Pregnancy is a period of profound physiological transformation. The mother’s body undergoes wide-ranging adaptations across virtually all organ systems, designed to support foetal growth, prepare for labour, and safeguard maternal well-being. These changes are primarily mediated by hormonal influences, particularly progesterone and oestrogen, and evolve as pregnancy progresses.
Cardiovascular system changes
From early pregnancy, rising progesterone levels cause a decrease in systemic vascular resistance, leading to a fall in diastolic blood pressure. This is most noticeable during the first and second trimesters. In compensation, the cardiovascular system increases cardiac output — a change that begins by week 8 and peaks between weeks 20 and 28, with a rise of up to 40%. This is achieved through increases in both stroke volume and heart rate, the latter typically climbing by 10 to 20 beats per minute.
Pregnancy also activates the renin–angiotensin–aldosterone system, contributing to sodium retention, plasma volume expansion, and overall fluid accumulation. The increased blood volume supports uteroplacental perfusion and cushions against the haemodynamic stresses of labour.
In late pregnancy, the enlarged uterus may compress the inferior vena cava when the woman is supine, leading to reduced venous return and hypotension — a condition that can be relieved by adopting the left lateral position.
Common cardiovascular findings on examination include a bounding or collapsing pulse, the presence of a third heart sound, and systolic flow murmurs. Normal ECG changes in pregnancy include left axis deviation, small Q waves with T wave inversion in lead III, nonspecific ST changes, and occasional atrial or ventricular ectopics.
Respiratory system changes
Pregnancy increases maternal metabolic demand and oxygen consumption, prompting physiological respiratory changes to maintain adequate gas exchange. Tidal volume and minute ventilation both rise, largely due to progesterone-driven stimulation of the respiratory centre. The result is a state of compensated respiratory alkalosis, characterised by reduced arterial pCO₂, elevated pO₂, and a mild fall in serum bicarbonate — changes that optimise placental gas transfer.
Anatomical shifts also occur: the diaphragm is elevated by the growing uterus, yet total lung capacity is preserved thanks to compensatory widening of the thoracic cavity. In the final weeks, diaphragmatic splinting may slightly reduce tidal volume.
Gastrointestinal system changes
Progesterone-induced smooth muscle relaxation slows gastrointestinal motility, extending transit time to enhance nutrient absorption but often resulting in constipation. The gallbladder also becomes hypomotile, predisposing to gallstone formation.
Anatomically, the expanding uterus displaces the stomach upwards and increases intra-abdominal pressure. Coupled with reduced lower oesophageal sphincter tone, this frequently leads to gastro-oesophageal reflux, nausea, and vomiting. The appendix may shift upwards, complicating diagnosis of appendicitis in later pregnancy.
Endocrine system changes
The maternal endocrine system undergoes major alterations. Progesterone and oestrogen levels rise steadily, initially produced by the corpus luteum and later by the placenta. Elevated oestrogen stimulates hepatic production of thyroid-binding globulin (TBG), increasing total but not free levels of T3 and T4. To maintain equilibrium, thyroid-stimulating hormone (TSH) secretion also increases. These changes ensure an adequate supply of maternal thyroxine to the foetus, which is essential until the foetal thyroid becomes functional in the second trimester.
The second trimester also brings rising levels of cortisol, human placental lactogen (hPL), and prolactin. These hormones exert insulin-antagonistic effects, promoting maternal insulin resistance. This physiological adaptation ensures a steady glucose supply to the foetus but may predispose the mother to gestational diabetes.
As maternal glucose utilisation decreases, lipolysis increases, raising plasma free fatty acid concentrations and the risk of ketogenesis. For this reason, pregnancy is a state more prone to ketoacidosis, especially in poorly controlled diabetes.
Renal and urinary system changes
Renal plasma flow and glomerular filtration rate (GFR) increase by up to 60% during pregnancy. This enhances renal clearance and typically lowers serum levels of urea, creatinine, and urate. Mild glycosuria or proteinuria may occur due to tubular reabsorption thresholds being exceeded.
Progesterone-induced smooth muscle relaxation affects the ureters and renal pelvis, causing dilatation and urinary stasis, which heightens the risk of urinary tract infections. The kidneys enlarge slightly, and ureters become more tortuous. Additionally, plasma osmolality falls due to fluid retention.
Haematological changes
Plasma volume expands by approximately 50%, while red cell mass increases more modestly, resulting in physiological (dilutional) anaemia. Erythropoietin levels rise, but haemoglobin levels remain lower than pre-pregnancy norms.
Iron requirements increase significantly, with around 1000 mg needed over the course of the pregnancy. While serum iron levels fall, transferrin and total iron-binding capacity increase to maintain supply.
Pregnancy induces a hypercoagulable state. Levels of clotting factors VII, VIII, IX, X and fibrinogen increase, while fibrinolysis decreases. These changes protect against haemorrhage but also raise the risk of thromboembolism. Because warfarin is teratogenic, low molecular weight heparin (LMWH) is the preferred anticoagulant during pregnancy when indicated.
Metabolic changes
The basal metabolic rate gradually rises by about 15–20% across pregnancy. Although energy demands remain fairly stable during the first two trimesters, they increase by an estimated 200 kcal per day in the third trimester.
Recommended total weight gain varies with pre-pregnancy BMI, but for women with a normal BMI, a gain of 11.4 to 15.9 kg is typical. Approximately 5 kg of this is attributable to the foetus, placenta, and amniotic fluid; the remainder consists of maternal tissue growth and fluid expansion. Routine weight monitoring is no longer a standard part of antenatal care, as it has limited predictive value for outcomes.
Dermatological changes
Hormonal shifts, particularly increases in melanocyte-stimulating hormone, contribute to hyperpigmentation, including linea nigra, darkening of the nipples, and facial melasma (chloasma). Spider naevi and palmar erythema may also appear, related to increased oestrogen levels and hyperdynamic circulation. Striae gravidarum (stretch marks) commonly develop due to dermal stretching and hormonal influences.
Musculoskeletal and postural changes
Pregnancy-related ligamentous laxity, driven by relaxin, enhances pelvic flexibility but may contribute to back pain and symphysis pubis dysfunction. As the uterus enlarges, the mother’s centre of gravity shifts, often producing lumbar lordosis and an altered gait — the characteristic “waddle” of late pregnancy.
Interpreting blood results in pregnancy
As a result of the wide-ranging physiological changes that occur during pregnancy, the following changes in normal blood results should be expected:
| Trend in normal pregnancy | Pregnancy normal values* | Abnormalities and possible interpretations | |
|---|---|---|---|
| Haemoglobin | Decreased | 10.5-13.5 g/dL | Consider dilutional anaemia of pregnancy |
| White cell count | Increased | 8-18 x 109/L | Can make infection more difficult to diagnose |
| Platelets | Unchanged/slightly increased | 200-600 x 109/L | Platelet levels can also fall and thrombocytopaenia in pregnancy is diagnosed when platelet count falls below 100 x 109/L |
| Sodium | Slightly decreased | 132-140 mmol/L | Always consider in the light of the patient’s clinical status |
| Potassium | Slightly decreased | 3.2-4.6 mmol/L | Always consider in the light of the patient’s clinical status |
| Urea | Decreased | 1.0-3.8 mmol/L | Increased in dehydration, hyperemesis, late stages of pre-eclampsia and renal impairment |
| Creatinine | Decreased | 40 – 80 μmol/L | Increased in renal impairment and the late stages of pre-eclampsia |
| Fasting glucose | Unchanged | 3.0-5.0 mmol/L | Increased in gestational diabetes |
| Total calcium | Decreased | 2.0-2.4 mmol/L | Total serum calcium decreased (due to reduced serum albumin secondary to haemodilution) but ionised calcium unchanged in pregnancy |
| Albumin | Decreased | 24-31 g/L | Decreased further if there is malnutrition, recurrent vomiting or hyperemesis gravidarum |
| Bilirubin | Decreased | 3-14 μmol/L | Increased in obstetric cholestasis, HELLP syndrome, the late stages of pre-eclampsia, acute fatty liver, viral hepatitis |
| TSH | Slight decrease in the first trimester, normal in the second trimester, slightly raised in the last trimester | 0.1-4.0 IU/L | Less than 0.05 in Graves’ disease or hyperemesis gravidarum |
| fT4 | Unchanged | 10-25 pmol/L | Increased in Graves’ disease or hyperemesis gravidarum |
| fT3 | Unchanged | 3.5-6 pmol/L | Increased in Graves’ disease or hyperemesis gravidarum |
*Local laboratory reference ranges should always be used
Header image used on licence from Shutterstock
Thank you to the joint editorial team of www.mrcgpexamprep.co.uk for this article.
