Cardiac Disease in Pregnancy BROWN

7/30/2019 Cardiac Disease in Pregnancy BROWN

http://slidepdf.com/reader/full/cardiac-disease-in-pregnancy-brown 1/58

Cardiac Disease in Pregnancy

Dr. Brown, M.D.



Diagnosis of Heart Disease In

Pregnancy Pregnant women with heart disease are at

greater risk for CV complications and neonatalcomplications

Various hemodynamic changes in pregnancymake diagnosis of certain CV disease moredifficult

Dyspnea, orthopnea, fatigability, syncope, anddizzy spells are common in pregnancy



Diagnosis Continued

Systolic murmurs occur in 95 percent of pregnantwomen

Dependent edema, rales in the lower lung fields, visibleneck veins, and cardiomegaly are all common inpregnancy

Certain findings suggestive of heart disease: Severe dyspnea, syncope with exertion, hemoptysis, paroxysmal

nocturnal dyspnea, and chest pain with exertion



Diagnosis Continued

Physical signs of organic heart disease include: Cyanosis

Clubbing

Diastolic murmur

Sustained cardiac arrhythmias

Loud, harsh systolic murmurs

Changes of normal pregnancy must be recognized



Preconception Counseling

Several fundamental principals are important

CVS undergoes specific changes to meet needsof mother and fetus which may worsen disease

Cardiac risk varies among specific forms of heartdisease

Some diseases negligible, some prohibitive




If condition can be cured, do so before pregnancy (ASD, PDA, some forms of coarctation)

If condition can be ameliorated, do so before pregnancy (MS, MR, AS, Tetralogy, VSD with mild pulmonary hypertension,

PS)

Pregnancy before valve replacement (prosthetic) shouldbe advised




Some CV disorders pose prohibitive risks to

mother and high maternal mortality, pregnancy

contraindicated

If already pregnant with such conditions,

termination recommended

D & E preferred to prostaglandins



Preconception Planning1. Dilated cardiomyopathy 15-60% MMR

2. Primary pulmonary HTN 50% MMR

3. Eisenmenger Syndrome 15-30% MMR

4. Marfan Syndrome with aortic root dilatation 25-50%

MMR

5. Coarctation of aorta 5%

6. Tetralogy of Fallot 12%



Preconception Planning

Mother’s heart condition determines likelihood of inheritance

Detailed family history important

Strong familial tendencies for PDA, ASD (and other diseaseslikelihood of inheritance well described)

Hypertrophic cardiomyopathy can be Mendelian in manner of inheritance

Risk of drugs needed for control of disease



Preconception Planning

Team approach important: Ob, MFM,cardiologist

Check and correct other medical

conditions thyroid, anemia, infection, hypertension,

vaccinations up to date



Maternal Cardiovascular

Adaptations to pregnancy Blood volume- plasma volume increases from 6-8 weeks

to 32 weeks by 45% Increase 1200-1600 mL

Increase greater in twins

Red cell mass increases 250-240mL-20-30% Iron supplements add to increase

Maternal demand of 500 mg, 300 mg for fetus, 200 mg for normal daily losses

Protects against hemodynamic instability with blood loss




Adaptations Cardiac Output= Heart rate x Stroke Volume

CO is the functional capacity of the heart

CO increases 30-50% during pregnancy

Increase is secondary to increase in both strokevolume and heart rate




Adaptations Stroke volume decreases after 32 weeks

Heart rate increases 15-20 bpm and maintains C.O.

in late third trimester

Maternal posture significantly affects C.O.

Supine position decreases C.O. 20-30% second tocaval compression and decrease venous return

8% demonstrate supine hypotensive syndrome




Adaptations Uterine blood flow increases 10x (500-800mL/min)

This represents 2-17% by term of total C.O.

Renal blood flow increases by 50%

Arterial blood pressure decreases in pregnancy

Peripheral vascular resistance falls greater than C.O.increases




Adaptations Nadir of BP occurs at 24-32 weeks

Rise to nonpregnant values by term

Diastolic fall greater than systolic

Always use same Korotkoff for diastolic pressure

Ambulatory BP measurement needs further pregnancystudy before use understood




Adaptations Systemic vascular resistance decreases from

five weeks secondary to progesterone, PG,endothelium derived relaxant factor

Venous complications increase progressively inpregnancy

* With decrease in venous vascular resistancemore sensitive to autonomic blockade




AdaptationsIncrease during pregnancy

1. Cardiac Output +40%

2. Heart rate +17%

Decrease during pregnancy

1. SVR -20%

2. PVR -35%

3. COP/PCWP -28%

4. COP -14%

(colloid osmotic pressure)

*CVP NS

*PCWP NS




Adaptations Intrapartum 1st stage of labor 12-31% increase in COsecondary to increase in stroke volume

2nd stage of labor CO increases by 50%

Left lateral decubitous position and pain control partiallyalleviate CO changes

Systolic and diastolic BP up 35 and 25 mm Hgrespectively in labor

For these reasons, women with CV disease

decompensate in labor, particularly during the 2nd

stage




Adaptations Postpartum- greatest risk for pulmonary edema

in women with CVD is immediately postpartum

Immediate puerperium-80% increase in COwithin 15 minutes of vaginal delivery with localanesthesia, 60% increase with caudalanesthesia

Decrease venocaval obstruction,autotransfusion from uterus mobilization of extravascular fluidvenous return




Adaptations Cardiac output returns to prelabor level one hour p.p.

Cesarean section does not cause as dramatic a shift in

hemodynamics, but still CO increases by 25%

Vaginal delivery 500 cc blood loss, Cesarean section1000 cc blood loss

SV, CO, SVR return to prepregnancy levels by 12 weekspostpartum



General Guidelines to management

Activity restrictions

Diet modifications

Team approach Infection control

Immunizations, SBE

prophylaxis,

prophylaxis against

Rheumatic fever

Interruption of

pregnancy

Counseling Contraception

CV surgery

CV drugs



Left to Right Shunt

Atrial Septal Defect May be undiscovered before pregnancy since symptoms often absent

Be alert to uncorrected defect in immigrant from underdeveloped

country

Surgical closure of ostium secundum ASD usually straight forwardand done before pregnancy

If no pulmonary hypertension usually no problem in pregnancy



Left to Right Shunt

Complicated ASD Advanced age, uncorrected large ASD, chronic arrhythmia (AF),

RV dysfunction, pulmonary hypertension

Pregnancy not advised if these sequelae present

SBE uncommon with ostium secundum and prophylaxisnot warranted

Ostium primum- Down’s syndrome, endocarditis,pulmonary hypertension



Left to right shunt

VSD- great spectrum and risk dependent upon size,location (muscular vs. membranous)

Echocardiogram is diagnostic

Usually tolerate pregnancy well with left to right shunt.SBE prophylaxis indicated

Higher the PVR, the greater the risk and patient may bebest served by early termination



Left to Right Shunt PDA

Loud continuous systolic diastolic machinery murmur

Usually corrected in infancy

Closure should be accomplished prior to pregnancy

SBE prophylaxis required

Uncomplicated PDA usually well tolerated but thedevelopment of pulmonary hypertension is anindication for termination



Eisenmenger Syndrome

Congenital communication between systemic andpulmonary circulation and increased PVR either wherePVR=SVR (no shunt) or PVR>SVR (right to left shunt)

Most common lesion is large VSD, followed by PDA

Once Eisenmenger pathophysiology in place, pulmonary

hypertension irreversible and VSD inoperable



Eisenmenger Syndrome Pregnancy carries 50% mortality

Fetal survival <50% (R L shunt creates cyanosis)

Sudden death common, perpartum period mostdangerous

Any decreased venous return yields inability of right

heart to pump through high PVR hypotension andshock unresponsive to medical management

Pregnancy management- maintain pulmonary blood flow

and venous return (preload)



Eisenmenger Syndrome Cause of death: “sudden death”, PE, CHF, pulmonary

artery rupture

Pregnancy management: bed rest, supplemental O2,

anticoagulants, low threshold for hospitalization

Intrapartum-epidural may increase right to left shunt andincrease hypoxia (low dose epidural or intrathecal

narcotics)

PPH causes hypotension and decreased venous return

Pulmonary artery catheter- many complications



Primary Pulmonary Hypertension

Same principles as Eisenmenger apply to

it’s management

Mortality 50%

Treatments include vasodilators

25% lower pulmonary artery pressure with

prostacylin infusion- favorable and predictsresponse to nifedipine and good prognosis



Valvular Heart Disease

In general, regurgitant valvular lesions are welltolerated. Stenotic lesions greater risk for decompensation

>60% have worsening of NYHA Class, 38%CHF, 23% adverse perinatal outcome (PTL,IUGR, stillbirth) Class I: Asymptomatic

Class II: symptoms with greater than normal activityClass III: symptoms with normal activity

Class IV: symptoms at rest



Valvular Lesions with High

Maternal or Fetal Risk Severe AS

AR Class III-IV

MS Class II-IV

AS or MS with severe pulmonary hypertension(pulmonary pressure > 75% of systemicpressure)

Aortic or mitral valve disease with LVEF <40%

Mechanical Valves requiring anticoagulation AR in Marfan’s Syndrome



Valvular Lesions with low Maternal

or Fetal Risk AS with low mean gradient ( <50 mmHg) with LVEF

>50%

AR class I-II with normal LV function

MR class I-II with normal LV function MVP with up to moderate MR and normal LV function

Mild to moderate MS (valve area > 1.5 cm2, gradient <50 mm Hg) and no pulmonary hypertension

Mild to moderate PS



Mitral Stenosis

More commonly results from rheumatic heartdisease

Complications: pulmonary edema, RV failure,arrhythmias, PE

Pregnancy detrimental to MS: increase blood

volume, increase risk of pulmonary edema,tachycardia decreases LV filling time elevatedLA pressure pulmonary edema



Mitral Stenosis

Severity of MS based on the valve area: 4-5cm^2 normal, >1.5 cm ^2 mild, <1 cm^2 severe

Likelihood of maternal or fetal complicationsassociated with severity based on valve areamore than NYHA class

Overall 35% maternal complications, 30% fetalor neonatal complications



Mitral Stenosis- Treatment If Rheumatic Heart history daily penicillin prophylaxis

Gentle diuresis, B blocker prn tachycardia

Typical AF management, remember anticoagulation

Percutaneous balloon mitral valvotomy ideally beforepregnancy, but safe in pregnancy

Labor: adequate pain control to prevent tachycardia,epidural lowers SVR in patient who has decreased abilityto increase CO hypotension

Intra-thecal narcotics ideal



Aortic Stenosis

Most common cause- congenital bicuspid valve

Much smaller number subaortic stenosis hypertrophic

cardiomyopathy

Severity graded by average valve area or peak gradientacross valve

Peak gradient >50 mm Hg and/or < or = to 1 cm squareddefines severe disease



Aortic Stenosis

AS creates fixed stroke volume and difficulty in achievingincreased CO of pregnancy

Rate control NB – bradycardia -> decreased CO andhypotensive tachycardia -> decreased ventricular fillingtime -> decreased CO and risk for myocardial ischemia

If severe AS – valvuloplasty before pregnancy.

Moderate to severe AS 70% maternal morbidity (CHF,angina, rarely sudden death)



Aortic stenosis

Mild to moderate AS- conservative management

Severe, symptomatic AS- balloon vavluloplasty consideration

During labor prevent hypotension and tachycardia with generoushydration, cautious epidural use

Shorten second stage

Active management of PPH to avoid hypotension and tachycardia



Mitral Valve Prolapse

MVP is the most common cardiac condition in Obstetrics

MVP affects 4% of the population and 12-17% of women of childbearing age

Redundant valve prolapse into ventricle during systole

Most asymptomatic, some: chest pain, dyspnea, weakness,palpitations

Little effect on pregnancy



Mechanical Heart Valves

Anticoagulant issues very difficult and controversial

Women who desire childbearing should consider valve

repair or biologic if possible

Warfarin safest for mother but poses greatest risk tofetus

ACC/AHA 1998 guidelines issues and recommendations



Coarctation of the Aorta Most commonly distal to the left subclavian artery, a discrete

narrowing

Proximal hypertension, distal hypoperfusion

Severity determined by gradient across the coarct

Open surgical repair vs. balloon angioplasty

Associated intracranial aneurysms and “intrinsic aortapathy” – dissection, aneurysm, rupture

Maternal mortality 5%

Vaginal delivery safe, epidural ideal, assisted delivery to shortensecond stage



Marfan’s Syndrome Autosomal dominant condition- multiple

mutations in fibrillin gene on chromosome 15

Manifestations: MVP, MR, aortic root dilatation, AR, dissection or rupture of aortic root

Mean age of death 32 years

Aortic root diameter critical, surgical replacement

if root diameter >5.5 cm



Marfan’s Syndrome

Aortic root diameter may predict pregnancy risk

As high has 50% mortality (root diameter > 4.5cm, AR, LVdysfunction, or coarctation)

Follow root with monthly echocardiography

Treat hypertension aggressively (B-blocker)

Uncomplicated- deliver vaginally, high risk (see above) electivecesarean section to minimize likelihood of hypertension dissection



Cyanotic Congenital Heart Disease

This category includes any malformations that involve aright to left shunt creating deoxygenated blood in thesystemic circulation and cyanosis

Tetralogy of Fallot, transposition of the great vessels,double outlet right ventricle, and others

With history of repair and no cyanosis currently andnormal ventricular function, may tolerate pregnancy



Cyanotic Congenital Heart Disease

Tetralogy of Fallot most common uncorrectedcyanotic congenital heart lesion (not previouslyrepaired)

1. Large defect high in the ventricular septum

2. Pulmonary stenosis

3. Dextraposition of the aorta-overrides the right

ventricle and sits outside the VSD4. Right ventricular hypertrophy



Tetralogy of Fallot

Special problem in pregnancy- decreased SVR causesgreater right to left shunt intensifying hypoxemia leadingto syncope or death

Maintenance of venous return critical (labor issues)

Pregnancy should be discouraged

Prognosis bleak with repeated syncope, hematocrit>60%, or RV systolic pressure >120 mm Hg



Peripartum Cardiomyopathy

(PPCM) First defined in 1971: Symptoms of CHF that become apparent in

last month of pregnancy or within 5 months postpartum with no pre-existing disease and no other etiology for heart failure

Echocardiographic criteria: ejection fraction <45% and end diastolicdimension >2.72 cm/m squared

Incidence 1/3000-1/4000 in USA

Usually older, multiparous, African descent, chronic hypertension,

pre-eclampsia, tocolytics



Peripartum Cardiomyopathy

Treatment similar to any cause of CHF

Preload reduction (Na and fluid reduction, diuretics,nitrates)

Afterload reduction (hydralazine, ACE inhibitors PP)

Inotropes- digoxin

Data on prognosis limited-echo after 6 mo?

18-50% mortality

50% recurrence in future pregnancies



Ischemic Heart Disease Rare <1/10,000 pregnancies

Rare risk with ergonovine, PGE, PGE2, ritodrine

Most cases with known cardiac risks

Delivery within 2 weeks= 50% mortality

Treatment of MI same as non-pregnant treatment(thrombolytics t-PA ect. Caution placental abruption,fetal intracranial bleeding)

Vaginal delivery preferred



Maternal Arrhythmias SVT common in young women without structural

heart disease

Pregnancy treatment of SVT unchanged

Vagal maneuvers first, then IV adenosine(adenosine associated with occasional fetal

bradycardia)

Frequent episodes- beta blockers, calciumchannel blockers, digoxin



Maternal Arrhythmias Atrial fibrillation and flutter usually associated

with underlying conditions: hyperthyroidism,

COPD, PE, cardiomyopathy, cardiac valve

lesions (AS, MS)

Treatment unaltered by pregnancy and depends

upon clinical scenario

Eg. new AF with MS can lead to pulmonary

edema, hemodynamic instability-cardioversion



Endocarditis Prophylaxis

See ACOG handout



Key Points

Preconception considerations

Optimization of maternal status: Repair defects prior to pregnancy if indicated,

medication adjustments

Discussion of fetal risks Awareness of risk of transmission of defect to

offspring

Patients need to understand maternal and fetal risks



Key Points

Antepartum Consideration

Maternal risks vary greatly, depending onthe specific lesion, severity of lesion, andprepregnancy functional status

Anticoagulation consideration



Key PointsIntrapartum considerations

Labor most dangerous time period for many types of heart disease.NB cardiac output increases

Vaginal delivery preferred over cesarean section for most patients:less blood loss, fewer postpartum infections, less VTE

Assisted second stage

SBE prophylaxis ACC/AHA

Telemetry for arrhythmias

Active third stage management, particularly if lesions preloaddependent (AS, MS)



Key Points

Anesthetic Considerations

Regional anesthetic appropriate for most with

cardiac disease: avoids tachycardia (NB in MS-Lventricular filling), decreased cardiac work,allows assisted vaginal delivery

Severe stenotic lesions will not tolerate suddendecrease in SVR; slow epidural or intrathecalnarcotics. GA for cesarean section?



Key Points

Postpartum considerations

Patients remain at high risk for VTE during

postpartum period; appropriate prophylacticanticoagulation important

Patients with certain cardiac conditions (eg,

Eisenmenger’s syndrome) have a higher risk of death during postpartum period and may requirehospitalization



Thank you

Documents

Cardiac Disease in Pregnancy BROWN