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CVPR > CVPR Week 9: Pathophysiology of congenital heart disease > Flashcards

CVPR Week 9: Pathophysiology of congenital heart disease Flashcards

1
Q

Objectives

A
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2
Q

What is the goal of all heart surgery?

A
  • separate the blue and red blood
  • relief of obstruction to flow
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3
Q

Congenital heart disease prevalence

A
  • 8/1000 live births have congenital heart disease
  • 2-3/1000 will require early cardiac surgery
  • ~50% are detected by prenatal ultrasound
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4
Q

Congenital heart disease symptoms at birth

A

most are asymptomatic at birth but become symptomatic with changes in PVR

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5
Q

How are Congenital heart diseases screened at birth

A

mandated pulse oximetry newborn screen (pre and pst ductal saturations ( normal < 4%)

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6
Q

Congenital heart disease comorbidity rate

A

25% of infants with CHD have extracardiac anomalies or chromosomal abnormality

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7
Q

Congenital heart disease recurrence risk

A

~3-6% if no gene abnormality found

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8
Q

Congenital heart disease subspecialty

A
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9
Q

Embryology of the heart

A
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10
Q

Congenital heart disease: congenital defects are caused by?

A
  • abnormal development
  • Abnormal growth (in response to flow pattern)
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11
Q

Highest oxygenated blood in the fetal circulation

A

Umbilical vein

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12
Q

Describe the ductus venosus

A
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13
Q

Describe streaming of flow in the fetal circulation

A
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14
Q

Describe foramen ovale

A
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15
Q

Describe ductus arteriosus in the fetal circulation

A
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16
Q

Describe the combined cardiac output in the fetal circulation

A

RV 65% LV 35%

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17
Q

What kind of lesion is a ventricular septal defect?

A

flow dependent lesion

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18
Q

Ventricular septal defect causes

A
  • decreased flow out of the aorta
  • poor growth of the aortic isthmus
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19
Q

Prominent Eustachian valve

A
  • the Eustachian valve is designed to direct IVC flow across the foramen ovale
  • If the Eustachian valve is too large it can interfere with SVC flow to tricuspid valve
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20
Q

What is the congenital defect associated with prominent Eustachian valve

A

Tricuspid atresia

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21
Q

Why does a prominent Eustachian valve lead to another congential heart defect?

A

the large Eustachian valve can reduce flow from SVC so tricuspid valve does not receive flow to encourage growth leading to Tricuspid atresia

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22
Q

Describe the heart tube and its derivatives

A
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23
Q

Right atrium

A
  • usually receives IVC, SVC and coronary sinus
  • broad atrial appendage
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24
Q

Left atrium

A
  • usually receives pulmonary veins
  • long narrow atrial appendage
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25
Q

Possible atria congenital defects

A
  • atrial situs inversus
  • ambiguous atria
  • cor triatriatum
  • single atrium
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26
Q
A
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27
Q

Ventricles right and left designations

A

“right” and “left” describe morphology and not position in the body

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28
Q

Ventricles anterior-posterior location

A

The RV is anterior the LV is posterior

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29
Q

The RV develops from?

A

the part of the heart tube closest to the truncus

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30
Q

Variations of the ventricles

A
  • Ventricular inversion
  • Single ventricle (LV or RV morphology)
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31
Q

Right ventricle valves

A

tricuspid valve

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32
Q

RV gross structural organization

A

Tripartite

  • Inlet
  • Body
  • Outflow (conus)
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33
Q

Right ventricle wall properities

A
  • Trabeculated
  • built for pulmonary (light work)
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34
Q

RV purpose

A

built for light work (pulmonary)

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35
Q

LV structure-function relationship

A

smooth walled, built for systemic work

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36
Q

LV valves

A

mitral valve

37
Q

LV general structural description

A
  • Bullet shaped
    • inlet
    • absent conus
38
Q

Great arteries

A

Normally related great arteries

  • pulmonary artery off RV
  • Aorta off LV
39
Q

Transposition of the great arteries

A

Pulmonary artery off the LV

Aorta off the RV

40
Q

Atretic arteries

A

During fetal life, either great artery can be atretic

The patent ductus arteriosus then supplies blood to both circulation

41
Q

Describe the transposition of the great arteries

A
42
Q

Conus or infundibulum

A
  • pulmonary artery - anterior and superior
  • Subaortic conus regresses
  • aortic valve posterior and inferior
  • abnormal regression of the conus causes many congenital heart defects
43
Q

If the conus regresses under both arteries it would by?

A

Double outlet left ventricle

If the conus regresses under both great arteries, they will arise posteriorly and inferiorly i.e. over the left ventricle

44
Q
A
45
Q

Types of atrial situs

A
  • situs solitus
  • situs inversus
  • situs ambiguous
46
Q

Ventricle defects

A
  • D-looped
  • L-looped (inverted)
47
Q

Great artery defects

A
  • normally related
  • inverted
  • transposition - D or L
    • aorta to right or left of PA
  • Malposition
    • partial resportion of the conus
48
Q

Resistance =

A

pressure

flow (Q)

49
Q

Vasofilation effect on resistance

A

lower resistance and increase flow

50
Q

vasoconstriction effect on resistance

A
  • increase resistance
  • decrease flow
51
Q

Pulmonary vasodilation is in response to?

A

oxygen

52
Q

Pulmonary vasoconstriction is in response to?

A

hypoxia

53
Q

What receptor is responsible for systemic vasoconstriction

A

alpha agonists

54
Q

Pulmonary hypertension

A

abnormal musculature around smaller pulmonary arterioles

55
Q

abnormal vascular resistance at birth

A
  • Hypoplastic lungs
  • Abnormal musculature
  • unable to vasodilate
56
Q

What is the Ao sat compared to the LA sat in a normal heart

A

Ao sat = LA sat

57
Q

Pulmonary vasodilation is in response to?

A

oxygen

58
Q

Pulmonary hypertension

A

abnormal musculature around smaller pulmonary arterioles

59
Q

Lack of regression or secondary remodeling in response to high blood flow to lungs

A

(eg VSD, ASD, other) and/or hypoxia

60
Q

Normal heart pressures in systole

A

pressures are equal when chambers are connected ventricle and aorta

61
Q

Normal heart pressures in diastole

A

atrium and ventricle pressures are equal when chambers connected

62
Q

Qp/Qs =

A

Ao Sat - MV sat

PV sat - PA sat

63
Q

Qp/Qs >1.5

A
  • volume overload
  • risk for irreversible pulmonary vascular changes if not repaired
64
Q

Clinical consequences of ASD

A

volume overload of right heart - well tolerated for 20+ years

  • atrial arrhythmia
  • exercise intolerance
  • congestive heart failure
  • pulmonary hypertension - Eisenmenger syndrome
  • Shorten lifespan; repair early to avoid above
65
Q

Clinical consequences of ASD physical exam findings

A
  • right ventricular lift or heave
  • wide splitting of S2 (late P2 closure)
  • +/- pulmonary flow murmur (can sound innocent)
    • murmurs can be heard when blood crosses an obstruction at high velocity or when a higher volume of blood crosses a normal structure (pulmonary valve annulus)
66
Q

Septal ductus arteriosus

A
67
Q

Ventricular septal defect locations

A
  • multiple locations
  • variable spontaneous closure, relationship to valves
68
Q

Ventricular septal defect flow depends on

A
  • size of the hole
  • relative systemic and pulmonary vascular resistance in systole
69
Q

Qp:Qs ratio in?

A

Ventricular septal defect

or

atrial septad defect

70
Q

Ventricular septal defect symptoms depend on?

A

depend on flow to lungs

71
Q

What are the Ventricular septal defect symptoms

A
  • tachypnea
  • tachycardia
  • poor growth
72
Q

High pulmonary resistance in ventricular septal defect

A

high pulmonary resistance = less flow = less symptoms

73
Q

Physical exam findings in ventricular septal defect

A

lateral displacement of apical impulse

harsh, high frequency murmur or loud P2; narrowly split S2

74
Q

ventricular septal defect indications for surgery

A
  • poor growth
  • persistent pulmonary hypertension
  • aortic valve prolapse into defect
  • most repaired in 1st 6-12 months of life with surgery
  • device closure available but conduction system issues
75
Q

Aortic stenosis effects

A

left ventricular hypertrophy

76
Q

Aortic stenosis gradient depends on

A
  • size of annulus
  • mobility of leaflets
  • cardiac contractility
77
Q

Clinical consequences of Aortic stenosis: symptoms

A

symptoms depend on how quickly the load develops

  • Exercise intolerance
  • risk of sudden death
  • left ventricular dysfunction (gradient decreases)
78
Q

Aortic stenosis physical exam findings

A

early systolic ejection click

systolic murmur, RUSB and radiating into the neck

79
Q

Tx options for aortic stenosis

A
80
Q

Coarctation of the aorta features

A
81
Q

Tetralogy of fallot: Shunt depends on?

A

resistance

82
Q

Tx of tetralogy of Fallot

A
83
Q

Single ventricle lesions

A
  • Staged palliation
  • 1st - assure appropriate systemic and pulmonary blood flow
  • 2nd start to separate blue and red blood (lower volume load on a single ventricle)
  • 3rd separate blue and red blood
84
Q

Single ventricle lesions prognosis

A
85
Q

Question

A
86
Q

Atrial shunting with PS

A
87
Q

2 questions

A
88
Q

Summary

A

CVPR (93 decks)

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