Non-ischemic cardiac

disease during pregnancy

Ruben J. Azocar, MD
Assistant Professor of Anesthesiology
Boston University Medical Center

Introduction

Although the prevalence of clinically

significant maternal heart disease during
pregnancy is probably less than 1% its
presence increases the risk of adverse
maternal, fetal, and neonatal outcomes

CV Physiology of Pregnancy

Blood volume increases 30 to 50%

Plasma volume increase more than RBC mass

leading to physiologic anemia
An estrogen mediated stimulation of the reninangiotensin system results in retention of NA and
water

HR increases 10 to 20 bpm

CV Physiology of Pregnancy

CO increase up to 45% by 24 wks

These increases begin during the 1st trimester

Peak by 20-24 wks and are sustained until term
In early pregnancy an increase in SV (20-30%) is
responsible to the increase in CO
Later in pregnancy, the increase in HR is responsible since
SV decreased due to IVC compression

Concurrently there is a substantial reduction in SVR

by 21% with decreases in BP and decreases in PVR
by 34%

CV Physiology of Pregnancy

Symptoms and PE of normal pregnancy

mimic cardiac disease

Exertional dyspnea and orthopnea

Fatigue and Presyncope
Lower extremity edema
a and v waves may be pronounced in CVP tracing
Maximal apical impulse is displaced
1st Heart sound the pulmonary component of 2 nd
might are accentuated
3rd HS is heard in 80% of pregnant women

CV Physiology of Pregnancy

Murmurs frequently develop during pregnancy

Soft, mid-systolic, and heard along the left sternal border is

heard in 90% women
Anemia might accentuate it
Intensity may increase as CO increases
Cervical venous hums and a continuous murmur due to
increased mammary blood flow may also be heard
Echocardiography is warranted if:

Diastolic, continuous, or loud systolic murmurs (>2/6)

A fixed split 2nd sound
Associated with symptoms or an abnormal EKG

CV Physiology of Pregnancy

In normal pregnant women, echocardiography

demonstrates:

Minor increases in the left and right ventricular

diastolic dimensions (within the normal range)
A slight decrease in the LVES dimension and a
minimal increase in the size of the left atrium
Increased transvalvular flow velocities due to the
increased BV
Minor degrees of atrioventricular valve regurgitation

CV Physiology of Pregnancy

During labor:

CO increases 45% above pre-labor values

Uterine contraction boluses the patient

It might increase CO up to 65% of pre-labor values

The BP increases with uterine contractions/pain

CV Physiology of Pregnancy

Immediately after delivery

The cardiac filling pressure increase dramatically

due to the decompression of the vena cava and
the return of uterine blood into the systemic
circulation

CO might increase to 80% of pre-labor values

The cardiovascular adaptations associated with

pregnancy regress by approximately 6 weeks
after delivery

Physiology of Pregnancy

Pregnancy is also a hypercoagulable state

Decreased in Protein S activity

Stasis
Venous hypertension

The problem

A Canadian analyses of the outcomes of pregnancy

identified predictors of adverse maternal and fetal
outcomes in a group of women with congenital or
acquired heart disease (546 women and 599
pregnancies)

Approximately 40% of the women had a primary valve

disorder
Adverse maternal outcomes included: pulmonary edema,
sustained brady or tachyarrhythmias, stroke, cardiac arrest,
or death
Adverse fetal outcomes included: premature birth,
intrauterine growth retardation, respiratory distress
syndrome, intraventricular hemorrhage, and death

Maternal outcomes

Incidence of adverse maternal cardiac events

13% of completed pregnancies
More likely if:
EF below 40%
Left heart obstruction (AS with a valve area of less than 1.5
cm2 or MS with a valve area of less than 2.0 cm2)

Previous cardiovascular events (heart failure, tia, or stroke)

NYHA class II or higher

These events occurred in:

4% of the women with none of these risk factors

27 % of those with one risk factor

62 % of those with two or more risk factors
The 3 women that died had two or more risk factors

Fetal outcomes

Abnormal functional capacity (NYHA class II or higher) and left

heart obstruction were also predictors of neonatal complications
Other predictors of adverse fetal outcomes included:
The use of anticoagulant drugs throughout pregnancy
Smoking during pregnancy
Multiple gestation
Mothers age (> 35 yrs or < 20 yrs)
Fetal mortality was:
4 % among pregnancies in women with one or more of
these risk factors,
2% among those with none of these risk factors

Evaluation

The evaluation of a woman with clinically significant

valvular heart disease should occur before conception
and entail a full cardiac assessment
The history should focus on the patient's exercise
capacity, current or past evidence of heart failure, and
associated arrhythmias
Cardiac hemodynamics, including PAP and the severity
of valve dysfunction, should be assessed by echo
Exercise testing may be useful if the history is
inadequate to allow an assessment of functional capacity
During pregnancy evaluation each trimester and
whenever there is a change in symptoms, in order to
assess any deterioration in maternal cardiac status is the
rule

Mitral Stenosis

Rheumatic MS is the most common valvular

abnormality in pregnant women (60%)
Associated with pulmonary congestion, edema, and
atrial arrhythmias during pregnancy or soon after
delivery

The increased BV load and CO associated with pregnancy

lead to an increase in left atrial volume and pressure,
elevated pulmonary venous filling pressures, dyspnea, and
decreased exercise tolerance
Increases in the maternal HR decrease the diastolic filling
period, further increasing left atrial pressure and
decreasing CO
The increased atrial pressure may cause arrhythmias

Mitral Stenosis

Mortality among pregnant women with

minimal symptoms is less than 1%
Predictors of adverse maternal outcomes

Mitral valve area less than 1.5 cm2

Abnormal functional class before pregnancy

Fetal mortality increases with deteriorating

maternal functional capacity

30 % when the mother has NYHA class IV

Mitral Stenosis

For women with mild or moderate symptoms

Medical therapy is directed to the treatment of volume

overload
Diuretic therapy but avoiding hypotension and
tachycardia
NA+ restriction
Reduction of physical activity
Beta-blockers decrease HR and prolong the diastolic
filling period which provides symptomatic benefit

Mitral Stenosis

Development of AF requires prompt treatment,

including cardioversion.
Beta-blockers and digoxin for rate control
Procainamide and quinidine are frequently used if
suppressive antiarrhythmic therapy is needed
Due to the increased risk of systemic embolism in
patients with MS and AF anticoagulant therapy is
indicated

Mitral Stenosis

NYHA class III / IV or a valve area of less than 1.0 cm 2

Percutaneous balloon mitral valvuloplasty (PBMV) or

valve surgery BEFORE conceiving appear to allow
pregnancy with fewer complications than women treated
medically
PBMV, during the 2nd trimester, has been associated with
normal deliveries and excellent fetal outcomes
Fetal risks associated with exposure to radiation may
be reduced by avoiding exposure during the first half
of pregnancy
The uterus must be shielded and the patient should be
informed about the possible risks
Mitral valvuloplasty has also been performed under
TEE guidance

Mitral Stenosis

Open cardiac surgery has been performed

during pregnancy for severe MS
Maternal outcomes are similar to the nonpregnant
Fetal loss in 10 to 30 % of cases

MS: Anesthesia management

Careful clinical evaluation early on in

conjunction with the OB team to have a clear
plan
ICU consultation
Vaginal delivery is the usual approach
Hemodynamic goals:

Avoidance of tachycardia and fluid overload

Preservation sinus rhythm
Increase of BV, CO and HR during pregnancy
and labor may result in pulmonary congestion,
tachycardia and atrial fibrillation

MS: Anesthesia management

Monitoring:

A-LINE and probably PAC

Labor and delivery is associated with an increase

of 8 to 10 mm Hg in the left atrial and pulmonary
wedge pressures

PAC used before and during delivery facilitates

the management of hemodynamics in women with
advanced disease

MS: Anesthesia management

Epidural anesthesia to achieve effective pain control

A mixture of LA and opioids is ideal

Pain control and minimization of BV/CO increase after
delivery

Assisted-delivery devices during the second stage

of delivery eliminate hemodynamic effects of
valsalva maneuver during pushing
Cesarean section should be performed when there
are obstetrical indications for it

Mitral Regurgitation

Most commonly due to mitral-valve prolapse and is

usually well tolerated during pregnancy because of
the reduction in SVR
Women with symptomatic MR may benefit from
mitral-valve surgery (preferably repair )before
becoming pregnant.

However, LV dysfunction associated with MR is unlikely to

improve after surgery and will increase maternal risk during
pregnancy
Diuretics and vasodilators may be indicated

Outcome data that would help to guide clinical

decision making in this area are lacking.

Aortic Stenosis

Congenital valvular abnormalities are usually the

cause of AS in young women in the US
Severe AS is poorly tolerated during pregnancy

Maternal and perinatal mortality of 17% and 32% have

been reported

The pressure gradient is responsible for the HD

changes seen in AS

The increased LVSP needed to maintain systemic arterial

blood pressure increases stress in the ventricular wall
Lt ventricular hypertrophy develops leading to diastolic
dysfunction, fibrosis, diminish coronary blood flow reserve
and late systolic failure

Aortic Stenosis

Patients who are symptomatic or who have a

peak outflow gradient of more than 50 mm Hg are
advised to delay conception until after surgical
correction
Termination of pregnancy should be strongly
considered if the patient is symptomatic before
the end of the 1st trimester
Aortic-valve replacement and palliative aortic
balloon valvuloplasty have been performed during
pregnancy with associated maternal and fetal risk

Aortic Stenosis

Hemodynamic goals:

Maintain normovolemia

NSR

Tachycardia decrease dyastolic filling time

Atrial kick is responsible for up to 40% of ventricular
filling in this patients

Baseline SVR

Aortic Stenosis

The normal physiological changes of pregnancy can

precipitate heart failure in patient with severe AS
The further increase of CO and BV during labor in
face of the fixed CO of AS patients may precipitate:

Tachycardia which decreased diastolic time (and

coronary perfusion time) and increases O2
consumption
Increases LVEDP
Ischemia might result

Aortic Stenosis

Vaginal delivery is preferred

Instrumental delivery to avoid hemodynamic

changes of the valsalva manuver
Oxytocin may decrease SVR an increase PAP

Monitoring:

A-line
?CVP ?PAC

Aortic Stenosis

Epidural analgesia

Pain control and also minimizes BV/CO increase

after delivery
Avoid epinephrine test dose
Careful titration to avoid sudden decrease of SVR
Dilute LA with opioids to minimize sympathectomy

Aortic Stenosis

Cesarean section

GA has traditionally being advocated to avoid sudden

decreases of SVR
Opiod based induction
Fetal depression. Pediatric team must be aware
Case reports of epidural anesthesia with positive outcomes
Careful titration of LA and fluid replacement/vasopressors
to counteract sympathectomy
Phenylephrine possible a better choice over ephedrine

Aortic Regurgitation

AI may be due to a dilated Ao annulus (as in

Marfan's syndrome), a bicuspid Ao valve, or
previous endocarditis

The reduced SVR of pregnancy reduces the

volume of regurgitated blood

Women with an abnormal functional capacity or

left ventricular dysfunction are predicted to have a
high risk of abnormal maternal outcomes, but few
data concerning this population are available

Aortic Insufficiency

Isolated AI can usually be managed with vasodilators

and diuretics
ACE inhibitors should be discontinued during
pregnancy, and other agents, such as hydralazine
or nifedipine, should be substituted
Clinical and echo assessment should be performed
before conception in women with AI due to Marfan's
syndrome
Even in the absence of overt cardiac abnormalities,
this syndrome predisposes women to
unpredictable, but increased, risk during pregnancy.

Pulmonary hypertension

PHTN is associated with high maternal mortality (33

to 40 %), as well as with an increased rate of
adverse neonatal events
Secondary PHTN due to valvular disease is
associated with an increased rate of adverse
maternal events, but the absolute risk of such
events is unclear.
A systolic pulmonary-artery pressure that is more
than 75 % as high as the systemic pressure places
the woman at high risk.

Pulmonary hypertension

Hemodynamic objectives

Maintain the PAP as low as possible and the

systemic pressure within the 15% above and
below the basal level (the systemic pressure
should always be higher than pulmonary
pressure)
Avoid dysrhythmias and tachycardia, and maintain
sinus rhythm

Pulmonary hypertension

Pregnancy and labor CV changes against goals:

Uterine contraction after delivery returns a large bolus

of blood to the circulation. This can be poorly tolerated
in patients with severe PHTN
The sudden hypervolemia can be treated with
vasodilators, such as nitroglycerine, and diuretics.
A BP cuff inflated between the arterial and venous
pressures around the thighs, can suddenly and
reversibly decrease RV filling by reducing venous
return
Air or amniotic fluid embolism could acutely increase
pulmonary pressure

Pulmonary hypertension

Monitoring:
a-line and CVP or PAC should be used for monitoring
or for drug administration

Vaginal delivery
Pain control with a mixture of local anesthetics in a low
concentration and opioids via epidural
Forceps delivery, which decreases patient effort and
hemodynamic consequences, is the technique of
choice.

Pulmonary Hypertension

Cesarean Delivery

Both general and epidural anesthesia have been

used for cesarean delivery in patients with
pulmonary hypertension.
The surgical procedure can lead to excessive
bleeding and hypovolemia

Pulmonary hypertension

Induction of general anesthesia

Based on opioids
Lidocaine (1 mg/kg) reduces pulmonary and
hemodynamic reactions during intubation
Induction can be complemented with pentothal,
propofol, or etomidate
Succinylcholine can be used for intubation
Anesthesia could be maintained with use of short
acting narcotic infusion, volatile anesthetics
and/or propofol infusion

Prosthetic Heart Valves

Bioprostheses are not as durable as mechanical

prostheses, but eliminate the need for anticoagulant
therapy
Women with mechanical valves have a higher rate
of thromboembolism and higher 10-year mortality,
despite a lower rate of valve loss

Pregnancy does not appear to increase the rate of failure of

mechanical prostheses or homograft nor accelerates the
deterioration of bioprosthetic valves
Pregnancy in a woman with a mechanical valve is
associated with an estimated maternal mortality of 1 to 4%
with death usually resulting from complications of
prosthetic-valve thrombosis.

Anticoagulation

There are no results of clinical trials to guide the

choice of anticoagulant therapy during pregnancy
Monitoring is required in order to assess whether the
antithrombotic effect is adequate
The effective doses of these drugs change during
pregnancy because of changes in intravascular
volume and body weight
In a series of 976 women with a total of 1234
pregnancies the use of any anticoagulant therapy
resulted in major bleeding in 2.5 % of the pregnancies,
with bleeding usually occurring at the time of delivery

Warfarin

In women with mechanical valves the use of

warfarin throughout pregnancy was associated with
the greatest maternal protection

Risk of thromboembolism, 3.9%, risk of death, 1.8%

Warfarin crosses the placenta

Fetal deformities and CNS abnormalities

High rate of fetal loss (30%) including spontaneous

abortions, stillbirths, and neonatal deaths
Exposure to warfarin between 6 -12 wks of gestation
was associated with a rate of fetal loss that was twice
that associated with the use of unfractionated heparin

Fetopathic effects of warfarin use (nasal hypoplasia and

bone stippling) occurred in approximately 6 % of cases,

Heparin

If heparin rather than warfarin was used during the 1st trimester,
the risks of maternal thromboembolism and maternal death more
than doubled (9.2% and 4.2% respectively)

The use of adjusted-dose heparin (titrated to a therapeutic

activated PTT) throughout pregnancy was associated with the
highest risks of maternal thromboembolism and maternal death
(25% and 7 % respectively)

A large proportion of the women had ball-and-cage valves or

older single-tilting-disk valves that are known to carry a high risk
of thromboembolism

Long-term use of heparin is associated with maternal risks of HIT

and osteopenia.

LMWH

Low-molecular-weight heparins have been used

successfully to treat DVT during pregnancy

Lower risks of thrombocytopenia and osteopenia than

unfractionated heparin
Probably safe for the fetus
There are insufficient data from studies of women with
prosthetic heart valves to support the efficacy of this
therapy or the use of any type of heparin throughout
pregnancy
Nor has the use of low-molecular-weight heparin been
studied in women with AF associated with valvular disease
during pregnancy.

Anticoagulation Guidelines

Although definitive data are lacking authors

recommend

Encourage education of the prospective parents and their

involvement in the decision-making process
Warfarin to achieve a target INR of 2.0 to 3.0 throughout
most of the pregnancy.
The only exceptions are the periods between 6 and 12
weeks of pregnancy and after 36 weeks of pregnancy,
when they would opt for the closely monitored use of
unfractionated heparin
This option was suggested because of medicolegal
concern relating to the "off-label" use of warfarin and the
risk of embryopathy.

Peripartum cardiomyopathy

Unknown etiology
Incidence 25-75/100000 in some series
Diagnosis:

Biventricular dilated cardiomyopathy in 3rd

trimester or in puerperium
Absence of prior cardiac disease
50% good prognosis if early reversion of
symptoms but 25-50% mortality

Treatment: Supportive

Questions?

Thank you