1
Forth stage
Obstetric
Lec-14
.د
احمد جاسم
1/1/1014
Heart Disease in Pregnancy
PHYSIOLOGY OF NORMAL PREGNANCY:
Cardiac output rises 30 to 50 percent above baseline during normal
pregnancy
Blood pressure typically falls early in gestation
Cardiovascular Physiology of Pregnancy
Normal pregnancy is associated with an increase of 30 to 50 percent in
blood volume
Blood volume increases, starting at the sixth week and rising rapidly until
mid-pregnancy; the levels peak by 20 to 24 weeks of pregnancy and then
are either sustained until term or decrease an
estrogen-mediated
stimulation of the renin-angiotensin system results in sodium and water
retention appears to be the mechanism underlying the blood volume
increase.
Increase in cardiac output is most significant change during pregnancy.
It begins to rise in first trimester and steadily rises to peak at 32 weeks
by 30 to 50%.
Cardiac output is normally 4.2 L/min., is 6.5 L/min. at 8-10 weeks of
pregnancy and remains so till near term.
Increase in cardiac output is achieved by rise in stroke volume (in early
pregnancy) and Heart Rate (in latter part of pregnancy) adjusting together
Incidence
1% of pregnancies.
2
Causes
Rheumatic heart (75%): mitral valve affection is the commonest followed
by aortic valve then both or others.
Congenital heart diseases (10%):
Acyanotic (left to right shunt): more common, includes septal defects
and patent ductus arteriosus.
Cyanotic (right to left shunt): e.g. Fallot’s tetralogy and Eisenmenger’s
syndrome which is more dangerous carries a maternal mortality rate
exceeding 25%.
Others (5%): e.g. ischaemic heart disease, arrhythmias and
cardiomyopathy.
Diagnosis
History of:
rheumatic fever,
heart lesion,
dyspnoea,
paroxysmal nocturnal dyspnoea,
orthopnoea,
haemoptysis,
Prophylaxis with long acting penicillin.
Examination may reveal:
murmur,
accentuated heart sound,
arrhythmia,
central cyanosis,
displaced apex beat,
Manifestations of left side heart failure e.g. gallop rhythm, crepitations
over lung bases and pleural effusion.
Manifestations of right side heart failure e.g. congested neck veins,
enlarged tender liver, ascitis and oedema lower limbs.
3
Investigations:
Chest X-ray: may show cardiac enlargement, pulmonary congestion or
pleural effusion.
Electrocardiography (ECG).
Echo cardiography: shows cardiac structure and function.
Misleading in Diagnosis during Pregnancy
Dyspnoea and tachycardia: are common physiological changes during normal
pregnancy.
Increased neck (jugular) venous pressure: during normal pregnancy up to +5
cm is not uncommon due to high cardiac output. This level is indicative of
right side heart failure in non-pregnant state.
Displacement of apex beat: 2-3 cm lateral to its normal position due to
rotation of the cardiac axis caused by elevation of the diaphragm.
Auscultation changes due to hyperkinetic circulation include:
Presence of third heart sound (50% of women).
Splitting of the first heart sound.
Systolic ejection murmur.
Early diastolic murmur due to increased velocity of the blood passing
through the aortic and pulmonary valves.
Mammary souffle or internal mammary murmur is a systolic murmur maximal
in the 2nd and 3rd intercostal spaces, especially on the left side due to flow
in the dilated internal mammary arteries.
Functional classification
According to New York Heart Association (1964);
Class I: No discomfort (i.e. dyspnoea, palpitation or anginal pain) on ordinary
activity.
Class II: Discomfort on ordinary activity.
Class III: Discomfort on less than ordinary activity.
Class IV: Dyspnoea at rest. Patient is decompensated.
4
Effect of Pregnancy on Heart Disease
Heart failure:
During pregnancy, heart failure can occur at any time but the maximum
incidence is between 32 and 34 weeks when the blood volume and cardiac
output are in their peaks. After that they have a plateau level up to full
term.
During the 2nd stage, heart failure may occur due to stress on the heart.
After delivery, failure may occur due to loading of the circulation by the
blood from the placental sinuses after retraction of the uterus.
Subacute bacterial endocarditis: may develop in the puerperium.
Effect of Heart Disease on Pregnancy
Abortion.
Intrauterine growth retardation.
Still birth.
Premature labour.
These complications are encountered especially in cyanotic heart diseases.
Management
General management:
More frequent antenatal visits.
More rest.
Diet is directed to restrict weight gain and prevent anaemia as it increases
cardiac strain.
Infection should be avoided and properly treated.
Hospitalisation: if signs of decompensation occur, the earliest evidence is
tachycardia exceeding 100 beats/ minute and crepitations at the lung
bases. Rest in a hospital is desirable in the last 2 weeks of pregnancy.
5
Specific management:
Medical treatment:
Digoxin: is indicated in atrial fibrillation to slow the ventricular response
and in acute heart failure to increase myocardial contractility.
Diuretics are used in acute and chronic heart failure with potassium
supplements in prolonged therapy.
Beta-adrenergic blockers: as propranolol may be indicated for arrhythmia
associated with ischaemic heart disease.
Aminophylline: relieves bronchospasm.
Heparin: is indicated in patients with artificial valves or atrial fibrillation.
N.B. Acute pulmonary oedema is urgently treated by:
Morphine 15 mg IV, to allay anxiety and reduce venous return.
Oxygen.
Digoxin 1 mg IV, except in severe mitral stenosis as the increase in
right heart output cannot be handled by the mitral valve.
Aminophylline 250 mg IV.
Venesection, removing 500 ml blood rapidly may be indicated in severe
cases.
Surgical treatment:
Therapeutic abortion: should be considered in class III and IV if the
patient is seen early in pregnancy.
Cardiac surgery: It may be an alternative to therapeutic abortion. The
principal indication is recurrent pulmonary oedema with mitral stenosis and
heart failure not responding to medical treatment. There is no increased
risk to the mother or the foetus in closed cardiac surgery e.g. mitral
valvotomy but there is higher incidence of foetal loss with open surgery.
Management of labour
There is no indication to induce labour because of cardiac disease.
If induction of labour is indicated for an obstetric cause e.g. antepartum
haemorrhage a low amniotomy + oxytocin in a concentrated glucose solution
is the best method. This minimises the incidence of infection and pulmonary
oedema.
6
Induction of labour never to be undertaken in patient with acute heart
failure.
Vaginal delivery is preferable to caesarean section but should be an easy
and not a prolonged one.
There is no place for “trial of labour" in cardiac patients.
Bed rest in semi-sitting position.
Oxygen mask or ventilation if heart failure or cyanosis develop.
Adequate analgesia pethidine or morphine can be used. Epidural anaesthesia
is preferable as it abolishes the bearing down desire so decreases the
effort load.
Shorten the second stage by forceps or ventouse.
Ergometrine is better avoided as it causes sudden load of the circulation
with blood from the uterus leading to acute heart failure. Oxytocin can be
used instead.
Prophylactic antibiotic is essential to guard against subacute bacterial
endocarditis.
Postpartum observation for 48 hours is essential as the risk of heart failure
is high in this period. Although bed rest is essential, early ambulation is
desirable to avoid thromboembolism.
Breast feeding is allowed unless there is heart failure. Oestrogens should
not be used to suppress lactation and bromocriptine or lisuride can be used.
Sterilisation may be advised if decompensation occurred in this pregnancy.