CVD in pregnancy Flashcards

1
Q

deaths attributable to cardiovascular diseases were

responsible for approximately — percent of all pregnancy-related deaths

A

deaths attributable to cardiovascular diseases were

responsible for approximately 26 percent of all pregnancy-related deaths

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2
Q

hemodynamicCardiovascular Physiological changes during pregnancy

A

CO increases approximately 40 % during pregnancy, Almost half of this total takes place by 8 weeks’ gestation and is maximal by midpregnancy 28 wks. Mediated by increase preload due to the increase of blood volume due to the estrogen medicated activation of the RAS leading to Na and H2O retention.
reduced afterload due to the decrease of systemic vascular resistance due to increase progesterone production.
a rise in maternal heart rate 10-15 beats per minute .
Red blood cell mass increase by 20-30 % due to the fall in HB concentration Causing physiologic anemia.

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3
Q

ECG physiological changes during pregnancy:

A

15-degree left-axis deviation is found as the diaphragm is elevated in advancing pregnancy, a reduced PR interval, inverted or flattened T waves, and a Q wave in lead III

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4
Q

Classification of Functional Heart Disease:

A

Class I. Uncompromised—no limitation of PA
not have symptoms of cardiac insufficiency or experience anginal pain.
• Class II. Slight limitation of PA: comfortable at rest, but if DLA is undertaken, discomfort in the form of excessive fatigue, palpitation, dyspnea, or anginal pain results.
• Class III. Marked limitation of PA: comfortable at rest, but less than DLA causes excessive fatigue, palpitation,
dyspnea, or anginal pain.
• Class IV. Severely compromised—inability to perform any PA without discomfort: Symptoms of cardiac insufficiency or angina may develop even at rest.

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5
Q

modified (WHO) Risk Classification of Cardiovascular Disease and Pregnancy:
WHO 1 ? Where No detectable increased risk of maternal mortality and no or mild increase in morbidity.

A

• Uncomplicated, small or mild o Pulmonary stenosis
o Patient ductus arteriosus o Mitral valve prolapse
• Successfully repaired simple lesions (atrial or ventricular septal defect, patent ductus arteriosus, anomalous pulmonary venous drainage).
• Atrial or ventricular ectopic beats, isolated

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6
Q

Simpson (2012) recommends cesarean delivery for

women with the following Cardiac conditions:

A

(1) dilated aortic root >4 cm or aortic aneurysm; (2)
acute severe congestive heart failure; (3) recent myocardial infarction; (4) severe symptomatic aortic stenosis; (5) warfarin administration within 2 weeks of
delivery (6) need for emergency valve replacement immediately after delivery.

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7
Q

epidural safe in cardiac patient but

A

Subarachnoid blockade is not generally recommended in women with significant heart disease due to associated hypotension.

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8
Q

Mitral valve vegetations—Libman-Sacks endocarditis—are relatively common in women with

A

antiphospholipid antibodies. These sometimes coexist with systemic lupus erythematosus.

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9
Q

In asymptomatic women with ASD, thromboembolism prophylaxis is problematic.

A

Compression stockings and prophylactic heparin have

also been recommended for a pregnant woman with an ASD who is immobile or has another risk factor for thromboembolism

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10
Q

Eisenmenger Syndrome

A

describes secondary pulmonary hypertension that arises from any cardiac lesion. The syndrome develops when pulmonary vascular resistance exceeds
systemic resistance and leads to concomitant right-to-left shunting. The most common underlying defects are ASD or VSD and persistent ductus arteriosus

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11
Q

Pregnant women with Eisenmenger syndrome tolerate hypotension poorly, and death usually is caused by

A

right ventricular failure with cardiogenic shock.
(Eisenmenger syndrome is considered to be an
absolute contraindication to pregnancy)

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12
Q

secondary Pulmonary arterial HTN causes

A

connective tissue disease.e.g. approximately 1/3 of women with scleroderma and 10 percent with systemic lupus erythematosus, in young women are (HIV) infection, sickle-cell disease, and thyrotoxicosis

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13
Q

What is the most common causes of secondary pulmonary venous hypertension In pregnant women?

A

caused by left-sided atrial, ventricular, or valvular disorders. A typical example is mitral stenosis.

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14
Q

pulmonary HTN symptoms:

A

dyspnea with exertion is the most frequent. orthopnea and nocturnal dyspnea are also usually present. Angina and syncope occur when right ventricular output is fixed, and they suggest advanced disease.

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15
Q

the standard way to measure pulmonary Pressure:

A

cardiac catheterization remains the standard

for measurement.

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16
Q

primary cardiomyopathies Examples

A

hypertrophic cardiomyopathy, dilated cardiomyopathies, and peripartum cardiomyopathy

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17
Q

Secondary cardiomyopathies

A

Diabetes, systemic lupus erythematosus, chronic hypertension, and thyroid disorders

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18
Q

peripartum (pregnancy-induced) cardiomyopathy diagnostic criteria:

A
  1. Development of cardiac failure in the last month of pregnancy or within 5 months after delivery,
  2. Absence of an identifiable cause for the cardiac failure.
  3. Absence of recognizable heart disease prior to the last month of pregnancy.
  4. Left ventricular systolic dysfunction demonstrated by classic echocardiographic criteria, such as depressed ejection fraction or fractional shortening along with a dilated left ventricle.
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19
Q

findings from the Registry on Pregnancy and Cardiac Disease indicate that women with preexisting heart
disease who develop preeclampsia have a __percent risk of developing heart failure during pregnancy

A

findings from the Registry on Pregnancy and Cardiac Disease indicate that women with preexisting heart
disease who develop preeclampsia have a 30-percent risk of developing heart failure during pregnancy

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20
Q

The most common arrhythmia seen in reproductive-aged women is

A

paroxysmal SVT. The prevalence during pregnancy is 24 cases per 100,000 hospital admissions, and approximately 20 percent will experience symptomatic
exacerbations during pregnancy.
approximately half of women with paroxysmal SVT had an initial onset during pregnancy

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21
Q

maternal paroxysmal SVT was associated with a —fold greater risk of septal cardiac defects, particularly secundum atrial septal defects, in their offspring.

A

maternal paroxysmal SVT was associated with a twofold greater risk of septal cardiac defects, particularly secundum atrial septal defects, in their offspring.

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22
Q

new-onset atrial fibrillation during pregnancy should prompt a search for underlying etiologies that include

A

cardiac anomalies, hyperthyroidism, pulmonary

embolism, drug toxicity, and electrolyte disturbances

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23
Q

aortic dissection risk factors:

A

1) Marfan syndrome or EDS.
2) aortic coarctation/bicuspid aortic valve
3) pregnancy > half of dissection cases in young women are related to pregnancy.
4) Turner or Noonan syndromes.

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24
Q

differential diagnosis of aortic dissection in pregnancy INCLUDES ?

A

myocardial
infarction, pulmonary embolism, pneumothorax, aortic valve rupture, and
obstetrical catastrophes, especially placental abruption and uterine rupture.

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25
Q

Marfan Syndrome, MODE OF INHERITANCE :

A

autosomal dominant connective tissue disorder has an incidence of 2 to 3 cases per 10,000 individuals

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26
Q

Marfan Syndrome CHARACTERSTICS

A

characterized by generalized tissue weakness that can result in dangerous cardiovascular
complications. joint laxity and scoliosis. Progressive aortic dilation causes aortic valve insufficiency, and there may be infective endocarditis and mitral valve prolapse with insufficiency.

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27
Q

Associated lesions with Aortic coarctation:

A

1/4 of affected patients have a bicuspid aortic valve, and another 10 percent have cerebral artery aneurysms. Other associated lesions are persistent ductus arteriosus, septal defects,
and Turner syndrome.

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28
Q

Major complications with aortic coarctation include:

A

CHF after long-standing severe HTN, bacterial endocarditis of the bicuspid AV, and aortic rupture. Because HTN may worsen in pregnancy,
antihypertensive therapy using β-blocking drugs is usually required. Aortic rupture is more likely late in pregnancy or early puerperium. Cerebral hemorrhage from circle of Willis aneurysms may also occur.

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29
Q

the risk of acute myocardial infarction is approximately —-fold higher in pregnant women compared with nonpregnant women of similar age

A

the risk of acute myocardial infarction is approximately Threefold higher in pregnant women compared with nonpregnant women of similar age

30
Q

What the incidence of cardiac disease in pregnancy?

A

1-4%

31
Q

What are the structural changes in the heart in pregnancy ?

A

Left ventricular end diastolic volume by 10%.
Left and right ventricular mass by 50 % and 40%.
the structural changes return to normal postpartum in Less than a year.

32
Q

What should counseling include for mother with cardiac dis?

A

1) pregnancy can contribute to a decline in cardiac status that may not return to baseline after the pregnancy.
2) Maternal morbidity and mortality is possible.
3) Fetal risk of congenital heart or genetic conditions , fetal growth restriction , preterm birth , IUFD and perinatal mortality.

33
Q

What are the physiological cardiovascular changes related to labor ?

A

CO increase by 50 % with each contraction.
Mean systemic pressure rises due to the catecholamines released due to pain and anxiety. Blood pressure and HR decrease 48 hours postpartum.

CO at it highest level where Dramatic increase in cardiac output due to uterine involution.

34
Q

What increases the risk of pulmonary edema at the time of delivery and postpartum ?

A

Increase hydrostatic pressure and decrease colloid osmotic pressure.

35
Q

Approach to pt with cardiac disease?

A

History :
Family history ( structural , vascular or rythm disorders and sudden unexplained death) Any genetic testing performed ( MYH7 for cardiomyopathy ).
Any current cardiovascular symptoms
Medication history.
Physical examination
Noninvasive testing : ECG ,Chest X-ray ( to check for cardiomegaly and pulmonary vascular prominence ) , echo ( mild valvular regurgitation and chamber enlargements are normal echo changes ) , exercise stress test , CT , MRI ( rarely when echo is non-diagnostic ) , Holter monitor ( if there is palpitations , light headedness, syncope).
+ BNP and NT-pro BNP, troponin.

36
Q

In what conditions does BNP increase significantly in pregnancy ?

A

In pregnant women with SOB related to HF from left ventricle systolic dysfunction. Diastolic dysfunction Hypertensive disorders including pre-eclampsia.

37
Q

Who are the candidates for infective endocarditis prophylaxis?

A

Prosthetic valve prosthetic or material used for cardiac valve repair
Prior endocarditis
Patients with CHD
Unrepaired cyanotic CHD, including palliative shunts and conduits.
Completely repaired congenital heart defect repaired with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure.
Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (both of which inhibit endothelialization)
Cardiac transplant recipients with valve regurgitation due to a structurally abnormal valve.

38
Q

What is the risk for fetal congenital heart disease in mothers with CHD?

A

3% With single gene defect and autosomal dominant ( Marfan syndrome ) 50 %.

39
Q

What are the minimal risk cardiac lesions?

A
VSD 
ASD
Bicuspid aortic valves without stenosis 
Aortic insufficiency  
Aortic enlargement .
40
Q

Moderate risk cardiac lesions?

A

Repaired TOF W/O significant pulmonary stenosis or insufficiency .
Complex CHD with an atomic right ventricle
Mild left side valve stenosis

41
Q

High risk cardiac lesions?

A

Eisenmenger syndrome
Severe Pulmonary hypertension
Severe aortic stenosis
left ventricle outflow tract dysfunction
Marfan syndrome with aortic dialation more than 45 mm
Symptomatic ventricular dysfunction with EF < 40%.

42
Q

What does TOF consists of ?

A

Right Ventricle Outflow obstruction
VSD
Right ventricle hypertrophic Overriding aorta Right to left shunt cyanosis.

43
Q

For Which group of pulmonary HTN pregnancy is contracindicated? What is its mortality rate?

A

Group 1, 23 %.

44
Q

What is the most common CHD in adults?

A

ASD

45
Q

What is the mortality rate of Eisenmenger syndrome ?

A

50 % with cyanosis.

46
Q

How would manage labor in patients with idiopathic hypertrophic subaortic stenosis?

A

1) inotropic Agents may exacerbate obstruction.
2) Medications that decrease systemic vascular resistance should be avoided or limited.
3) Cardiac rhythm should be monitored and tachycardia treated promptly.
4) The patient should undergo labor in the left lateral position with the second stage shortened by operative delivery .

47
Q

Pregnancy in women after surgical correction of TGA is associated with?

A

Arrhythmia HF NYHA class deterioration High incidence of serious obstetrics Complications 65%/ Mortality is 11%.

48
Q

is pregnancy discouraged after heart transplant?

A

No , if stable for 1 year post transplant.

49
Q

Whats the incidence of peripartym cardiomyopathy ?

A

25-100 per 100,000 patient.

50
Q

Peripartum cardiomyopathy presents as?

A

1) Late in pregnancy of the first few months postpartum.
2) EF less than 45%
3) No previous history of heart disease.
4) No ischemic cardiomyopathy

51
Q

whats the outcome of peripartum cardiomyopathy ?

A

Most women recover mostly if EF is more than 30%.. Some will develop chronic cardiomyopathy and heart failure if EF less than 30%.

52
Q

What is the most common cause of pregnancy associated acute coronary syndrome?

A

Coronary artery dissection.

53
Q

What is the most common cause for maternal cardiac arrest in women admitted for delivery ?

A

Hemorrhage , 38.1% followed by amniotic fluid embolism 13.3% Coronary artery syndrome is 10% Venous thromboembolism 4%.

54
Q

antepartum management principles of cardiac patient?

A
  • Delivery at a tertiary hospital.
  • A comprehensive plan for pregnancy , delivery and postpartum should be available in the medical record.
  • Should be treated by pregnancy heart team.
  • Fetal echocardiograph in women with CHD at 18-22 weeks.
  • Fetal growth assessment either by serial clinical examination or ultrasound.
  • Daily lose dose asprin prophylaxis for women with high risk for developing pre eclampsia started at 12-28 weeks and continued till delivery .
  • Antihypertensives if needed.
  • Echo for women with pulmonary edema.
55
Q

Intra-partum management principles for cardiac patient?

A
  • detailed delivery plan should be determined between 20-30 weeks.
  • Should include management of induction , delivery and postpartum concerns and a surveillance plan.
  • Women with stable cardiac disease can undergo vaginal delivery at39 weeks , with cesarean delivery for obstetric indications.
  • In the absence of spontaneous labor , a scheduled induction should be done at 39-40 weeks.
  • For women who are receiving LMWH d/c at least 12 hours before induction or cesarean section.
  • For women with arrhythmia , intrapartum cardiac monitoring.
  • IE prophylaxis as indicated.
56
Q

What is the most common intra-partum cardiac complication?

A

Pulmonary edema.

Arrhythmia.

57
Q

Cardiovascular assessment and follow up at 3 months postpartum is recommended in women with which conditions?

A
  • Hypertension, chronic/essential or hypertensive disorder of pregnancy (ie, gestational hypertension, preeclampsia, eclampsia, hemolysis, elevated liver enzymes, and low platelet syndrome, chronic hypertension [with or without superimposed preeclampsia])
  • Gestational diabetes mellitus- Intrauterine fetal growth restriction (particularly less than the 5th percentile for gestational age or less than 2,500 g at term)
  • Idiopathic preterm birth
  • Placental abruption
  • Obesity/excessive pregnancy weight gain/post- partum weight retention
  • Sleep disorders/moderate-to-severe obstructive sleep apnea (193–197)
  • Maternal age older than 40 years
58
Q

ongoing postpartum care after the 3 month cardiovascular assessment visit should include? .

A

-contraception-Weight reduction to pre-pregnancy weight ( referral to dietician , peer support , physical activity , programs that provides child care with no or low cost ).-Counseling regarding risk of future CVS-disease and overt diabetes in women who had pregnancy complications such as PET or GDm.-Considering low dose asprin with patients with history of PET for future pregnancies.-Early screening for GDM if positive history.-Breastfeeding

59
Q

Patients should be counseled to avoid pregnancy or consider induced abortion if they have severe heart disease, including an

A

ejection fraction less than 30% or class III/IV heart failure, severe valvular stenosis, Marfan syndrome with aortic diameter more than 45 mm, bicuspid aortic valve with aortic diameter more than 50 mm, or pulmonary arterial hypertension.

60
Q

Cardiac patient counselling

A

Discussion of cardiovascular disease with the woman should include the possibilities that 1) pregnancy can contribute to a decline in cardiac status that may not return to baseline after the pregnancy; 2) maternal morbidity or mortality is possible; and 3) fetal risk of congenital heart or genetic conditions, fetal growth restriction, preterm birth, intrauterine fetal demise, and perinatal mortality is higher when compared with risk when cardiovascular disease is not present.

61
Q

Whats the incidence of early pregnancy loss ?

A

10%. 80% of cases in the first trimester. For women aged 20-30&raquo_space; 9-17%. At 35 yo 20%. At 40 yo 40%. At 45 yo 80%.

62
Q

Patients with Marfan syndrome (MS) face a high risk of aortic dissection during pregnancy. A dilated aortic root (———) is considered a relative contraindication for pregnancy

A

Patients with Marfan syndrome (MS) face a high risk of aortic dissection during pregnancy. A dilated aortic root (>40 to 45 mm) is considered a relative contraindication for pregnancy

63
Q

In a patient with Marfan syndrome, the risk of aortic dissection associated with pregnancy has been estimated as approximately ? percent

A

In a patient with Marfan syndrome, the risk of aortic dissection associated with pregnancy has been estimated as approximately 3 percent

64
Q

management for atrioventricular (AV) conduction disorders

A

pacing during pregnancy usually not needed

vaginal delivery reportedly not associated with adverse outcomes in women with congenital AV block

65
Q

The Five Groups of pulmonary HTN

A

Group 1: Pulmonary Arterial Hypertension (PAH)
Group 2: Pulmonary Hypertension Due to Left Heart Disease.
Group 3: Pulmonary Hypertension Due to Lung Disease.
Group 4: Pulmonary Hypertension Due to Chronic Blood Clots in the Lungs.
Group 5: Pulmonary Hypertension Due to Unknown Causes.

66
Q

Modified WHO classification of maternal cardiovascular risk

A

(cardiac lesions classification)

67
Q

Stage I cardiac lesions of Modified WHO classification of maternal cardiovascular risk

A
68
Q

the most frequent cause of heart failure in pregnancy

A

Chronic hypertension with superimposed preeclampsia

69
Q

Heart failure diagnosis

A

Echocardiography may show an ejection fraction <0.45 or a fractional shortening <30 percent, or both, and an end-diastolic dimension >2.7 cm/m2

70
Q

merican College of Cardiology and the American Heart Association estimate that the risk of embryopathy is dose dependent, and the risk is < ?percent if the warfarin dose is ≤5 mg/d

A

merican College of Cardiology and the American Heart Association estimate that the risk of embryopathy is dose dependent, and the risk is <3 percent if the warfarin dose is ≤5 mg/d, If the dosage is >5 mg/d, the risk of embryopathy exceeds 8 percent.

71
Q

Effect of normal pregnancy physiology on patient with mitral Stenosis

A

With more severe stenosis, the left atrium dilates, left atrial pressure is chronically elevated, and significant pulmonary hypertension develops. These women have a relatively fixed cardiac output, and thus the increased preload of normal pregnancy and other factors that raise cardiac output may cause ventricular failure and pulmonary edema.

72
Q

most mitral stenosis lesions caused by

A

Rheumatic endocarditis