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KULIAH MAGISTER

Cardiac Diseases AND


Pregnancy
dr. Ary A Permana
Pembimbing : dr. Cut Aryfa Andra, SpJP
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OUTLINES
 Incidence & mortality
 CV physiology of pregnancy
 Management area
 Pre-conceptional counseling
 Risk assessment
 Antepartum care
 Anti coagulation theraphy
 Peripartum care
 Recurrence of congenital lesion in neonates
 Specific congenital heart defect
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The incidence and changing pattern of heart disease


 It ranges from 0.1% to 4%.

 Hospital statistics - industrialized countries  


in the incidence from 0.9% to 0.3%

 Sharp decline in the incidence of chronic


rheumatic heart disorders.

 Advances in the medical and surgical treatment of


patients with congenital heart defects  
survival to reproductive age.
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Maternal mortality from heart disease


 Statisticshave demonstrated a decline in maternal
mortality from cardiac disease since 1950 from 5.6
to 0.3 per 100 000 births.

 Besides of improved medical care of the pregnant


cardiac patient and a sharp decrease in the
incidence of rheumatic heart disease.
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MATERNAL MORTALITY FROM HEART DISEASE

 Confidential enquiry of latest report on maternal deaths


in the United Kingdom, has shown that cardiac disease
accounted for the greatest number of maternal deaths

 accounting for 35 (16.5%) of all maternal deaths over the


period 1997–1999*

* de Swiet M. Cardiac disease. In: Lewis G, Drife J, eds. Why Mothers Die 1997–1999. The
Confidential Enquiries into Maternal Deaths in the United Kingdom. London: Royal College of
Obstetricians and Gynaecologists, 2001; 153–64
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Cardiac diseases is also the leading cause


of indirect maternal death. Of the cardiac
deaths reported to the Confidential enquiry
between 2000-2002, 40% were noted to
have substandard care.

Deans CL, Uebing A, Steer PJ. Cardiac disease in pregnancy. In Progress in Obstetrics and
Gynaecology, Vol 17, Edi Studd J, Tan S L, Chervenak FA.Churchill Livingstone 2007, 164-182.
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CV PHYSIOLOGY OF PREGNANCY
 Normal pregnancy is associated with an increase of 30
to 50 percent in blood volume

 Blood volume increases, starting at the sixth week and


rising rapidly until mid pregnancy; the levels peak by
20 to 24 weeks of pregnancy and then are either
sustained until term or decrease

 An estrogen-mediated stimulation of the renin-


angiotensin system results in sodium and water
retention appears to be the mechanism underlying the
blood volume increase.
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CV PHYSIOLOGY OF PREGNANCY
 Increase in cardiac output is most significant change
during pregnancy.

 Itbegins to rise in 1st trimester and steadily rises to


peak at 32 weeks by 30 to 50%.

 Cardiac output is normally 4.2 L/min., is 6.5 L/min.


at 8-10 weeks of pregnancy and remains so till near
term.

 Increase in cardiac output is achieved by rise in


stroke volume (in early pregnancy) and Heart Rate (in
latter part of pregnancy) adjusting together
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Cardiovascular Physiology of Pregnancy

 Due to rise in endogenous circulating


catecholamine, there is positive inotropic and
chronotropic myocardial response.

 Later in pregnancy, the rise is related to an


acceleration of heart rate (25%), since stroke
volume decreases as a result of vena caval
compression.
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 BloodPressure remains almost to prepregnant levels except a


tendency to fall during pregnancy (particularly during
midtrimester) as the systemic vascular/peripheral resistance
falls

(due to large arteriovenous shunts at placental bed and


physiologic vasodilation secondary to endothelial prostacyclin
and circulating progesterone)
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 Colloid oncotic pressure is another important


variable

 Bothplasma and interstitial colloid oncotic pressure


 throughout pregnancy

 Thereis accompanying increase in capillary


hydrostatic pressure.

 An hydrostatic pressure or  in colloid oncotic


pressure may overcome the delicate balance that
favors oedema formation
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Colloid oncotic pressure

 After delivery, decrease in plasma colloid oncotic


pressure takes place reaching a peak between 6 to
16 hours and returns towards intrapartum level
after 24 hours.

 Thesechanges can lead to dependant oedema


complicating diagnosis of cardiac
decompensation.
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Simulating cardiac disease


Owing to these normal changes, many healthy pregnant
women have symptoms mimicking those of cardiac disease,
Including :

fatigue, dyspnea, and light-headedness,


& number of “abnormal” findings on physical
examination, electrocardiography, and echocardiography
Table 1. Normal physiological changes of pregnancy
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that mimic symptoms and signs of cardiac disease
Symptoms
Tiredness
Dyspnoea
Orthopnoea
Syncope
Light-headedness
Physical signs
Peripheral oedema
Hyperventilation
Distended neck veins with prominent A and V
waves
Brisk, diffuse, and displaced left ventricular
impulse
Palpable right ventricular impulse
Increased S1 intensity
Persistent splitting of S2
Early ejection systolic murmurs at lower left
sternal edge or pulmonary area
Cervical venous hum
Mammary souffle
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Contd..
Table 1. Normal physiological changes of pregnancy
that mimic symptoms and signs of cardiac disease

Electrocardiogram
Left axis deviation
ST segment and T wave changes
Small Q, inverted P or T wave in lead III
Increased R wave amplitude in lead V2
Atrial or ventricular ectopics
Chest X-ray
Straightened left upper cardiac border
Horizontal heart position
Increased lung markings
Echocardiogram
Increased left/right ventricular dimensions
Mild increase in left/right atrial size
Slightly improved left ventricular systolic function
Functional tricuspid/pulmonary insufficiency
Small pericardial effusion
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Management areas
Areas be considered in the clinical approach to the woman with heart
disease who is pregnant or considering pregnancy:

• Risk stratification, pre-conceptional


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• Antepartum management
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• Peripartum management
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• Recurrence of congenital lesion in neonate


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 This is an important aspect of management or the


cardiac patient planning a pregnancy.
1.a. Pre-conceptional counseling
 Ideally,the obstetrician and cardiologist should work
together to help the patient make an informed decision.

 Prevent an unwanted pregnancy and avoid the risks


associated with pregnancy continuation or termination.
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1.b Risk stratification


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1.bA cardiac
• Riskevent
stratification
(arrhythmia, stroke, transient ischemic attack,
or pulmonary edema) before pregnancy but since a prior
cardiac surgical procedure.

• Siu developed a risk index incorporating these factors. In a


woman with heart disease and no other risk factors, the
likelihood of a cardiac event during pregnancy is about 5%,
increasing to 25% with one risk factor & 75% with more than
one risk factor.
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Table 2. Maternal mortality risk and cardiac disease
Group Cardiac disease Associated mortality risk
I Atrial septal defect* <1%
Ventricular septal defect*
Patent ductus arteriosus*
Pulmonary/tricuspid valve disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Mitral stenosis, NYHA Class I, II
II Coarctation of aorta without valvular involvement 5% - 15%
Uncorrected tetralogy of Fallot
Marfan’s syndrome with normal aorta
Mechanical prosthetic valve
Mitral stenosis with atrial fibrillation or NYHA Class III, IV
Aortic stenosis
Previous myocardial infarction
III Pulmonary hypertension—primary or secondary 25% - 50%
Coarctation of aorta with valvular involvement
Marfan’s syndrome with aortic involvement
Peripartum cardiomyopathy
*Uncomplicated
Table 3.NEW YORK HEART ASSOCIATION
24 FUNCTIONAL
CLASSIFICATION OF CARDIAC DISEASE

CLASS I No functional limitation of activity.


No symptoms of cardiac decompensation with activity.

CLASS II Mild amount of functional limitation.


Patients are asymptomatic at rest. Ordinary physical activity
results in symptoms.

CLASS III Limitation of most physical activity.


Asymptomatic at rest
Minimal physical activity results in symptoms.

CLASS IV Severe limitation of physical activity results in symptoms.


Patients may be symptomatic at rest/heart failure
at any point of pregnancy.

CLASS V If patient is on ionotropic support, ventilator, Assisted


circulation or having comprised renal or pulmonary function
necessitating dialysis/EMCO to
maintain vital signs.

The criteria committee of the New York Heart Association, Nomenclature and criteria for diagnosis of diseases of heart and great vessels, Edi 8,
New York Association,1979.
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2. Antepartum Management
 The chief aim of management of the patient in pregnancy is to keep
patient within her cardiac reserve.
 It is preferable to have detailed baseline information prior of
pregnancy.
 Limiting activity is helpful in severely affected women with
ventricular dysfunction, left heart obstruction, or class III or IV
symptoms.
 Hospital admission by mid-second trimester may be advisable for
some
 Problems should be identified early and treated aggressively,
especially pregnancy induced hypertension, hyperthyroidism,
infection, and anemia.
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Intervention in a mother during


pregnancy
Angiography :
 4th month 2nd trimester, Heparin has to be given
at 40–70 U/kg, targeting an activated clotting time
of at least 200 s, but not exceeding 300 s.
 gravid uterus should be shielded from direct
radiation.
 Fluoroscopy should be as brief as possible
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Cardiac surgery with CPB :


 neurological impairment in 3–6% of children
 when medical therapy or interventional procedures fail
and the mother’s life is threatened. The best period for
surgery is between the 13th and 28th week
 At 26 weeks, survival is generally 80%, with 20%
having serious neurological impairment.
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CV Drugs Safety Profile in Pregnancy


Beta-blockers safe
Digoxin safe
Diuretics Use judiciously
Ace-i unsafe
Calcium antagonist Use judiciously
Adenosine safe
Lidocaine safe
Procainamide safe
Quinidine Safe
Amiodarone unsafe
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Antepartum Care (2)


Beta-blockers rather than digoxin should be used to
control the heart rate for patients with functionally
significant mitral stenosis.

Empiric therapy with beta-blockers is offered to


patients with coarctation, Marfan syndrome and
ascending aortopathy for other reasons (eg, a bicuspid
aortic valve).
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Antepartum care (2)


Sustained tachyarrhythmias, such as
atrial flutter or atrial fibrillation, should be
treated promptly.

If possible, all antiarrhythmic drugs should


be avoided during the first trimester, and those
known to be teratogenic should be avoided
throughout pregnancy.

Because of their safety profiles, preferred drugs include


digoxin, beta-blockers and adenosine.
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Antepartum care (3)


 Anticoagulation therapy. No current strategy is equally
safe for both mother and fetus.
 Oral therapy with warfarin is effective and logistically
easy.
 However, it can affect embryonic organ development,
although some evidence shows that a dosage of 5 mg per
day may not be teratogenic.
 Fetal intracranial bleeding is a risk throughout pregnancy,
particularly during vaginal delivery, unless warfarin is
stopped before labor
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Anticoagulation therapy
* Heparin in adjusted subcutaneous doses
does not cross the placenta and so has no teratogenic
effects.

However, it may cause maternal


thrombocytopenia and osteoporosis and is
less effective in preventing thrombosis in
patients with prosthetic valves.
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Anticoagulation therapy
More recent guidelines recommend either
(1) adjusted-dose heparin during the entire pregnancy or

(2) adjusted-dose heparin until the 13th week of


gestation, warfarin from the 14th week to the middle of
the 3rd trimester, and then restart adjusted-dose
heparin.

* Low-molecular-weight heparin in adjusted


doses is easier to administer and has been
suggested as an alternative to adjusted-dose
unfractionated heparin.
Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic agents during pregnancy. Chest 2004;

126:627S–644S .
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Anticoagulation therapy
At week 36 #
*Discontinue warfarin
*Change to UFH titrated to a therapeutic aPTT or anti-factor
Xa level.

At Delivery:
*Restart heparin therapy 4 to 6 hr after delivery if no
contraindications
*Resume warfarin therapy the night after delivery if no
bleeding complications
#if labor begins while the woman is receiving warfarin,
anticoagulation should be reversed and caesarean delivery
performed
Ginsberg JS, Greer I, Hirsh J. Use of antithrombotic agents during pregnancy. Chest 2001;119:Suppl:122S-131S
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Anticoagulation therapy
Monitoring
 With LMWH administered sc. twice daily
maintain anti-Xa level between 0.7 and
1.2 U/ml 4 hours after admn.
 With dose adjusted UFH, the aPTT should be at
least twice control.
 those on warfarin, the INR goal should be
3.0(range 2.5 to 3.5)
Chan WS, Anand S, Ginsberg JS. Anticoagulation of pregnant women with mechanical heart valves: a systematic review

of the literature. Arch Intern Med 2000;160:191-196


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3. Peripartum management
Timing & mode of delivery :
preferable to induced labour for the majority of women
with heart disease. Timing is individualized, according to
the gravida’s cardiac status

Cesarean section is indicated only :


 Aortic dissection
 Marfan syndrome with dilated aortic root
 Taking warfarin within 2 weeks of labor.
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Preterm induction is uncommon.


 However, once fetal lung maturity is assured, planned
induction and delivery may be warranted for high-risk
patients to ensure that appropriate staff and equipment are
available.

Antibiotic prophylaxis for endocarditis is


not routine. AHA guidelines do not recommend routine
endocarditis prophylaxis for cesarean section delivery or
for uncomplicated vaginal delivery without infection 
but some center do
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Positioning the patient on her left side  lessens the


hemodynamic fluctuations associated with contractions when
the patient is supine.

Forceps or vacuum extraction should be


considered at the end of the second stage of labor to shorten
and ease delivery.
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Postpartum monitoring
 Because hemodynamics do not return to baseline for
many days after delivery, patients at intermediate or high
risk may require monitoring for at least 72 hours
postpartum.

 A slow i.v. infusion of oxytocin (,2 U/min), which avoids


systemic hypotension, is administered after placental
delivery to prevent maternal haemorrhage. Prostaglandin
F analogues are useful to treat post-partum haemorrhage,
unless an increase in pulmonary artery pressure (PAP) is
undesirable.
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 Methylergonovine is contraindicated because of


the risk (.10%) of vasoconstriction and
hypertension.

Lactation should be encouraged unless patient is in


failure.
Cardiac output is not compromised during
lactation. Lactation is a pathway for fluid
excretion and diuretic requirement may actually
fall.
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4. Recurrence of congenital lesion in


neonate
 Contaception : Monthly injectables that contain
medroxyprogesterone acetate are inappropriate for
patients with heart failure because of the tendency
for fluid retention.
 Lowdose oral contraceptives containing 20 mg of
ethinyl estradiol are safe in women with a low
thrombogenic potential, but not in women with
complex valvular disease
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 Progesterone only pill have better side effect


profile & long acting slow releasing as Mirena
(levonogestrel) intrauterine system have improved
efficacy.

 Sterilization
where family completed.
(Laparoscopic clip sterilization carries risk).

Deans CL, Uebing A, Steer PJ. Cardiac disease in pregnancy. In Progress in Obstetrics and Gynaecology, Vol 17, Edi
Studd J, Tan S L, Chervenak FA.Churchill Livingstone 2007, 164-182.
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 Pregnancy termination should be discussed with


women in whom gestation represents a major
maternal or fetal risk.

 The first trimester is the safest time for elective


pregnancy termination, which should be
performed in hospital, rather than in an outpatient
facility, so that all emergency support services are
available.
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Specific congenital heart


disease
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