Normal pulmonary physiological changes
Hormonal changes in pregnancy produce hyperaemia and oedema of the upper airway, resulting in symptoms of rhinitis. Placental growth hormone and oestrogens are likely to be responsible for many of these effects (1).
These changes will have implications for endotracheal intubation and other upper airway interventions, increasing the risk of the procedures and necessitating smaller endotracheal tubes. The thoracic cage is altered both by the enlarging uterus and hormonal effects producing ligamentous laxity. The diaphragm is elevated by up to 4 cm, but an increase in the anteroposterior and transverse diameters and widening of the subcostal angle help partially offset the loss of total lung capacity. Diaphragmatic function remains normal and diaphragmatic excursion is not reduced.Although total lung capacity is only minimally decreased, the changes in the chest wall produce a progressive decrease in functional residual capacity (FRC) by 10-25% by term (2). FRC is made up of the residual volume and the expiratory reserve volume, both of which demonstrate a decrease (2). These changes can be measured as early as 16-24 weeks of gestation and progress to term. Vital capacity remains unchanged, and measurements of airflow and lung compliance are not affected by pregnancy. Measurements of air flow, such as the forced expiratory volume in 1 second (FEVi) are thus valuable in assessing dyspnoea during pregnancy. Chest wall and total respiratory compliance are reduced in the third trimester due to the chest wall changes and increased abdominal pressure.
The most striking respiratory physiological changes are the functional effects, namely an increase in respiratory drive mediated by progesterone (3). Minute ventilation increases markedly in pregnancy, produced mainly by an increase in tidal volume of approximately 30-35%. These effects begin in the first trimester and minute ventilation reaches 20-40% above baseline by term (Figure 25.1).
The respiratory rate is unchanged initially and rises only about 10% later in pregnancy. A respiratory alkalosis occurs with partial arterial pressure of carbon dioxide (Pac02) decreasing to 3.8-4.3 kPa (2832 mmHg), despite increased carbon dioxide production. Acidbase balance is compensated for by renal excretion of bicarbonate, with plasma bicarbonate falling to 18-21 mEq/L (4). Alveolar-to- arterial oxygen tension differences (PAO2 - PaO2) are not changed by pregnancy, and mean PaO2 usually exceeds 13 kPa (100 mmHg) throughout pregnancy (at sea level). An increased alveolar-arterial gradient may develop in the supine position because of airway closure, as FRC diminishes near term. Oxygen consumption increases by 20-33% in pregnancy, due to both maternal and fetal metabolic demands. The combination of a reduction in FRC and an increase in oxygen consumption makes the pregnant patient susceptible to the rapid development of hypoxia in response to apnoea (5).During labour, pain and anxiety may produce hyperventilation resulting in marked respiratory alkalosis, which may be aggravated by volume depletion and/or vomiting. Alkalosis adversely affects uterine blood flow and therefore fetal oxygenation. In some patients, mild hypoxaemia may result from severe pain and anxiety producing rapid, shallow breathing with alveolar hypoventilation, and atelectasis. Pain relief with narcotics or epidural analgesia blunts this ventilatory response and can correct these gas exchange abnormalities associated with active labour.
More on the topic Normal pulmonary physiological changes:
- Normal pulmonary physiological changes
- Arulkumaran S., Ledger W., Denny L., Doumouchtsis S. (eds.). Oxford Textbook of Obstetrics and Gynaecology. Oxford University Press,2020. — 928 p., 2020
- Physiological changes to thekidney during healthy pregnancy
- REFERENCES
- Acute Abdominal Pain in Pregnancy
- Cardiopulmonary Resuscitation
- Obstetric Anaesthesia in Multiple Pregnancy
- Immunodeficiency
- Antiphospholipid syndrome in obstetrics
- Indications