Cardiac Disease in Pregnancy

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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

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Objectives

• Provide an overview of normal cardiac 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 

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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

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Maternal Cardiac PhysiologyCardiovascular
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

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Maternal Cardiac PhysiologyCardiovascular
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

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Maternal Cardiac PhysiologyCardiovascular
Alterations
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Maternal Cardiac PhysiologyCardiovascular
Alterations

• Decreased systemic vascular resistance
• Decreased blood pressure
• Decreased pulmonary vascular resistance
• Increased heart rate
• Increased cardiac output
• CO SV x HR

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Maternal Cardiac PhysiologyCardiovascular
Alterations
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Maternal Cardiac Disease

• Valvular Cardiac Disease
• Mitral Stenosis
• Mitral Insufficiency
• Aortic Stenosis
• Aortic Insufficiency
• Pulmonic Stenosis

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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
• Ebsteins Anomaly

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Maternal Cardiac Disease

• Pulmonary Hypertension
• Eisenmenger syndrome
• Mitral Valve Prolapse
• Marfan Syndrome/Aortic Dissection
• Aortic Coarctation
• Infective Endocarditis
• Ischemic Heart Disease
• Myocardial Infarction

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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

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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 lt 2cm²
• Aortic valve area lt 1.5cm²
• Aortic valve peak gradient gt 30mm Hg
• Ejection fraction lt 40
• NYHA Class III or IV prior to pregnancy

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Mitral Stenosis

• Most commonly caused by rheumatic 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

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Mitral Stenosis
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Mitral Insufficiency

• Incomplete coaptation of the mitral valve allows
  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

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Mitral Insufficiency
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Aortic Stenosis

• May be congenital (i.e., bicuspid aortic valve)
  or acquired (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, a-
  adrenergic blockade from epidural, hemorrhage,
  etc.) may result in stroke or sudden cardiac
  death
• Maternal mortality 5-15 depending on severity of
  lesion

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Aortic Stenosis
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Aortic Insufficiency

• Mostly rheumatic in origin but may also be
  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

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Aortic Insufficiency
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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

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Pulmonic Stenosis
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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

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Atrial Septal Defect (ASD)
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Ventricular Septal Defect(VSD)

• Size of defect is most important factor in
  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

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Ventricular Septal Defect
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Patent Ductus Arteriosus(PDA)

• Uncommon in pregnant women due to high rate 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

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Patent Ductus Arteriosus
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Cyanotic Heart Disease

• Congenital heart lesions that shunt blood from
  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

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Tetralogy of Fallot

• The most common cyanotic heart lesion encountered
  in pregnancy
• VSD
• Overriding aorta (receives blood from RV and LV)
• RV hypertrophy
• Pulmonary stenosis
• Surgical correction allows for excellent
  obstetrical outcomes
• Uncorrected Tetralogy of Fallot is associated
  with 4-15 maternal and 30 fetal mortality

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Tetralogy of Fallot
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Ebsteins Anomaly

• Few women with uncorrected Ebsteins 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

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Ebsteins Anomaly
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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

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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

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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

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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

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Eisenmengers Syndrome

• Occurs in the presence of pulmonary 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
• Eisenmengers 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

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Eisenmengers Syndrome
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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.

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Marfan Syndrome

• Autosomal dominant connective tissue disorder
• Manifestations include ocular, skeletal, and
  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

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Aortic Coarctation

• Associated with VSD and PDA as well as
  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

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Aortic Coarctation
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Infective Endocarditis
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Ischemic Heart Disease/ Myocardial Infarction

• Incidence of pregnancy complicated by ischemic
  heart 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