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Cardiovascular System > Session 3 - Congenital heart defects > Flashcards

Session 3 - Congenital heart defects Flashcards

1
Q

What are the groups of causes of congenital heart defects?

A
  • Genetic factors
  • Environmental factors
  • Maternal infections
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2
Q

Provide an example of genetic disease which has heart defects?

A
  • Downs

- Marfans

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3
Q

Provide examples of enviornmental factors which can cause of heart defects

A
  • Drugs

- Alcohol

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4
Q

Give examples of maternal infections which can cause congenital heart defects

A
  • Rubella

- Toxoplasmosis

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5
Q

What are the most common heart defects?

A
  • ASD

- VSD

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6
Q

What two groups can congenital heart defects be broken into?

A
  • Acyanotic

- Cyanotic

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7
Q

What are the characteristical features of acyanotic heart defects

A
  • Require a hole in the heart
  • Shunting of blood from LH to RH
  • Blood oxygen levels not effected
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8
Q

What commonly causes acyanotic defects?

A

-Structural defects such as ASD, VSD and PDA

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9
Q

Apart from structural defects, what other things can cause acyanotic defects?

A
  • Aortic, mitral and pulmonary stenosis

- Coarctation of the aorta

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10
Q

What happens to the blood in the LH in a structural acyanotic defect?

A

-Returned to the lungs instead of the body

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11
Q

What is an ASD?

A

-Artial septal defect-> opening anywhere along the atrial septum which persists after birth

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12
Q

What is the most common place for ASD to occur?

A

-Foreman ovale

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13
Q

What happens to the flow of blood when an ASD is present?

A

-The blood is shunted from left atrium to right atrium and thus pulmonary bloodflow is greater

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14
Q

What are the haemodynamic effects of an ASD?

A
  • Increased pulmonary blood flow
  • RV volume overload
  • Pulmonary hypertension (rare)
  • Eventually RH failure
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15
Q

Why is there no mixed blood pumped around the body with an ASD?

A
  • There is higher pressure within the LA and thus blood flows from left to right
  • Therefore oxygenated blood mixes with deoxygenated blood in the RA which gets pumped to the RV then the lungs to become oxygenated
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16
Q

What is the name for when the foreman ovale doesnt close?

A

-Patent foreman ovale

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17
Q

Why is PFO not a true ASD?

A

-Remains clinically silent

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18
Q

What is a paradoxical embolism and how does it occur?

A
  • An embolism of the venous system which enters the systemic circulation
  • Occurs when there is an ASD (including PFO) and RA pressure increases, even transiently, allowing blood to flow from right to left, ie allowing passage of the embolus
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19
Q

What is a VSD?

A
  • Ventricular Septal Defect

- An opening anywhere along the interventricular septum

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20
Q

How common are VSD?

A

150-350/100,000 live births

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21
Q

How common are ASD?

A

67/100,000 live births

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22
Q

Which way does blood flow with a VSD?

A

-From left to right

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23
Q

Why is there no cyanosis with VSD?

A

-Blood flows from L->R and thus oxygenated blood mixes with deoxygenated blood in the RV and thus is pumped to the lungs, not the systemic circulation

24
Q

Where does the most common VSD occur?

A

-In the membranous portion of the septum

25
Q

What are the haemodynamic effects of a VSD?

A
  • RV volume overload
  • Pulmonary venous congestion
  • Eventual pulmonary hypertension
26
Q

What is a PDA?

A
  • Patent ductus arteriosus

- Failed closure of the ductus arteriosus

27
Q

What happens to blood flow with a PDA?

A

-Blood flows from the aorta into the pulmonary artery (High to low pressure)

28
Q

When can PDA become cyanotic?

A
  • Constant L->R shunting can cause vascular remodelling of the pulmonary circulation with increased pulmonary resistance
  • If the resistance becomes so great the shunt can reverse
29
Q

What is eisenmenger syndrome?

A
  • Pulmonary hypertension, when associated with a septal defect, causes blood to flow from the right side of the heart to the left or from the pulmonary artery to aorta
  • Deoxygenated blood enters circulation and pt becomes cyanotic
30
Q

What is coarctation of the aorta?

A

-Narrowing of the aortic lumen in the region of the ligamentum arteriosum

31
Q

What consequences does coarctation of the aorta have on the left ventricle?

A

-Increases the afterload of the LV which can lead to LV hypertrophy

32
Q

What parts of the body are not comprimised in coartcation of the aorta and why?

A

-The head and upperlimb as the arteries emerge proximal to the coarctation

33
Q

Why can the severity of symptoms of coarctation of the aorta vary?

A

-It is dependant on how narrowed the aorta is

34
Q

What are clinical signs of coarctation of the aorta?

A
  • Weak and delayed femoral pulses

- Upper body hypertension

35
Q

In very severe cases, how do infants present after birth with coarctation of the aorta?

A

-With symptoms of heart failure shortly after delivery

36
Q

Which way is blood shunted in cyanotic congenital heart diseases?

A

-From RH to LH

37
Q

What are the general features of a cyanotic heart disease?

A
  • Structural hole
  • Distal obstruction
  • Cyanosis of skin and mucus membranes
38
Q

What is tetrology of fallot?

A
  • A group of 4 lesions as a result of a single developmental defect of rotation
  • Over-riding aorta
  • Pulmonary stenosis
  • VSD
  • RV hypertrophy
39
Q

Which lesions in tetralogy of fallot are variable?

A
  • Pulmonary stenosis

- RV hypertrophy

40
Q

What is an over-riding aorta?

A

-The aorta is laced above both ventricles

41
Q

How does over-riding aorta cause pulmonary stenosis?

A

-Displaces the pulmonary artery out of the way making it smaller

42
Q

Why does RV hypertrophy occur in tetralogy of fallot?

A

-Pulmonary stenosis increases the afterload of the RV so the RV must operate at a higher pressure causing hypertrophy

43
Q

Why does cyanosis occur with tetralogy of fallot?

A
  • Increased pressure on the right side of the heart, along with the VSD causes right to left shunting
  • Mixed blood is pumped into systemic circulation from LV
44
Q

What determines the magnitude of severity of tetralogy of fallot?

A

-The severity of pulmonary stenosis as this determines the level of shunting of blood

45
Q

What is tricuspid atresia?

A

-Lack of development of the tricuspid valve, leaving no inlet to the RV

46
Q

What must be present in order for tricuspid atresia to be compatible with life?

A
  • A complete right to left shunt of the entire venous return to right atrium (ASD of PFO)
  • A VSD of PDA to allow blood to flow to the lungs
47
Q

What is pulmonary atresia?

A

-Lack of development of the pulmonary outflow valve meaning there is no RV outlet

48
Q

What must be present for pulmonary atresia to be present with life?

A
  • A right to left shunt of venous return eg ASD/VSD

- PDA in order to allow bloodflow to the lungs

49
Q

What is transposition of the great vessels?

A
  • The great vessels are not connected to the right chambers, ie the RV is connected to the aorta and the LV connected to the pulmonary artery
  • This produces two unconnected parallel circulations
50
Q

How does transposition of the great vessels occur?

A

-The conotruncal septum within the truncus arteriosus does not a spiral course, instead it is straight

51
Q

What is necessary for transposition of the great arteries to be compatible with life?

A

-A shunt between the two sides of the heart VSD/PDA to allow the two circulations to communicate

52
Q

How is transposition of the great arteries treated?

A

-A shunt must be maintained or created immediately following birth until permanent surgical correction can be made

53
Q

What is hypoplastic left heart?

A

-Underdevelopment of the LV and ascending aorta

54
Q

What must occur for hypoplastic left heart to be viable?

A
  • There must be a left to right shunt (PFO/ASD) so the RV can support the systemic circulation (blood returning from lungs shunts right)
  • PDA must be present in order to supply the systemic circulation with adequate blood, as PDA connects at descending aorta which is Okay
55
Q

Why does cyanosis occur in hypoplastic left heart?

A

-PDA from pulmonary artery provides mixed-oxygenated blood into descending aorta -> cyanosis due to insufficient oxygen

56
Q

How common are congenital heart defects?

A

6-8/1000 live births

Cardiovascular System (19 decks)

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