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MIDS 187 > Ch 9 Abnormal Heart > Flashcards

Ch 9 Abnormal Heart Flashcards

1
Q

What is considered tachycardia + bradycardia in fetuses?

A

Tachy: over 180 bpm
Brady: under 100 bpm

(if sustained they can have severe clinical consequences)

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2
Q

We primarily assess arrhythmias using what?

A

M-mode

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3
Q

Is atria or ventricular rate assessed using m-mode?

A

Both!

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4
Q

What is the m/c benign arrhythmia?

A

PACs (premature atrial contractions)

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5
Q

Can PACs be conducted + non-conducted?

A

Yes!

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6
Q

What does it mean when PACs are conducted?

A

-They affect the ventricle
-Can lead to sustained tachy
-Occurs 2-3% of the time

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7
Q

What does it mean when PACs are non-conducted?

A

It stops at the AV node

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8
Q

Rate of SVT?

A

180-300 bpm

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9
Q

What is the ratio of atrial + ventricular beats with SVT?

A

1:1 ratio

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10
Q

What is SVT associated with in 10% of cases?

A

Structural cardiac lesions

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11
Q

If a fetus has SVT, what medication can be administered to the mother to treat it?

A

Digoxin (if structural)

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12
Q

A fetus with SVT that does not respond to treatment is at risk for what?

A

-Nonimmune hydrops
-Heart failure

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13
Q

What is the rate of atrial flutter?

A

300-400 bpm

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14
Q

What is the ratio of atrial to ventricular beats with atrial flutter?

A

2:1

-2 atrial beats for each ventricular beat
-there are dropped ventricular beats at a set rate

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15
Q

Is A-FIB rare?

A

Extremely rare!!

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16
Q

What is the rate of A-FIB?

A

Over 400 bpm

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17
Q

What is A-FIB? How does it differ from flutter?

A

-Irregular atrial rate (unlike flutter)
-No set ventricular conduction pattern (unlike flutter)

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18
Q

What heart condition are we concerned about when a fetus has bradycardia?

A

Heart block

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19
Q

What is the most severe form of a heart block?

A

3rd degree AV block

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20
Q

What would a 3rd degree AV block look like in terms of the atrial + ventricular HR?

A

-Normal atrial rate (120-180 bpm)
-Ventricular rate of approx 70 bpm or slower

(use m-mode to evaluate atria + ventricles)

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21
Q

If a fetus has a 3rd degree AV block, how will we treat this?

A

May deliver baby + do external pacing of the fetus

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22
Q

What is transient fetal bradycardia? Is it common?

A

-Slow HR that comes + goes
(heart can completely stop too)

-Very common

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23
Q

Can probe pressure cause the heart to slow down or stop?

A

Yes! In transient fetal bradycardia

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24
Q

What is the m/c cardiac malformation?

A

Isolated VSDs - ventricular septal defects

(accounts for 30% of cardiac abnormalities, incidence of 1-2%)

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25
Q

Are VSDs m/c in isolation? When else would they occur?

A

-Yes, 60% isolated
-Other 40% are apart of a chromosomal disorder

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26
Q

If we see a VSD, what other abnormalities should we look for?

A

Extracardiac abnormalities

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27
Q

75% of VSDs occur in what?

A

The membranous/perimembranous section of the septum

(common with tetralogy of fallot - TOF)

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28
Q

List the 4 types of VSD muscular defects?

A

-Inlet
-Outlet (aka subarterial or conal)
-Trabecular (aka midmuscular or central)
-Apical

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29
Q

Where do inlet defects affect?

A

Portion of septum extending from TV leaflets

(think going into heart we hit the TV first)

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30
Q

Where do outlet defects affect?

A

Most superior portion of septum, close to AoV + PV

(think going out of heart through AoV + PV,
aka subarterial/conal defects)

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31
Q

Where do trabecular defects affect?

A

Midportion of septum

(aka midmuscular/central defects)

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32
Q

Where do apical defects occur?

A

Close to apex of heart, past insertion point of moderator band

(think apical = apex)

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33
Q

VSDs are best detected with the u/s beam parallel or perpendicular to the IVS in a 4 ch view?

A

-Perpendicular
-Always demonstrate in 2 views so we know it is not just dropout

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34
Q

What other views can assist in finding VSDs?

A

LVOT + RVOT

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35
Q

What u/s function can we use to help detect VSDs?

A

CD

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36
Q

Do we want to set our PRF/scale high or low when using CD to evaluate VSDs?

A

Low b/c we want to detect low flow

(may not show well b/c RV + LV are relatively equal pressure in the fetus)

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37
Q

If CD flow is seen in the membranous portion of the IVS, is this a true VSD?

A

No, is likely artifact

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38
Q

How common are ASDs?

A

-1 in 1,500 births
-5th m/c congenital cardiac anomaly

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39
Q

What is the m/c type of ASD?

A

Ostium secundum defect

(80% of cases, is in middle of atrial septum)

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40
Q

What is the 2nd m/c type of ASD?

A

Ostium primum defect

(is the bottom portion of atrial septum)

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41
Q

Which type of ASD usually occurs as part of a complex anomaly such as an AV defect?

A

Ostium primum

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42
Q

Sinus venous ASDs involve a defect adjacent to the SVC or IVC, which leads to what?

A

Leads to right to left shunts

(top portion of atrial septum)

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43
Q

ASDs are best seen in what view?

A

4 chamber subcostal view

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44
Q

What are ASDs often confused by?

A

The normal foramen ovale

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45
Q

Why is color flow limited in utility when looking for ASDs?

A

Due to the turbulent flow caused by the foramen ovale

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46
Q

What are ASDs frequently associated with?

A

Other complex anomalies

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47
Q

If a fetus has transposition of the great vessels, would an ASD be a good thing in this case?

A

-Yes b/c without an ASD when the foramen ovale closes at birth the baby will result in death

-This is b/c the ASD allows the only route for pulmonary return to enter the left side of the heart

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48
Q

Other terms for atrioventriculer septal defects (AVSDs)?

A

-AV canal defects
-Endocardial cushion defects

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49
Q

When do AVSDs occur?

A

When the endocardial cushions of the heart fail to fuse properly

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50
Q

AVSDs are associated with what?

A

-All 3 major trisomies
-Variety of syndromes + chromosomal abnormalities

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51
Q

45% of heart lesions in a fetus with trisomy 21 (down syndrome) are what?

A

AVSDs

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52
Q

Are AVSDs easily recognized? What view should we look in?

A

-Yes b/c they are large defects
-Look in subcostal or apical 4 ch view

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53
Q

If we see an AVSD, what else should we look for?

A

Nuchal fold + other down syndrome indicators

54
Q

What is the most severe left sided obstructive lesion?

A

Hypoplastic left heart syndrome

55
Q

What is the m/c cause of death from congenital heart defect (CHD) in the neonatal period?

A

Hypoplastic left heart syndrome

56
Q

What does hypoplastic left heart syndrome include?

A

-Hypoplastic/underdeveloped LV
-AO atresia/narrowing
-Hypoplasia/underdevelopment of asc AO
-MV atresia + hypoplasia
-Sometimes a small LA

(image shows LV really small + AO really narrow)

57
Q

What is the first finding of hypoplastic left heart syndrome?

A

MV stenosis

58
Q

When will findings of hypoplastic left heart syndrome be fully present?

A

Late 2nd trimester

59
Q

What should we do if we suspect the left sided heart structures are smaller compared to the right side? Or if there is concern about the MV function?

A

Imaging should be repeated again later in gestation

60
Q

Does the hypoplastic left heart maintain the normal cardiac axis?

A

Yes!

61
Q

Which view will show the size discrepancy b/w the right + left side with hypoplastic left heart syndrome?

A

4 ch view

(moderator band should be noted in the RV to confirm that it is the LV that is hypoplastic)

62
Q

The degree of AO atresia or hypoplasia can be assessed in which 2 views?

A

-SAX right outflow tract
OR
-3VV

63
Q

Is the MV generally stenotic or atretric with hypoplastic left heart syndrome?

A

Yes

64
Q

What should we use to document the patency + direction of the ductus arteriosis + foramen ovale?

A

Doppler

65
Q

Is RV hypoplasia common?

A

No, extremely uncommon!

66
Q

What does RV hypoplasia result from generally?

A

From pulmonary atresia with an intact ventricular septum

67
Q

RV hypoplasia from pulmonary atresia can be diagnosed by identification of what?

A

Unusually small RV in either an apical or subcostal 4 ch view

68
Q

Which 2 views will show a small hyperechoic PA with RV hypoplasia/pulmonary atresia?

A

-LAX of PA
-SAX right outflow tract

69
Q

RV hypoplasia results in what type of lesion?

A

A ductal-dependent lesion

(the ductus arteriosus + foramen ovale should be inspected)

70
Q

What does tricuspid atresia result in?

A

RV hypoplasia due to lack of inflow from RA

71
Q

What is tricuspid atresia?

A

A progressive lesion that gets worse as pregnancy progresses

72
Q

With TV atresia, the presence of a VSD may allow for a left to right shunt. This may preserve what?

A

Some of the RV development

73
Q

SF of TV atresia?

A

-Hyperechoic
-Thick
-No CD flow on either side of valve

74
Q

What is present in approx 25% of cases of TV atresia?

A

PV atresia

(PV + PA should be assessed using SAX right outflow tract views)

75
Q

In the presence of a normal foramen ovale, is the LA + ventricles expected to be larger or smaller?

A

Larger - some degree of LA + ventricular enlargement is expected

76
Q

What is coarction of the AO?

A

-Narrowing of the AO along the AO arch
-Results in outflow obstruction (depending on how narrow the AO is)

77
Q

3 types of AO coarction?

A

-Preductal (top)
-Ductal (in middle)
-Postductal (bottom)

78
Q

What happens in severe cases of AO coarction?

A

A complete interruption can occur

(normally is just narrowing of the AO tho)

79
Q

Explain where type A, B + C lesions occur in regards to AO coarction?

A

A: occur just distal to left subclavian
B: occur b/w left carotid + left subclavian
C: occur b/w innominate + left carotid

80
Q

70% of AO coarction is associated with what 2 things?

A

-Vascular anomalies (berry aneurysms)
-Extracardiac anomalies (m/c genitourinary)

81
Q

Is AO coarction difficult to diagnose prenatally?

A

Yes! One of the most difficult

82
Q

What would AO coarction look like?

A

If there is RV enlargement in the 4 ch view w/o visualization of other abnormalities, this will indicate high suspicion

(evaluate AO arch diameter in SAG for subtle signs of narrowing)

83
Q

What view should we evaluate in to assess for AO coarction?

A

SAX right outflow tract view

(b/c bicuspid AoV is associated with cases of coarction)

84
Q

How common is tetralogy of fallot (TOF)?

A

-1 in 3,600 births
-7% of congenital heart defects

85
Q

What is the m/c form of cyanotic heart disease?

A

TOF

86
Q

What are the 4 classic features of tetralogy?

A

1: perimembranous/conal VSD
2: overriding AO (encompasses the defect)
3: pulmonary stenosis or atresia
4: RV hypertrophy

87
Q

What views can we assess for TOF?

A

-Perimembranous VSD can be seen in either apical or subcostal 4 ch view

-VSD + AO override can be assessed in LAX of LVOT

88
Q

What pathology can be confused with TOF?

A

DORV (double outlet right ventricle)

-If more than 50% of the AO overrides the RV, DORV is more likely the case

89
Q

What are the 3 types of PA abnormalities with TOF?

A

-Pulmonary stenosis
-Pulmonary atresia with a patent ductus
-Pulmonary atresia with major aortopulmonary collaterals

(evaluate using SAX right outflow tract views)

90
Q

If the PA is present but small in diameter compared to the AO root, what diagnosis does this support?

A

TOF

91
Q

Is RV hypertrophy always apparent on an initial prenatal u/s with TOF?

A

No, commonly seen postnatally

92
Q

50% of fetuses with TOF have chromosomal abnormalities, what are they?

A

-Trisomy 21
-DiGeorge syndrome

93
Q

What is ebstein anomaly?

A

When the posterior + septal TV leaflets are apically displaced from their normal location (at the AV junction into the RV)

94
Q

Which chamber is abnormally large + pathologically small with ebstein anomaly?

A

Large: RA
Small: RV

95
Q

The aberrant (unusual) TV leaflets with ebstein anomaly may be adherent to the ventricular wall, what will this result in?

A

Abnormally small mobile portions of the valve cusps

96
Q

Ebstein anomaly frequently causes severe dysfunction in uteruo, list 3 dysfunctions it includes?

A

-Cardiomegaly
-Hydrops
-Arrhythmias

97
Q

What is associated with a 28x increased risk of ebstein anomaly if ingested by the mom?

A

Lithium carbonate

(has huge impact on development of fetal heart)

98
Q

Is ebstein anomaly associated with chromosomal abnormalities?

A

Yes - trisomy 13, 18 + 21

99
Q

What number is the diagnostic offsets for fetuses with ebstein anomaly usually greater than?

A

8mm

(measure the offset b/w septal leaflets of MV + TV)

100
Q

2 types of transposition of the great arteries?

A

-Complete (d-transposition)

-Congenitally corrected (CCTGA or I-transposition)

101
Q

What does the “d” + “I” represent with transposition of the great arteries?

A

Denotes location of AO in relation to PA

d: right
I: left

102
Q

In which condition/category of transposition of the great arteries does the PA arise from the LV + the AO arise from the RV?

A

Both!!

(we will find this during our sweeps of the outflow tracts. normal = cross, abnormal = parallel)

103
Q

What happens in complete transposition of the great arteries?

A

The connection b/w atria + ventricles is concordant (normal):
-RA connects with the RV
-LA connects with LV

Abnormal (is flipped):
-AO comes off RV (causing deoxygenated blood to circulate systemically)
-PA comes off LV

104
Q

What does transposition of the great arteries result in, in regards to circulation?

A

In systemic + pulmonary circulation that functions in parallel rather than in sequence

105
Q

Complete TGA has a higher incidence in males or females?

A

Males

106
Q

What do we “need” for oxygenated blood from LV to reach RV/systemic circulation so that fetus can live until correction can be performed with TGA?

A

Need at least an ASD or VSD

107
Q

In complete transposition, will the apical + subcostal 4 ch view usually look completely normal or abnormal?

A

Normal

(know this, was on midterm)

108
Q

How would TGA look in short + long axis?

A

Short axis of right outflow tract: PA encircling central AO is lost

Long axis of outflow tracts: AO + PA run parallel (w/o normal crossing pattern)

109
Q

Should we assess the ventricular septum with TGA?

A

Yes! A VSD is present in 20% of cases

110
Q

Is complete or congenitally corrected (CCTGA) transposition m/c?

A

Complete (CCTGA is extremely rare)

111
Q

What is CCTGA?

A

-RA connects to LV, which connects to PA
-LA connects to RV, which connects to AO

(RA/LA are usually in correct locations on top, but dextrocardia is present in up to 20% of cases)

112
Q

In CCTGA, is the moderator band + TV seen connecting to the LA or RA?

A

LA (think is opposite than normal)

113
Q

What is truncus arteriosis?

A

-Rare
-When the truncoconal ridges that normally divide the truncus arteriosis into AO + pulmonary trunks fails to fuse
-A single great vessel arises just above IVS

114
Q

What is uniformly present within the upper portion of the septum, just below the location of the truncus with truncus arteriosis?

A

A VSD

115
Q

A single valve is present with truncus arteriosis, where is it?

A

-Directly above VSD
or
-Above RV

116
Q

Does the truncus arteriosis receive blood from both RV + LV?

A

Yes, it perfuses into pulmonary, systemic + coronary systems

117
Q

List associated cardiac anomalies with truncus arteriosis?

A

-Valvular insufficiency/stenosis
-Absent ductus arteriosis (50-75%)
-Right sided AO arch (30%)

118
Q

Why is diagnosing truncus arteriosis often missed?

A

B/c often only abnormality seen on views is VSD

119
Q

With truncus arteriosis, what would be seen in LAX of LVOT + SAX of RVOT?

A

LAX of LVOT: single vessel overriding VSD

SAX of RVOT: single truncal valve seen (encircling PA is absent)

120
Q

What is the m/c prenatally diagnosed cardiac tumor?

A

Rhabdomyoma

(echogenic mass in RV, LV or IVS)

121
Q

Several pt’s with rhabdomyomas are subsequently diagnosed with what?

A

Tuberous sclerosis

122
Q

Cardiac tumors are rare + can result in arrhythmias, m/c which one?

A

Supraventricular (SVT)

123
Q

Rhabdomyomas that obstruct the MV, TV, PV or AoV can cause what?

A

Valvular stenosis

124
Q

What is a double outlet right ventricle (DORV)?

A

Group of disorders where the AO + PA arise from the RV (above a perimembranous VSD)

125
Q

The VSD with DORV is m/c where?

A

Below AO, with AO + PA lateral to each other

126
Q

4 main types of DORV?

A

-VSD type
-Fallot type
-TGA type
-Noncommittal VSD type

127
Q

DORV is hard to differentiate b/w what other 2 conditions?

A

-Tetralogy (fallot type)
-HLHS (hypoplastic left heart syndrome)

128
Q

Does DORV have parallel or crossing outflow tracts?

A

Parallel (similar to TGA)

129
Q

Why does the 4 ch view often look normal when a fetus has DORV?

A

B/c the VSD is m/c anterior + may not be apparent on the apical/subcostal views

(confirm there is both MV + TV, as AVSDs often only have 1 valve present)

130
Q

Are other cardiac anomalies, poorly controlled diabetes + chromosomal abnormalities associated with DORV?

A

Yes

(cardiac 65-70%, extracardiac 47%)

MIDS 187 (19 decks)

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