Download The impact of pregnancy on heart diseases. Recommendations for

Heart diseases in pregnancy
Cardiovascular changes during
pregnancy:
intravascular volume and cardiac output
increase by 50%



Decrease in peripheral vascular resistance and blood
pressure (endothelium dependent factors)
Physiologic high output (HR 10-20 bpm and ejection
fraction – early increase in ventricular wall muscle
mass, increased end- diastolic volume, heart is
phisiologicly dilatated and has higher contractility))
Peak during the second trimester (20-28)
 The increased blood volume serves two purposes. First, it
facilitates maternal and fetal exchanges of respiratory gases,
nutrients and metabolites. Second, it reduces the impact of
maternal blood loss at delivery. Typical losses of 300-500 ml
for vaginal births and 750-1000 ml for Caesarean sections are
thus compensated with the so-called "autotransfusion" of
blood from the contracting uterus
 Aortocaval Compression - enlarged uterus compresses both the
inferior vena cava and the lower aorta when the patient lies
supine cousing reducton in return to the heart and cosequent
fall in stroke volume and cardiac output (up to 25 %). Pregnant
woment should lie on the side or the pelvis should be rotated so the uterus drops on the side.
Reduced cardiac uotput is associated with reduction in uterine
blood flow, and lower placental perfusion = deceleration in
FHR on CTG
Pulmonary vascular resistance like systemic
vascular resistance in diminished
 PCWP – pulomary capillary wedge
pressure is the same, but colloid oncotic
pressure is reduced - making pregnant
women susceptible to pulmonary oedema
(espessialy if there is increse in cardiac preload - i.v. Fluides or increased in
pulomnary capillary permeability preeclampsia)

LABOUR:
 Futher increase in cardiac uotput ( 15% in the first stage
and 50 % in the second stage)
 Uterine contractions lead to autotransfusion of 300 – 500
ml of blood into circulation
 Sympathetic response to pain and anxiety elevates futher
HR and blood pressure
 After delivery there is immediate rise in cardiac output –
relife of IVC and contracting uterus empties the blood to
systemic circulation
 Women with cardiovascular disease are most at risk of
pulmonary oedema during second satge of labour and
immediate postpartum period
 Cardiac output returns to normal in 2 weeks.
 Symptoms mimicking cardiac disease in healthy pregnant
women:
fatigue, dyspnea, light-headedness

„Abnormal” cardiac findings in pregnancy: displaced
apical impulse, prominent jugular venous pulsations,
widely split I and II heart sounds, soft ejection systolic
murmur

ECG findings:
sinus tachycardia, premature atrial/ ventricular ectopic
beats, right/left axis deviation,
ST-segment depression, T-wave changes
Echocardiographic findings

Mild increase in left ventricular diastolic
dimension with preservation of ejection
fraction

Functional tricuspid and mitral regurgitation

Small pericardial effusion
Pathology
Outcomes vary with different cardiac
lesions
Ability to tolerate pregnancy depends on :
 Precence of pulmonary hypertention
 Functional class – NYHA
 Heamodynamic significance of any lesion
 Presence of cyyanosis (arterial oxygen sauration < 80%)
High risk of death during pregnancy: Eisenmenger
syndrome, pulmonary vascular obstructive disease,
Marfan syndrome with aortopathy, mitral stenosis(
pulmonary oedema)
 Other complications: heart failure, arrythmias, stroke
 Fetal complications: spontaneus abortion, premature
birth, IUGR, low birth weight, intrauterine fetal death
Left-to-right cardiac shunts:
atrial septal defect, ventricular septal defect,
patent ductus arteriosus
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The incidence of congenital heart disease in pregnancy is
increasing - beter corresctive surgery in children
Higher cardiac output does not increase shunting becouse
of attenuating effect of the decrease in peripheral vascular
resistance

Pregnancy, labour and delivery – well tolerated unless
pulmonary hypertension exists

Risk of paradoxical embolism! with atrial shunts (patent
foramen ovale)
Aortic stenosis
Left ventricular outflow tract
obstruction

Heart failure / ischemia developement in severe
stenosis (aortic valve area <1 cm² or transvalvular
pressure gradient > 64mmHg)

Hypertrophic and noncompliant left ventricle

Complications with severe stenosis because of
restricted ability to increase cardiac output
Management:

Symptomatic aortic stenosis: surgical
correction first! then pregnancy

Absence of symptoms does not guarantee good
tolerance of pregnancy!

If necessary: baloon valvuloplasty during labor
and delivery
Coarctation of the aorta

Associated with: bicuspid aortic valve, aneurysms
of the circle of Willis, ventricular septal defects,
Turner syndrome
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Risk of aortic rupture in the III trimester and
during labor if CoA not corrected

If CoA corrected before pregnancy – risk of PIH
developement due to residual abnormalities in
aortic complience
Pulmonary valve stenosis

Classification - according to the peak pressure
gradient across the valve:
mild <50mmHg; moderate 50-70mmHg; severe
>80mmHg

Pregnancy well tolerated if stenosis mild or
treated by valvuloplasty or surgery

Right-sided heart failure or atrial arrhythmias in
severe stenosis (including asymptomatic!)
Management:

Severe pulmonary valve stenosis requires
correction before pregnancy

If symptoms progress during pregnancy –
baloon valvuloplasty
Tetralogy of Fallot
If not corrected/palliated:
- fall in systemic vascular resistance and
rise in cardiac output
exacerbate right-to-left shunting
- results: increased maternal hypoxemia and
cyanosis
- poor fetal outcomes (loss rate ~30%)
- maternal mortality risk 4 – 15%

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If succesfully corrected: low risk; pregnancy well
tolerated
Marfan syndrome

Connective tissue disorder

Autosomal-dominant
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Complications due to medial aortopathy: dilation,
dissection, valvular regurgitation

Aortic root replacement before pregnancy does
not eliminate the risk of dissection of the residual
native aorta!
Management
Recent data: maternal mortality rate: 1%; fetal
mortality rate ~ 22%
 Aortic root involvement: preconception
counseling – risk in pregnancy
 Little cardiovascular involvement; aortic root
diameter < 40mm – good tolerance of pregnancy
 Serial echocardiography to monitor for
progressive aortic root dilation
 Beta-blockers prophylactically – reduce aortic
dilatation

Eisenmenger syndrome &
pulmonary vascular obstructive
disease

ES: pre-existing left-to-right shunt; pulmonary
pressure rise to systemic level; shunt flow rightto-left

Pregnancy complications: at term and during 1st
postpartum week

High frequency of: spontaneous abortion, IUGR,
preterm labor

Maternal mortality rate: primary pulmonary
hypertention ~ 30%; Eisenmenger syndrome
~36%; secondary vascular pulmonary
hypertention ~56%
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Perinatal mortality due mainly to prematurity
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Neonatal mortality rate: 12%

Preconception counseling: extreme risk from
pregnancy; pregnancy is contraindicated!
Acquired heart disease - Mitral stenosis
The most common valvular lesion in pregnancy
 Hypervolemia and tachycardia exacerbate
transmitral gradient
 Symptoms: asymtomatic, dyspnoea, cough
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Even asymptomatic patients (mild to moderate
stenosis) can develope atrial fibrillation and heart
failure in antepartum/peripartum period! Pulmonary
oedema.
Outcomes

No maternal mortality

Morbidity (heart failure and arrhytmias)

Risk of complications higher in patients with a
history of cardiac events: arrhytmias, stroke,
pulmonary oedema
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Fetal/neonatal outcomes: risk increases with
severity of mitral stenosis
Management

In patients in NYHA class III or IV (despite
optimal medical therapy), percutaneous
mitral valvuloplasty during pregnancy
should be considered
Other rheumatic lesions

Rheumatic aortic stenosis: risk similar to
congenital aortic stenosis

Aortic or mitral regurgitation – well tolerated
during pregnancy

Function may deteriorate (NYHA
classification)
Peripartum cardiomyopathy
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Idiopathic dilated cardiomyopathy, involves
ventricular systolic dysfunction that developes
during the last month of pregnancy or in the first
5 months after delivery in patients with no known
underlying disease
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Heart failure – the most common manifestation;
others: arrhytmias, embolic events

Outcomes: improvement in NYHA functional
status postpartum or persisting/worsening heart
lesion

Relapse rate in subsequent pregnancy:
Substantial in women with persisting cardiac
enlargement / left ventricular dysfunction
Possibility of persistent subclinical dysfunction
(despite of recovered systolic function)
-
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Atheromatous coronary artery disease

If possible – assessment (exercise testing) and
treatment (coronary bypass surgery) before
pregnancy

Risk in pregnancy: angina developement,
myocardial infarction, especially in the peripartum
period
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Coronary angiography: recognition of mechanism
of the infarct
Management

Thrombolytics shoul be avoided if coronary artery
dissection occured

Percutaneous intervention (PCI) with stenting is
optimal
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Differentiate with: congenital coronary
anomalies, disease with aneurysm formation,
coronary arteriitis, autoimmune vascular diseases
Clinical approach general recommendations:
1.
Risk stratification
2.
Antepartum management
3.
Peripartum management
4. Recurrence of congenital lesion in the
neonate
5. Site of antepartum and peripartum care
Risk assessment
Cardiovascular history and examination
 12-lead electrocardiogram
 Transthoracic electrocardiogram
 Arterial oxygen saturation measurement by
percutaneous oximetry in cyanotic patients
 Define underlying cardiac lesion
 Assess: ventricular function, pulmonary pressure,
severity of obstructive lesions, persistence of
shunts, hypoxemia

Low risk
Small left-to-right shunt
 Repaired lesions without residual cardiac
dysfunction
 Isolated mitral valve prolapse without significant
regurgitation
 Bicuspid aortic valve without stenosis
 Mild/moderate pulmonic stenosis
 Valvular regurgitation with normal ventricular
systolic function
 Patient can be managed in a community hospital

High risk
Significant pulmonary hypertention
 Marfan syndrome with aortic root or major
valvular involvement
 Peripartum cardiomyopathy with residual left
ventricular systolic dysfunction
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Patient should be managed in a high-risk
pregnancy unit by a multidisciplinary team
staffed by obstetricians, cardiologists,
anesthesiologists and pediatricians
Antepartum management
Limiting activity in severely affected patients;
hospital admission by mid-second trimester
 Pregnancy complications: early identification,
aggresive treatment (ie. PIH, hyperthyroidism,
infections, anemia)
 Mitral stenosis: rather beta-blockers than digoxin
 Coarctation, Marfan syndrome, ascending
aortopathy: empiric therapy with beta-blockers
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Arrhytmias: if possible, avoid drugs in the 1st trimester,
but:
Drugs administration for patients with severe symptoms or
poor tolerance of sustained arrhytmias
Antiarrhytmic drugs:
preferred: digoxin, cardio-selective beta-blockers,
adenosine;
limited use: quinidine, sotalol, lidocaine, flecainide,
propafenone;
contraindicated: amiodarone
Electrical cardioversion is save
Implantable cardioverter-defibrillator
Anticoagulation therapy
Oral warfarin: non teratogenic in dose <5mg per
day; risk of fetal intracranial bleeding throughout
pregnancy, especially during vaginal delivery unless
warfarin stopped before labor
 Heparin: less effective in patients with prosthetic
valves, safe for the fetus 6-12 Hbd
 Low-molecular-weight heparin: more stable
anticoagulation level
 Low-dose aspirin in women with prosthetic valves
as a part of antithrobotic regimen

Peripartum management
Elective cesarean section - indicated for: aortic
dissection, Marfan syndrome with dilated aortic
root, taking warfarin within 2 weeks of labour
 Preterm planned induction: in high-risk patients to
ensure that appropriate staff and equipment are
avaliable; uncommon
 Hemodynamic monitoring: no consensus on using
invasive procedures during labor and delivery

Replace anticoagulants by heparine at 36 Hbd
 Give up heparin at least 12 hours before induction
 Routine antibiotic prophylaxis for endocarditis:
controversial in cesarean section or uncomplicated
vaginal delivery; indicated in patients with
prosthetic valves or previous endocarditis
 Pain control: epidural anaesthesia and adequate
volume preloading is recommended
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Positioning the patient on her left side lessens
hemodynamic fluctuations associated with
contractions
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Forceps or vacuum extractor at the end of
second stage to shorten delivery

Postpartum monitoring of patients at
intermediate or high risk: for at least 72 hours
Risk of congenital heart disease in
offspring

0.4 - 1% in general population

10 - fold increase if a first-degree relative is
affected

Patients of reproductive age with congenital heart
disease should be offered genetic assessment and
counseling: estimation of transmission risk and
information of the options for prenatal diagnosis