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
Are VSDs m/c in isolation? When else would they occur?
-Yes, 60% isolated -Other 40% are apart of a chromosomal disorder
26
If we see a VSD, what other abnormalities should we look for?
Extracardiac abnormalities
27
75% of VSDs occur in what?
The membranous/perimembranous section of the septum (common with tetralogy of fallot - TOF)
28
List the 4 types of VSD muscular defects?
-Inlet -Outlet (aka subarterial or conal) -Trabecular (aka midmuscular or central) -Apical
29
Where do inlet defects affect?
Portion of septum extending from TV leaflets (think going into heart we hit the TV first)
30
Where do outlet defects affect?
Most superior portion of septum, close to AoV + PV (think going out of heart through AoV + PV, aka subarterial/conal defects)
31
Where do trabecular defects affect?
Midportion of septum (aka midmuscular/central defects)
32
Where do apical defects occur?
Close to apex of heart, past insertion point of moderator band (think apical = apex)
33
VSDs are best detected with the u/s beam parallel or perpendicular to the IVS in a 4 ch view?
-Perpendicular -Always demonstrate in 2 views so we know it is not just dropout
34
What other views can assist in finding VSDs?
LVOT + RVOT
35
What u/s function can we use to help detect VSDs?
CD
36
Do we want to set our PRF/scale high or low when using CD to evaluate VSDs?
Low b/c we want to detect low flow (may not show well b/c RV + LV are relatively equal pressure in the fetus)
37
If CD flow is seen in the membranous portion of the IVS, is this a true VSD?
No, is likely artifact
38
How common are ASDs?
-1 in 1,500 births -5th m/c congenital cardiac anomaly
39
What is the m/c type of ASD?
Ostium secundum defect (80% of cases, is in middle of atrial septum)
40
What is the 2nd m/c type of ASD?
Ostium primum defect (is the bottom portion of atrial septum)
41
Which type of ASD usually occurs as part of a complex anomaly such as an AV defect?
Ostium primum
42
Sinus venous ASDs involve a defect adjacent to the SVC or IVC, which leads to what?
Leads to right to left shunts (top portion of atrial septum)
43
ASDs are best seen in what view?
4 chamber subcostal view
44
What are ASDs often confused by?
The normal foramen ovale
45
Why is color flow limited in utility when looking for ASDs?
Due to the turbulent flow caused by the foramen ovale
46
What are ASDs frequently associated with?
Other complex anomalies
47
If a fetus has transposition of the great vessels, would an ASD be a good thing in this case?
-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
48
Other terms for atrioventriculer septal defects (AVSDs)?
-AV canal defects -Endocardial cushion defects
49
When do AVSDs occur?
When the endocardial cushions of the heart fail to fuse properly
50
AVSDs are associated with what?
-All 3 major trisomies -Variety of syndromes + chromosomal abnormalities
51
45% of heart lesions in a fetus with trisomy 21 (down syndrome) are what?
AVSDs
52
Are AVSDs easily recognized? What view should we look in?
-Yes b/c they are large defects -Look in subcostal or apical 4 ch view
53
If we see an AVSD, what else should we look for?
Nuchal fold + other down syndrome indicators
54
What is the most severe left sided obstructive lesion?
Hypoplastic left heart syndrome
55
What is the m/c cause of death from congenital heart defect (CHD) in the neonatal period?
Hypoplastic left heart syndrome
56
What does hypoplastic left heart syndrome include?
-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
What is the first finding of hypoplastic left heart syndrome?
MV stenosis
58
When will findings of hypoplastic left heart syndrome be fully present?
Late 2nd trimester
59
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?
Imaging should be repeated again later in gestation
60
Does the hypoplastic left heart maintain the normal cardiac axis?
Yes!
61
Which view will show the size discrepancy b/w the right + left side with hypoplastic left heart syndrome?
4 ch view (moderator band should be noted in the RV to confirm that it is the LV that is hypoplastic)
62
The degree of AO atresia or hypoplasia can be assessed in which 2 views?
-SAX right outflow tract OR -3VV
63
Is the MV generally stenotic or atretric with hypoplastic left heart syndrome?
Yes
64
What should we use to document the patency + direction of the ductus arteriosis + foramen ovale?
Doppler
65
Is RV hypoplasia common?
No, extremely uncommon!
66
What does RV hypoplasia result from generally?
From pulmonary atresia with an intact ventricular septum
67
RV hypoplasia from pulmonary atresia can be diagnosed by identification of what?
Unusually small RV in either an apical or subcostal 4 ch view
68
Which 2 views will show a small hyperechoic PA with RV hypoplasia/pulmonary atresia?
-LAX of PA -SAX right outflow tract
69
RV hypoplasia results in what type of lesion?
A ductal-dependent lesion (the ductus arteriosus + foramen ovale should be inspected)
70
What does tricuspid atresia result in?
RV hypoplasia due to lack of inflow from RA
71
What is tricuspid atresia?
A progressive lesion that gets worse as pregnancy progresses
72
With TV atresia, the presence of a VSD may allow for a left to right shunt. This may preserve what?
Some of the RV development
73
SF of TV atresia?
-Hyperechoic -Thick -No CD flow on either side of valve
74
What is present in approx 25% of cases of TV atresia?
PV atresia (PV + PA should be assessed using SAX right outflow tract views)
75
In the presence of a normal foramen ovale, is the LA + ventricles expected to be larger or smaller?
Larger - some degree of LA + ventricular enlargement is expected
76
What is coarction of the AO?
-Narrowing of the AO along the AO arch -Results in outflow obstruction (depending on how narrow the AO is)
77
3 types of AO coarction?
-Preductal (top) -Ductal (in middle) -Postductal (bottom)
78
What happens in severe cases of AO coarction?
A complete interruption can occur (normally is just narrowing of the AO tho)
79
Explain where type A, B + C lesions occur in regards to AO coarction?
A: occur just distal to left subclavian B: occur b/w left carotid + left subclavian C: occur b/w innominate + left carotid
80
70% of AO coarction is associated with what 2 things?
-Vascular anomalies (berry aneurysms) -Extracardiac anomalies (m/c genitourinary)
81
Is AO coarction difficult to diagnose prenatally?
Yes! One of the most difficult
82
What would AO coarction look like?
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
What view should we evaluate in to assess for AO coarction?
SAX right outflow tract view (b/c bicuspid AoV is associated with cases of coarction)
84
How common is tetralogy of fallot (TOF)?
-1 in 3,600 births -7% of congenital heart defects
85
What is the m/c form of cyanotic heart disease?
TOF
86
What are the 4 classic features of tetralogy?
1: perimembranous/conal VSD 2: overriding AO (encompasses the defect) 3: pulmonary stenosis or atresia 4: RV hypertrophy
87
What views can we assess for TOF?
-Perimembranous VSD can be seen in either apical or subcostal 4 ch view -VSD + AO override can be assessed in LAX of LVOT
88
What pathology can be confused with TOF?
DORV (double outlet right ventricle) -If more than 50% of the AO overrides the RV, DORV is more likely the case
89
What are the 3 types of PA abnormalities with TOF?
-Pulmonary stenosis -Pulmonary atresia with a patent ductus -Pulmonary atresia with major aortopulmonary collaterals (evaluate using SAX right outflow tract views)
90
If the PA is present but small in diameter compared to the AO root, what diagnosis does this support?
TOF
91
Is RV hypertrophy always apparent on an initial prenatal u/s with TOF?
No, commonly seen postnatally
92
50% of fetuses with TOF have chromosomal abnormalities, what are they?
-Trisomy 21 -DiGeorge syndrome
93
What is ebstein anomaly?
When the posterior + septal TV leaflets are apically displaced from their normal location (at the AV junction into the RV)
94
Which chamber is abnormally large + pathologically small with ebstein anomaly?
Large: RA Small: RV
95
The aberrant (unusual) TV leaflets with ebstein anomaly may be adherent to the ventricular wall, what will this result in?
Abnormally small mobile portions of the valve cusps
96
Ebstein anomaly frequently causes severe dysfunction in uteruo, list 3 dysfunctions it includes?
-Cardiomegaly -Hydrops -Arrhythmias
97
What is associated with a 28x increased risk of ebstein anomaly if ingested by the mom?
Lithium carbonate (has huge impact on development of fetal heart)
98
Is ebstein anomaly associated with chromosomal abnormalities?
Yes - trisomy 13, 18 + 21
99
What number is the diagnostic offsets for fetuses with ebstein anomaly usually greater than?
8mm (measure the offset b/w septal leaflets of MV + TV)
100
2 types of transposition of the great arteries?
-Complete (d-transposition) -Congenitally corrected (CCTGA or I-transposition)
101
What does the "d" + "I" represent with transposition of the great arteries?
Denotes location of AO in relation to PA d: right I: left
102
In which condition/category of transposition of the great arteries does the PA arise from the LV + the AO arise from the RV?
Both!! (we will find this during our sweeps of the outflow tracts. normal = cross, abnormal = parallel)
103
What happens in complete transposition of the great arteries?
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
What does transposition of the great arteries result in, in regards to circulation?
In systemic + pulmonary circulation that functions in parallel rather than in sequence
105
Complete TGA has a higher incidence in males or females?
Males
106
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?
Need at least an ASD or VSD
107
In complete transposition, will the apical + subcostal 4 ch view usually look completely normal or abnormal?
Normal (know this, was on midterm)
108
How would TGA look in short + long axis?
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
Should we assess the ventricular septum with TGA?
Yes! A VSD is present in 20% of cases
110
Is complete or congenitally corrected (CCTGA) transposition m/c?
Complete (CCTGA is extremely rare)
111
What is CCTGA?
-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
In CCTGA, is the moderator band + TV seen connecting to the LA or RA?
LA (think is opposite than normal)
113
What is truncus arteriosis?
-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
What is uniformly present within the upper portion of the septum, just below the location of the truncus with truncus arteriosis?
A VSD
115
A single valve is present with truncus arteriosis, where is it?
-Directly above VSD or -Above RV
116
Does the truncus arteriosis receive blood from both RV + LV?
Yes, it perfuses into pulmonary, systemic + coronary systems
117
List associated cardiac anomalies with truncus arteriosis?
-Valvular insufficiency/stenosis -Absent ductus arteriosis (50-75%) -Right sided AO arch (30%)
118
Why is diagnosing truncus arteriosis often missed?
B/c often only abnormality seen on views is VSD
119
With truncus arteriosis, what would be seen in LAX of LVOT + SAX of RVOT?
LAX of LVOT: single vessel overriding VSD SAX of RVOT: single truncal valve seen (encircling PA is absent)
120
What is the m/c prenatally diagnosed cardiac tumor?
Rhabdomyoma (echogenic mass in RV, LV or IVS)
121
Several pt's with rhabdomyomas are subsequently diagnosed with what?
Tuberous sclerosis
122
Cardiac tumors are rare + can result in arrhythmias, m/c which one?
Supraventricular (SVT)
123
Rhabdomyomas that obstruct the MV, TV, PV or AoV can cause what?
Valvular stenosis
124
What is a double outlet right ventricle (DORV)?
Group of disorders where the AO + PA arise from the RV (above a perimembranous VSD)
125
The VSD with DORV is m/c where?
Below AO, with AO + PA lateral to each other
126
4 main types of DORV?
-VSD type -Fallot type -TGA type -Noncommittal VSD type
127
DORV is hard to differentiate b/w what other 2 conditions?
-Tetralogy (fallot type) -HLHS (hypoplastic left heart syndrome)
128
Does DORV have parallel or crossing outflow tracts?
Parallel (similar to TGA)
129
Why does the 4 ch view often look normal when a fetus has DORV?
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
Are other cardiac anomalies, poorly controlled diabetes + chromosomal abnormalities associated with DORV?
Yes (cardiac 65-70%, extracardiac 47%)