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Semester 2 > CVS Session 3 > Flashcards

CVS Session 3 Flashcards

0
Q

Where does septation occur?

A

Interarterial septum
Interventricular septum
Septation of ventricular outflow

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1
Q

What does septation achieve?

A

Creation of 4 chambers

Selective outflow

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2
Q

Where do endocardial cushions develop?

A

Point of constriction in the atrioventricular region - AV canal

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3
Q

In which direction do the endocardial cushions grow?

A

From dorsal and ventral walls towards middle

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4
Q

What is the function of the endocardial cushions?

A

Divide developing heart into right and left channels

Contribute tissues

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5
Q

What is the path of the septum primum?

A

Moves down to fused endocardial cushions

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6
Q

What is the ostium primum?

A

Hole present before septum primum fuses

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7
Q

What forms the ostium secundum?

A

Programmed cell death

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8
Q

When does the ostium secundum form?

A

Before ostium primum closes

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9
Q

Describe septum secundum formation.

A

Crescent-shaped septum grows with foramen ovale

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10
Q

How many holes and septa are involved in atrial septation?

A

3 holes

2 septa

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11
Q

Where does the muscular portion in ventricular septation grow upwards from?

A

Same platform as atrial septum

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12
Q

What is the primary interventricular foramen?

A

Small gap left by growth of muscular portion towards endocardial cushions in ventricular septation

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13
Q

What fills the primary interventricular foramen and forms the membranous portion of the interventricular septum?

A

Connective tissue from endocardial cushions

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14
Q

What are the stages of atrial septation?

A

Septum primum –> ostium secundum appearing –> ostium secundum complete –> septum secundum –> septum secundum complete w/foramen ovale –> R to L shunt

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15
Q

Where are the left and right auricles of the L and R atria derived?

A

Primitive atrium

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16
Q

What is the fossa ovalis?

A

Adult remnant of foramen ovale

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17
Q

What is the purpose of the foramen ovale?

A

In utero shunt to bypass lungs

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18
Q

How is the difference in atrial development identified in the developed heart?

A

R atrium has smooth but largely trabeculated walls

L atrium largely smooth walled

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19
Q

What is visible in the right and left atria?

A

R: fossa ovalis
L: pulmonary vein entrances

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20
Q

Describe the formation of the conotruncal septum.

A

Endocardial cushions appear staggered in the truncus arteriosus –> grow towards and twist around each other –> forms spiral septum

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21
Q

Are septation of the outflow tract and atrial septation simultaneous?

A

Yep

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22
Q

What is the result of successful outflow tract septation?

A

Left ventricle pumps to aorta
Right ventricle pumps to pulmonary trunk
Blood circulates in spiral flow

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23
Q

How does foetal blood return to the placenta?

A

Via umbilical arteries

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24
Q

What occurs to the foetal circulation during birth?

A 
Respiration begins 
Left atrial pressure increases
Foramen ovale closes
Ductus arteriosus contracts
Ductus venosus closes structurally
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25
Q

What prevents L to R bloodflow in the neonatal heart?

A

p(LA) > p(RA)

Septum primum pushed against septum secundum w/specific non-alignment

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26
Q

Under what circumstance does blood move through the foramen ovale?

A

p(LA)<p(RA)

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27
Q

What are the fates of each of the foetal shunts after birth?

A

Foramen ovale –> fossa ovalis
Ductus arteriosus –> ligamentum arteriosum
Ductus venosus –> ligamentum venosum
Umbilical vein –> ligamentum teres (hepatis)

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28
Q

What are the fates of each of the parts of the primordial heart tube?

A

Sinus venosus –> RA except L horn
Atrium –> auricles of atria
Ventricle –> left ventricle
Bulboventricular sulcus –> primary IV foramen

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29
Q

How does the bulbus cordis change during development?

A

Proximal third –> trabeculated RV
Conus cordis –> outflow tract of L and R ventricles
Truncus arteriosus –> roots of pulmonary trunk and proximal aorta

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30
Q

Why are congenital heart defects common?

A

Due to complexity of septation

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31
Q

Which type of congenital heart defect is most common?

A

Ventricular septal defects

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32
Q

What causes transposition of great vessels?

A

Conotruncal septum is not spiral

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33
Q

What causes tetralogy of Fallot?

A

Conus cordis not equally split into 2 therefore four separate defects arise

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34
Q

What are the three causes of congenital heart disease?

A

Genetics
Environmental
Maternal infections

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35
Q

Does glycaemia in maternal diabetes directly cause predisposition to congenital heart defects?

A

No

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36
Q

What is the normal physiology of the heart?

A

R ventricle pumps deoxygenated blood to lungs
Pulmonary circulation has low resistance
L ventricle pumps oxygenated blood at systemic BP to aorta
Each ventricle morphological lay adapted to task

37
Q

What is the approximate oxygen saturation of blood in the right side of the heart?

A

67%

38
Q

What happens to the blood flow in an acyanotic shunt?

A

L –> R

Blood from L heart returned to lungs instead of body

39
Q

What must the heart do to maintain cardiac output in the event of an acyanotic shunt?

A

Pump harder

40
Q

What is damaging to the lungs in the instance of a L–>R shunt?

A

Increased pulmonary artery and venous pressure

41
Q

What can cause an acyanotic shunt?

A

Atrial/ventricular septal defects
Patent ductus arteriosus
Aortic/pulmonary/mitral stenosis
Coarctation of the aorta

42
Q

What do both acyanotic and cyanotic shunts require?

A

A hole

43
Q

What happens to the passage of blood in a cyanotic shunt?

A

R –> L

Deoxygenated blood bypasses the lungs

44
Q

At what oxygen saturation is cyanosis seen?

A
45
Q

What can cause a cyanotic shunt?

A 
Pulmonary stenosis
Tetralogy of Fallot
Transposition of great arteries
Total anomalous pulmonary venous drainage
Univentricular heart
46
Q

Why do atrial septal defects eventually lead to right heart failure?

A

Increased pulmonary blood flow –> right ventricle volume overload

47
Q

What three locations are the common sites for an atrial septal defect?

A

Sinus venous defect
Secundum atrial defect
Primum atrium defect

48
Q

Why is pulmonary resistance not usually damaged by an atrial septal defect?

A

Blood is at low pressure - pulmonary hypertension is rare

49
Q

In which direction does blood flow in an atrial septal defect?

A

L –> R

50
Q

Why does a ventricular septal defect lead to eventual pulmonary hypertension?

A

Left ventricle volume overload –> pulmonary venous congestion

51
Q

Why is pulmonary resistance usually damaged in a ventricular septal defect?

A

Blood at high pressure

52
Q

Why is a patent foramen ovale not a true ASD?

A

Usually clinically silent due to higher left atrial pressure closing flap

53
Q

How does a patent foramen ovale allow the passage of a venous embolism into the systemic circulation?

A

Right heart pressure increases –> flap opens

54
Q

Why is oxygenated and deoxygenated blood pumped to the lungs at high pressure in an atrio-ventricular septal defect?

A

Blood mixes in atria and ventricles as common AV valve leaks blood back into upper chambers

55
Q

What causes an atrio-ventricular septal defect to form?

A

Faulty development of the embryonic endocardial cushions

56
Q

Why do the ventricle muscle walls thicken in aortic stenosis?

A

To be able to contract with more force to push blood through narrowed aorta

57
Q

What causes aortic stenosis?

A

Congenital defect

Calcium deposits in aortic valve

58
Q

What predisposes aortic stenosis by calcium deposits in the aortic valve?

A

Abnormal aortic/bicuspid valves

59
Q

Is aortic stenosis more common in men or women?

A

3x more common in men

60
Q

Why must L–> R shunting be treated?

A

To avoid vascular remodelling of the pulmonary circulation

61
Q

What happens if pulmonary vascular remodelling causes pulmonary resistance to increase beyond systemic circulation resistance?

A

Right heart pressure increases causing shunt to become R–> L
Eisenmenger syndrome

62
Q

Why does coarctation of the aorta cause LV hypertrophy?

A

More muscle needed to push blood through narrowing in ductus arteriosus area

63
Q

What vasculature in the body is affected by coarctation of the aorta?

A

All except head and upper limb

64
Q

What signs related to the systemic circulation can be detected clinically in coarctation of the aorta?

A

Femoral pulse weak and delayed

Upper body hypertension

65
Q

In what range can the extent of symptoms of coarctation of the aorta be found?

A

Ranging from neonate heart failure to detection only in adulthood

66
Q

Which four congenital heart defects are present in Tetralogy of Fallot?

A

Overriding aorta
Ventricular septal defect
Pulmonary stenosis
Thickened R ventricle

67
Q

What does the magnitude and severity of the shunt depend on in Tetralogy of Fallot?

A

Severity of pulmonary stenosis

68
Q

What is an overriding aorta?

A

Aorta comes off both ventricles

69
Q

In which direction is the blood shunted in Tetralogy of Fallot?

A

R–> L

70
Q

What can overcome the excess bloodflow present in Tetralogy of Fallot?

A

Pulmonary stenosis

71
Q

What is tricuspid atresia?

A

Absence of RV inlet causing R–> L atrial shunt of entire venous return

72
Q

How is blood flow to the lungs achieved in tricuspid atresia?

A

Drugs followed by surgery to keep central septal defect or patent ductus arteriosus shunts open

73
Q

What is a univentricular heart?

A

Only one giant ventricle present

74
Q

Is univentricular heart seen with or without transposition of great arteries?

A

Either

75
Q

What is hypoplastic left heart?

A

Left ventricle is underdeveloped and ascending aorta is very small

76
Q

What supports the systemic circulation in hypoplastic left heart?

A

Right ventricle

77
Q

How is hypoplastic left heart treated?

A

ASD or PDA must be kept open for short term survival to enable surgery to reconstruct R ventricle as pump

78
Q

How are the great arteries arranged in transposition of the Great Arteries?

A

Aorta connected to R ventricle

Pulmonary artery connected to L ventricle

79
Q

What must be present for transposition of the great arteries to be viable?

A

Atrial/ventricular/ductal shunt so two circuits can communicate

80
Q

What is transposition of the great arteries an example of?

A

Bi-directional shunting

81
Q

How is transposition of the great arteries treated?

A

With immediate surgery or use of drugs to keep shunts open until surgery can be performed

82
Q

What is pulmonary atresia?

A

Absence of R ventricle outlet causing R–> L shunt of entire venous return

83
Q

How is bloodflow to lungs achieved in pulmonary atresia?

A

PDA

84
Q

How does an ASD usually present?

A

Asymptomatic late into adulthood
Late onset arrhythmia
R heart failure

85
Q

How does a VSD usually present?

A

Unless v. small seen in infancy w/left heart failure
Very common
Causes heart murmurs

86
Q

What does an untreated VSD lead to?

A

Inoperable pulmonary hypertension

87
Q

What complicates coarctation of the aorta in adulthood?

A

Renal hypertension –> left ventricle hypertrophy

88
Q

What is often associated with coarctation of the aorta in adulthood?

A

Aortic valve stenosis

89
Q

How does Tetralogy of Fallot usually present?

A

In infancy/early childhood w/cyanotic spells

Mild cases compatible w/adulthood

90
Q

Which congenital heart defects are neonatal emergencies due to reduced pulmonary bloodflow?

A

Transposition of the great arteries
Hypoplastic left heart
Preductal coarctation of the aorta
Pulmonary atresia

Semester 2 (45 decks)

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