Obstetrics and Gynaecology chapters
Maternal physiological and hormonal changes in pregnancy, and fetal physiology
The hormones of pregnancy (hCG, progesterone, oestrogens, human placental lactogen, prolactin) and how they change the mother's heart, blood, lungs, kidneys, gut, thyroid and metabolism, plus the key facts of fetal circulation, haemoglobin and lung maturity.
- hCG from the syncytiotrophoblast rescues the corpus luteum (peaks at 10-12 weeks); the placenta takes over progesterone at about 8 weeks; hPL makes the mother insulin resistant to spare glucose for the fetus.
- Blood volume rises (about 30% by term) more than red cell mass → dilutional fall in Hb; cardiac output rises 30-40%, SVR and BP fall mid-pregnancy; the blood becomes hypercoagulable (more factors VIII, IX, X, fibrinogen; less protein S and antithrombin).
- Minute ventilation rises about 50% (progesterone) so PaCO2 falls; GFR rises up to 50%; TBG rises and TSH dips in the first trimester; the fetus relies on four shunts and HbF (higher oxygen affinity).
On this page
Overview
Pregnancy changes almost every system in the mother. Most changes are driven by placental hormones and by the needs of the growing fetus and placenta. Knowing what is normal stops you calling a physiological finding a disease (for example a low haemoglobin, a raised heart rate or a soft systolic flow murmur), and explains why some diseases get worse in pregnancy.
Hormones of pregnancy
hCG (human chorionic gonadotrophin)
- A glycoprotein made by the syncytiotrophoblast; shares an alpha subunit with LH, FSH and TSH.
- Detectable in maternal blood about 8-9 days after ovulation, soon after implantation; a sensitive urine test can be positive just before the missed period.
- In a viable early pregnancy it roughly doubles every 48 hours; it peaks at about 10-12 weeks, then falls to a lower plateau by 16-20 weeks.
- Main job: acts on LH receptors to rescue the corpus luteum, which keeps making progesterone and oestrogen and prevents menstruation.
- Also stimulates fetal testes to make testosterone (male development) and weakly stimulates the maternal thyroid (TSH receptor).
- Very high hCG: multiple pregnancy, molar pregnancy; both are linked with hyperemesis.
Progesterone
- From the corpus luteum until about 8 weeks, then from the placenta (luteo-placental shift). Removing the corpus luteum before about 7-8 weeks usually causes miscarriage; progesterone support is given if it must be removed.
- Rises about 10-fold over pregnancy.
- Actions: decidualises the endometrium, relaxes the myometrium (keeps the uterus quiet), relaxes smooth muscle elsewhere (gut, ureters, veins), increases the respiratory centre's sensitivity to CO2, prepares breast lobules.
Oestrogens
- Placental oestrogen output rises to about 30 times non-pregnant levels.
- The placenta cannot make oestrogen from scratch. It converts DHEA (and 16-hydroxy-DHEA) from the fetal adrenal (and maternal adrenal) into oestrogens, mainly oestriol. This partnership is the fetoplacental unit.
- Actions: growth of the uterus, breast ducts and external genitalia; relaxation of pelvic ligaments and the symphysis; raises liver binding proteins (TBG, SHBG) and clotting factors.
A fetus with anencephaly has little fetal adrenal stimulation, so maternal oestriol is very low. Low unconjugated oestriol is also a marker used in Down syndrome screening.
Human placental lactogen (hPL, human chorionic somatomammotropin)
- Made by the syncytiotrophoblast from about 5 weeks; rises in proportion to placental mass.
- Structure similar to growth hormone.
- Actions: anti-insulin (raises maternal blood glucose), lipolysis (fatty acids released as maternal fuel), helps breast development. Net effect: glucose is spared for the fetus. (See the chapter on metabolism in pregnancy.)
Other hormones
| Hormone | Change | Effect |
|---|---|---|
| Prolactin | Rises steadily to 10-20 times normal at term (pituitary enlarges at least 50%) | Prepares breast for milk; milk blocked by oestrogen and progesterone until delivery |
| FSH, LH | Suppressed | No new follicles mature in pregnancy |
| Cortisol | Moderately raised | Mobilises amino acids |
| Aldosterone | About doubled | Sodium and water retention |
| Relaxin | From corpus luteum and placenta | Softens the cervix; relaxes ligaments; contributes to early vasodilatation |
| Thyroid hormones | TBG up; TSH dips in first trimester; FT4 rises then falls | See below |
| PTH | Rises if calcium intake is low | Maintains maternal calcium while the fetus mineralises bone |
Cardiovascular system
| Variable | Change |
|---|---|
| Cardiac output | Rises 30-40%, mostly by the end of the second trimester |
| Heart rate | Rises |
| Systemic vascular resistance | Falls (marked peripheral vasodilatation) |
| Blood pressure | Falls slightly in the first trimester, lowest in the mid-trimester, back to pre-pregnancy level near term |
| Uterine blood flow | Rises greatly at term |
- Aortocaval compression: lying flat in late pregnancy, the uterus presses on the IVC and aorta; venous return and cardiac output fall, and she may become faint (supine hypotension). Use left lateral tilt or semi-prone positions, and manual uterine displacement in resuscitation.
- Swelling of the ankles is common.
- Women with fixed cardiac output lesions (for example mitral or aortic stenosis) or pulmonary hypertension tolerate these changes poorly. In Eisenmenger physiology, falling SVR increases right-to-left shunting.
Blood
| Variable | Change |
|---|---|
| Plasma volume and blood volume | Rise; blood volume about 30% above normal near term (an extra 1-2 litres) |
| Red cell mass | Rises, but less than plasma |
| Haemoglobin | Falls (haemodilution) |
| MCV | May rise slightly |
| White cell count | Rises (more in labour) |
| Platelets | May fall slightly; gestational thrombocytopenia in about 7-8% |
| Clotting factors | VIII, IX, X and fibrinogen rise |
| Natural anticoagulants | Protein S and antithrombin fall |
| Fibrinolysis | Reduced |
- Anaemia cut-offs: Hb below 110 g/L in the first trimester, below 105 g/L in the second and third, below 100 g/L postpartum.
- Iron needs: about 375 mg for the fetus plus about 600 mg for the mother's extra red cells (Guyton), more than most women have in stores, so iron deficiency is common without supplements.
- Hypercoagulability protects against haemorrhage at delivery but raises VTE risk about 6-10 times; worse with venous stasis from the uterus and immobility after birth. VTE is a leading direct cause of maternal death in the UK.
Dilutional anaemia is physiological; but in Pakistan, true iron deficiency is common and must not be dismissed as "dilution". Check the Hb against the trimester-specific cut-off.
Hypercoagulability plus venous stasis (uterine pressure on the IVC, immobility) explains the high VTE risk, which continues into the puerperium.
Respiratory system
- Oxygen consumption rises (about 20% near term).
- Progesterone increases the respiratory centre's sensitivity to CO2 → minute ventilation rises about 50%, mainly through a larger tidal volume.
- Result: PaCO2 falls → mild respiratory alkalosis, compensated by renal loss of bicarbonate. The lower maternal PaCO2 helps CO2 pass from fetus to mother.
- The diaphragm rises and functional residual capacity falls; with higher oxygen use this makes pregnant women desaturate quickly during apnoea (relevant to anaesthesia).
- Many women feel breathless (physiological dyspnoea).
A PaCO2 that would be normal for a non-pregnant woman may mean respiratory failure in a pregnant asthmatic.
Renal and urinary tract
- Renal blood flow and GFR rise (GFR up to about 50%), so creatinine and urea fall; a "normal" non-pregnant creatinine may be abnormal in pregnancy.
- Tubular sodium and water reabsorption rise (aldosterone, oestrogen), so there is net fluid retention.
- Glycosuria is common because the higher GFR lowers the renal threshold for glucose; still check blood glucose.
- Smooth muscle relaxation and pressure slow urine flow; asymptomatic bacteriuria (about 8%) can progress to pyelonephritis if untreated, so it is screened for and treated.
Gastrointestinal system
- Progesterone relaxes smooth muscle: heartburn (lower oesophageal sphincter), constipation (slower gut).
- Gastric emptying is slowed in labour, especially with opioids; this raises aspiration risk under general anaesthesia.
Endocrine and metabolic
- Thyroid: TBG rises (oestrogen) so total T4 and T3 rise; measure FT4 and TSH using pregnancy ranges. In the first trimester hCG stimulates the thyroid: TSH falls and FT4 rises, then FT4 drifts down later. Relative iodine deficiency also occurs.
- Glucose: mild fasting hypoglycaemia, insulin resistance in the second half, rising insulin needs in diabetics.
- Basal metabolic rate rises about 15% in the second half of pregnancy; women often feel hot.
Because GFR rises, a serum creatinine that is normal for a non-pregnant woman may already reflect kidney impairment in pregnancy.
- Weight gain averages about 11 kg (Guyton gives 24 lb): fetus, placenta, liquor, uterus, breasts, extra blood and fluid, and some fat.
- Uterus grows from about 50 g to about 1,100 g.
Skin and musculoskeletal
- Pigmentation (face, areolae, midline), spider naevi, striae; itching needs liver tests to exclude obstetric cholestasis.
- Ligament laxity, lordosis → backache, symphysis pubis pain; swelling → carpal tunnel syndrome.
Fetal physiology
Fetal circulation: four shunts
| Shunt | Route | Closure after birth |
|---|---|---|
| Umbilical vessels | Two arteries carry deoxygenated blood to the placenta; one vein returns oxygenated blood | Cord clamped |
| Ductus venosus | Umbilical vein blood bypasses the liver to the IVC | Closes as umbilical flow stops → ligamentum venosum |
| Foramen ovale | Oxygenated IVC stream crosses right atrium → left atrium, then to the brain and heart | Left atrial pressure rises with lung blood flow → flap closes |
| Ductus arteriosus | Pulmonary artery → descending aorta, bypassing the fluid-filled lungs | Functional closure within days (oxygen, fall in prostaglandin) → ligamentum arteriosum |
- The duct is kept open by prostaglandin E2 and prostacyclin; NSAIDs (cyclo-oxygenase inhibitors) given to the mother can close it early.
- Failure of pulmonary resistance to fall after birth gives persistent fetal circulation (persistent pulmonary hypertension) with cyanosis.
- A single umbilical artery (about 0.5%) is linked to growth restriction and anomalies.
The four shunts in order of blood flow: "Vein, Venosus, Ovale, Arteriosus" (umbilical vein → ductus venosus → foramen ovale → ductus arteriosus).
Oxygen transfer and haemoglobin
- HbF (alpha2 gamma2) has a higher oxygen affinity than adult HbA, and fetal Hb concentration is higher (about 18 g/dL at birth); together with the double Bohr effect, this lets the fetus load oxygen at low PO2.
- HbF is about 90% of fetal Hb from 10 to 28 weeks; a switch to HbA starts around 28-34 weeks; at term HbF:HbA is about 80:20; by 6 months only about 1% is HbF.
- Blood formation: yolk sac, then liver (from about 6-8 weeks, peak 12-16 weeks), then bone marrow (main site by about 20 weeks).
Lungs
- Type II pneumocytes make surfactant from about 30 weeks; about 80% is phosphatidylcholine (lecithin).
- Surfactant production is increased by cortisol (hence antenatal corticosteroids before preterm birth) and delayed by maternal diabetes.
- Fetal breathing movements and enough amniotic fluid are needed for lung growth; oligohydramnios (for example renal agenesis) causes pulmonary hypoplasia.
Other systems
- Liver: immature bilirubin conjugation (low glucuronyl transferase); the placenta clears unconjugated bilirubin in utero → physiological neonatal jaundice. Glycogen stores build mainly in the third trimester (growth-restricted and preterm babies are prone to hypoglycaemia).
- Kidney and gut: fetal urine forms most of the amniotic fluid; the fetus swallows it, so upper gut atresia causes polyhydramnios. Meconium in the liquor is linked to post-term pregnancy and hypoxia.
- Immunity: maternal IgG crosses the placenta (passive immunity); IgM does not, so IgM in the newborn means fetal infection.
- Endocrine: fetal thyroid makes T4 from about 10-12 weeks; fetal testes make testosterone in the first trimester.
Expect: hCG source, timing (detectable at 8-9 days, doubling 48 hours, peak 10-12 weeks) and function (corpus luteum rescue, thyroid stimulation); luteo-placental shift at about 8 weeks; oestriol and the fetoplacental unit; hPL as anti-insulin; plasma volume rising more than red cell mass (physiological anaemia) with the trimester Hb cut-offs; raised factors VIII, IX, X and fibrinogen with low protein S; cardiac output up and SVR down; aortocaval compression; minute ventilation up 50% with low PaCO2; GFR up, creatinine down, glycosuria; TBG up and TSH down in the first trimester; fetal shunts, HbF and surfactant (lecithin, steroids, diabetes delay).
Quick revision
- hCG: syncytiotrophoblast; rescues corpus luteum; peak 10-12 weeks.
- Progesterone: placenta takes over at about 8 weeks; relaxes smooth muscle; drives breathing.
- Oestriol needs fetal adrenal DHEA (fetoplacental unit).
- hPL: anti-insulin, lipolysis, glucose for the fetus.
- Blood volume up about 30%; Hb falls by dilution; anaemia under 110/105/100 g/L.
- Hypercoagulable: VIII, IX, X, fibrinogen up; protein S, antithrombin down.
- CO up 30-40%; SVR and BP down mid-pregnancy; avoid supine position late.
- Ventilation up 50%; PaCO2 down; GFR up 50%; creatinine down.
- TBG up; TSH dips in first trimester.
- Fetus: four shunts; HbF; surfactant from 30 weeks.
Written by The House Job from standard references (Obstetrics by Ten Teachers; Gynaecology by Ten Teachers; Guyton and Hall Textbook of Medical Physiology; Davidson's Principles and Practice of Medicine).
FAQ
Why does haemoglobin fall in a healthy pregnancy?
Plasma volume expands more than red cell mass, so the blood is diluted; this is normal within the trimester cut-offs, but true iron deficiency must still be excluded.
Why is a pregnant woman's PaCO2 lower than normal?
Progesterone makes the respiratory centre more sensitive to CO2, so she breathes more deeply, raising minute ventilation and washing out CO2.
Why should a pregnant woman not lie flat on her back in late pregnancy?
The heavy uterus compresses the inferior vena cava and aorta, cutting venous return and cardiac output, which can cause fainting and reduce placental blood flow.
Why are thyroid results interpreted differently in pregnancy?
Oestrogen raises thyroxine-binding globulin, so total hormone levels rise, and hCG stimulates the thyroid early on, lowering TSH; unbound T4 and TSH with pregnancy-specific ranges are used.