help in hypercyanotic spells of TOF

A

It increases SVR->shunting more blood to lungs

78
Q

Management of infant with unremitting cyanosis of TOF

A

surgical shunt + extracorporeal membrane oxygenation (ECMO)

79
Q

Management of infant with severe cyanosis and limited pulmonary flow

A

Alprostadil and supportive->fluid, morphine, bicarb, oxygen

80
Q

Ongoing/long term management of TOF

A

Surgical repair Monitoring with possible pulmonary valve replacement Endocarditis prophylaxis

81
Q

Endocarditis prophylaxis

A

Cephalexin in cardiac or amox/ampicillin preferred for dental

82
Q

What is the most common cyanotic heart disease of the neonate

A

Transposition of the great arteries

83
Q

Pathophysiology of TGA

A

parallel pulmonary and systemic circulations ƒƒsystemic: body  RA  RV  aorta  body ƒƒpulmonary: lungs  LA  LV  pulmonary artery  lungs ƒƒsurvival is dependent on mixing through PDA and/or atrial or ventricular septal defects

84
Q

Physical examination in TGA

A

With closure of the PDA->rapid progression to severe hypoxemia, unresponsive to oxygen therapy VSD: murmur, cyanosis not prominent->progression to CHF in first few weeks No VSD: absent murmur

85
Q

Investigations and findings in VSD

A

ECG: RAD/RVH, or may be normal CXR: egg on a string appearance

86
Q

Management of TGA

A

ƒƒsymptomatic neonates: prostaglandin E1 infusion to keep ductus open until balloon atrial septostomy followed by switch procedure ƒsurgical repair: arterial switch performed in the first two weeks in those without a VSD while LV muscle is still strong

87
Q

Commonest cause of death from CHD in first month of life

A

LV hypoplasia may include atretic or stenotic mitral and/or aortic valve, small ascending aorta, and coarctation of the aorta with resultant systemic hypoperfusion systemic circulation is dependent on ductus patency; upon closure of the ductus, infant presents with circulatory shock and metabolic acidosi

88
Q

Management of Hypoplastic left heart syndrome

A

Intubate Correct metabolic acidosis IV infusion of alprostadil Surgical palliation or heart transplant

89
Q

Characteristics of innocent murmurs

A

Systolic and musical No clinical significance Do not radiate Change with position. Soft <3/6. The rest of the examination is normal

90
Q

Venous hum

A

Blowing continuous in systole and diastole Heard below the clavicles Disappears on lying down

91
Q

Pulmonary flow murmur

A

Brief high pitched Best heard with child lying down

92
Q

History taking with a murmur

A

Fatigue Breathlessness Family history Antenatal->maternal medications, syndromes etc

93
Q

Physical examination in murmur

A

Murmur Signs of heart failure-> FTT, poor growth, tachyC/P, crepitations, hepatomegaly Pulse and BO Sternal heave Cyanosis->unlikely finding in children presenting with a murmur

94
Q

Investigations in CHD

A

Echocardiograph CXR ECG 24 hr ECG->if palpitations/syncope Cardiac catheterisation

95
Q

What is this murmur

A

Aortic stenosis

96
Q

What is this murmur

A

Mitral regurgitations

97
Q

What is this murmur

A

Aortic insufficiency

98
Q

What is this murmur

A

Mitral stenosis

99
Q

What is this murmur

A

ASD

100
Q

What is this murmur

A

Benign

101
Q

What is this murmur

A

VSD

102
Q

What is this murmur

A

PDA

103
Q

What is this murmur

A

S3

104
Q

What is this murmur

A

S4

105
Q

What is this murmur

A

Split S2

106
Q

Why is polycythemia important in cyanosis

A

Can lead to to more apparent cyanosis

107
Q

What CHD can cause cyanosis in first 24 hours of life

A

TGA

Pulmonary atresia

Tricuspid atresia

108
Q

Which cyanotic CHD is more common in the diabetic mother

A

TGA is 20 times more common in diabetic mothers

109
Q

Categories of CHD severity

A
  1. Minor

Little ot no hemodynamic impact/no functional impact

Small VSD

Trivial PVS

Bicuspid aortic valve

Small ASD

  1. Moderate

HemoD impact may produce long term complications, intervention required

ASD w/ V dilation

Coarctation >few months of age

VSD impeding flow

Anomalous pulmonary venous return

  1. Severe

Major hemodynamic impact

Single ventricle

TGA

TOF

Large VSD

110
Q

Clinical features in early weeks may suggest CHD

A
  1. Cyanosis
  2. Dusky
  3. Dysmorphic
  4. TachyP
  5. Poor feeding, poor weight gain
  6. Overactive praecordium
  7. Murmur

Pediatrics (58 decks)

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