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Cardiology > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

1
Q

what occurs in atrial septal defect?

A

the atrial septum remains open

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2
Q

the atrial septal defect causes what change to bloodflow?

A

Pressure difference between left (higher) and right (lower) causes blood to be shunted from left atrium to right atrium

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3
Q

what are the consequences of shunting in ASD?

A

cyanotic as less oxygenated blood being in left ventricle

Extra blood volume pulmonic valve causes a delay

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4
Q

what normally occurs to the atrial septum at birth?

A

o At birth septum secundum and septum primum slap shut and then fuse and close off this foramen ovale

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5
Q

what is the first step of atrial septum development?

A

Formation of ostium primum

Septum primum between left and right atria grows downwards and fuses with endocardial cushion and closes gap completely

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6
Q

what is the third step of atrial septum development?

A

Formation of makeshift valve which allows blood to flow through foramen ovale and ostium primum – one way blood flow from right to left atrium

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7
Q

what is the second step of atrial septum development?

A

ostium secundum opens up on the upper septum primum
septum secundum which grows downwards just right to septum primum and covers ostium secundem, leaving a small opening called foramen ovale

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8
Q

what are the 3 categories of causes of ASD?

A

problems with ostium secundum (70%)
problems with ostium primum
foetal alcohol syndrome

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9
Q

What is the cause of problems with the ostium secundum in ASD?

A

o Doesn’t grow enough in development

o Associated with Holt-Oram syndrome

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10
Q

what is the cause of problems with the ostium primum in ASD?

A

o Associated with abnormal AV valves

o Doesn’t grow the whole way down

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11
Q

what are the clinical features of atrial septal defects?

A

Pulmonary hypertension, Cyanosis, Arrhythmias, Haemoptysis, Chest pain, AF, Raised JVP, Increased frequency of migraines

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12
Q

what heart sounds may be heard in atrial septal defect

A
  • Fixed split of S2 pulmonary ejection systolic murmur

* PH may cause pulmonary or tricuspid regurgitation

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13
Q

what investigations can be done for atrial septal defects?

A

ECG, CXR, echo, Cardiac catherization

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14
Q

what are the ECG features of ASD caused by problems with Ostium Secundum?

A

RBBB with RAD

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15
Q

what are the ECG features of ASD caused by problems with Ostium Primum?

A

RBBB with LAD, prolonged PR interval

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16
Q

what are the CXR features of ASD?

A

small aortic knuckle, pulmonary plethora, progressive atrial enlargement

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17
Q

which investigations is diagnostic for ASD?

A

Echo

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18
Q

what will cardiac catherization show in ASD?

A

increased O2 sats in atrium

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19
Q

what is the treatment of small ASD?

A

watch and wait, may close on their own

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20
Q

what is the treatment of large ASDs?

A

transcatheter closure more common than surgery

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21
Q

what is a complication of ASD?

A

embolisms

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22
Q

how does the ventricular septum form?

A

o Septum forms as a muscular ridge tissue that grows upward from the apex
o Fuses with a membranous region growing downwards from endocardial cushion

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23
Q

what is the mechanism of ventricular septum defect?

A

if the septum doesn’t grow or fuse there will be a gap

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24
Q

what is the consequence of VSD?

A

oxygenated blood flows from left atrium to right atrium - less oxygenated blood pumped to body

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25
Q

what changes occur in the heart as a result of VSD?

A

Higher o2 saturation in right ventricle and pulmonary artery

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26
Q

what can be heard in VSD?

A

Harsh pan systolic murmur at left sternal edge with systolic thrill and left parasternal heave

27
Q

what are the causes of VSD?

A
  • Congenital – down syndrome
  • Acquired – post MI
  • Foetal alcohol syndrome
  • Other cardiac deformities
28
Q

what are the clinical features in small VSD?

A

asymptomatic

29
Q

what clincial features are present in large VSDs?

A

earlier onset, more severe
pulmonary hypertension
cyanosis

30
Q

what investigations can be done in VSD?

A

ECG, CXR, echo, cardiac catheterization

31
Q

what are the features of an ECG in VSD?

A

normal
LAD + LVH
LVH + RVH

32
Q

what are the CXR features of VSD?

A

normal heart size + mild pulmonary plethora

33
Q

what will cardiac catherization show in VSD?

A

raised O2 in right ventricle?

34
Q

what are the treatment options for VSD?

A

watch and wait
medical management
surgical management

35
Q

what are the epidemiological factors of PDA?

A
  • 5-10% of congenital heart defects

* 3x more common in females

36
Q

PDA is more common in…

A

premature infants

37
Q

what is the ductus arteriosus?

A

Blood vessel that connects pulmonary artery to aorta during fetal development - bypasses lungs

38
Q

what normally happens to the ductus arteriosus?

A

• Normally closes after birth and becomes a ligament – ligamentum arteriosum

39
Q

when does PDA occur?

A

if the ductus arteriosus remains open after birth

40
Q

what keeps the ductus arteriosus open during development

A

vasodilator – prostaglandin E2 (made by placenta and DA)

41
Q

what causes the ductus arteriosus to close at birth?

A

At birth O2 levels go up and lungs become main source of oxygenated blood
Foramen ovale closes and prostaglandin E2 fall, causing ductus arterious to close
Lungs release bradykinin which constricts smooth muscle wall of ductus arteriosus

42
Q

what are the causes of PDA?

A
  • 90% isolated

* 10% other causes – rubella

43
Q

what sound is heard in PDA?

A

Holosystolic machine like murmur

44
Q

what are the clinical symptoms of small PDAs?

A

asymptomatic

45
Q

what are the clinical features of large PDAs?

A

Premature infants – respiratory distress, apnoea, critically unwell
Other infants/children – signs of HF (Tachycardia, tachypnoea, poor feeding, failure to thrive, SOB on feeding)

46
Q

What investigations ca be done in PDA?

A

Echo, ECG, CXR

47
Q

which investigation is diagnostic in PDA?

A

Echo

48
Q

what ECG features are present in PDA?

A

signs of LVH

49
Q

what signs on CXR are present in PDA?

A

enlarged heart

50
Q

what is the medical management of PDA?

A

Indomethacin – NSAID, inhibits prostaglandin E2

51
Q

what is the surgical management of PDA?

A

Surgical Ligation via cardiac catheterisation

52
Q

how does PDA alter blood flow in the heart?

A

Blood from aorta with go either to body or into ductus
oxygenated blood therefore goes from aorta to pulmonary vessels to lungs
right side of heart unaltered (low pressure)

53
Q

what is the long term effect of PDA?

A

pulmonary hypertension

54
Q

What is Fallots Teratology?

A

Condition with four heart abnormalities

55
Q

what are the four heart abnormalities of Fallots Teratology?

A

Stenosis of right ventricular outflow tract
right ventricular hypertrophy
ventricular septal defect
aorta overrides ventricular septal defect

56
Q

what are the features of Stenosis of right ventricular outflow tract in Fallots teratology?

A

 Either valve itself or infundibulum (area below valve)
 Makes it hard for deoxygenated blood to reach lungs
 Degree of this determines degree of disease

57
Q

what are the features of right ventricular hypertrophy in Fallots teratology?

A

 In response to pulmonary valve stenosis

 Looks boot shaped on Xray

58
Q

what are the features of the ventricular septal defect in Fallots teratology?

A

 In TOF right ventricular outflow obstruction causes high right sided pressure
 Blood shunts from right to left

59
Q

what are the features of the aorta override in Fallots teratology?

A

 If deoxygenated blood is shunted will immediately flow into body
 won’t miss branching arteries of aorta (all body affected)
 Sats can be as low as 80%

60
Q

what is the cause of Fallots teratology?

A

chromosome 22 deletion - DiGeorge Syndrome

61
Q

What are the clinical features of Fallot’s Teratology

A

o Cyanosis
o Clubbing of fingers and toes
o Any decrease in O2 – range of symptoms: Feeding difficulty, Failure to gain weight, Failure to develop normally
o Cyanotic spell

62
Q

what is a cyanotic spell in Fallots Teratology?

A

When increased O2 demand heart pumps more deoxygenated blood - cyanosis
If baby squats, increased vascular resistance reduces cyanosis

63
Q

what investigations can be done in Fallots Teratology?

A

Echo, CXR

64
Q

What is the management of Fallot’s Teratology?

A

Cardiac repair surgery - Septal defect closed + RV outflow tract enlarged
Long term beta blockers
Endocarditis prophylaxis

Cardiology (9 decks)

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