Pregnancy is associated with several maternal physiological adaptations that both assist foetal survival as well as aiding the mother to meet the demands of pregnancy and prepare for labour.
Cardiovascular system changes
The increase in progesterone levels that occurs during pregnancy results in a fall in systemic vascular resistance. This, in turn, results in a decrease in diastolic blood pressure during the first and second trimesters of pregnancy.
In response to this, there is a steady increase in cardiac output. The cardiac output increases by 20% by week 8 and then up to 40% by weeks 20-28. There is an increase in both stroke volume and heart rate to achieve increased cardiac output. The heart rate increases on average by approximately 10-20 beats per minute.
Pregnancy also results in the activation of the renin-angiotensin-aldosterone system, which result in an increase in sodium levels, water retention, and an increase in total blood volume.
Venous return in the inferior vena cava can be compromised in late pregnancy if a woman lies flat on her back due to pressure from the uterus, resulting in reduced stroke volume and cardiac output. This can be relieved by lying the mother in the left lateral position.
The following cardiovascular examination findings are commonly found in pregnancy
- A bounding or collapsing pulse
- A third heart sound (from mid-pregnancy onwards)
- Systolic flow murmurs are common
The following ECG changes are considered normal in pregnancy:
Left axis deviation
- Small Q waves and inverted T wave in lead III
- ST depression and inversion or flattening of the T wave in inferior and lateral leads
- Atrial and ventricular ectopics
Respiratory system changes
The metabolic rate and oxygen consumption of pregnant women increase during pregnancy, and this, in turn, results in increased oxygen demand. There is an accompanying increase in the tidal volume and the minute ventilation rate that help the mother meet these oxygen demands.
A state of compensated respiratory alkalosis usually occurs, with a fall in arterial pCO2 and a rise in arterial pO2. This is accompanied by a decrease in bicarbonate levels that prevents any change in pH. The resultant lower maternal pCO2 also facilitates oxygen/carbon dioxide transfer to and from the foetus. This is thought to be, at least partly, driven by maternal hyperventilation caused by progesterone driven increased respiratory drive.
Anatomically, as the foetus grows throughout pregnancy, there is an upward causes displacement of the diaphragm. Total lung capacity, however, does not decrease significantly due to a compensatory increase in the transverse and anterior-posterior diameters of the thorax. Some splinting of the diaphragm with a reduction in tidal volume can occur in the later stages of pregnancy, though.
Gastrointestinal system changes
The increase in progesterone levels during pregnancy causes smooth muscle relaxation, which decreases gut motility. This increases transit time allowing for more time for nutrient absorption but can also result in constipation. Relaxation of the gallbladder also occurs secondary to increased levels of progesterone. Because of this, the gallbladder can consequently dilate and empty less completely, predisposing the mother to gallstones.
Several anatomical changes to the gastrointestinal tract occur secondary to the growth of the uterus. As the uterus grows, the stomach is displaced upwards. This increases intragastric pressure, predisposing the mother to gastrointestinal reflux, as well as nausea and vomiting. In addition, increased progesterone levels result in relaxation of the lower oesophageal sphincter, which further increases the risk of gastro-oesophageal reflux.
The growth of the uterus may also displace the appendix into the right upper quadrant of the abdomen.
Endocrine system changes
Profound changes occur in the mother’s endocrine system during pregnancy. Progesterone and oestrogen levels rise throughout pregnancy, oestrogen produced by the placenta and progesterone produced by the corpus luteum, and later on by the placenta.
The increase in oestrogen levels causes an increase in the hepatic production of thyroid-binding globulin (TBG). Consequently, there is an increase in the binding of free T3 and T4 to TBG, which, in turn, causes more thyroid-stimulating hormone to be released from the anterior pituitary gland. Therefore, free T3 and T4 levels remain unchanged overall, but there is an absolute rise in total T3 and T4 levels. Thyroxine is essential for foetal neural development, but the foetal thyroid gland is not functional until the second trimester of gestation. Therefore, the elevated maternal total T3 and T4 levels ensure a constant supply of thyroxine to the foetus early in pregnancy.
During the second trimester of pregnancy, there is also an increase in human placental lactogen, prolactin and cortisol levels.
These hormones have an anti-insulin effect, which results in insulin resistance in the mother and reduces the peripheral uptake of glucose. This ensures a continuous supply of glucose for the foetus but predisposes the mother to the development of gestational diabetes.
Lipids provide an alternative source of energy for the mother via lipolysis. This, however, results in increased levels of free fatty acids in the plasma, which can result in ketogenesis. Because of this, pregnancy is associated with an increased risk of ketoacidosis.
Urinary system changes
During pregnancy, the increase in blood volume and cardiac output causes an increase in renal plasma flow, which results in a 50-60% increase in glomerular filtration rate (GFR). This causes an increase in renal excretion and consequent reduction in blood levels of urea, creatinine, urate and bicarbonate.
Mild glycosuria and/or proteinuria may also occur because the increase in GFR may exceed the ability of the renal tubules to reabsorb glucose and protein. In addition, increased water retention causes a reduction of plasma osmolality.
The increased progesterone levels cause the smooth muscle of the renal pelvis and ureter to become relaxed and dilated, kidneys increase in length, and ureters become longer, more curved and with an increase in residual urine volume. It also causes relaxation of the muscles of the bladder. These changes result in urinary stasis, which increases the risk of urinary tract infection during pregnancy.
Throughout pregnancy, there is an approximate 50% increase in plasma volume, which results in dilutional anaemia. Erythropoietin levels rise, increasing the total red cell mass by the end of the second trimester, but haemoglobin concentrations are never restored to pre-pregnancy levels.
A normal pregnancy creates a demand for about 1000 mg of additional iron. This equates to 60 mg elemental iron or 300 mg ferrous sulfate per day. Serum iron falls during pregnancy, while transferrin and total iron-binding capacity rise.
Levels of some clotting factors (VII, VIII, IX and X) and fibrinogen increase while fibrinolytic activity decreases. Also, due to an increase in progesterone levels, stasis of blood and venodilation occurs. The combination of these changes are protective against haemorrhage at delivery but also make pregnancy a hypercoagulable state with an increased risk of thromboembolism. Warfarin cannot be given to pregnant women to counteract this as it is teratogenic. Therefore, low molecular weight heparin (LMWH) is usually the anticoagulant of choice during pregnancy if administration of one is required.
The basal metabolic rate increases slowly throughout pregnancy, to a maximum of around 15-20%. It is thought that the overall energy requirement does not increase significantly during the first or second trimesters but increases by approximately 200 kcal per day in the third trimester.
The recommended normal weight gain in pregnancy is 11.4 to 15.9 kg for a woman of normal body mass index (BMI). The foetus placenta, membranes and amniotic fluid account for around 5 kg of this, and the remainder is maternal stores of fat and protein and increased intra- and extra-vascular volume. Weight is no longer monitored in pregnancy as it does not affect the outcome and is affected by several factors.
Hyperpigmentation of the umbilicus, nipples, abdominal midline (linea nigra) and face (melasma or chloasma) are common during pregnancy and relate to the hormonal changes that occur.
The hyperdynamic circulation and high levels of oestrogen can cause spider naevi and palmar erythema. Striae gravidarum (‘stretch marks’) are also common.
Increased ligamental laxity caused by increased levels of relaxin contributes to back pain and pubic symphysis dysfunction. A shift in posture with exaggerated lumbar lordosis results in the typical gait that is commonly seen in 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
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Thank you to the joint editorial team of www.mrcgpexamprep.co.uk for this article.