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MFM Written Boards (Andrews) > Maternal cardiac > Flashcards

Maternal cardiac Flashcards

1
Q

What is NYHA (New York Heart Association) class 1?

A

No cardiac symptoms

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2
Q

What is NYHA (New York Heart Association) class II?

A

Cardiac symptoms with greater than normal activity (e.g., carrying packages)

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3
Q

What is NYHA (New York Heart Association) class III?

A

Cardiac symptoms with normal activity (e.g., getting dressed)

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4
Q

What is NYHA (New York Heart Association) class IV?

A

Cardiac symptoms with bedrest

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5
Q

With which two NYHA classes is pregnancy not advised?

A

NYHA 3-4

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6
Q

How does cardiac dysfunction present?

A

Fatigue, limited activity, palpitations, tachycardia, SOB, chest pain, dyspnea on exertion, cyanosis

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7
Q

What 4 cardiac conditions are contraindications to pregnancy?

A

Pulmonary hypertension
Severe ventricular dysfunction
Aortic root dilation (>4cm)
Severe left-sided obstructive lesions

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8
Q

While cardiac disease complicates 1-4% of pregnancies, it accounts for what % of maternal mortality?

A

Up to 25%

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9
Q

For women with congenital heart disease, what is the risk of fetal transmission?

A

5% (from 8/1000 background risk)

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10
Q

What features of pregnancy physiology can exacerbate cardiac disease?

A

Increased intravascular volume
Hypercoagulability
Decreased SVR

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11
Q

What are the general guidelines for pregnancy management in women with cardiac disease?

A 
Relative bedrest
Treat other medical conditions
Multidisciplinary approach
Monitor fetal growth q 4-6w
NST >34w
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12
Q

What are the general guidelines for labor management in women with cardiac disease?

A 
Lateral decubitus position
EpiduralO2
\+/- Endocarditis prophylaxis
Avoid hypotension (keep women ?wetter?) 
C/S for obstetric indications
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13
Q

While most cardiac conditions benefit from relative hypervolemia and relative hypotension intrapartum, what is the exception?

A

Mitral stenosis

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14
Q

Why is fluid overload (ie post-partum autotransfusion) bad for mitral stenosis?

A

The associated restricted LV filling can lead to pulmonary edema

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15
Q

What are the indications for c/s with maternal cardiac disease?

A

Aortic root dilation >4cm
Maternal Coumadin
Recent MI
Severe aortic stenosis

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16
Q

Which cardiac patients/diagnoses may benefit from invasive monitoring in labor?

A

Women with preload dependent conditions (aortic stenosis, PHTN)

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17
Q

Should women with prospthetic cardiac valves receive endocarditis prophylaxis?

A

Yes (during endothelialization)

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18
Q

After what time period after repair of CHD with prosthetic material should women receive endocarditis prophylaxis with delivery?

A

6 months

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19
Q

Does completely repaired CHD (with repair >6m ago) require endocarditis prophylaxis?

A

No

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20
Q

Does unrepaired cyanotic CHD require endocarditis prophylaxis?

A

Yes

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21
Q

If your patient had repair of CHD with prosthetic material remotely but there are residual defects, should they receive endocarditis prophylaxis?

A

Yes

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22
Q

How do we manage a patient with prior infective endocarditis in labor?

A

With endocarditis prophylaxis

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23
Q

When endocarditis prophylaxis is indicated, what antibiotic is used?

A

Ampicillin 2g IV

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24
Q

For PCN allergic women who need endocarditis prophylaxis, what antibiotics can be used?

A

clindamycin, cefazolin, cetriaxone

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25
Q

Is there an ACOG resource to guide endocarditis prophylaxis?

A

Yes - committee opinion 421, Antibiotics prophylaxis for infective endocarditis

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26
Q

What is the workup for palpitations?

A

Thyroid function
Rule out drugs/caffeine/tobacco
EKG
Echo

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27
Q

Are PACs and PVCs more common in pregnancy and typically benign?

A

Yes

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28
Q

What is the risk of complication or death in pregnancy with isolated VSD, repaired or unrepaired (high, moderate, or low)?

A

Low, <1%

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29
Q

When you have a patient with a long-standing large VSD, what should you rule out prior to becoming pregnant?

A

Pulmonary hypertension

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30
Q

Why is decreased SVR bad with pulmonary HTN caused by a VSD?

A

If pulmonary pressures exceed systemic pressures, the typical L-> R shunt can reverse, resulting in cyanosis

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31
Q

How should patients with VSD be managed intrapartum?

A

Avoid fluid overload

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32
Q

How is pulmonary hypertension defined? (What peak pulmonary artery pressures and mean PA pressures?)

A

Pulmonary artery pressure >30 mmHg, or mean pulmonary artery pressure >25 mmHg

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33
Q

What % of women with PHTN on echo have a normal pulm artery cath? (ie. What is the false + rate of a TTE?)

A

30%

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34
Q

What is thought to cause the delayed PP death in pulm HTN?

A

Loss of pregnancy associated hormones and increased pulm vascular resistance

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35
Q

Why is hypotension dangerous with PHTN?

A

Pulmonary perfusion depends on preload

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36
Q

Are patients with PHTN better managed wet or dry?

A

Wet (to avoid hypotension and decreased preload)

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37
Q

How is inhaled NO helpful in PHTN?

A

Inhaled NO selectively reduces pulmonary vascular resistance while sparing SVR (maintaining preload)

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38
Q

What are the goals for medical management of pulmonary HTN (think PVR and ventricular function)?

A

Avoid increasing pulmonary vascular resistance
Maintain RV preload
Maintain RV contractility

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39
Q

What medication is used in the treatment of pulmonary HTN by decreasing pulmonary vascular resistance?

A

Inhaled NO (which causes selective vasodilation of the pulmonary vascular bed)

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40
Q

What is the maternal mortality associated with pulmonary HTN?

A

17-28%

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41
Q

What is the ideal mode of delivery for patients with pulmonary HTN?

A

Vaginal

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42
Q

What are 4 genetic causes of dilated aortic roots?

A

Marfans
Ehlers-Danlos
Loeys-Dietz
Turner syndrome

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43
Q

When is aortic root repair recommended (what dilation, and rate of dilation)?

A

Repair outside of pregnancy is recommended for dilation >5.0 cm, or a rapidly dilating dilation (>0.5 cm per year)

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44
Q

Does pregnancy accelerate pathologic aortic root dilation?

A

Yes

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45
Q

What medication is used in pregnancy to reduce strain on the ascending aorta and reduce the rate of aortic dilation, ie in cases of Marfan’s?

A

B-blockade

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46
Q

When is vaginal delivery safe for a patient with Marfan’s?

A

With epidural, aortic root <4cm, and assisted second stage

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47
Q

What is the mortality associated with Marfan’s if aortic root is <4cm?

A

<1%

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48
Q

What is the risk of aortic dissection or death associated with Marfan’s if aortic root is >4cm?

A

20-50%

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49
Q

How should we evaluate patients with Marfan’s (or FH of Marfan’s) on initial presentation (cardiac, ophtho)?

A

Echocardiogram

Slit lamp study for ectopia lentis

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50
Q

How should we follow patients with Marfan’s in pregnancy?

A

Serial evaluation of the aortic root by echo
B-blockade
Avoid HTN

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51
Q

What spinal anomaly is present in 90% of pt with Marfans that may affect epidural placement?

A

Dural ectasia (widening of the dural sac at the lumbar spine)

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52
Q

Which genetic condition is associated with aortic dissection at diameters smaller than Marfan’s?

A

Loeys-Dietz

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53
Q

What non-genetic conditions predispose women to aortic dissection?

A

Bicuspid aortic valve
CHTN
Aortic coarctation

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54
Q

What is the pregnancy outcome with corrected asymptomatic aortic coarctation?

A

Good

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55
Q

When is aortic coarctation associated with increased risk for maternal mortality

A

With aneurysmal dilation and associated cardiac disease

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56
Q

How should cases of aortic coarctation be managed in labor?

A

Avoid hypotension and bradycardia

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57
Q

In general, how is cardiomyopathy treated?

A 
Oxygen
Diuretics
B-blockers (to avoid tachycardia)
Vasodilators
Inotropes (digoxin)
Anticoagulation
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58
Q

What principles should guide intrapartum management of hypertrophic CM?

A

Avoidance of hypotension, hypovolemia, and tachycardia

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59
Q

How is hypertrophic cardiomyopathy inherited?

A

AD (with variable penetrance)

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60
Q

What is the classic echo finding in hypertrophic cardiomyopathy?

A

Asymmetric LV hypertrophy

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61
Q

What physiologic changes in pregnancy result in worsening cardiac function in patients with hypertrophic cardiomyopathy?

A

Decreased SVR worsens outflow obstruction, and tachycardia decreases diastolic filling time -> decreases cardiac output

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62
Q

Do young asymptomatic women with hypertrophic cardiomyopathy tolerate pregnancy well?

A

Yes

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63
Q

With hypertrophic CM, at what LV gradient do patients become symptomatic?

A

30 mmHg

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64
Q

With hypertrophic CM, at what LV gradient are patients at risk for heart failure and sudden death?

A

100 mmHg

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65
Q

What are the causes of dilated cardiomyopathy?

A 
Myocarditis
Ischemia
CHTN
Alcohol
Familial
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66
Q

With dilated CM, what ejection fraction is concerning for adverse outcome?

A

<40%

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67
Q

Peripartum cardiomyopathy is defined as new onset left ventricular dysfunction (EF <45%) at what time points relative to delivery?

A

1 mo prior to delivery and 5 mos post-partum

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68
Q

When, relative to delivery, does peripartum CM most commonly occur?

A

2 months postpartum

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69
Q

What % of peripartum cardiomyopathy cases occur before delivery?

A

10%

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70
Q

What are the risk factors for peripartum cardiomyopathy?

A 
Age>30
Obesity
CHTN
Multiparity
Multiples
Terbutaline
Preeclampsia
Low socioeconomic status
African American race
71
Q

What is the mortality associated with peripartum CM?

A

25-50%

72
Q

What % of patients fully recover from peripartum CM?

A

35-50%

73
Q

What are poor prognostic factors for peripartum cardiomyopathy (LV size, EF, and status at 6 months)?

A

Large LV EDV and EF <30% at initial diagnosis, and failure of LV function to normalize by 6 months

74
Q

What % of women with peripartum CM and EF <25% will require a transplant?

A

57%

75
Q

What is the recurrence risk of peripartum CM?

A

35%

76
Q

What is the medical management of peripartum CM?

A 
Inotropic therapy (digoxin)
Afterload reduction (hydralazine +/- B-blockade)
ACE inhibitors (postpartum)
Anticoagulation (for  EF <35%)
Bromocriptine
77
Q

When in pregnancy is the risk of MI the greatest?

A

In the first days post-partum (6x increase)

78
Q

Does pregnancy increase the risk of MI?

A

Yes (by 2-4x)

79
Q

Which study identifies ischemia and ventricular dysfunction in patients at risk for MI?

A

Stress echo

80
Q

Which cardiac enzymes should not be ordered in the peripartum state to assess for cardiac ischemia?

A

CK (as CK is increased 2x in labor)

only TROPONINs are helpful

81
Q

How can we treat stable angina in pregnancy?

A

Nitrates
Ca channel blockers
B-blockers

82
Q

What is “stable” angina?

A

Chest pain with exertion that resolves with rest and nitrates

83
Q

How do we treat ischemic heart disease (MI)?medications and other therapy?

A 
Morphine
Low dose Aspirin
Nitrates
B-blockers
Ca channel blockers
Heparin
Coronary angioplasty
84
Q

If cardiac catheterization is indicated for MI, what should you tell your IR colleagues is the max dose of radiation considered safe in pregnancy?

A

1 Rad

85
Q

Is thrombolysis considered a safe management option for MI in pregnancy?

A

No ? use only if no other options

86
Q

How should women with history of MI be counseled on future pregnancy?

A

Best not to become pregnant! (but may be considered if EF and coronaries are normal one year s/p MI)

87
Q

What are the main causes of aortic stenosis in developed countries?

A

Bicuspid aortic valve

88
Q

What are the main causes of aortic stenosis in developing countries?

A

Rheumatic heart disease

89
Q

Women with aortic stenosis can expect good pregnancy outcomes if which criteria are met (what symptoms, what testing, what drop in aortic valve peak pressure)?

A

Asymptomatic
Normal EKG/stress test
Good EF
Aortic valve peak pressure drop <80 mmHg

90
Q

When should pt with aortic stenosis undergo repair prior to childbearing (what aortic valve peak gradient, and what EF)?

A

Peak gradient >50 mmHg (possibly >30 mmHg), or EF <30%

91
Q

If aortic valve replacement is required during pregnancy, what is the risk for fetal death with ECMO

A

20%

92
Q

What intervention may be used to temporize patients with severe aortic stenosis during pregnancy in anticipation of valve replacement?

A

Balloon valvuloplasty

93
Q

At what aortic diameter do people become symptomatic from aortic stenosis?

A

<1 cm

94
Q

What are the potential bad outcomes associated with aortic stenosis

A

Angina, MI, syncope, sudden death

95
Q

Why is it important to avoid hypovolemia with aortic stenosis

A

In aortic stenosis, cardiac output is preload dependent. Hypovolemia causes decreases CO, and inadequate coronary/cerebral perfusion

96
Q

Why is cardiac output fixed in aortic stenosis

A

Outflow obstruction leads to LV hypertrophy and subsequent poor filling (diastolic dysfunction)

97
Q

Why is the fixed cardiac output of aortic stenosis dangerous in pregnant states of increased preload and HR?

A

Without the ability to increase output, coronary and carotid perfusion decreases

98
Q

Is it better to keep pt with aortic stenosis wet or dry?

A

Wet (as preload dependent)

99
Q

What effect does the fixed cardiac output of aortic stenosis have on fetal growth?

A

10%

100
Q

How is aortic stenosis managed in pregnancy

A

Bedrest and B-clockers (to decrease HR and increase LV ejection time to maximize coronary filling)

101
Q

What is the main cause of mitral stenosis?

A

Rheumatic heart disease

102
Q

How does mitral stenosis present?

A

Pulmonary edema and a-fib

103
Q

How is mitral stenosis treated in pregnancy?

A

Restricted activity

Diuretics B-blockers (rate control)

104
Q

Women with mitral stenosis but valve area greater than what value have a good outcome?

A

> 1.5 cm2

105
Q

How does mitral stenosis lead to a fixed cardiac output?

A

Prevention of LV filling

106
Q

Why should patients with mitral stenosis be managed on the ?dry side

A

With fluid overload, CO cannot increase, and pulmonary edema can result

107
Q

When in pregnancy is mitral stenosis likely to decompensate, due to the peak maternal blood volume levels?

A

30-32w

108
Q

Why should tachycardia be avoided in patients with mitral stenosis?

A

Poor LV filling may result -> hypotension

109
Q

When should B-blockers be given to pt with mitral stenosis to prevent tachycardia-associated poor CO?

A

HR of 90-100

110
Q

At what mitral valve area should pt be offered pre-pregnancy intervention?

A

<1.2 cm (or if pt is symptomatic)

111
Q

Can balloon mitral valvuloplasty be performed in pregnancy for failed medical management?

A

Yes

112
Q

What is the maternal mortality associated with mitral stenosis?

A

5%

113
Q

What types of mechanical heart valves are the highest risk?

A

Ist generation: Starr-Edwards and Bjork-Shiley in Mitral position

114
Q

Do women with mechanical heart valves need prophylactic or therapeutic anticoagulation during pregnancy?

A

Therapeutic (with weekly blood levels)

115
Q

Which types of heart valves require anticoagulation in pregnancy ? bioprosthetic or mechanical?

A

Mechanical

116
Q

Why do mechanical heart valves require anticoagulation?

A

Due to the shearing effects of the valve on circulating blood (which can result in platelet activation and thrombus formation)

117
Q

When using heparin for anticoagulation, when can an epidural be placed after the last dose?

A

4-6h (good to check a PTT first)

118
Q

Aside from mechanical heart valves, which cardiac conditions may require anticoagulation?

A

Afib and PHTN

119
Q

What is the therapeutic range for heparin?

A

Heparin: PTT 60-80 sec.

120
Q

What is the therapeutic range for Coumadin, and Lovenox?

A

Coumadin: INR 2-3.

121
Q

What is the therapeutic ranges for Lovenox (peak and trough)?

A

Peak (4h after 4th dose) anti-Xa 0.8-1.2. Trough 0.6-0.7

122
Q

What is the risk of warfarin teratogenicity (%) with first trimester exposure?

A

10-15%

123
Q

How does warfarin teratogenicity present after first trimester exposure?

A

Nasal hypoplasiaOptic atrophyDigital anomaliesMental impairment

124
Q

Is Coumadin or heparin a better at preventing thromboembolism in women with a mechanical valve?

A

Coumadin

125
Q

To minimize both teratogenicity and risk for VTE with mechanical heart valves, how should women be anticoagulated during pregnancy?

A

Heparin in first trimester and >36w, and Coumadin from 12-36w

126
Q

What is the risk of complication or death in pregnancy with L->R shunt with pulm HTN (high, moderate, or low)?

A

High >25%

127
Q

What is the risk of complication or death in pregnancy with Eisenmenger?s (high, moderate, or low)?

A

High >25%

128
Q

What is the risk of complication or death in pregnancy with Uncorrected aortic coarctation with proximal aortic dilation (high, moderate, or low)?

A

High >25%

129
Q

What is the risk of complication or death in pregnancy with left heart obstructive lesions like severe aortic stenosis and hypertrophic CM (high, moderate, or low)?

A

High >25%

130
Q

What is the risk of complication or death in pregnancy with mild-mod aortic stenosis (high, moderate, or low)?

A

Moderate (5-15%)

131
Q

What is the risk of complication or death in pregnancy with a systemic right ventricle (high, moderate, or low)?

A

Moderate (5-15%)

132
Q

What is the risk of complication or death in pregnancy with well functioning Fontan palliation for hypoplastic ventricles (high, moderate

A

Moderate (5-15%)

133
Q

What is the risk of complication or death in pregnancy with an isolated ASD or VSD, repaired or unrepaired (high, moderate, or low)?

A

Low (<1%)

134
Q

What is the risk of complication or death in pregnancy with pulmonic or tricuspid valve disease (high, moderate, or low)?

A

Low (<1%)

135
Q

What test can be recommended before conception to predict clinical outcome in pregnancy in moms with congenital heart disease?

A

Exercise stress test and echo

136
Q

What is the indication for a FONTAN procedure

A

Any anatomic abnormality in which a two-ventricle repair is unfeasible (tricuspid or pulm atresia, hypoplastic heart)

137
Q

What is the Fontan procedure (ie what vascular structures does it connect, and divert)?

A

From the RA (systemic venous return) to the pulmonary arteries, bypassing the RV

138
Q

What is the risk of maternal death in asymptomatic women s/p Fontan with good vent function and no pulm HTN?

A

2%

139
Q

What are the 4 features of TOF?

A

VSD
Overriding aorta
RVH
Pulmonary stenosis

140
Q

What is the risk of complication or death in pregnancy with uncorrected cyanotic defects like TOF (high, moderate, or low)?

A

Moderate (5-15%) (high with severe pulm regurg or RV dysfunction)

141
Q

What is the risk of complication or death in pregnancy with repaired TOF with normal RV function and competent pulmonic valve (high, moderate, or low)?

A

Low (<1%)

142
Q

What is the risk of complication or death in pregnancy with palliated TOF with pulm regurg and RV dysfunction (high, moderate, or low)?

A

Moderate (5-15%)

143
Q

What complications are seen with repaired TOF in pregnancy?

A

SVT, right heart failure

144
Q

Left sided obstruction = mitral valve area less than?

A

2 cm^2

145
Q

Left sided obstruction = aortic valve area less than?

A

1.5 cm^2

146
Q

Left sided obstruction = peak LV outflow tract gradient above?

A

30 mm Hg

147
Q

What 4 CV changes are likely to be poorly tolerated by a pregnant woman with cardiac disease?

A
  1. The 50-percent increase in blood volume and cardiac output by the early third trimester
  2. Further fluctuations in volume and cardiac output in the peripartum period (and postpartum increase from “auto transfusion”)
  3. A decline in systemic vascular resistance, reaching a nadir in the second trimester, and then rising to 20 percent below normal by late pregnancy (can allow for a L to R shunt)
  4. Hypercoagulability, which is of special importance in women requiring anticoagulation before pregnancy with coumarin derivatives.
148
Q

What are the drawbacks of bioprosthetic heart valves?

A

-Valvular dysfunction, deterioration, or failure are common, and develop in 5 to 25 percent of pregnancies. -Bioprostheses are not as durable as mechanical ones, and valve replacement averages every 10 to 15 years.

149
Q

What is the normal mitral valve surface area?

A

4.0 cm^2

150
Q

At what surface area do symptoms result from mitral stenosis?

A

2.5 cm^2

151
Q

What is the most prominent symptom of mitral stenosis? Why?

A

Dypsnea due pulmonary venous hypertension and edema.

Fatigue, palpitations, cough, and hemoptysis are also common

152
Q

How is peripartum cardiomyopathy defined?

A

This is defined as cardiomyopathy (with EF <45%) occurring during last four weeks of pregnancy or within five months postpartum (peaks at 2 months postpartum), without other cause.

153
Q

What are risk factors for peripartum cardiomyopathy?

A 
Older maternal age
multiparity
African-American race
multiple gestations
hypertensive disorders of pregnancy
154
Q

How is peripartum cardiomyopathy managed?

A

Serial echocardiography
digoxin
diuretics
afterload reduction—hydralazine and/or beta-blockers in pregnancyACE inhibitors postpartum
anticoagulation if EF is <35%,
possible intrapartum PAC
The addition of bromocriptine to standard heart failure therapy appears to improve left ventricular EF and a composite clinical outcome in women with acute severe peripartum cardiomyopathy, but the number of patients studied was too small to make any recommendation

155
Q

How should women with peripartum cardiomyopathy be counseled about future pregnancies?

A
  • Persistent dilated cardiomyopathy with abnormal EF predicts a high risk (19%) of mortality and symptoms of cardiac failure (44%) with subsequent gestation, and should be discouraged.
  • Even women with “normal” echo- cardiograms (EF > 45–50%) after recovering from peripartum cardiomyopathy can have persistent “subclinical” low contractile reserve (61), with up to 21% risk of developing symptoms of CHF, but no mortality reported in one study.
  • Of women with EF < 25%, 57% require a cardiac transplant or are on a transplant list because of progressive symptoms of heart failure at a mean of 3.4 years of follow-up postpartum.
156
Q

Risk of VSD in fetus if mother affected?

A

10-15%

157
Q

Risk of aortic stenosis in fetus if mother affected?

A

15-18%

158
Q

Risk of pulmonary stenosis in fetus if mother affected?

A

6-7%

159
Q

Risk of ASD in fetus if mother affected?

A

5-10%

160
Q

Risk of aortic coarctation in fetus if mother affected?

A

15%

161
Q

Risk of Marfan in fetus if mother affected?

A

50%

162
Q

Risk of PDA in fetus if mother affected?

A

4%

163
Q

Risk of IHSS (hypertrophic cardiomyopathy) in fetus if mother affected?

A

50% (autosomal dominant disorder)

164
Q

What does a Swan-Ganz catheter (flow directed pulmonary artery catheter) measure?

A 
Pressures in the:
Right atrium
Right ventricle
Pulmonary artery
Can estimate left atrial pressure by measuring pulmonary artery wedge pressure
165
Q

In what clinical situations is a Swan-Ganz useful?

A

Shock
Resp failure
Cardiac failure

166
Q

How is pulmonary artery wedge pressure measured?

A
  • A balloon is inflated at the tip of the catheter, allowing the balloon to occlude a branch of the PA, and then measure the pressure during occlusion.
  • This creates a static column of blood between the catheter tip and the left atrium. Pressure at both ends of the column equilibrates, after which the pressure at the distal end of the catheter is equal to the pressure of the left atrium.
  • The pressure at the distal end of the catheter is termed the pulmonary artery wedge pressure (PAWP), which is also known as the pulmonary capillary wedge pressure or pulmonary artery occlusion pressure
167
Q

What is the range of normal PAWP?

A

6-15 mm Hg, with a mean of 9 mm Hg

168
Q

What exactly is PAWP estimating?

A

The PAWP usually estimates the left ventricular end-diastolic pressure (ie, the left ventricular preload) if there is no obstruction to flow between the left atrium and left ventricle.

169
Q

Is ASD in young women associated with heart failure?

A

No, so diuretics & extreme limitation of IV fluids are not warranted. A small percentage of pts have atrial flutter or fibrillation.

170
Q

What are possible complications of a large uncorrected ASD?

A

Chronic afib
RV dysfunction
Pulmonary hypertension
Pregnancy not advised if these complications are present

171
Q

What is Eisenmenger syndrome?

A

A congenital communication between the systemic and pulmonary circulations and increased pulmonary vascular resistance, either to systemic level (so that there is no shunt across the defect) or exceeding systemic (allowing right-to- left shunting).
The most common underlying defect is a large VSD, followed in prevalence by a large PDA.
Eisenmenger pathophysiology is less common in ASD.
The woman with Eisenmenger syndrome must be informed that pregnancy carries a mortality risk of about 50%

172
Q

What is tetralogy of Fallot?

A
  1. VSD
  2. Pulmonary stenosis
  3. Aorta overrides the VSD
  4. RVH
173
Q

What does the repair of TOF involve? Is it curative?

A

Repair = Closing the VSD and relieving the pulmonic stenosis. But not curative bc pts can still have arrhythmia or conduction defects requiring pacemaker or defibrillator, or can still have partial defects like continued RV obstruction or pulmonic regurg.

174
Q

What is Ebstein anomaly?

A

Malformation of the tricuspid valve - the septal leaflet is displaced apically and the anterior leaflet is abnormally large in size.
Deformed valve may be incompetent or stenotic.
Freq associated with WPW.

MFM Written Boards (Andrews) (33 decks)

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