Chapter 82 – Maternal Physiology during Pregnancy


It comes as no surprise that there are major endocrine changes during pregnancy. These endocrine changes are the driving force for many of the other physiological and anatomical changes associated with pregnancy.

Chapter 82 Maternal Physiology during Pregnancy

How does endocrine function alter during pregnancy?

It comes as no surprise that there are major endocrine changes during pregnancy. These endocrine changes are the driving force for many of the other physiological and anatomical changes associated with pregnancy.

The main hormones involved are:

  • β-human chorionic gonadotropin (β-hCG), a glycoprotein hormone with a structure similar to that of luteinising hormone, follicle-stimulating hormone and thyroid-stimulating hormone (TSH). It is secreted by the placenta shortly after implantation of the embryo and can be detected in the maternal circulation from the second week of pregnancy. β-hCG levels rise rapidly, doubling every 2 days until a peak is reached at 10 weeks’ gestation. Its main role is to prolong the life of the corpus luteum:

    1. In the second half of the menstrual cycle, the corpus luteum secretes progesterone and a small amount of oestrogen.

    2. After 14 days, in the absence of an implanted embryo, progesterone secretion stops and the corpus luteum degenerates into the corpus albicans. The decline in progesterone triggers sloughing of the uterine lining (the endometrium).

    3. If an embryo implants in the endometrium (or fallopian tube in the case of an ectopic pregnancy), the syncytiotrophoblast cells of the newly formed placenta produce progressively increasing amounts of β-hCG, which stimulates the corpus luteum to continue secreting progesterone. This prevents sloughing of the endometrium, which would cause miscarriage.

    4. After 10 weeks’ gestation, the placenta slowly takes over oestrogen and progesterone synthesis from the corpus luteum. β-hCG concentration then falls and the corpus luteum degenerates.

    β-hCG is also thought to be involved in suppressing the maternal immune response, protecting the placenta and embryo from immune destruction.

  • Human placental lactogen (hPL), a polypeptide hormone whose structure is similar to that of growth hormone. Like β-hCG, hPL is secreted by the syncytiotrophoblast cells of the placenta. Throughout pregnancy, hPL concentration increases in proportion to foetal and placental growth, peaking near term. Its function is to ensure adequate provision of nutrients for the growing foetus through manipulation of maternal metabolism:

    1. Increased maternal lipolysis increases the availability of free fatty acids.

    2. Decreased maternal peripheral insulin sensitivity results in decreased peripheral utilisation of glucose and thus increased maternal plasma glucose concentration. It is important that the foetus has access to ample glucose, as this is its primary source of energy. hPL is implicated in the development of gestational diabetes.

    3. Stimulation of breast growth and development. As the name suggests, hPL mimics the action of prolactin (PRL); whilst it has a much weaker effect than PRL, the high concentration of hPL is thought to be partly responsible for breast development during pregnancy.

  • Progesterone, a steroid hormone often referred to as the ‘pregnancy hormone’, reflecting its many important roles. Progesterone is secreted by the corpus luteum in early pregnancy and by the placenta in the second and third trimesters. The main functions of progesterone are:

    1. Preparing the endometrium for implantation and promoting growth of the endometrium following implantation;

    2. Uterine muscle relaxation, suppressing myometrial contractions and preventing miscarriage;

    3. Formation of a cervical mucus plug, thus protecting the developing foetus from ascending infection;

    4. Development of milk glands in preparation for lactation.

    In addition, progesterone is responsible for many of the other physiological changes associated with pregnancy, which are discussed in more detail below.

  • Oestrogen. Three oestrogens are synthesised by the placenta: oestradiol, oestrone and oestriol. Each oestrogen comes from a different precursor, and the amount of each oestrogen produced is proportional to the amount of each precursor delivered to the placenta. The main oestrogen produced in pregnancy is oestriol, whose main role is to increase uteroplacental blood flow (in contrast, oestradiol dominates the menstrual cycle). Importantly, oestriol is produced from a foetal adrenal precursor called dehydroepiandrosterone sulphate. Consequently, uteroplacental blood flow is under the control of the growing foetus. Other roles of oestrogens include:

    1. Stimulation of uterine growth;

    2. Sensitisation of the myometrium to oxytocin in preparation for labour.

    In addition, oestriol is responsible for the increased risk of thromboembolic disease associated with pregnancy.

Other pregnancy-related endocrine changes include:

  • Thyroid hormones. In pregnancy, oestriol stimulates the liver to synthesise additional thyroxine-binding globulin. Therefore, one might expect unbound triiodothyronine (T3) and thyroxine (T4) concentrations to decrease. However, thyrotropin-releasing hormone secretion increases as a result of the negative-feedback loop, which increases TSH secretion by the pituitary. Increased TSH stimulates the thyroid to secrete additional T3 and T4, bringing the free fractions of thyroid hormones back to normal.

  • PRL. Oestrogen stimulates a dramatic increase in the pituitary secretion of PRL, whose role is the preparation of the breasts for lactation. The pituitary gland doubles in size to accommodate the number of extra lactotrophs required. Because of the increased metabolic demands of the enlarged pituitary gland, it becomes vulnerable to ischaemia. Pituitary infarction can occur if the patient suffers prolonged hypotension, as may result from post-partum haemorrhage – this is known as Sheehan’s syndrome.

  • Parathyroid hormone (PTH). Ca2+ is transferred across the placenta to meet the requirements of the growing foetus. As maternal absorption of dietary Ca2+ cannot meet this placental loss, one might expect maternal ionised Ca2+ concentration to fall. However, the maternal parathyroid glands sense the fall in plasma Ca2+ and respond by increasing secretion of PTH. PTH increases plasma Ca2+ concentration by increasing bone resorption, renal tubular Ca2+ reabsorption and activation of vitamin D. Of clinical significance, pregnant patients at high thromboembolic risk, such as those with prosthetic heart valves, may be treated with low-molecular-weight heparin (LMWH). LMWH has the undesirable effect of worsening the PTH-related reduction in bone mineral density, potentially leading to osteopenia.

Which other physiological changes of pregnancy are of interest to anaesthetists?

This is best answered using a system-by-system approach:

Respiratory system. Changes to the respiratory system begin by as early as 4 weeks’ gestation, but the most significant changes occur from 20 weeks’ gestation:

  • Airway. Pregnancy-related capillary engorgement causes oedema of the oropharyngeal mucosa and larynx. In pre-eclampsia, the change in capillary dynamics can significantly worsen airway oedema.

  • Minute ventilation. From early pregnancy, progesterone stimulates the respiratory centre in the medulla:

    1. E increases by 50% at term: the increase in VT is substantially greater (40%) than that of respiratory rate (10%). E increases further in labour due to pain.

    2. Anatomical dead space increases due to bronchodilatation; that is, progesterone-induced smooth muscle relaxation.

    3. A mild reduction in PaCO2 (typically 4.3 kPa) due to progesterone-induced maternal hyperventilation. This mild respiratory alkalosis triggers a compensatory renal HCO3‾ loss (typical plasma HCO3‾ concentration is 20 mmol/L), which usually corrects the pH disturbance.

    This is of clinical significance when anaesthetising a pregnant patient: special attention should be paid to E. One should aim for a PaCO2 of ~4.3 kPa, which represents a normal value for pregnancy:

    1. The foetus cannot correct a pH disturbance by respiratory or renal compensation. Therefore, maternal respiratory acidosis can cause foetal acidosis.

    2. Likewise, maternal alkalosis should be avoided: the oxyhaemoglobin dissociation curve is shifted to the left, reducing O2 transfer to the foetus with the potential for foetal hypoxia.

  • Lung volumes. The gravid uterus causes an upwards displacement of the diaphragm and flaring of the lower ribs: the anterior–posterior diameter of the ribs increases by 2–3 cm. Diaphragmatic contraction is not restricted, but lung volumes are affected:

    1. Functional residual capacity (FRC) is reduced by 20% when standing and by a further 30% in the supine position. The reduction in FRC is mainly due to a reduction in residual volume.

    2. Vital capacity remains unchanged.

  • O2 consumption. The O2 requirements of the growing foetus result in a 20% increase in O2 consumption at term. O2 consumption is further increased during labour due to uterine contractions.

  • Respiratory compliance. Lung compliance is unaffected by pregnancy, but thoracic wall compliance is reduced by 20%. This is another consequence of the upward displacement of the diaphragm.

Sep 27, 2020 | Posted by in ANESTHESIA | Comments Off on Chapter 82 – Maternal Physiology during Pregnancy
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