Transcript Cardiac Disease in Pregnancy

Cardiac Disease in Pregnancy
John G. Harkins M.D., F.A.C.O.G.
Assistant Professor
Department of Obstetrics and Gynecology
The University of Texas Southwestern School
of Medicine
Austin, Texas
Objectives
• Provide an overview of normal cardiac
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physiology in pregnancy and how it differs from
the nonpregnant state
Identify common maternal cardiac diseases
(anatomic and physiologic)
Discuss rational and evidence based treatment
algorithms for these maternal cardiac issues and
strategies for optimizing maternal and fetal
outcome
Maternal Cardiac Physiology
Maternal cardiac and circulatory
adaptations to pregnancy begin early
in the first trimester and do not
return to baseline until at least 6
weeks postpartum
Maternal Cardiac Physiology
Cardiovascular Alterations
• Increased blood volume
– Average 40-45% increase in volume by third
trimester; individual variation apparent with
some nearly doubling
– Marked increases with twins and higher order
gestations
Maternal Cardiac Physiology
Cardiovascular Alterations
• Expansion of maternal blood volume
provides the following benefits:
– Allows the perfusion of the hypertrophied uterus and
associated vasculature
– Protects maternal and fetal circulation against
postural hypotension and impaired venous return to
the heart
– Allows for significant blood loss during parturition
Maternal Cardiac Physiology
Cardiovascular Alterations
Maternal Cardiac Physiology
Cardiovascular Alterations
• Decreased systemic vascular resistance
• Decreased blood pressure
• Decreased pulmonary vascular resistance
• Increased heart rate
• Increased cardiac output
CO = SV x HR
Maternal Cardiac Physiology
Cardiovascular Alterations
Maternal Cardiac Disease
• Valvular Cardiac Disease
– Mitral Stenosis
– Mitral Insufficiency
– Aortic Stenosis
– Aortic Insufficiency
– Pulmonic Stenosis
Maternal Cardiac Disease
• Congenital Heart Disease
– Septal Defects
• Atrial Septal Defects
• Ventricular Septal Defects
• Atrioventricular Septal Defects
– Patent Ductus Arteriosus
• Cyanotic Congenital Heart Disease
– Tetralogy of Fallot
– Ebstein’s Anomaly
Maternal Cardiac Disease
• Pulmonary Hypertension
– Eisenmenger syndrome
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Mitral Valve Prolapse
Marfan Syndrome/Aortic Dissection
Aortic Coarctation
Infective Endocarditis
Ischemic Heart Disease
Myocardial Infarction
New York Heart Association (NYHA)
Classification (1979)
• Class I – uncompromised
– No symptoms of cardiac disease
• Class II – limited symptomatology
– These patients are asymptomatic at rest but develop
symptoms (chest pain, shortness of breath, fatigue,
palpitations) with physical exertion
• Class III – marked symptomatology
– These patients are asymptomatic at rest but become
symptomatic with even minimal physical activity
• Class IV – symptoms at rest
Maternal Cardiac Disease
• Predictors of cardiac complications in
pregnancy include:
– Prior heart failure, transient ischemic attack,
stroke, or arrythmia
– Left sided obstruction as defined by:
• Mitral valve area < 2cm²
• Aortic valve area < 1.5cm²
• Aortic valve peak gradient > 30mm Hg
– Ejection fraction < 40%
– NYHA Class III or IV prior to pregnancy
Mitral Stenosis
• Most commonly caused by rheumatic
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endocarditis
Relatively fixed cardiac output
Degree of stenosis is directly associated with risk
Patients with mitral stenosis are at risk for atrial
fibrillation, mural thrombi, pulmonary edema,
and passive pulmonary hypertension
Epidurals and SVD generally advisable but must
avoid drops in preload to maintain CO
Mitral Stenosis
Mitral Insufficiency
• Incomplete coaptation of the mitral valve allows
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regurgitation of blood from LV back into LA
leading to LV hypertrophy
Usually caused by Rheumatic fever, MVP, or LV
dilatation (cause AND effect)
Usually asymptomatic in nonpregnant patients
Extremely well tolerated in pregnancy due to
decrease in SVR (afterload) resulting in less
regurgitation
Mitral Insufficiency
Aortic Stenosis
• May be congenital (i.e., bicuspid aortic valve) or acquired
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(rheumatic fever)
A disease of fixed cardiac output
In severe cases, cardiac output may not be able to
adequately maintain cerebral or cardiac perfusion
Limitation of physical activity during pregnancy is
essential
Any decrease in preload (orthostasis, α- adrenergic
blockade from epidural, hemorrhage, etc.) may result in
stroke or sudden cardiac death
Maternal mortality 5-15% depending on severity of
lesion
Aortic Stenosis
Aortic Insufficiency
• Mostly rheumatic in origin but may also be
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secondary to connective tissue disease or
congenital
LV hypertrophy and dilatation are secondary to
AI
Very well tolerated in pregnancy due to:
– Decrease in SVR (afterload)
– Physiologic increase in HR allows less time for
regurgitant backflow
Aortic Insufficiency
Pulmonic Stenosis
• Usually congenital
• Can be associated with Tetralogy of Fallot
or Noonan syndrome
• Can cause RA and RV enlargement
• Severe stenosis associated with right sided
heart failure and atrial arrythmias
Pulmonic Stenosis
Septal Defects
• Atrial Septal Defect (ASD)
– Most common congenital lesion seen in
pregnancy
– Rarely symptomatic
– Characterized by high pulmonary blood
flow and normal pulmonary artery
pressure
– Paradoxical embolism
Atrial Septal Defect
(ASD)
Ventricular Septal Defect
(VSD)
• Size of defect is most important factor in
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determining severity and 90% close in childhood
If effective size exceeds that of aortic valve,
symptoms develop rapidly and must be
surgically corrected
Adults with unrepaired sizable VSDs can develop
LV hypertrophy, LV failure, and pulmonary
hypertension
Ventricular Septal Defect
Patent Ductus Arteriosus
(PDA)
• Uncommon in pregnant women due to high rate
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of detection and repair in childhood
Severity is related to size of PDA
As with all high pressure left to right shunting,
pulmonary hypertension can develop
Sudden drops in SVR (massive hemorrhage,
epidural, etc.) may cause reversal of flow
through PDA and be fatal
Patent Ductus Arteriosus
Cyanotic Heart Disease
• Congenital heart lesions that shunt blood from
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the right heart to the left heart and bypass the
pulmonary capillary bed
This results in deoxygenated blood being placed
back into the systemic circulation
The magnitude of the shunting, and hence the
degree of cyanosis, is inversely related to SVR
When hypoxemia stimulates erythropoetic
centers such that hematocrit is at or above 65%,
pregnancy wastage is virtually 100%
Tetralogy of Fallot
• The most common cyanotic heart lesion
encountered in pregnancy
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VSD
Overriding aorta (receives blood from RV and LV)
RV hypertrophy
Pulmonary stenosis
• Surgical correction allows for excellent
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obstetrical outcomes
Uncorrected Tetralogy of Fallot is associated with
4-15% maternal and 30% fetal mortality
Tetralogy of Fallot
Ebstein’s Anomaly
• Few women with uncorrected Ebstein’s
anomaly reach their reproductive years
• Pregnancy increases volume overload and
hence exacerbates RV failure and cyanosis
• In the absence of significant cyanosis,
pregnancy is otherwise well tolerated
Ebstein’s Anomaly
Pulmonary Hypertension
• WHO Classification 2004
– Class I
• Idiopathic
• Familial
• Associated with collagen vascular disorders,
congenital left to right shunts, HIV disease,
thyrotoxicosis, SCA, antiphospholipid antibody
syndrome, portal hypertension
– Class II – associated with left sided heart
disease
Pulmonary Hypertension
– Class III – associated with lung disease
• Chronic obstructive pulmonary disease (COPD)
• Interstitial lung disease
– Class IV – Pulmonary hypertension due to
chronic thromboembolic disease
• Class I disorders have poorest prognosis in
pregnancy and 80% of maternal deaths
occur postpartum
Pulmonary Hypertension
• Class II disorders are the most common in
pregnancy (VSD, PDA, severe mitral
stenosis) and are associated with better
maternal outcome
• Severe disease regardless of class is
associated with at least a 50% chance of
maternal mortality
Pulmonary Hypertension
• Management
– Minimizing activity
– Avoiding supine position as gestation progresses
– Use of diuretics, O², and vasodilators to treat
symptoms
– At delivery, avoiding hypotension is critical as most
maternal deaths in patients with pulmonary
hypertension are due to decreased venous return to
the heart
Eisenmenger’s Syndrome
• Occurs in the presence of pulmonary
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hypertension caused by an underlying congenital
left to right shunt (usually ASD, VSD, or PDA)
As pulmonary hypertension worsens, PA
pressure equals systemic pressure and the shunt
becomes bidirectional or entirely right to left
Eisenmenger’s syndrome is associated with a
30-50% chance of maternal mortality during
pregnancy, delivery, or postpartum
RV failure and cardiogenic shock is the most
common cause of maternal mortality
Eisenmenger’s Syndrome
Mitral Valve Prolapse
• Cardiac complications from MVP are rare
• Pregnancy outcomes are excellent
• ACOG specifically refers to MVP and states
that MVP “never needs infective
endocarditis prophylaxis”
– ACOG Committee Opinion #421, Nov. 2008.
Marfan Syndrome
• Autosomal dominant connective tissue disorder
• Manifestations include ocular, skeletal, and
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cardiovascular abnormalities
In pregnancy, aortic root or splenic artery
aneurysm or dissection is most common site of
complications
Aortic root dilatation of 40 mm is associated with
up to a 50 % risk of maternal mortality
Aortic Coarctation
• Associated with VSD and PDA as well as
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intracranial aneurysms in the circle of Willis
NYHA Class I or II have 3-4% risk of mortality
Anomalous or bicuspid aortic valves, other
associated cardiac lesions, aneursms in the circle
of Willis or aortic aneurysms all increase
maternal mortality to 15%
Aortic Coarctation
Infective Endocarditis
Ischemic Heart Disease/ Myocardial
Infarction
• Incidence of pregnancy complicated by ischemic heart
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disease increasing
Incidence of acute myocardial infarction in pregnancy
estimated to be 1-6/100,000
Risk factors appear to be consistent with nonpregnant
population
Mortality risk adversely affected by pregnancy and
increases with advancing gestational age
Treatment is essentially standard and intervention
warranted only for obstetrical indications