Maternal changes in pregnancy
Maternal adaptation to pregnancy: cardiovascular, respiratory, renal, haematological and metabolic
Almost every maternal system changes in pregnancy, mostly under progesterone, oestrogen and the low-resistance placental circulation. These normal changes alter the reference ranges for blood tests and examination findings, and explain supine hypotension, rapid desaturation at anaesthesia and the high risk of thrombosis. CPSP asks the direction and size of each change and its mechanism.
Cardiovascular
| Variable | Change | Mechanism or note |
|---|---|---|
| Plasma volume | Up 40–50% | Oestrogen and RAAS activation retain sodium and water |
| Red cell mass | Up 20–30% | Erythropoietin; so haemoglobin falls (dilutional anaemia) |
| Cardiac output | Up 30–50%, mostly by 20–24 weeks | Stroke volume and heart rate (up 10–15 beats/min) both rise |
| Systemic vascular resistance | Falls | Progesterone, NO, prostacyclin, low-resistance placental bed |
| Blood pressure | Falls in the second trimester (diastolic most), back to normal by term | Vessels become refractory to angiotensin II; loss of this precedes pre-eclampsia |
| Uterine blood flow | About 500–750 mL/min at term | Unregulated: falls if maternal pressure falls |
- Cardiac output rises further in labour (each contraction returns about 300–500 mL to the circulation) and peaks immediately after delivery, the most dangerous time for women with heart disease.
- The heart is pushed up and to the left: left axis deviation and an apparently large heart on X-ray. A soft ejection systolic murmur and a third heart sound are normal; diastolic murmurs are not.
- Aortocaval compression from about 20 weeks: lying supine, the uterus compresses the IVC, venous return and cardiac output fall, and the woman becomes pale, sweaty and hypotensive. Treatment: left lateral position or tilt.
- Oedema of the ankles: higher femoral venous pressure plus a lower plasma oncotic pressure (albumin falls to about 30 g/L).
Respiratory
- Progesterone sensitises the respiratory centre to CO2: tidal volume up 30–40%, minute ventilation up 40–50%, respiratory rate almost unchanged.
- PaCO2 falls to about 4 kPa (30 mmHg); kidneys excrete bicarbonate (18–22 mmol/L): compensated respiratory alkalosis with pH about 7.44. The steeper gradient helps fetal CO2 to cross to the mother.
- The diaphragm rises about 4 cm: functional residual capacity falls about 20% (expiratory reserve and residual volumes fall), while vital capacity, FEV1 and peak flow are unchanged.
- Oxygen consumption rises about 20%; with low FRC, a pregnant woman desaturates quickly during apnoea at induction of anaesthesia.
- Capillary engorgement of the airway makes intubation harder. Progesterone lowers lower oesophageal sphincter tone; with raised intragastric pressure and slow emptying in labour, this raises the risk of acid aspiration (rapid sequence induction).
Renal
| Variable | Change |
|---|---|
| Renal plasma flow | Up 50–80% |
| GFR | Up about 50% by the early second trimester |
| Creatinine and urea | Fall; a creatinine of 85 micromol/L (0.96 mg/dL) is abnormal in pregnancy |
| Uric acid | Falls by about a third (higher clearance); rises again in pre-eclampsia |
| Glucose | Glycosuria with normal blood glucose: filtered load exceeds tubular reabsorption |
| Plasma osmolality | Falls about 10 mOsm/kg (osmostat reset); sodium slightly low |
- Kidneys enlarge; pelvicalyceal and ureteric dilatation, right more than left (progesterone relaxes smooth muscle; the uterus compresses the right ureter at the pelvic brim; the sigmoid cushions the left). Urinary stasis favours pyelonephritis.
- High aldosterone does not cause hypokalaemia because progesterone blocks the mineralocorticoid receptor.
Haematological
- Hypercoagulable state: fibrinogen, factors VII, VIII, X and von Willebrand factor rise; protein S falls; fibrinolysis is reduced (placental plasminogen activator inhibitor). With venous stasis and delivery trauma, thrombosis risk is highest after delivery.
- White cells rise (neutrophilia up to about 15 x 10^9/L, more in labour); ESR rises.
- Platelets fall slightly; gestational thrombocytopenia is mild, late, asymptomatic and benign.
- Iron: about 1,000 mg extra is needed; the largest share expands the maternal red cell mass, the rest goes to fetus and placenta and to losses. Iron absorption increases.
Metabolic and gastrointestinal
- Weight gain about 12 kg; basal metabolic rate up about 15–20%.
- First half anabolic (fat storage); second half insulin resistant with accelerated starvation (details in the adrenal and insulin chapter).
- Triglycerides rise 2–3 times: oestrogen increases hepatic VLDL production and adipose lipoprotein lipase activity falls. Women with familial hypertriglyceridaemia may develop pancreatitis.
- Albumin falls; alkaline phosphatase rises (placental isoenzyme); transaminases and bilirubin stay normal, so a rise is abnormal.
- Intrahepatic cholestasis: oestrogen and progesterone metabolites impair bile acid export; commoner with twins (more placental steroid).
- Progesterone relaxes gut and gallbladder smooth muscle: constipation, heartburn, biliary sludge and stones.
- Total body water rises by several litres; binding proteins (TBG, CBG, SHBG) rise under oestrogen.
Remember In pregnancy: volume up, output up, resistance down, PaCO2 down, GFR up, clotting up.
Exam trap A "normal" non-pregnant creatinine or PaCO2 is abnormal in pregnancy.
Exam trap Vital capacity does not change in pregnancy; the functional residual capacity falls.
Test yourself on this topic
5 of the 19 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
In normal pregnancy, plasma renin activity and aldosterone rise several-fold, yet women do not become hypokalaemic or hypertensive. Which hormone competes with aldosterone at the renal mineralocorticoid receptor?
Answer: Progesterone
Progesterone binds the mineralocorticoid receptor in the distal nephron and acts as an antagonist, promoting natriuresis. This natriuretic tendency, together with the fall in vascular resistance, stimulates the renin–angiotensin–aldosterone system. The high aldosterone balances progesterone's effect so that sodium is retained overall, supporting plasma volume expansion without potassium loss. Cortisol also binds the receptor but is normally inactivated in the kidney by 11β-HSD2.
RAAS in pregnancy
- Renin and aldosterone rise
- Progesterone blocks the MR
- Net sodium retention
- No hypokalaemia
Remember Progesterone is a natural anti-aldosterone.
Exam trap High aldosterone in pregnancy is physiological and does not mean primary hyperaldosteronism.
Why the other options are wrong
- Oestradiol Tends to retain sodium; not an aldosterone antagonist.
- Human placental lactogen Metabolic hormone; no mineralocorticoid action.
- Relaxin Causes vasodilatation; does not block the receptor.
- Cortisol Inactivated by renal 11β-HSD2 and an agonist if not.
At 36 weeks, a normotensive woman has pitting ankle oedema by evening. Urine shows no protein, and her serum albumin is 30 g/L, lower than before pregnancy. Apart from raised femoral venous pressure from the uterus, which change favours fluid moving into her tissues?
Answer: Fall in plasma oncotic pressure
Plasma volume expands by about 40–50% in pregnancy, and albumin synthesis does not keep pace, so serum albumin falls by about 10 g/L. Albumin generates most of the plasma colloid oncotic pressure, which holds fluid in capillaries. A lower oncotic pressure, together with raised venous pressure in the legs from uterine compression of the iliac veins and IVC, shifts the Starling balance toward filtration. Physiological oedema is therefore common, but oedema with hypertension or proteinuria needs assessment for pre-eclampsia.
Physiological oedema
- Plasma volume up 40–50%
- Albumin falls by dilution
- Oncotic pressure falls
- Plus raised leg venous pressure
Remember Dilute albumin, leaky ankles.
Exam trap Oedema alone is common in pregnancy; with hypertension or proteinuria it is not.
Why the other options are wrong
- Rise in capillary permeability Increased permeability is a feature of pre-eclampsia, not normal pregnancy.
- Lymphatic obstruction by the uterus The uterus compresses veins, not lymphatics, to cause this.
- Rise in interstitial oncotic pressure Not the normal change.
- Raised arterial blood pressure Her blood pressure is normal; arterial pressure falls in mid-pregnancy.
A woman in a village clinic is told she needs about 1000 mg of extra iron over a singleton pregnancy. Which single use accounts for the largest share of this?
Answer: Expansion of maternal red cell mass
Maternal red cell mass rises by about 25–30% in pregnancy, needing roughly 450–500 mg of iron. The fetus and placenta take about 300 mg, and basal losses add around 200 mg, while menstrual losses stop. Blood loss at delivery is partly offset by iron returned from the red cells as the red cell mass falls afterwards. Demand is greatest in the second half of pregnancy, when absorption also increases.
Iron in pregnancy
- Red cell mass: about 500 mg
- Fetus and placenta: about 300 mg
- Basal losses: about 200 mg
- Total about 1000 mg
Remember The mother's own new red cells need the most iron.
Exam trap Plasma volume rises more than red cell mass, but the red cells, not the plasma, use iron.
Why the other options are wrong
- Iron stored in the fetus and placenta About 300 mg, less than the red cell increase.
- Blood lost at delivery Partly offset by post-delivery fall in red cell mass.
- Ongoing basal losses from gut and skin About 200 mg over pregnancy.
- Iron secreted into amniotic fluid Negligible.
A woman carrying twins develops generalised itching, worst on her hands and feet, in the third trimester. Liver tests show high bile acids, and everything returns to normal within a week of delivery. Why is she, with twins, especially prone to this?
Answer: More sex steroids impair bile export
Intrahepatic cholestasis of pregnancy occurs when the high levels of oestrogen and progesterone metabolites in late pregnancy impair canalicular transport of bile acids, mainly through the bile salt export pump, in genetically susceptible women. Bile acids accumulate in blood, causing itching, and the condition resolves rapidly once the placenta is delivered. It is more common in twin pregnancy, when hormone levels are higher. High bile acids are linked to fetal risks such as preterm birth and stillbirth.
Cholestasis of pregnancy
- Itching of palms and soles
- Raised bile acids
- Sex steroids impair bile salt export
- Resolves after delivery
Remember Itchy palms in late pregnancy: check bile acids.
Exam trap The itching has no rash; a rash points to a skin disease of pregnancy instead.
Why the other options are wrong
- Autoimmune destruction of bile ducts Primary biliary cholangitis; does not resolve after delivery.
- Gallstones obstructing the bile duct Causes pain and obstructive jaundice.
- Fatty infiltration of hepatocytes Acute fatty liver of pregnancy; the woman is unwell.
- Haemolysis with liver enzyme rise HELLP syndrome; causes low platelets and haemolysis.
A woman at 34 weeks has a thrombophilia screen after a family member's DVT. Fibrinogen, factor VIII and von Willebrand factor are all raised. Which other result is a normal physiological change of late pregnancy?
Answer: Reduced free protein S
Pregnancy is a hypercoagulable state that prepares the mother for placental separation. Fibrinogen, factors VII, VIII, X and von Willebrand factor rise, while free protein S falls and fibrinolysis is reduced, partly by placental plasminogen activator inhibitor type 2. Antithrombin and protein C are largely unchanged. A low protein S in late pregnancy should not be labelled protein S deficiency without retesting after delivery.
Clotting in pregnancy
- Up: fibrinogen, VII, VIII, X, vWF
- Down: free protein S
- Fibrinolysis reduced (PAI-2)
- Antithrombin and protein C unchanged
Remember Pregnancy tilts the balance toward clotting.
Exam trap Do not diagnose protein S deficiency during pregnancy; the level falls normally.
Why the other options are wrong
- Raised antithrombin Antithrombin is largely unchanged.
- Platelets below 50 × 10⁹/L Platelets may fall mildly, but not this low.
- Increased fibrinolytic activity Fibrinolysis is reduced.
- Reduced factor VII Factor VII rises.
Where this sits in the CPSP syllabus
- Obstetrics & Gynaecology, Paper 2: Reproduction, pregnancy and labour, Maternal adaptation to pregnancy: cardiovascular, respiratory, renal, haematological and metabolic
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