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 renin-

angiotensin 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 2nd

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 Mother’s 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 cm2

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 non-

pregnant 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?

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