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CARDIOVASCULAR DISORDERS IN PREGNANCY

Ina S. Irabon, MD, FPOGS, FPSRM, FPSGE Obstetrics and Gynecology

Reproductive Endocrinology and InfertilityLaparoscopy and Hysteroscopy

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REFERENCE

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 25th edition; 2018; chapter 49 Cardiovascular Disorders

OUTLINE

PHYSIOLOGICAL CONSIDERATIONS IN PREGNANCY DIAGNOSIS OF HEART DISEASE PERIPARTUM MANAGEMENT CONSIDERATIONS VALVULAR HEART DISEASE CONGENITAL HEART DISEASE PULMONARY HYPERTENSION INFECTIVE ENDOCARDITIS

PHYSIOLOGICAL CONSIDERATIONS IN PREGNANCY

Cardiovascular Physiology The marked pregnancy-induced anatomical and functional changes in cardiac physiology can have a profound effect on underlying heart disease cardiac output increases approximately 40 percent during pregnancy.

takes place by 8 weeks’ gestation and is maximal by midpregnancy This early rise stems from augmented stroke volume, which results from lowered vascular resistance. greater end-diastolic ventricular volume that results from pregnancy hypervolemia gives rise to higher resting pulse and stroke volume normal left ventricular function is maintained during pregnancy à pregnancy is not characterized by hyperdynamic function or a high cardiac-output state.


HEMODYNAMIC CHANGES IN NORMAL PREGNANT WOMEN AT TERM


PHYSIOLOGICAL CONSIDERATIONS IN PREGNANCY

Ventricular Function in Pregnancy Ventricular volumes and mass increase to accommodate pregnancy-induced hypervolemia.

This is reflected by greater end-systolic and end-diastolic dimensions. All of these adaptations return to prepregnancy values within a few months postpartum.


DIAGNOSIS OF HEART DISEASE

Symptoms

Progressive dyspnea orthopnea Nocturnal cough

Hemoptysis

Syncope Chest pain

SignsCyanosis Clubbing of fingers Persistent neck vein distention Systolic murmur grade 3/6 or greater Diastolic murmur Cardiomegaly

▪ Persistent tachycardia and/or arrhythmia

▪ Persistent split second sound

▪ Fourth heart sound ▪ Criteria for pulmonary

hypertension


NORMAL CARDIAC EXAM FINDINGS IN A PREGNANT WOMAN


DIAGNOSTIC STUDIES

12L ECG 2D ECHO Chest xray


ECG FINDINGS IN A PREGNANT WOMAN


CHEST XRAY AND 2D ECHO FINDINGS

CXRAY: use a lead apron/abdominal shield to minimize fetal radiation exposure;

heart silhouette normally is larger in pregnancy. This is accentuated further with a portable AP chest radiograph.

2D ECHO: permits accurate diagnosis of most heart diseases during pregnancy.

Some normal pregnancy-induced changes include a small increase in the dimensions of all cardiac chambers, a slight but significant growth in left ventricular mass, and greater tricuspid and mitral valve regurgitation


CLASSIFICATION OF FUNCTIONAL HEART DISEASE

The New York Heart Association (NYHA)clinical classification is based on past and present disability and is uninfluenced by physical signs:

Class I. Uncompromised—no limitation of physical activity: do not have symptoms of cardiac insufficiency or experience anginal pain. Class II. Slight limitation of physical activity: comfortable at rest, but if ordinary physical activity is undertaken, discomfort in the form of excessive fatigue, palpitation, dyspnea, or anginal pain results. Class III. Marked limitation of physical activity: comfortable at rest, but less than ordinary activity causes excessive fatigue, palpitation, dyspnea, or anginal pain. Class IV. Severely compromised—inability to perform any physical activity without discomfort: Symptoms of cardiac insufficiency or angina may develop even at rest.


WORLD HEALTH ORGANIZATION (WHO) RISK CLASSIFICATION OF CARDIOVASCULAR DISEASE AND PREGNANCY WITH MANAGEMENT RECOMMENDATIONS


LABOR AND DELIVERY

vaginal delivery is preferred, and labor induction is usually safe Cesarean delivery recommended for women with the following:

(1) dilated aortic root >4 cm or aortic aneurysm; (2) acute severe congestive heart failure; (3) recent myocardial infarction; (4) severe symptomatic aortic stenosis; (5) warfarin administration within 2 weeks of delivery; (6) need for emergency valve replacement immediately after delivery. During labor, the mother should be in a semirecumbent position with a lateral tilt.


LABOR AND DELIVERY

PR >100 beats per minute and RR> 24 per minute + dyspnea ----> ventricular failure. Delivery does not necessarily improve the maternal condition Doing emergency cesarean delivery may be particularly hazardous.


ANALGESIA AND ANESTHESIA

Relief from pain and from apprehension is important. à continuous epidural analgesia is recommended

major problem with conduction analgesia is maternal hypotension à dangerous in women with intracardiac shunts in whom flow may be reversed.

Hypotension can also be life-threatening if there is pulmonary arterial hypertension or aortic stenosis because ventricular output is dependent on adequate preload.

narcotic regional analgesia or general anesthesia may be preferable. Subarachnoid blockade (spinal anesthesia)is not recommended in women with significant heart disease due to associated hypotension. For cesarean delivery, epidural analgesia is preferred by most clinicians


PUERPERIUM

Women who have shown little or no evidence of cardiac compromise during pregnancy, labor, or delivery may still decompensate postpartum.

Fluid mobilized into the intravascular compartment and reduced peripheral vascular resistance place higher demands on myocardial performance. Postpartum hemorrhage, anemia, infection, and thromboembolism may push patient to decompensation

May delay postpartum tubal sterilization after vaginal delivery


ANTICOAGULATION

• Critical for pregnant women with mechanical prosthetic valves. • Warfarin is the most effective anticoagulant for preventing maternal thromboembolism

but causes harmful fetal effects • Heparin is less hazardous for the fetus, but the risk of maternal thromboembolic

complications is much higher • Warfarin is teratogenic and causes miscarriage, stillbirths, and fetal malformations.


ANTICOAGULATION

• Anticoagulation for mechanical valves using low-dose unfractionated heparin is definitely inadequate and carries a high associated maternal mortality rate • if full anticoagulation with dose-adjusted UFH or LMWH is used, meticulous

monitoring is recommended. • The activated partial thromboplastin time (aPTT) should be at least 2 times

control or anti-Xa levels should be 0.8 to 1.2 U/mL at 4 to 6 hours postdose


RECOMMENDATIONS FOR ANTICOAGULATION

Any of four regimens is recommended: adjusted-dose LMWH is given twice daily, with a peak anti-Xa level drawn 4 hours after dosing. adjusted UFH is dosed every 12 hours to keep the midinterval aPTT twice control or anti Xa level between 0.35–0.70 U/mL. LMWH or UFH is given as just described until 13 weeks, and then warfarin is substituted until near delivery, at which time it is replaced by LMWH or UFH. in women judged to carry a high risk of thrombosis and for whom the efficacy and safety of heparins are concerns, warfarin is suggested throughout pregnancy. Heparin is then substituted close to delivery. In addition, aspirin, 75 to 100 mg, is given daily.


RECOMMENDATIONS FOR ANTICOAGULATION

Heparin is discontinued just before delivery.

If delivery happens during heparin administration, and extensive bleeding is encountered, then protamine sulfate is given intravenously.

Anticoagulant therapy with warfarin or heparin may be restarted 6 hours following vaginal delivery, usually with no problems. The American College of Obstetricians and Gynecologists (2017) advises resuming unfractionated or low-molecular-weight heparin 6 to 12 hours after cesarean delivery. These anticoagulants are compatible with breastfeeding


Valvular heart disease

CARDIAC VALVE DISORDERS: POSSIBLE CONSEQUENCES DURING PREGNANCY


MITRAL STENOSIS

Usually due to Rheumatic endocarditis; The contracted valve impedes blood flow from the left atrium to the ventricle. The normal mitral valve surface area is 4.0 cm2, and when stenosis narrows this to <2.5 cm2, symptoms usually develop. With more severe stenosis, the left atrium dilates, left atrial pressure is chronically elevated, and significant passive pulmonary hypertension develops increased preload of normal pregnancy and other factors that raise cardiac output may cause ventricular failure and pulmonary edema. The resulting pulmonary venous hypertension and pulmonary edema create symptoms of dyspnea, fatigue, palpitations, cough, and hemoptysis.


MITRAL STENOSIS: MANAGEMENT

Limited physical activity is recommended If with symptoms of pulmonary congestion: activity is further reduced, dietary sodium is restricted, and diuretics are given β-blocker drug therapy slows the ventricular response to activity. For new-onset atrial fibrillation: intravenous verapamil (5 to 10 mg )or electrocardioversion For chronic fibrillation: digoxin, a β-blocker, or a calcium-channel blocker can slow ventricular response. Surgical intervention is considered for women with symptomatic severe mitral stenosis and in those with lesser degrees of mitral stenosis complicated by recurrent systemic embolization or severe pulmonary hypertension.


MITRAL STENOSIS: MANAGEMENT

Labor and delivery: Epidural analgesia for labor is ideal, but fluid overload is avoided. Most prefer vaginal delivery in women with mitral stenosis. With severe stenosis and chronic heart failure, insertion of a pulmonary artery catheter may help guide management.


MITRAL INSUFFICIENCY

• Acute mitral insufficiency is caused by chordae tendineae rupture, papillary muscle infarction, or leaflet perforation from infective endocarditis.

• Chronic mitral regurgitation may derive from rheumatic fever, connective tissue diseases, mitral valve prolapse, or left ventricular dilation of any etiology

• Mitral valve vegetations —Libman-Sacks endocarditis—are relatively common in women with antiphospholipid antibodies

• During pregnancy, mitral regurgitation is similarly well tolerated, probably because the lowered systemic vascular resistance yields less regurgitation.


MITRAL VALVE PROLAPSE

• Usually involves a pathological connective tissue disorder— myxomatous degeneration—which may involve the valve leaflets themselves, the annulus, or the chordae tendineae.

• Usualy asymptomatic and are diagnosed during routine examination or echocardiography. • The few women with symptoms have anxiety, palpitations, atypical chest pain, dyspnea

with exertion, and syncope • Pregnant women with mitral valve prolapse rarely have cardiac complications. • Hypervolemia may even improve alignment of the mitral valve, and women without

pathological myxomatous degeneration generally have excellent pregnancy outcomes


AORTIC STENOSIS

aortic stenosis in younger women is most likely a congenital lesion. A normal aortic valve has an area of 3 to 4 cm2, with a pressure gradient <5 mm Hg. If the valve area is <1 cm2, there is severe obstruction to flow and a progressive pressure overload on the left ventricle à Concentric left ventricular hypertrophy develops. Characteristic manifestations develop late and include chest pain, syncope, heart failure, and sudden death from Mild-to-moderate degrees of stenosis are well tolerated, however, severe disease is life- threatening


AORTIC STENOSIS

The principal underlying hemodynamic problem is the fixed cardiac output associated with severe stenosis. During pregnancy, several common events acutely lower preload further and thus aggravate the fixed cardiac output. complication rates were higher if the aortic valve area measured <1.5 cm2 Women with valve pressure gradients >100 mmHg appear to be at greatest risk.


AORTIC STENOSIS: MANAGEMENT

For asymptomatic women: no treatment except close observation is required. For symptomatic women: strict limitation of activity and prompt treatment of infections. If symptoms persist despite bed rest, surgical intervention may be considered. Abrupt drops in end-diastolic volume may result in hypotension, syncope, myocardial infarction, and sudden death --> avoiding diminished ventricular preload and maintaining cardiac output are key. During labor and delivery, affected women are best managed on the “wet” side

provides a margin of safety in intravascular volume in anticipation of possible hemorrhage. During labor, narcotic epidural analgesia seems ideal and avoids potentially hazardous hypotension.


AORTIC INSUFFICIENCY

Frequent causes of abnormal insufficiency are rheumatic fever, connective tissue abnormalities, congenital lesions, bacterial endocarditis or aortic dissection. aortic and mitral valve insufficiency have both been linked to the appetite suppressants fenfluramine and dexfenfluramine and to the ergot-derived dopamine agonists cabergoline and pergolide. With chronic insufficiency, left ventricular hypertrophy and dilation develop and are followed by slow-onset fatigue, dyspnea, and pulmonary edema, although rapid deterioration usually follows Aortic insufficiency is generally well tolerated during pregnancy. Like mitral valve insufficiency, diminished vascular resistance is thought to improve hemodynamic function. If symptoms of heart failure develop, diuretics are given and bed rest is encouraged.


PULMONIC STENOSIS

usually congenital and may be associated with Fallot tetralogy or Noonan syndrome. hemodynamic burden of pregnancy can precipitate right-sided heart failure or atrial arrhythmias in women with severe stenosis. Surgical correction ideally is done before pregnancy, but if symptoms progress, a balloon valvuloplasty may be necessary antepartum


Congenital heart disease

ATRIAL SEPTAL DEFECTS

Most atrial septal defects (ASDs) are asymptomatic until the third or fourth decade. Pregnancy is well tolerated unless pulmonary hypertension has developed, but this is uncommon Treatment of ASD during pregnancy is indicated for congestive heart failure or an arrhythmia. With the potential to shunt blood from right to left, a paradoxical embolism, that is, entry of a venous thrombus through the septal defect and into the systemic arterial circulation, is possible and may cause an embolic stroke Compression stockings and prophylactic heparin have also been recommended for a pregnant woman with an ASD who is immobile or has another risk factor for thromboembolism


VENTRICULAR SEPTAL DEFECTS

These lesions usually close spontaneously during childhood if the defect measures <1.25 cm2, pulmonary hypertension and heart failure do not develop. If the effective defect size exceeds that of the aortic valve orifice, symptoms rapidly develop. Adults with unrepaired large defects develop left ventricular failure and pulmonary hypertension and have a high incidence of bacterial endocarditis Pregnancy is well tolerated with small-to-moderate sized shunts. If pulmonary arterial pressures reach systemic levels, however, there is reversal or bidirectional flow—Eisenmenger syndrome

When this develops, the maternal and fetal mortality rates are significantly higher, and thus, pregnancy is not generally advisable.


EISENMENGER SYNDROME / “EISENMENGERIZATION”

This describes secondary pulmonary hypertension that arises from any cardiac lesion. The syndrome develops when pulmonary vascular resistance exceeds systemic resistance and leads to concomitant right-to-left shunting. The most common underlying defects are atrial or ventricular septal defects and persistent ductus arteriosus


Pulmonary hypertension

PULMONARY HYPERTENSION

Normal resting mean pulmonary artery pressure is 12 to 16 mmHg. Pulmonary hypertension is defined in nonpregnant individuals as a resting mean pulmonary pressure >25 mmHg.


Comprehensive Clinical Classification of Pulmonary Hypertension


DIAGNOSIS

Symptoms may be vague, and dyspnea with exertion is the most frequent. With group 2 disorders, orthopnea and nocturnal dyspnea are also usually present. Angina and syncope occur when right ventricular output is fixed, and they suggest advanced disease. Chest radiography often shows enlarged pulmonary hilar arteries and attenuated peripheral markings.

It also may disclose parenchymal causes of hypertension. Noninvasive echocardiography can provide an estimate of pulmonary artery pressures, although cardiac catheterization remains the standard for measurement.


PROGNOSIS

pregnancy is contraindicated with severe disease, especially in women with pulmonary arterial changes—most cases in group 1. With milder disease from other causes—group 2 being the most common—the prognosis is better and all tolerated pregnancy reasonably well. Regardless of the etiology, the final common pathway of pulmonary hypertension is right heart failure and death. The average survival length after diagnosis is <4 years


MANAGEMENT

Treatment of symptomatic pregnant women includes activity limitation and avoidance of the supine position later in gestation. Diuretics, supplemental oxygen, and pulmonary vasodilator drugs are standard therapy for symptoms. Some experts recommend anticoagulation


MANAGEMENT

May use intravenous pulmonary artery vasodilators: Prostacyclin analogues that can be administered parenterally include epoprostenol and treprostinil; iloprost is inhaled. Inhaled nitric oxide is an option that has been employed in cases of acute cardiopulmonary phosphodiesterase-5 inhibitors, such as sildenafil, cause vasodilation of both the pulmonary and systemic vascular beds and have an inotropic effect on the hypertrophic right ventricle. Bosentan, an endothelin-receptor antagonist, is teratogenic in mice and contraindicated in pregnancy


MANAGEMENT

During labor and delivery, these women are at greatest risk when venous return and right ventricular filling are diminished.

To avoid hypotension, assiduous attention is given to epidural analgesia induction and to blood loss prevention and treatment at delivery


Infective Endocarditis

INFECTIVE ENDOCARDITIS

greatest risk for endocarditis are those with congenital heart lesions, intravenous drug use, degenerative valve disease, and intracardiac devices Among intravenous drug abusers and those with catheter-related infections: Staphylococcus aureus predominates. Prosthetic valve infections: Staphylococcus epidermidis


DIAGNOSIS AND MANAGEMENT

Fever with chills

anorexia, fatigue, and other constitutional symptoms Clinical clues include murmurs, anemia, proteinuria, and manifestations of embolic lesions that include petechiae, focal neurological changes, chest or abdominal pain, and ischemia in an extremity. In some cases, heart failure develops. Diagnosis is made using the Duke criteria, which include positive blood cultures for typical organisms and evidence of endocardial involvement


ENDOCARDITIS PROPHYLAXIS

The American Heart Association recommends prophylaxis for dental procedures in those with: (1) a prosthetic valve or prosthetic material used in a valve repair, (2) prior endocarditis, (3) unrepaired cyanotic heart defect or repaired lesion with residual defect at prosthetic sites, and (4) valvulopathy after heart transplantation The American College of Obstetricians and Gynecologists (2016) does not recommend endocarditis prophylaxis for either vaginal or cesarean delivery in the absence of pelvic infection except with the lesions cited above. prophylactic regimens are administered as close to 30 to 60 minutes before the anticipated delivery time as is feasible.


ANTIBIOTIC PROPHYLAXIS FOR INFECTIVE ENDOCARDITIS IN HIGH-RISK PATIENTS

American College of Obstetricians and Gynecologist Standard (IV): ampicillin 2 g or cefazolin or ceftriaxone 1 g Penicillin-allergic (IV): cefazolin or ceftriaxone 1 g or clindamycin 600 mg Oral: amoxicillin 2 g

American Heart Association/European Society of Cardiology

Standard: amoxicillin 2 g PO or ampicillin 2 g IV or IM

Penicillin-allergic: clarithromycin or azithromycin 500 mg PO; cephalexin 2 g PO; clindamycin 600 mg PO, IV, or IM; or cefazolin or ceftriaxone 1 g IV or IM


SUMMARY

PHYSIOLOGICAL CONSIDERATIONS IN PREGNANCY DIAGNOSIS OF HEART DISEASE PERIPARTUM MANAGEMENT CONSIDERATIONS VALVULAR HEART DISEASE CONGENITAL HEART DISEASE PULMONARY HYPERTENSION INFECTIVE ENDOCARDITIS

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