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CVPR > Embryology and Congenital Heart Defects > Flashcards

Embryology and Congenital Heart Defects Flashcards

1
Q

Layers in a blastocyst

A

Outer cell is tophoblast Inner cell is Embryoblast Central cavity is called blastocyst

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2
Q

Embyoblast layers

A

External: epiblast which gives rise of embryonic disc Internal: hypoblast

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3
Q

Blastocyst stage

A

precordial cells are in epiblast portion of embryonic disc on either side of the primitive stread. They migrate downward to give rise of intraembryonic mesoderm

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4
Q

Gastrula Stage

A

formation of the three layers 1) endo 2) mesoderm - which contains the precardial cells that migrate anteriorly and laterally (cranially) 3) ectoderm

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5
Q

what happens on day 16 gestation

A

precardiac cells are most cranial and surround neural plate in the cardiogenic area.

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6
Q

where are cardiac cells dervied

A

mesoderm

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7
Q

Day 19 in gestation

A

cardiogenic cells migrate ventrally to forebrain and foregut. Formation of two endothelial lined heart tubes begins and the splancnic mesoderm surrounds the heart cells

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8
Q

Day 21 and 22

A

cardiac cells fuse due to cephalic and lateral folding to form the primitive heart tube. and heart begins to beat

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9
Q

when do the heart tubes begin to form? when do they fuse?

A

day 19 - form and fuse by day 22

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10
Q

when does the heart start to beat?

A

day 22

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11
Q

what cells give rise to the endocardium

A

endothelial layer of heart tub

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12
Q

what cells give rise to the myocardium

A

outer tube mesoderm

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13
Q

what cells give rise to the epicardium

A

outer tube mesoderm

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14
Q

where is the cardiac jelly

A

in between endocardium and myocardium to facilitate in looping and separation

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15
Q

General order form head to tail of the cardiac loop

A

Dorsal Aorta - Truncus - Conus - Bulbus Cordis - Primitive Ventricle - antrioventricular sulcus - primitive atria - sinus venosus

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16
Q

what does the truncus form?

A

aortic sac and aorta, Pulmonic trunk, Aortic and pulmonic valves

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17
Q

what does the conus from?

A

infundibula of ventricles

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18
Q

what does the bulbus cordis form?

A

Trabeculated RV

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19
Q

what does the primitive ventricle form?

A

Traveculated LV

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20
Q

What does the atrioventricular sulcus form?

A

IV septum

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21
Q

what forms the aorta and pulmonary a.?

A

Truncus

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22
Q

what forms the trabeculated RV

A

Bulbus cordis

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23
Q

what forms the trabeculated LV

A

Primitive ventricle

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24
Q

Looping stage days

A

Day 23-25

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25
Q

Looping stage

A

day 23-25 loops right. Cranial to caudal and posterior to anterior.

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26
Q

Blood flow at day 25

A

Entry itno sinus venosus via three veins. 1) Umbillical 2) vitelline 3) cardinal

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27
Q

Umbillical Vein

A

From the placenta

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28
Q

Vitelline vein

A

from the yolk sac

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29
Q

Cardinal Vein

A

From the embryo

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30
Q

What happens to the umbillical vein?

A

Right disappears, Left forms ductus venosus

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31
Q

what happens to the vitelline vein?

A

R form the superior mesenteric artery distal and proximal suprahepatic a. and IVC L forms hepatic sinusoids

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32
Q

what happens to the cardinal veins?

A

R fors SVC, brachiocephalic V and innominate L forms ligament of marshall

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33
Q

how do the pulmonary veins form?

A

splanchnic plexus forms the pulmonary venous plexus –> pulmonary veins. An endothelial projection form LA connects to pulmonary venous venous plexus to form a common pulmonary vein that branches into R and L

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34
Q

Cushions in the conus

A

Dextrodorsal conal crest Sinistroventral conal crest

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35
Q

Cushions in the truncus

A

Dextrosuperior CC Sinistroinferior Right and Left intercalated swellings

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36
Q

Sinistroventral conal crest is contiuous with..

A

the sinstrosuperior conal crest of the truncus

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37
Q

dextrosuperior conal crest is continuous with..

A

the dextrodorsal conal crest of the conus

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38
Q

which is unique about the great artery formation?

A

it happens in a rotation. So pulmonary outlet in to the right and anterior of the aortic.

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39
Q

Right intercalated swelling forms part what valve?

A

aortic cusp

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40
Q

Left intercalated swelling forms part of what valve?

A

pulmonic cusp (anterior)

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41
Q

when do the great arteries form?

A

35-56 day

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42
Q

what doe the aortic arches give rise to?

A

vascullature of head, neck and upper thorax

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43
Q

First aortic arch

A

gives rise to maxillary and external carotid a. First to disappear

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44
Q

Second aortic arch

A

proximal disappears and distal gives rise to stapedial a.

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45
Q

3rd aortic arch

A

carotid a.

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46
Q

4th aortic arch

A

Right gives rise to Right brachiocephalic and rt. subclavian. Left gives rise to transverse aortic arch

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47
Q

5th aortic arch

A

disappears

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48
Q

6th aortic arch

A

Proximal Right: Proximal Pulm a. Proximal Left: pulmonary a. Distal L: ductus arteriosus

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49
Q

what arch gives rise to the external carotid a.

A

1st

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50
Q

what arch gives rise to the maxillary a.

A

1st

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51
Q

what arch gives rise to the cartod a.

A

3rd (1st external carotid)

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52
Q

what arch gives rise to the right brachiocephalic a.?

A

4th fight aortic arch

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53
Q

what arch gives rise to the Rt subclavian a?

A

4th right aortic arch

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54
Q

what arch gives rise to the transverse aortic arch?

A

left 4th aortic arch

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55
Q

what gives rise to the proximal pulmonic artery?

A

Proximal Right and left 6th aortic arch

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56
Q

what gives rise to the ductus arteriosis?

A

distal L 6th aortic arch

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57
Q

Ductus venosus

A

connects placenta with hepatic artery at IV before going into RA. Mixes oxygenated blood from placenta with deoxygenated blood from fetal circulation

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58
Q

what portion of blood pumped into the RA gets pumped out RV?

A

2/3 - gets pumped through the pulmonary valve (not all into the lungs though). 1/3 goes through foramen ovale into the LA.

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59
Q

Ductus arteriosus

A

shunt from Right pulmonary A to the aorta.

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60
Q

what percent of Ventricular blood goes through the ductus arteriosus?

A

55-60%; only 6-8% goes through the lungs

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61
Q

Risk factors for patent ductus arteriosus?

A

Premature if less than 29 weeks or under 1000 grams has higher than 70% incidence. High elevation. Maternal rubella infection

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62
Q

Usual closure of ductus arteriosus

A

occurs 10-15 hours with functional closure, then anatomic closure 2-3 weeks old. >98% are closed completely at 1 year

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63
Q

Functional closure vs. Anatomic closure of ductus arteriosus.

A

Functional: contraction and cellular migration to lumen of medial smooth muscle. Anatomical: vascular remodeling. Proliferation of elastic membrane of ductus imtima and media to form mucoid lakes that form a **hyaline mass to occlude y lumen.

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64
Q

why does the ductus close?

A

ductus has fewer elastic fibers than aortic or pulmonic arteries. Increase in pulmonary artery oxygen pressure causes contraction of spiral muscle fibers

65
Q

why does the ductus stay open?

A

prostaglandin due to metabolism of arachidnoic acid (PGE2) from local or placental source.

66
Q

when does the septum form?

A

days 28-42

67
Q

atrial septum formation

A

septum primium begins to grow towards the valve and closes the ostium primum. Ostium secundum is due to apoptosis in the primum. The septum secundum in the RA begins to grown and sovers the ostium secundum to from the foramen ovale which is a one way shunt from Right to left.

68
Q

Ventricular septum formation

A

fusion of the septum primus from the atrium with the endothelial cushions and primitive intraventricular septum. Superior and inferior endocardial cushions fuse and leave two aterioventricular canals.

69
Q

Right endocardial cushion forms

A

Tricuspid valve and ventricular spteum

70
Q

Left endocardial cushion forms

A

mitral valve and ventricular septum

71
Q

Membranous part of IV spteum

A

Right under aortic valve. thinner area forms the inferior endothelial cushion

72
Q

Superior Endocardial cushion

A

Left surface of the outlet protion of the intraventricular septum Part of MV

73
Q

Inferior endocardial cushion froms..

A

Inlet protion of IV septum membranous part of septum Part of Tricuspid and mitral valve

74
Q

Right endocardial cushion forms

A

part of tricuspid valve

75
Q

Left endothelial cushion forms

A

posterior leaflet of mitral valve.

76
Q

what cushions form the mitral valve?

A

Superior, inferior and left endocardial cushions

77
Q

what cushions form the tricuspid valve?

A

Right and Inferior endocardial cushions

78
Q

Epidemiology of Congenital heart Defects

A

5-8/1000 Boys over girls Equal for races and parental ages

79
Q

Risk factors of congenital heart defects

A

Maternal diabetes (X3), Family Hx with first degree relative. Recommended with fetal echo - focus on structural abnormalities

80
Q

Most common congenital heart defects

A

VSD> PDA > TOF >ADS> Coarch

81
Q

Percentage for VSD

A

15.6%

82
Q

PDA percent

A

5%

83
Q

TOF percent

A

2.6

84
Q

ASD percent

A

2.4

85
Q

Coarch percent

A

1.4

86
Q

Shunt type for PDA

A

Left to right shunt from Aorta into pulmonary artery. Decreased pressure relative to aorta of pulmonary a cause flow back to lungs.

87
Q

Risk factors of PDA

A

maternal rubella, premature, high elevation at birth

88
Q

Magnitude of PDA shunt is based on..

A

size, resistance and pressure in aorta and pulmonary A.

89
Q

What is the long term structural heart changes in PDA

A

overload of LA and LV due to increase pulmonary blood flow to cause dilation and heart failure.

90
Q

Clinical Signs of PDA

A

Small: asymptomatic Large: respiratory problems, pulmonary edema, Left sided CHF, feeding intolerance, renal insufficiency, intraventricular hemorrhage, rarely death. If found in older infant/child: hoarse cry due to largyngeal nerve, hx of pneumonia, failure to thrive, increased WOB, diaphoresis,

91
Q

Physical Exam with PDA

A

Wide pulse pressure and bounding pulses (can feel in hands). Hyperactive precrodium increased WOB Continuous murmur on LUSB in both systolic and diastolic

92
Q

CXR for PDE

A

normal if asymptomatic Pulmonary edema with dilated LA and LV for severe symptomatic

93
Q

Treatment of symptomatic PDA in infants

A

NSAIDS (IV indomethacin or IV ibuprofen) if fail, surgery

94
Q

Treatment of symptomatic vs. asymptomatic child with PDA

A

Sym: percutaneous occlusion in the Cath lab Asymptomatic with murmur: percutaneous occlusion.

95
Q

what is the biggest risk of PDA?

A

pulmonary hypertension and subacute bacterial endocarditis if untreated

96
Q

Types of ASD

A

Ostium Secundum and Steum Secundum

97
Q

Ostium secundum

A

most common type of ASD - too large a central hole to becovered

98
Q

Spteum secundum

A

second type of ASD: due to inadequte development to cover regular size ostium secundum

99
Q

Magnitude of ASD is determined by

A

size and resistance of LV and RV. Moves from LA to RA because it is more compliant and lower resistance.

100
Q

Clinical Presentation of ASD

A

RARE in infancy because LV is approximately equal to RV pressure due to fluid filled lungs. Long term: pulmonary hypertension, atrial arrhythmia, CHF

101
Q

PE of ASD

A

large: increased respiratory rate, sweating, hepatomegaly Murmur that is not due to shunt blood flow. Systolic ejection murmur and disatolic rumble with side split S2

102
Q

Systolic ejection murmur in ASD is due to

A

excess flow across Pulmonary valve

103
Q

Diastolic murmur in ASD is due to

A

excess flow across tricuspid valve

104
Q

ASD Murmur

A

Systolic Ejection murmur due to excess flow across PV Diastolic rumble due to excess flow across TV Split S2 (accentuated with both exhalation and inhalation) due to increased RV pressure

105
Q

CXR on ASD

A

Variable size heart, pulmonary artery elargement, pulmonary vascular markings

106
Q

Treatment of ASD

A

in infants: diuretics Adults or children or symptomatic infants: fix the hole!

107
Q

VSD cuases

A

75% due to preimembranous portion 10% due to muscular Some due to infundibular

108
Q

magnitude of VSD

A

size and systemic and pulmonic vascular resistance

109
Q

Pathophysiology of VSD

A

left to right shunt, increased lung flow, increased LA flow, increased EDV, increased muscle length, increased contraction, increased LV output.

110
Q

Clinical Presentation of VSD

A

asymptomatic until pulmonary pressure decreases significnatly (delayed at elevation). Large VSD: causes respiratory distress, diaphoresis, failure to thrive Small VSD: tachypnea, diaphoresis

111
Q

PE of VSD large vs. small

A

large: active precordium, holosystolic murmur, diastolic murmur 2nd heart sound delay small: normal precordial cells, normal S2, early systolic murmur. no diastolic murmur.

112
Q

Murmur in VSD

A

Holosystolic murmur represents shunting of blood form LV to RV. Decreases to early systolic in small VSDs. Diastolic murmur represtsns increased flow across MV in large VSD cases. Delayed S2 due to increased RV volume in large VSDs

113
Q

Is a quiet VSD murmur good?

A

not necessary - could mean equalization of LV and RV pressures OR increased Pulmonary Vascular Resistance.

114
Q

Is a loud VSD murmur bad?

A

not necessarily - could bean closure or increase in pressure change.

115
Q

CXR in VSD

A

RV and LV hypertrophy, pulmonary edema, enlarged pulmonary a.

116
Q

which murmur, ASD or VSD, is due to blood flow in shunt?

A

VSD only

117
Q

long term remodeling in VSD

A

RV and LV hypertrophy - no dilation because blood goes directly into pulmonary a.

118
Q

Treatment of VSD

A

Diuretics for HF or pulmonary edema Surgery if persistent symptoms despite treatment, poor growth, or secondary complications.

119
Q

Eisenmenger’s

A

when it starts a Left to right shunt, but pulmonary hypertension gets so severe that RV pressure exceeds LV to shunt from Right to left and cuase cynaosis and clubbing.

120
Q

Tetralogy of Fallot

A

cyatonic defect with Pulmonary Stenosis, RVH, Aorta overrides VSD to receive blood from LV and RV, and VSD. RV pressure equals LV pressure, but flow in from right to left.

121
Q

Embryology of TOF

A

conal crest abnormality to displace infundibular septum anteriorly, rightward, and superiorly

122
Q

Magnitude of TOF

A

source of pulmonary BF, severity of pulmonary stenosis, balance of RV and LV pressures

123
Q

Pink vs blue baby in TOF

A

Pink: if with mild pulmonic stenosis and patent DA Blue if severe stonisis and no PDA (right to left)

124
Q

Tet spells

A

hypoxic and hypercyanotic at 2-6 months that is alleviated by squatting. Infundibular spasm to decreased pulmonary Blood flow Usualy triggered by crying, anemia,, dehydration,

125
Q

why does squatting help in TOF

A

increases systemic vascular resistance to decreases the Right to left shunt.

126
Q

Tx of Tet spells

A

Knees to chest, phenylephrine to increase systemic vascular resistance and pulmonary blood flow, fluids, morphine. Can be prevented by beta blockers

127
Q

Diagnosis of TOF

A

RV domination of precordial impulse Systolic Pulmonic stenosis murmur RVHypertrophy

128
Q

Treatment of TOF

A

propanolol to prevent tet spells Surgury at 2-4 months to close VSD and open Pulmonary A. at expense of AV Prostaglandin to keep DA open

129
Q

If untreated TOF

A

cyanosis, clubbing, poor enamel and teeth, increased bleeding, limited exercise tolerance, arrhythmias, cerebral abcesses

130
Q

Cerebral Abcesses

A

complication of TOF and other cyanotic cogential defects. Occurs after 1.5-2 years. Causes unexplained fevers and behavior changes

131
Q

What conditions is coarctation of the aorta associated with?

A

bicuspid AV and Turners

132
Q

Embryology of CoArch

A

extension of ductal tissue to aortic arch Subclavian a. distruvance decreased blood flow through isthmus as fetus Intraluminal projection

133
Q

Clinical presentaiton of coarch

A

necrotizing enterocolitis, leg claudication with exercise, decreased kidney flow–> rebound hypertension with ductus patent - asymptomatic at 1-2 weeks: tachypnic, diaphoretic, decreased feeding, shock with HF, Lack of femoral pulses Systmic hypertension in childhood

134
Q

Physical Exam of CoArch

A

tachycardia, higher BP in arms than legs, pulmonary rales, hypatomegaly, absent or weak femoral pulses. Murmur: systolic click over bicupsid AV soft systolic murmur S2 with S3 gallop

135
Q

CXR of coarch

A

signs of cardia failure Rib notching from dialted intercostal a. aortic knob post stenotic dilation

136
Q

Untreated Coarch

A

HF>aortic rupture or dissection>infective endocarditis > cerebral hemorrhage

137
Q

Pressure and O2 sat for PDA

A

increase in O2 sat between RV and PA Increased diastolic pressure in PA. Increased systolic Pressure in RV, PA, LA, LV, Aorta

138
Q

Pressure and O2 sat for ASD

A

increased O2 sat in RA vs IVC/SVC

139
Q

Pressure and O2 sat for VSD

A

increased O2 sat in RV compared to RA

140
Q

Pressure O2 sat for TOF

A

decreased O2 sat between LA and LV. Increase pressure in RV compared to low PA pressure

141
Q

Primary vs secondary congenital heart defect

A

primary - genetic secondary - extrinsic or environmental

142
Q

Left to right shunts

A

ASD, VSD, AVSD

143
Q

Most common left to right shunts

A

VSD

144
Q

Down syndrome defects

A

ASD, VSD, AVSD, AV valve malformations

145
Q

Rubella leads to

A

PDA in child

146
Q

Turner causes…

A

CoArch, Bicuspid AV, hypoplastic LH

147
Q

Digeorge (del 22) causes.

A

TOF, truncus arteriosus, aortic arch deficit

148
Q

where is infundibular VSD?

A

below pulmonary valve

149
Q

What is transpositon of Great vessels assoicated with?

A

VSD, PFO, PDA

150
Q

infantile Coarch

A

hypoposia of aortic arch

151
Q

Adult CoArch

A

infodling of ligamentum arteriosum

152
Q

AV stenosis - congenital

A

Sub, valvular, and supra which are all due to mineralization and fibrosis.

153
Q

Valvular AV stenosis

A

atretic or severe, associated with hypoplastic LH syndrome

154
Q

PV stenosis congenital

A

isoalted or with TOF

155
Q

Moderate congeital Aortic Stenosis

A

25-49 mmHg decrease intense exercise

156
Q

Intermediate congenital Aortic stenosis

A

50-79 mmHg Depends on doctor

157
Q

Severe congenital aortic stenosis

A

>80 mmHg balloon, or valve replacement

158
Q

Hypolastic Left heart

A

underdevelopment of Aorta, AV, LV, LA, MV to cuase blood flow to go out PDA and leads to cyanosis

CVPR (12 decks)

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