CARDIAC DISEASES IN PREGNANCY

1. MINISTRY OF HEALTH OF UKRAINE
DONETSK NATIONAL MEDICAL UNIVERSITY
CARDIAC DISEASE IN PREGNANCY
TEACHER: LARISA PETRIVNA SHELESTOVA
BY: SRISHTI GUPTA
GROUP: 603 A.M.
KROPYVNYTSKYI
2022

2. INCIDENCE
At present, cardiac disease complicates 0.2–4% of all pregnancies in Western countries. In developing
countries like India, cardiac diseases complicate 2% of pregnancies and contribute to about one-fifth of all
maternal deaths.
Congenital heart disease is the most frequent cardiovascular disease present during pregnancy (75–82%) in
the industrialized world, with shunt lesions being predominant (20–65%)
Rheumatic valvular heart disease is most common cause in developing countries, comprising 56–89% of all
cardiovascular diseases in pregnancy. The commonest cardiac lesion is of rheumatic origin followed by the
congenital ones.
The ratio between the two has fallen over the past two decades from 10: 1 to about 3: 1 or even 1: 1 in
advanced countries.
Rheumatic valvular lesion predominantly includes mitral stenosis (80%).

3. Predominant congenital lesions include patent ductus arteriosus, atrial or ventricular septal defect,
pulmonary stenosis, coarctation of aorta and Fallot’s tetralogy
Rare causes are hypertensive, thyrotoxic, syphilitic or coronary cardiac diseases.
Cardiomyopathy is uncommon, but represents severe cause of cardiovascular complications in pregnancy.
Peripartum cardiomyopathy (PPCM) is the most frequent cause of severe complications.
Maternal heart disease is now the major cause of death during pregnancy in developed countries.

4. EFFECT OF CARDIOVASCULAR PHYSIOLOGY ON HEART
LESION
• A normal heart has got enough reserve power so that the extra load can well be tackled. While a
damaged heart with good reserve can even withstand the strain but if the reserve is poor, cardiac
failure occurs sooner or later.
• Cardiac failure occurs during pregnancy around 30 weeks, during labor and mostly soon following
delivery.

5. FACTORS RESPONSIBLE FOR CARDIAC FAILURE
• Advanced age
• Cardiac arrhythmias or left ventricular hypertrophy
• History of previous heart failure
• Appearance of “risk factors” in pregnancy like infection, anemia,
• hypertension, excessive weight gain and multiple pregnancy.
• Inadequate supervision

7. EFFECTS OF HEART LESION ON PREGNANCY
• There is tendency of preterm delivery and prematurity.
• IUGR is quite common in cyanotic heart diseases

9. CLASSIFICATION OF CONGENITAL HEART DISEASES
• Patent ductus arteriosus
• Atrial septal defect
• Ventricular septa I defect
• Coarctation of the aorta
• Pulmonary stenosis
• Fallot’s tetralogy
• Aortic stenosis
• Eisenmenger’s syndrome
• Cardiomyopathy of pregnancy
• Supraventricular tachycardia
• Wolf-Parkinson-White syndrome.

10. RISK OF MATERNAL AND FETAL MORBIDITY
ASSOCIATED WITH PREGNANCY
• Low Risk
1 . Mitral valve prolapse without severe regurgitation
2 . Atrial and ventricular septal defect previously repaired or without pulmonary hypertension
3 . Corrected congenital heart disease without residual cardiac dysfunction
4 . Patent ductus arteriosus
5 . Pulmonary stenosis
6 . Mild mitral or aortic valvular disease ( stenosis or regurgitation ) with normal left ventricular function :
class I o r II

11. • Moderate Risk
1. Marfan’s syndrome with normal aorta
2. History of peripartum cardiomyopathy with no residual ventricular dysfunction
3. Previous myocardial infarction

12. • High Risk
1.AnyconditionwithNewYorkHeartAssociationclassIIIorIV.Moderatetoseveresystemicventriculardysfunction
2.Pulmonaryhypertensionfromanycause
3.TetralogyofFallot;uncorrectedorwithresidualdisease
4.Coarctationoftheaorta
5.Mitralstenosiswithatrialfibrillation
6.Severeaorticstenosis
7.Mechanicalvalverequiringanticoagulation
8.Marfan’s syndrome with aortic involvement
9.History of peripartum cardiomyopathy with residual ventricular dysfunction

13. MATERNAL PROGNOSIS
1. Nature of lesion .
2. Functional capacity of the heart.
3. Quality of medical supervision provided during pregnancy, labor and
puerperium.
4. Presence of other risk factors .
5. Whether patient has undergone corrective surgery or not

15. • Maternal mortality is lowest in rheumatic heart lesions and acyanotic group of
heart diseases—less than 1%.
• With elevation o f pulmonary vascular resistance especially with cyanotic
heart lesions, the mortality may be raised to even 50% (Eisenmenger’s
syndrome).
• Most of the deaths occur due to cardiac failure and the maximum deaths
occur following birth

16. • Low maternal mortality (< 1 % risk of death): atrial and ventricular septal detects, patent ductus
arteriosus, minimal mitral stenosis, porcine heart valve, and corrected tetralogy of Fallot.
• Intermediate maternal mortality (5–15 % risk of death): mitral stenosis with atrial fibrillation, artificial
heart valve, uncorrected tetralogy of Fallot, and Marfan syndrome with normal aortic root diameter.
• High maternal mortality (25–50 % risk of death): pulmonary hypertension,
Eisenmenger’s syndrome, Marfan syndrome with aortic root more than 40 mm diameter, and peripartum
cardiomyopathy.

17. • The other causes of death are—
(a) pulmonary edema
(b) pulmonary embolism
(c) active rheumatic carditis
(d) Subacute bacterial endocarditis
(e) rupture of cerebral aneurysm in coarctation of aorta.
• Pregnancy does not affect the long term survival of a woman with rheumatic heart lesion provided she
survives pregnancy itself.

18. FETAL PROGNOSIS
• In rheumatic heart lesions , the fetal outcome is usually good and in no way different from the patients
without any heart lesion
• In cyanotic group of heart lesion , there is increased fetal loss (45%) due to abortion , IUGR and
prematurity.
• Fetal congenital cardiac disease is increased by 3–10% if either of the parents have congenital lesions.
• Fetal problems are mainly due to a restriction of maternal cardiac output and hence placenta perfusion,
maternal cardiac output, resulting in fetal growth retardation.

20. SYMPTOMS

21. MANAGEMENT
Principles:
• Early diagnosis and evaluation of anatomical type and functional grade of the
case.
• To detect the high risk factors and to prevent cardiac failure.
• Multidisciplinary team approach (obstetrician, cardiologist and neonatologist)
and mandatory hospital delivery.

22. PRE-PREGNANCY
• Ideally in patients with significant hear t disease , pregnancy is a planned event.
• The patient’s cardiologist should be an active participant.
• Maternal disease status should be determined.
• A careful history is obtained to identify previous cardiac complications , including
arrhythmias.
• The patient’s functional status should also be established by New York Heart Association
(NYHA) classification system.

23. • Most cases falls in groups I & II disease with favorable outcomes , but deterioration may
occur.
• Grade III & IV disease have very high maternal mortality, nearly 85%.
• Coexisting conditions that may aggravate preexisting heart disease, such as anemia,
arrhythmias, and hypertension, should be appropriately treated and controlled.
• Ideally, necessary cardiac surgery is carried out before conception

24. THERAPEUTIC TERMINATION
• Absolute indications:
 Primary pulmonary hypertension
 Eisenmenger’s syndrome and
 Pulmonary veno-occlusive disease.
• Relative indications:
 Parous woman with grade III and IV cardiac lesions
 Grade I or II with previous history of cardiac failure in early months or in between pregnancy.
The termination should be done within 12 weeks by suction evacuation (MVA) or by conventional D & E.

25. • The patients with heart disease should be supervised in a tertiary care hospital.
• Initial assessment should be made in consultation with a cardiologist.
• During prenatal care, the patient should be routinely questioned and examined for signs or symptoms
of cardiac failure:
 Infections—Urinary tract, dental and respiratory tract.
 Anemia, Obesity, Hypertension, Arrhythmias , Hyperthyroidism, Drugs— Betamimetics.
 Dietary indiscretion: Excess intake of caffeine, alcohol, high calorie diet, excess salt

26. • Injection Penidure LA-12 (benzathine penicillin) is given at intervals of 4 weeks throughout pregnancy
and puerperium to prevent recurrence of rheumatic fever.
• Counseling is to be done regarding prognosis and risks.
• Anticoagulants are indicated in cases with:
(a) Congenital heart disease,
(b) pulmonary hypertension,
(c) mechanical heart valve,
(d) atrial fibrillation.

27. • The patient taking warfarin should discontinue it as soon as pregnancy is diagnosed and to
replace it by heparin 5,000 units twice daily subcutaneously up to 12th week.
• Low molecular weight heparin (LMWH) can also be used. This is then replaced by warfarin
tablet 3 mg. daily to be taken at the same time each day and continued up to 36 weeks.
• Thereafter it is replaced by heparin up to 7 days postpartum. Warfarin is then to be
continued.
• UFH, LMWH and Warfarin therapy do not contraindicate breast-feeding.

28. EMERGENCY
• Deterioration of the functional grading
• Appearance of dyspnea or cough or basal crepitations or tachyarrhythmias
• Appearance of any pregnancy complication like anemia, preeclampsia.

29. DURING LABOR
Most patients with cardiac disease go into spontaneous labor and deliver
without any difficulty. Induction (vaginal PGE2 ) may be employed in very
selected cases for obstetric indications. One should guard against infection and
pulmonary edema due to fluid overload.

30. Usually Vaginal delivery is encouraged unless indication for Cesarean:
• Coarctation of aorta
• Aortic dissection or aneurysm
• Aortopathy with aortic root >4cm
• Warfarin treatment within 2 weeks
• Preferred choice or anaesthesia is Epidural or General anaesthesia

31. PUERPERIUM:
Observation closely for the first 24 hours.
Oxygen is administered.
Hourly pulse, BP and respiration are recorded.
Diuretic may be used if there is volume overload.
Breastfeeding is not contraindicated unless there is heart failure.
Anticoagulant therapy is not a contraindication of breastfeeding.

32. MANAGEMENT OF CARDIAC FAILURE IN PREGNANCY
• Propped up position
• O2 administration
• Monitoring with ECG and pulse oximetry
• Diuretic: Frusemide (Loop) (40–80 mg) IV (anticipatory aggressive diuresis is needed to avoid pulmonary
congestion)
• Mechanical ventilation
• Injection morphine 15 mg IM
• Digoxin 0.5 mg IM followed by tab digoxin 0.25 mg P.O. (Digoxin crosses the placenta and is excreted in
breast milk)
• Dysrhythmias—quinidine or electrical cardioversion
• Tachyarrhythmias—Adenosine (3–12 mg) IV or DC conversion

33. RHEUMATIC HEART DISEASE
• Asia, Africa, and South America have high prevalence rates.
• Rheumatic heart disease is a complication of rheumatic fever.
• Cardiac valve damage results from an immunologic injury initiated by a group A β-hemolytic
streptococcal infection.
• During pregnancy, the increased maternal blood volume and heart rate can lead to heart failure and
pulmonary edema. Arrhythmias also frequently complicate pregnancy.
• Rates o f IUGR and prematurity are increased with complicated rheumatic hear t disease .

35. MANAGEMENT
• Aim is to prevent cardiac failure and bacterial endocarditis.
• Volume status is monitored, and activity should be limited.
• Antibiotics can be given prior to cesarean section.

36. MITRAL STENOSIS
• Either alone or in combination with other lesions, is the most common valvular disorder associated with
rheumatic heart disease.
• Normal mitral valve area ranges between 4 and 6 cm2 .
• Symptoms usually appear when stenosis narrows this to less than 2.5 cm2 .
• Women with mitral valve area ≤1 cm2 , have the high rate of pulmonary edema (55%) and arrhythmia
(33%).
• In pregnancy, the increased intravascular volume can further elevate pressures and lead to pulmonary
edema and arrhythmias, even in previously asymptomatic patients.
• In asymptomatic cases, the mortality is < 1% but once it is significantly symptomatic, mortality ranges
between 5% and 15%.
• The severity of the stenosis is the best predictor of cardiac compromise.

38. MANAGEMENT
PREPREGNANCY
• Define the severity of cardiac compromise.
• Two-dimensional echocardiography and color-flow Doppler are used to determine cardiac
function and the degree of stenosis.
• Severe stenosis is defined by a valve area of less than 1.0 cm.
• Valve areas of 1.2 cm or less are associated with an increased risk of complications during
pregnancy.

39. • In symptomatic patients or those with severely stenotic valves , surgical correction should take place be
fore conception.
1. Surgical commissurotomy (traditional treatment modality) .
2. Percutaneous mitral valve commissurotomy (an alternative in patients without calci fied valves or signi
ficant regurgitation)

41. • It can be congenital or rheumatic in origin, or it may be due to an agerelated calcification of the aortic
valve .
• It accounts for only 5% to 10% of cases of rheumatic heart disease in pregnancy and is usually seen in
conjunction with mitral valve disease.
• Normal aortic valve area is 3–4 cm2 . When it is reduced to less than or equal to 1 cm2 , stenosis is
significant.

43. LABOR AND DELIVERY AND POSTNATAL
• Fluid management is the critical component of intrapartum care.
• Patients should labor and deliver in the lateral position .
• Epidural anesthesia is contraindicated.
• During labor, fluid therapy (125–150 mL/h) should not be restricted.
• Blood loss to be monitored closely and replaced as necessary.

44. CARDIOMYOPATHIES
Peripartum cardiomyopathy
• Cardiac failure within last month of pregnancy or within 5 months postpartum.
• No determinable cause for failure.
• Absence of previous heart disease.
• Left ventricular dysfunction as evidenced on echocardiography—
 Ejection fraction less than 45% and
 Left ventricular end diastolic dimension more than 2.7 cm/m2 .
Peripartum cardiomyopathy is a diagnosis of exclusion.
Pregnancy is poorly tolerated in women with dilated cardiomyopathy.

46. MANAGEMENT
• Pregnancy is strongly discouraged in patients with a history of peripartum cardiomyopathy, particularly
those with residual cardiac dysfunction.
• The patient should be informed of the potential for worsening cardiac function during pregnancy, which
may not completely resolve postpartum.
• Combined hormonal contraceptives should be avoided in patients with residual ventricular dysfunction.
• Depo-Provera or IUDs can be safely used.
• Permanent sterilization may also be considered

47. MANAGEMENT
PREPREGNANCY
•Before pregnancy, the severity of aortic stenosis should be determined by echocardiography.
•Severe disease should be corrected surgically before conception.
PRENATAL
•Physical activity should be limited.
•Patients should be observed for signs of congestive heart failure or arrhythmias.
•Serial fetal ultrasounds should be scheduled to detect evidence of growth restriction.

48. Prenatal
If pregnancy occurs, echocardiography should be performed to document ventricular size and function as
well as the presence of mural thrombi.
Termination should be offered, especially to patients who have persistent echocardiographic
abnormalities.
Treatment
• Bed rest,
• Digoxin,
• Diuretics (preload reduction),
• Hydralazine or ACE inhibitors (postpartum) (afterload reduction),
• β blocker
• Anticoagulant therapy

49. • Vaginal delivery is preferred.
• Epidural anesthesia is ideal.
• There is no contraindication of breastfeeding.
• Mortality is high (20–50%)—due to CCF, arrhythmia or thromboembolism.
• It may recur in subsequent pregnancies