Heart Disease and the Pregnant Patient Vanita Jain, MD FACOG

Heart Disease and the Pregnant
Patient
Vanita Jain, MD FACOG
Delaware Center for Maternal & Fetal Medicine
Disclosures
• Deny any relationship with companies who
manufacture products used in the treatment of
the subjects under discussion;
• Deny any relationship between the planner and
faculty and commercial supporters(s) of the
activity
• I do not intend to discuss unlabeled uses of a
commercial product, or an investigational use of
a product not yet approved for this purpose.
Objectives
• Cardiac Physiology in Pregnancy
• Counseling the patient with cardiac disease
• Management of the pregnant patient with
cardiac disease
– Valvular lesions
– Congenital lesions
– Myocardial infarction
– Cardiomyopathy/heart failure
• Medication use in pregnancy
Introduction
• Advances in diagnosis and treatment of cardiac
conditions have led to dramatically improved survival
rates in reproductive age women
• The number of women postponing child bearing
beyond age 40 has grown, increasing the likelihood of
co-morbid conditions such as cardiac disease
• Cardiac disease complicates 4% of pregnancies, yet
accounts for 34% of all maternal deaths
• Obstetric patients with cardiac disease are susceptible
to a number of potential complications resulting from
significant physiologic changes associated with
pregnancy and delivery
Ullery JC. Management of pregnancy complicated by heart disease AJOG 1954
Chang C et al. Pregnancy-related mortality surveillance, US. MMWR CDC 2003
Physiologic Changes
Measurement
Normal Value
Change in
Pregnancy (%)
Heart rate (bpm)
71 ± 10
 20%
Stroke Volume (mL)
73.9 ± 9
 30%
Cardiac output (L/min)
4.3 ± 0.9
 50%
5
 20%
Systemic Vascular Resistance (dyne/cm/s)
1530 ± 520
 20%
Mean Arterial Pressure (mmHg)
86.4 ± 7.5
No change
Oxygen consumption (mL/min)
250
 20%
Blood Volume (L)
Clark SL et al. Central hemodynamic assessment of normal term pregnancy. AJOG 1989
Elkayam U et al. Hemodynamics and cardiac function during normal pregnancy and puerperium.
Cardiac Problems in pregnancy 3rd ed. NY 1998
Physiologic Changes
Measurement
Normal Value
Change in
Pregnancy (%)
Heart rate (bpm)
71 ± 10
 20%
Stroke Volume (mL)
73.9 ± 9
 30%
Cardiac output (L/min)
4.3 ± 0.9
 50%
5
 20%
Systemic Vascular Resistance (dyne/cm/s)
1530 ± 520
 20%
Mean Arterial Pressure (mmHg)
86.4 ± 7.5
No change
Oxygen consumption (mL/min)
250
 20%
Blood Volume (L)
Clark SL et al. Central hemodynamic assessment of normal term pregnancy. AJOG 1989
Elkayam U et al. Hemodynamics and cardiac function during normal pregnancy and puerperium.
Cardiac Problems in pregnancy 3rd ed. NY 1998
Physiologic Changes
Measurement
Normal Value
Change in
Pregnancy (%)
Heart rate (bpm)
71 ± 10
 20%
Stroke Volume (mL)
73.9 ± 9
 30%
Cardiac output (L/min) 4.3 ± 0.9  50%
5
 20%
Systemic Vascular Resistance (dyne/cm/s)
1530 ± 520
 20%
Mean Arterial Pressure (mmHg)
86.4 ± 7.5
No change
Oxygen consumption (mL/min)
250
 20%
Blood Volume (L)
Clark SL et al. Central hemodynamic assessment of normal term pregnancy. AJOG 1989
Elkayam U et al. Hemodynamics and cardiac function during normal pregnancy and puerperium.
Cardiac Problems in pregnancy 3rd ed. NY 1998
Physiologic Changes
Measurement
Normal Value
Change in
Pregnancy (%)
Heart rate (bpm)
71 ± 10
 20%
Stroke Volume (mL)
73.9 ± 9
 30%
Cardiac output (L/min)
4.3 ± 0.9
 50%
5
 20%
1530 ±
520
 20%
Mean Arterial Pressure (mmHg)
86.4 ± 7.5
No change
Oxygen consumption (mL/min)
250
 20%
Blood Volume (L)
Systemic Vascular
Resistance
(dyne/cm/s)
Clark SL et al. Central hemodynamic assessment of normal term pregnancy. AJOG 1989
Elkayam U et al. Hemodynamics and cardiac function during normal pregnancy and puerperium.
Cardiac Problems in pregnancy 3rd ed. NY 1998
Physiologic Changes
• Total blood/plasma volume increases by 50%
• Red cell mass increases by only 33%
• Results in functional anemia (decreased
hemoglobin/hematocrit)
• Heart accommodates this because of the decreased
SVR
• Decreased SVR results in systolic and diastolic blood
pressure drop in pregnancy (nadir 24-32 weeks)
• Cardiac output increases shortly thereafter 50% by 32
weeks, and an additional 50% in the second stage of
labor
Capeless EL et al. Cardiovascular changes in early phases of pregnancy. AJOG 1989
Gei AF Cardiac Disease and pregnancy. Obstet Gynecol Clin 2001
Clotting Factor Changes in pregnancy
Factor
Change
Factor II (prothrombin)
No change
Factor 7, 8, 9, 12
 increase
Fibrinogen
Increase
Platelets
No change
Clotting Factor Changes in pregnancy
Factor
Change
Factor II (prothrombin)
No change
Factor 7, 8, 9, 12
Fibrinogen
 increase
Increase
Platelets
No change
Physiologic Changes
• Four fundamental alterations
1)
2)
3)
4)
Increased volume of blood
Increased cardiac output
Decreased systemic vascular resistance
Hypercoagulability
Changes in cardiovascular tests in
pregnancy
Cardiovascular Exam
Findings in Pregnancy
Chest X-Ray
Cardiomegaly
Enlarged Left Atrium
Increased pulmonary vasculature
Small bilateral pleural effusions
(postpartum)
EKG
Left axis deviation (15°)
Right Bundle Branch Block
Q waves – leads III, aVF
T wave inversions – leads III, V2, V3
Shortening of PR/QT intervals
Echocardiography
Mild TR
Mild PR – difficult to calculate PASP
Increased left atrium size (15%)
Increased LVED dimension (10%)
Mild MR
Small pericardial effusion
Cardiac Physiology
Antepartum
• CO increases to 50% by
28 weeks
• HR increases 15 bpm by
32 weeks
• Stroke volume increases
30% by 32 weeks
• SVR decreases 20% by
24 weeks
Cardiac Physiology
Intrapartum
• CO increases another 50%
(up to 11 L/min) in labor
• HR increases due to pain
• MAP can increase due to
pain
• Contractions result in
autotransfusion of 500cc
blood from uterus
increases preload/stroke
volume
Cardiac Physiology
Postpartum
• CO increases by 50%
within 1 hour of delivery
• Stroke volume increases
by 70% within 1 hour of
delivery
• Reflex bradycardia
• Postpartum diuresis 2-5L
over 2-7 days
• Cardiac status returns to
baseline 2-6 weeks
Maternal Mortality associated with Pregnancy
Group
Lesion
Risk of Mortality
1
ASD, VSD, PDA
Mitral stenosis (NYHA I/II)
Pulmonary valve disease
Corrected TOF
Bioprosthetic valves
< 1%
2–A
Mitral stenosis (NYHA III/IV)
Aortic stenosis
Coarctation of Aorta, normal valves
Uncorrected TOF
History of MI
Marfan syndrome, normal aorta
5-15%
2–B
Mitral stenosis (NYHA III/IV) & AFIB
Artificial mechanical valves
15%
3
Pulmonary Hypertension
Coarctation of aorta, abnormal valves
Marfan syndrome, abnormal aorta
Peripartum CM with persistent LV
dysfuncton
25%
Maternal Mortality associated with Pregnancy
Group
Lesion
Risk of Mortality
1
ASD, VSD, PDA
Mitral stenosis (NYHA I/II)
Pulmonary valve disease
Corrected TOF
Bioprosthetic valves
< 1%
2–A
Mitral stenosis (NYHA III/IV)
Aortic stenosis
Coarctation of Aorta, normal valves
Uncorrected TOF
History of MI
Marfan syndrome, normal aorta
5-15%
2–B
Mitral stenosis (NYHA III/IV) & AFIB
Artificial mechanical valves
15%
3
* Pulmonary Hypertension
* Coarctation of aorta, abnormal valves
* Marfan syndrome, abnormal aorta
* Peripartum CM with persistent LV
dysfxn
25%
Predicting Adverse Events
• CARPREG Score
– First study 1997 (Siu et al) – identifies
independent risk factors for cardiac complications
(CHF, CVA, arrythmia), 252 pregnant patients,
variety of lesions
– Most significant risk factors for complications
appear to be NYHA ¾, cyanosis, historyo f
arrhythmia, pulmonary vascular disease, EF < 40%
or significant mitral/aortic valve obstruction
Siu SC et al. Risk and predictors for pregnancy related complications in
women with heart disease. Circulation 1997
Predicting Adverse Events
• CARPREG Score
– 2001 study, Siu et al: prospective evaluation 617
pregnancies complicated by maternal cardiac
disease to characterize 4 predictors of maternal
complications:
• 1) History of CHF/TIA/CVA/arrythymia
• 2) Prepregnancy NYHA class II-IV or cyanosis
• 3) Left heart obstruction (MVA <2cm; AVA <1.5cm,
LVOT gradient > 30mmHg)
• 4) EF < 40%
Siu SC et al. Prospective multicenter studyo f pregnancy outcomes in women with
heart disease. Circulation 2001
Predicting Adverse Events
Number of Risk Factors
0
1
2 or more
Risk of adverse event (%)
5
27
75
Siu SC et al. Prospective multicenter study of pregnancy outcomes in women with heart disease.
Circulation 2001
Counseling the patient
Increased risk for the following:
– Miscarriage
– Preterm labor
– Stillbirth
– Preeclampsia
– Growth restriction
– NICU admission – neonatal complications
– If mother had CHD, risk to fetus of CHD
Risk of Fetal Congenital Heart Defect
Cardiac Lesion
Prior affected
Sibling
Father Affected
Mother Affected
TOF
2.5%
1.5%
2.6%
Aortic Coarctation
14.1%
ASD
2.5%
1.5%
4.6 – 11%
VSD
3%
2%
9.5 – 15.6%
Pulmonary stenosis
2%
2%
6.5%
Aortic stenosis
2%
3%
15 – 18%
Driscoll DJ et al. Occurrence risk for congenital heart defects in relatives of patients with
aortic stenosis, pulmonary stenosis or ventricular septal defect. Circulation 1993
Lupton M et al. Cardiac disease in pregnancy. Curr Opin Obstet Gynecol 2002
Teerlink JR et al. Valvular heart disease in pregnancy Cardiol Clin 1998.
Valvular Heart Lesions
Mitral Stenosis
– Flow across valve is fixed, progressive increase in preload results in
increase LA – LV pressure gradient; leads to increased LA pressure, can
result in pulmonary edema or pulmonary hypertension
– Baseline echocardiogram to determine severity of lesion, presence of
LAE
– Baseline EKG to rule out afib/LAE/RVH (suggest PHTN)
– Ideally recommend repair PRIOR to pregnancy
– Severe lesions can be repaired during pregnancy (case reports suggest
percutaneous balloon valvuloplasty is safe/effective; however medical
management should be clearly exhausted before assuming these risks
in pregnancy)
– Complications typically around 30-32 weeks: pulmonary edema (60%
risk), atrial tachyarrhythmia (20% risk), LA clot -> CVA
– GOALS: prevent tachycardia, diuretics for pulmonary edema, antiarrythmics if afib occurs, manage pain, consider assisted 2nd stage
– Avoid terbutaline
Valvular Heart Lesions
Aortic Stenosis
– Stenotic valve obstructs flow from LV to aorta – causes LVH; CO
is fixed regardless of the high output situation (pregnancy);
sensitive to preload changes
– Increased preload will cause transmission of pressure back to
LA, pulmonary system causing edema
– Decreased preload will result in underperfusion
– Baseline echocardiogram to assess AVA and pressure gradient,
LVH, EF
– Baseline EKG to assess LVH, LV ischemia, LAE, arrhythmias
– Careful with physical activity – angina, syncope, CHF
– Avoid hypotension (hemorrhage) – decreased perfusion to
coronary arteries/infarction
– Correct BEFORE pregnancy if possible
– Anesthesia assistance for epidural (slow)
– Assisted 2nd stage
Valvular Heart Lesions
Mechanical Heart Valves - 3 options:
- Warfarin:
crosses placenta, warfarin embryopathy (nasal hypoplasia,
limb hypoplasia, epiphyseal stippling), intracranial
hemorrhage, miscarriage
but lowest rates of VTE
- Heparin
does not cross placenta
adjusted dose regimen with/without warfarin
- Lovenox
does not cross placenta
however black box warning after 2 maternal/fetal deaths
occurred in 2002 – may have been insufficient dosing
Mechanical Valves continued..
• Altered pharmacodynamics of medications in
pregnant patients, alterations in coagulation
cascade
• Need to monitor peak/trough levels with antiXa measurements and aPTT
• PTT is hard to monitor due to pregnancy
induced changes – elevation of factor VIII (8)
• Anesthesia considerations
Valvular Heart Disease
Number of
women
Pregnancies
Fetal loss
Preterm delivery
Valve
deterioration
VTE
Mechanical Valve
31
Porcine Valve
57
56
27%
5.9%
5.3%
95
12%
7.7%
7.0%
5.3%
Lee C. Pregnancy following cardiac prosthetic valve replacement
Mechanical Valves
• 0-12 weeks (First Trimester)
– Heparin/Lovenox (dose adjusted)
• 12-36 weeks (Second/Third Trimesters)
– Warfarin (INR 2.5 – 3.5) + dose adjusted heparin/lovenox (PTT goal 6080, anti Xa goal 0.7-1.2)
• 36 weeks – delivery
– Stop Warfarin
– Continue heparin (no lovenox) dose adjusted
• Delivery
– Stop heparin at least 12 hours prior to delivery/regional anesthesia
• Postpartum
– Restart heparin/lovenox 6 hours post vaginal delivery, 12 hours post csection
– Restart Warfarin 12-24 hours
Bonow RO et al. ACC guidelines Circulation 2008
Obstetric Issues with anticoagulation
• General issues
– Full reversal of anticoagulation is not needed
– Make sure not supratherpeutic at least
– Full reversal is needed if maternal hemorrhage
• If on heparin at time of delivery
– Try to delay delivery 6 hours
– Prefer vaginal delivery (less bleeding)
– Protamine if emergency and fully anticoagulated
• If on warfarin at time of delivery
–
–
–
–
Prefer c-section (fetal hemorrhage)
Delay delivery to give vitamin K (INR <2)
Given FFP in OR prior to c-section (INR <2)
Notify peds neonate may need FFP/vitamin K
Butchart EG et al. Recommendations for management of patients after
heart valve surgery. Eur Heart J 2005.
SBE prophylaxis
ACC Guidelines to use SBE
prophylaxis during
labor/delivery
- Prosthetic cardiac valve
- History of endocarditis
- CHD with
- Cyanotic disease
- Repaired <6 months ago
- Repaired with residual
defects
ACOG recommendations
for antibiotics for SBE
prophylaxis during
labor/delivery
- Ampicillin 2g IV
- Cefazolin 1g IV
- Ceftriaxone 1g IV
- Clindamycin 600mg IV
- Amoxicilllin 2g PO
ACOG Committee Opinion No. 421 Obstet Gynecol 2008
ACC 2006 Guidelines. Circulation 2006
Maternal Congenital Heart Disease
• Aortic Coarctation:
–
–
–
–
–
If possible correct PRIOR to pregnancy
Screen for other co-existing lesions
Increased risk for intracranial aneurysm (screen)
Increased risk for preeclampsia (screen)
Concerns about risk of aortic rupture/aortic dissection
has prompted some to recommend elective c-section
– however can have assisted 2nd stage vaginal delivery
and manage pain carefully with epidural, control
blood pressure, maintain preload and minimize
valsalva
Maternal Congenital Heart Disease
• VSD/ASD/PDA
– Isolated VSD or corrected VSD do not increase the risk
of adverse outcomes in pregnancy, unless pulmonary
hypertension exists (screen)
– ASD do not increase risk to pregnant patient even if
unrepaired unless arrhythmias or pulmonary
hypertension occurs. However there is a risk for
paradoxical embolism (screen)
– Repaired PDA post no risk, unrepaired PDA pose risk
only if develop pulmonary hypertension (screen)
Maternal Congenital Heart Disease
• Ebstein Anomaly
– Uncommon in pregnancy, pregnancy is well tolerated
• TGV
– If uncorrected – 90% mortality rate, if corrected then
pregnancy can be tolerated with careful management
for RV dysfunction and dysrhythmia
• TOF
– If corrected overall tolerate pregnancy well, increased
risk for CHF, arrythymia (screen)
Maternal Congenital Heart Disease
• Eisenmenger Syndrome/Pulmonary Hypertension
– Unrepaired congenital intracardiac shunt with flow right to left
and pulmonary HTN
– Increased volume and decreased preload from decreased SVR
challenges the RV and precipitates RV failure
– Decreased SVR lowers peripheral resistance versus pulmonary
resistance worsening hypoxia/cyanosis
– Hypercoaguable state of pregnancy increased risk of clot
– Maternal mortality rates 30-50%
– Recommend termination of pregnancy
– If continues pregnancy – minimize cardiac demands (hospitalize,
bed rest), maximize oxygenation (supplemental oxygen),
anticoagulate, try pulmonary vasodilators
Maternal Congenital Heart Disease
• Marfan Syndrome
– 50% risk of passing to children
– 3-5% risk of dissection in pregnancy, greatest risk is those
with Ao Root Diameter > 4.5cm
– ACC/AHA recommends discouraging pregnancy if Ao Ro >
or = to 4cm
– Recommend repair PRIOR to pregnancy – even if no
symptoms
– Recommend beta blockers during pregnancy
– Vaginal delivery if Ao Root <4cm and no signs of heart
failure and pain is managed
– Controversial if Ao Root is >4cm – assisted 2nd stage? Or csection
Pyeritz RE. The Marfan Syndrome: diagnosis & management. NEJM 1979
Rossiter JP et al. Longitudinal evaluation of pregnancy in Marfan syndrome. AJOG 1995
Shores J et al. Progression of aortic dilatation and the benefit of long term beta blockade in Marfan’s syndrome. NEJM 1994
Maternal Arrhythmias
• Depends of arrhythmia – get information to characterize
the type
• History of SVT increases risk of SVT in pregnancy
• History of afib/flutter should prompt evaluation for
structural disease (baseline echo, screen)
• Pharmacologic management should NOT be altered due to
pregnancy
• If unstable acute arrythmia in pregnancy not responding to
medical management can perform electrical cardioversion
• Ideally prefer evaluation PRIOR to pregnancy to determine
if need ablation, pacemaker or ICD, and to review risks of
fetal exposure to maternal cardiac medications
Acute Myocardial Infarction
• Rare (1/35,000), mortality rate 7.3%
• History of AMI is more common
• Same management as non pregnant patient:
– Oxygen, aspirin, nitroglycerin, heparin
– Careful with fibrinolytics
• Vaginal delivery can be performed – minimize
myocardial demand, control heart rate, maintain
blood pressure, control volume shifts
• Careful with Pitocin, Methergine or Misoprostil
Cardiomyopathy
• Peripartum CM is the development of heart
failure between 36 weeks and 5 months
postpartum in the absence of preexisting heart
disease
• Risk Factors include: multiparity, AMA, multiples,
preeclampsia, CHTN
• Echo criteria:
– EF < 45%
– LV shortening fraction < 30%
– LV end diastolic dimension > 2.7 cm/m2 BSA
Pearson GD et al. Peripartum cardiomyopathy – NIH recommendations. JAMA 2000
Cardiomyopathy
• Management is focused on reducing preload, reducing
afterload, improving contractility
• Delivery counseling
• Careful postpartum management
• Anesthesia evaluation
• Postpartum counseling – prognosis depends on return
of LV function within 6 months of delivery (expected in
50% of patients)
• In subsequent pregnancy if if EF does not recover to at
least > 25 % should counsel to avoid pregnancy
Cardiac Medications in Pregnancy
Agent
Uterine Effect
Fetal Effect
Inotropes:
Epinephrine
Dopamine
Digoxin
Decreases uterine flow
Decreases uterine flow
No change
None
None
Crosses placenta
Vasodilators:
Hydralazine
Nitroglycerin
Nitroprusside
Decreases uterine flow
Decreases uterine flow
No change
None
None
Fetal cyanide toxicity
Beta blockers
Labetalol/Propranolol
Decreases uterine flow
Can cross placenta – IUGR
Calcium channel blockers
Nifedipine/Verapmail
None
None
Cardiac Medications in Pregnancy
Agent
Uterine Effect
Fetal Effect
No change
No change
Amiodarone
None
Teratogenic – bradycardia,
prolonged QT
AV nodal agents
Adenosine
None
None
Anti-arrhythmic
Lidocaine
Procainamide
Quinidine
Standard of Care
• Accurate Diagnosis of the cardiac condition
• baseline echocardiogram, then follow every trimester
(pending lesion, severity, cardiology input)
• Mode of delivery based on obstetrical indications
only
• Discuss mode of delivery with cardiology ahead of time
(risks/benefits c-section versus VAVD/FAVD)
• Medical management initiated early in labor
(schedule delivery if possible)
• avoid prolonged labor; plan induction with a favorable
cervix
Standard of Care
• Anesthesia consultation is paramount to help with pain/anxiety,
hypertension (CSE/epidural – use fentanyl), assist with central
lines/art line
• Maintain hemodynamic stability
• Telemetry on admission, through labor and 12 hours postpartum
(when risk of CHF is highest)
• Replete electrolytes on admission and postpartum
• VTE prophylaxis labor/postpartum
• Continue cardiac medications in labor
• Prophylactic antibiotics (SBE) if at risk for endocarditis
• Avoid maternal blood loss
• Careful with pitocin, hemobate, methergine
• Have plan for active management of third stage of labor (in event
of PPH)
Family Planning
• Reproductive age women
presenting with cardiac
disease unique situation
– Preconception counseling
regarding risks with
undertaking pregnancy
– Contraception until they are
ready to undertake pregnancy
– Postpartum contraceptive
counseling to assist in
pregnancy spacing
– Discussion regarding surgical
correction prior to pregnancy
• Refer to MFM
Breast-feeding
• Most medications are
safe
• In general our principle
is that healthy mother is
healthy baby – so
certain cardiac
medications may be
necessary for maternal
health
• Discuss with
pediatrician
Thank you
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