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Year 3 - Congenital Heart Disease > Cardiac pathology: congenital heart disease Evelina Physiology Team > Flashcards

Cardiac pathology: congenital heart disease Evelina Physiology Team Flashcards

1
Q

Which congenital heart defects are cyanotic?

A

-ToF
-Transposition of the Great Arteries (TGA)

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2
Q

Reasons for increased survival in congenital heart defects

A

-Improved surgical techniques
-Greater access to surgical intervention
-Advanced non-surgical intervention
-Improved diagnostic tools (echo, MRI, CT, CPET)
-Better access to paediatric and adult congenital heart disease (ACHD) services
-Access to prenatal diagnosis

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3
Q

What day does primitive heart tube form and what does it develop into?

A

-Primitive heart tube forms at day 21 of gestation
-Heart tube -> formation of septum and endocardial cushions
-Form atria, ventricles and valves

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4
Q

Structures of the embryonic heart and their derivatives in the adult

A
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5
Q

Inside of heart 28 days vs 8 weeks

A
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6
Q

What are the 2 streams of flow in fetal circulation?

A

-Right to left across the foramen (PFO)
-PDA sends oxygenated blood from PA -> aortic arch -> body/brain

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7
Q

What happens when baby is born?

A

-O2 trigger to close the duct
-Decrease in RA pressure/Increase in LA pressure
-Pushes the foramen closed

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8
Q

Examples of things going which cause congenital heart defects

A

-Folding, bending, twisting of heart tube in the wrong direction
-If sinus venosus doesn’t join to atria
-Septum/duct doesn’t close

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9
Q

Acyanotic congenital cardiac defects

A

-O2 levels delivered to body remain normal
-Normal or increased blood flow to lungs
-Left to right shunt
-Normal saturations, pink
-Asymptomatic or symptoms of CCF, breathlessness, failure to thrive
-Can present late in children and adults

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10
Q

Cyanotic congenital cardiac defects

A

-Less than normal levels of O2 are delivered to the body
-Decreased blood flow to the lungs
-Right to left shunt
-Low saturation, blue
-Sick, hypoxic, tachypnoeic
-Present as babies

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11
Q

Signs of cyanosis in older child

A

Clubbing

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12
Q

Causes of PDA

A

-Prematurity
-Genetic mutation
-Maternal illness (rubella)
-Complex CHD
-Unknown

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13
Q

Presentation of PDA

A

Small duct:
-Well tolerated left to right shunt
-No symptoms
-Murmur

Moderate duct:
-Symptomatic early in life
-Failure to thrive
-HF due to pulmonary congestion

Large duct:
If untreated can cause:
-Pulmonary hypertension
-Reduced lung compliance
-Right to left shunt

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14
Q

Diagnosis for PDA

A

Echo
-Size
-Haemodynamic effect on heart
-Associated defects

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15
Q

Treatment for PDA

A

-May spontaneously close (watch and wait)
-PDA closure device in cath lab
-Surgery to tie or clip the duct

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16
Q

Treatment for Eisenmenger’s syndrome (right to left shunt)

A

-Medicate
-Trial occlusion
-Heart and lung transplant

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17
Q

Surveillance in PDA

A

Watch
-Repeat echo every 6-12 months
-Review post surgery
-Review post catheter closure to ensure device is well seated
-Very good outcomes
-Lifelong follow up not required

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18
Q

What will significant left to right shunt cause in ASD?

A

-Right heart dilatation (RA, RV, PA)
-Increase flow across tricuspid valve
-Increase flow across pulmonary valve

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19
Q

What is the most common defect of the atrial septum?

A

-Deficiency of the flap valve of the foramen ovale
-Perforated or too small to overlap oval foramen (PFO)
-Known as Secundum defects

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20
Q

What is a Vestibular defect?

A

-Rare
-Occurs at the hinge point of the oval fossa

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21
Q

3 main types of ASD?

A

-Ostium secundum defects (PFO)
-Ostium primum defects (top)
-Sinus venosus defects (bottom - AV valve)

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22
Q

Prevalence of ASDs

A

-ASDs are common and can present at any age
-Females constitute 65% to 75% of patients with secundum ASDs
-Common arrhythmias

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23
Q

Symptoms of ASD

A

-No symptoms - although most will become symptomatic at some point - breathlessness
-Exercise intolerance - exertional dyspnoea/fatigue
-Atrial fibrillation/flutter reflects atrial dilation/stretch
-Decompensated right heart failure
-Eisenmenger syndrome - irreversible pulmonary HTN

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24
Q

How to diagnose ASDs?

A

Echocardiogram
-Easily seen
-PFO can be tricky, sometimes requires bubble study

MRI
-Can be used to quantify the right heart size

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25
Q

Features of transcatheter ASD closure?

A

-Simple ASDs
-No significant PHT
-Risks of embolisation/wire perforation

26
Q

Features of surgical ASD closure?

A

-Larger more complex ASDs
-Redirection of other vessels, such as pulmonary veins
-Surgical complications
-Sternotomy scar

27
Q

What does a significant left to right shunt cause?

A

-Left heart dilation

28
Q

Features of coarctation of the aorta

A

-Common - 5-10% of congenital heart disease
-Aorta is narrowed - restricted blood flow to the body
-Discrete and long length
-Usually occurs after subclavian branch

29
Q

Types of CoA

A

Mild - hypertensive
Discrete coarctation
Aortic arch hyperplasia

30
Q

Presentation of CoA

A

-Depends upon severity of coarctation
-Severe CoA - present as a baby
-Mild CoA - present as an adult

31
Q

Symptoms of CoA

A

-Baby with severe CoA may present collapsed with poor peripheral pulses
Adult symptoms:
-Uncontrolled hypertension
-Headaches
-Exercise intolerance (cold feet/legs after exercise)
-SOB
-Chest pain

32
Q

Diagnosis of CoA

A

-First line - Echo
-Direct visualisation of the coarctation
-More clear imaging in babies than adults
-Bigger patients - Colour wave doppler

33
Q

CoA on ECG

A

ECG:
-LVH - Tall QRS, ST changes

34
Q

Cardiac MRI in CoA

A

-Clear 3D imaging of the whole of the aorta, including visualisation of collateral vessels
-Gives flow and anatomical information
-Measurements to allow for procedural planning (e.g. custom made stent)

35
Q

Long term effects of CoA

A

-Life long hypertension
-Stroke
-Early onset CAD
-Aortic dissection and rupture
-CoA often occurs with bicuspid aortic valve - can become stenotic

36
Q

Repairs for CoA

A

Discrete: End-end repair
-Transcend aorta
-Cut out narrowed section
-Stitch it back together

Hyperplasia: End-side repair
-Open up aorta
-Place Fillet patch
-Widen aorta

37
Q

Presentation of VSD

A

> 80% close spontaneously
-May present with pansystolic murmur
-Cardiac failure in infancy if large
-Common cause of breathlessness

38
Q

Where can VSD occur in ventricular septum?

A

-Perimembranous
-Muscular
-Doubly committed

39
Q

Why is there left heart volume overload in VSD?

A

-Blood goes from left to right
-Extra blood in right heart goes straight from RV to lungs
-Extra blood volume is received by the LA and expands left side
-Blood shunts across VSD in systole as RV contracts and goes straight to lungs

39
Q

VSD classifications

A
40
Q

Symptoms/signs of VSD

A

-Asymptomatic
-Murmur
-Cyanosis in severe cases where shunting is right to left
-PHT with large defects untreated into adulthood
-Left heart dilation

41
Q

ECG in VSD

A

-Normal in small VSDs
-LA and LV hypertrophy in large defects
-Right axis deviation and RV hypertrophy in pulmonary HTN

42
Q

Chest X ray in VSD

A

-Normal with small VSDs
-Large defects - Well visualised small pulmonary arteries in the periphery of both lungs
-PHTN - Enlargement of proximal pulmonary arteries

43
Q

Diagnosis of VSD

A

TTE/TOE
-Location and size of defect - 3D echo
-Left heart size and volume loading
-Shunt direction

CMR
-Very useful with complex associated lesions

Cardiac catheterisation
-Used in treatment and closure of small VSDs

44
Q

Treatment of VSD

A

Medically managed:
-Small VSDs, conservative (watch and wait), spontaneous closure
-Not suitable for surgery - comorbidities, right heart pressures (PHT), part of more complex VSD

Transcatheter closure: (usually muscular VSD)
-Small VSDs
-Location needs to be away from surrounding cardiac structures to avoid impingement

Surgical closure:
-Most common technique
-Cardiac bypass and sternotomy

45
Q

What are the 4 major defects in Tetralogy of Fallot

A

-VSD
-RVH
-Pulmonary stenosis
-Overriding aorta

46
Q

What is the most common form of cyanotic CHD?

A

ToF

47
Q

What percentage of children with ToF have a chromosomal abnormality?

A

25%

48
Q

ToF on ECG

A

-RAD
-RVH
-RBBB
-After repair QRS width >180ms reflects RV dilation, risk factor for VT

49
Q

What does ToF look like on chest X ray?

A

Boot shaped heart

50
Q

When do you use cardiac cath in ToF?

A

-Not usually required
-Used in more extreme forms of ToF
=>Very small PA branches or no PA branches
=>Pulmonary blood flow via collateral vessels to the lungs which come off aorta
-Can delineate coronary artery, now often done by CT

51
Q

Surgical correction for ToF

A

Tube
-Connects aorta and PA
-Supplies blood flow to lungs

Definitive
-Patching VSD
-Cutting away muscle that sits in outflow tract
-Dilate pulmonary valve

52
Q

Sequelae following ToF repair

A

Transannular patch repair
-severe pulmonary regurgitation
-right heart dilation +/- impaired function
-Ventricular arrhythmias and SCD (ICD)

Lifelong surveillance
-Arrhythmia
-Exercise intolerance
-Heart failure

Seen in clinic
-RV function
-Assess pulmonary valve for stenosis/regurgitation

53
Q

What is the gold standard for assessing intervention in ToF?

A

MRI
-Pulmonary valve replacement?
-Anatomical and flow info in 3D real time
-RV EDV 150ml/m^2 cut off

54
Q

What happens in TGA?

A

-Deoxygenated blood gets pumped around body instead of going to lungs
-Oxygenated blood gets pumped to the lungs instead of around the body

55
Q

What is mortality rate in TGA?

A

-Without intervention, mortality rate is ~90% by 6 months of age

56
Q

How is mixing promoted in TGA?

A

PDA
-usually closes after birth
-Prostaglandin given to keep duct open

ASD
-Atrial septostomy to increase size

VSD
-Can’t be enlarged

57
Q

Symptoms of TGA

A

-Reduced O2 saturations
-Patient can appear blue
-SOB
-Weak pulse
-Lack of appetite/poor weight gain

58
Q

Diagnosis of TGA

A

Echo
-Usually detected before birth, after birth, within first few weeks

59
Q

Treatment for TGA

A

Arterial Switch Operation (ASO)
-swap the great arteries back to their usual position
-Aorta and PA are detached from their native roots and reattached to the opposite root
-Coronary arteries taken off their normal position on aorta and transplanted into new aorta

60
Q

What is the Lecompte manoeuvre?

A

-During Arterial Switch Operation, main PA is cut and moved anterior to the aorta before re-attaching the PA

61
Q

How would adults be followed up?

A

-Echo
-CPET
-MRI

Year 3 - Congenital Heart Disease (1 decks)

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