MEDICAL DISORDER IN

PREGNANCY-HEART
DISEASE AND THYROID
HEART DISEASE IN PREGNANCY

Pregnancy place an additional strain on the heart due to

CVS changes that occur due to physiological adaptation
 Cardiovascular changes during
pregnancy
• Increased maternal blood volume and
increase in heart rate
• Increased cardiac output
• Cardiac output increases by 20–50%, starting
as early as 5 weeks of gestation and peaking
by mid- to late pregnancy ( from about 5L/min
to 7.0L/min)
 Blood pressure during pregnancy
• Total peripheral resistance decreases throughout
pregnancy ( 30% decrease as early as 8 weeks
gestation)
• Systolic blood pressure decreases 5-10 mmHg
• Diastolic blood pressure is decreased initially (15-20
mmHg), reaching its lowest point around the second
trimester, before increasing back to baseline during the
late last trimester
• In addition, increase secretion of various vasodilators,
such as nitric oxide (NO) and prostaglandins, which
cause a drop in the peripheral resistance
 Common cardiac problem
• Rheumatic heart disease-mitral stenosis, mitral
incompetence
• Congenital heart disease-ex cyanotic, acyanotic,
pulmonary hypertension and Eisenmenger’s
syndrome
• Marfan syndrome
• Hyperthrophic cardiomyopathies
• Cardiac arryhtmia-AF, SVT
• Coronary heart disease
 Complication
• Cardiac disease is a major cause of maternal
mortality due to heart failure and increase
incidence of venous thrombosis and
pulmonary embolism
• Unless heart failure develop cardiac disease
does not alter perinatal mortality but there is
high incidence of IUGR and preterm labour
 Management
• Involve multidisciplinary approach
• Prenatal/ pre-pregnancy counselling:
• Advice on contraception to avoid unwanted pregnancy
• Counsel for those wanting pregnancy
• Increased risk of maternal mortality
• Possible reduction of maternal life expectancy
• Effects of pregnancy on cardiac disease
• Congenital heart disease in the fetus
• Risk of preterm labour and FGR
• Need for increased medical surveillance during pregnancy
 Management
• Determine the patient functional status
• Use NYHA classification

• Class I and II low risk while class III and IV are at high
risk
 Management
• Antenatal
– Managed jointly by the obstetrician and cardiologist
– Vital sign
– Evaluate sign and symptoms of heart failure
• Ask if mother has symptoms like dyspnea, orthopnea, PND,
• Thorough clinical examination and cardiovascular assessment
- the presence of anaemia
- the presence of any dental caries
- the blood pressure
- the presence of any arrhythmia
- any evidence of subacute bacterial endocarditis
– Determine the factors that can precipitate heart failure like twin pregnancy,
polyhydramnios, anaemia, hyperthyroidism, PIH/ Pre-eclampsia, respiratory
infections, arrhythmias.
– Prevention of anemia, infection, hypertension
 Management
• Assess other factors :
- A history of previous cardiac failure
- Type of cardiac lesion
- Presence of any arrhythmia such as AF
- Presence of any valve replacement and whether
she is on anticoagulants
- Socioeconomic status of patient, distance of
house from hospital and availability of home help
 Management
• Optimise mother’s condition
• Investigations like :-
• baseline haemoglobin level
• urea and electrolytes
• ECG
• Echocardiogram (ejection fraction; less than
40% carries a poor prognosis.
 Mode of delivery
• Always best to wait for spontaneous labour
• Only induced if there is obstetric indication like IUGR,PIH.
• General principle is to minimise cardiac stress
– Vaginal delivery
• In labour, frequent assessment of vital signs, urine output, pulse
oximetry, put on continuous ecg monitoring.
– Propped up in bed, nursed in the left-lateral position to prevent
aortocaval compression, oxygen freely available.
– Adequate pain relief is important – often slow infusion
• epidural or parenteral opiates such as morphine.
• 2nd stage of labor: assisted delivery is indicated to avoid
maternal pushing increasing stress on heart.
. 3rd stage, iv ergometrine should be avoided to prevent sudden
increase in venous return when the uterus contract, syntocinon
should be used instead.
 Mode of delivery
• Caesarean delivery
• Dependent on obstetric reasons
• If cardiologist decides that the mother may not be able to withstand the
• Best delivered by an elective Caesarean section at 38 weeks.

– Antibiotic prophylaxis should be started in patients with

high risk of endocarditis e.g prosthetic cardiac valves,
previous history of endocarditis, mitral valve prolapse
with regurgitation.
- a combination of amoxicillin/cephalosporin and
gentamycin gives adequate protection.
 Management of postpartum
• Close monitoring
– careful fluid balance and watch for sign of heart failure
– Manage in high dependency unit for at least 24 hours postpartum
• In early puerperium, the mother must get
adequate rest
. Breastfeeding discouraged if she physically cannot
cope with it.
. Continue antibiotics, discuss about family planning
or sterilisation.
 Heart failure management
Multidisciplinary team consisting of cardiologist, obstetrician and
paediatrician.
Non-pharmacological
• Limiting strenuous exercise
• Adequate rest
• Maintaining low salt diet
• Treating anemia and infections early
• Frequent antenatal examinations
Pharmacological
• Nitroglycerine can be used in pregnancy for after load reduction.
• Digoxin is safe in pregnancy and during breastfeeding.
• Diuretic may be used for preload reduction. Used with caution as it
impair uterine blood flow particularly placental perfusion. No
teratogenic effects have been described.
• Selective B-blocker such as atenolol or metoprolol are generally
preferred. Otherwise, B-blocker may result in IUGR, apnea at birth, fatal
fetal bradycardia, hypoglycemia and hyperbilirubinemia.
• Contraindicated:-
-ACE-I and ARB.
• Other treatment
• Patients with atrial fibrillation who are
hemodynamically unstable should be promptly
electrically cardioverted.
• Anticoagulation is indicated in the presence of
atrial fibrillation, dilated left atrium or mechanical
prosthetic heart valve.
• Patients with valvular lesions who remain
symptomatic despite optimal medical treatment
may be considered for percutaneous valve
intervention or surgery.
THYROID DISEASE IN PREGNANCY
 Physiological Changes Of Thyroid
Hormone In Pregnancy
• To meet the increased metabolic needs during a
normal pregnancy, there are changes in thyroid
physiology .
– TBG d/t estrogen
– hCG and thyroid function
• hCG is one of a glycoprotein hormones (similar to TSH) with a
common alpha-subunit and a unique beta-subunit
• Suppressed TSH, but T3 & T4
• TSH gradually returns to its normal range (0.4-4.0mIU/L)
• Iodine
• increase iodine requirements (150 >> 200 microgram/day)
• increased renal iodine clearance
( GFR & renal blood flow during pregnancy)
• *To compensate, thyroid gland must increase uptake of iodine 
hyperplasia physiologic goitre
 Thyroid Function In Fetus
• For the first 8-10 weeks of pregnancy, the baby is
completely dependent on the mother for the
production of thyroid hormone.
• By 12 week, the baby’s thyroid begins to produce
thyroid hormone on its own. However, remains
dependent on the mother for ingestion of
adequate amounts of iodine, which is essential to
make the thyroid hormones.
• 30% of maternal T4 can be found in the cord
blood.
• It is important for fetal brain development
• 2nd trimester :
Neuronal multiplication, migration, structural
organization
• 3rd trimester :
Glial cell multiplication, migration, myelinisation

Inadequate thyroid hormones leads to (irreversible):

Disruption of brain growth
Development of brain damage
Eg. Poor cognitive development, mental retardation, CP.
 Hyperthyroidism in pregnancy
( TSH < 0.1mIU/L )
Causes
• Graves’ disease (80-85%)
• Multinodular goiter
• hCG-mediated hyperthyroidism
- Gestational transient thyrotoxicosis
- Hyperemesis gravidarum
- Trophoblastic hyperthyroidism
 History:
weight loss despite good
appetite Investigation
excessive sweating especially
at night, in cold weather • TSH ↓
excitability, irritability, • Free T4 & T3 ↑
tremulousness
palpitations

Physical examination:
goitre (usually with/without
bruit) in Graves’ disease
proximal muscle weakness,
hyperreflexia
warm, sweaty palms
fine finger tremors
lid retraction, lid lag
resting tachycardia
Effect on mother Effect on fetus
• PIH,Pre-eclampsia • fetal tachycardia
• Miscarriage • premature birth
• Premature labour • IUGR
• Thyroid storm • stillbirth
• Maternal CCF • Goiter
• Heart failure
• Growth restriction
Management
• Antithyroid drug
– Propylthiouracil (PTU)
– Carbimazole
• If 1st diagnosed in pregnancy,carbimazole 15mg/PTU 150mg 8 hourly for 4-5w. Dose
progressively reduced until maintenance dose of 15mg carbimazole/150mg PTU daily
achieve satisfactory control.
• Monitor TFT monthly in mother, adjust dose accordingly.
• If adequate control and mother euthyroid, drugs stopped at 36w POG to avoid effects on
fetal thyroid
*Lowest possible dose should be used as it can cross placenta and cause goitre and
hypothyroidism in the fetus
* PTU is more preferred as carbimazole may cause scalp defects in newborn,
agranulocytosis / ototoxicity in mother

• Beta blocker – to relieve symptoms

(Long term usage results in IUGR, fetal bradycardia, neonatal hypoglycemia)
• Radioactive iodine treatment is C/I as it can damage the fetal thyroid gland.
• Rarely, surgery to remove all or part of the thyroid gland is considered for women
who cannot tolerate antithyroid medications. If required, optimal time is at 2nd tri.
• If the patient chooses ATD therapy, the following recommendations should
be given: 1) Risks associated with both propylthiouracil (PTU) and
methimazole (MMI) should be discussed; 2) PTU should be used in the first
trimester of pregnancy, because of the risk of MMI embryopathy; and 3)
consideration should be given to discontinuing PTU after the first trimester
and switching to MMI in order to decrease the incidence of liver disease.

• Beta adrenergic blocking agents, such as propranolol 20–40 mg every 6–8

hours may be used for controlling hypermetabolic symptoms. The dose
should be reduced as clinically indicated. In the vast majority of cases the
drug can be discontinued in 2–6 weeks. Long-term treatment with beta
blockers has been associated with intrauterine growth restriction, fetal
bradycardia and neonatal hypoglycemia

• Thyroidectomy should be considered in cases of allergies/contraindications

to both ATDs, in women requiring large doses of ATDs, and for patients
who are not compliant with drug therapy. If surgery is indicated, second
trimester is the optimal time. A determination of serum TRAb titers is of
value at the time of surgery in order to assess the potential risk of fetal
hyperthyroidism (101). Preparation with beta-blocking agents and a short
course of potassium iodine solution (50–100 mg/d) are recommended
• At delivery, cord blood of baby should be taken for free T4 & TSH.
Newborn should be examined for goiter, hypothyroidism or thyrotoxicosis.
• PTU is drug of choice for breastfeeding mother
• Graves’ disease typically worsens in the postpartum period, usually in the
1st 3 months after delivery. Higher doses of anti-thyroid medications are
frequently required during this time.
 Hypothyroidism in Pregnancy
( TSH > 6.6mIU/L)
Primary
– Over treated hyperthyroidism
– Autoimmune Hashimoto’s thyroiditis (TPOAb)
– Surgical ablation (total thyroidectomy)
– Iodine deficiency
(TSH high, T4 low)

Secondary
– Hypothalamic-pituitary dysfunction
Screening
• Symptoms of hypothyroidism
• Goiter
• Family History of thyroid disease
Signs & symptoms
• Fatigue
• Dry skin
• Coarse hair
• Constipation
• Weight gain
• Cold intolerance
• Decreased concentration
• Depression
• Memory and mental impairment
• Myalgia

• Irregular/heavy menses, infertility

Risk to mother
• Anaemia
• Preterm labour
• Miscarriage
• IUD
• Spontaneous abortion
• Gestational hypertension
• Abruptio placentae
• PE
• Cardiac dysfunction

Risk to baby
• Low birth weight
• Stillbirth
• Impaired brain development
• Preterm birth
• Increase morbidity and mortality
• Cong. Hypothyroidism –cognitive, neurological & developmental
abnormalities
*These can largely be prevented if the disease is recognized and treated
immediately after birth.
Management
• Thyroid hormone replacement: Levothyroxine
(when TSH > 10mIU/L OR TSH 5-10mIU/L & goiter +/- TPOAb)
• Women with known hypothyroidism should test for TFT as
soon as pregnancy is detected and their dose adjusted to
maintain a TSH in the normal range. (0.3-3.0mIU/L)
• TFT should be checked every 6-8 weeks during pregnancy to
ensure that the woman has normal thyroid function
throughout pregnancy.
• After delivery, the woman may go back to pre-pregnancy dose
of levothyroxine
• It is also important to recognize that prenatal vitamins contain
iron and calcium that can impair the absorption of thyroid
hormone from the gastrointestinal tract. Consequently,
levothyroxine and prenatal vitamins should not be taken at
the same time and should be separated by at least 2-3 hrs.