The respiratory system

Tidal volume rises by ~30% in early pregnancy to 40-50% above non-pregnant values by term, with a fall in expiratory reserve and residual volume (Fig. 2.3) [6]. Neither FEV1 nor peak expiratory flow rate are affected by pregnancy, even in women with asthma. The rise in tidal volume is largely driven by progesterone, which appears to decrease the threshold and increase the sensitivity of the medulla oblongata to carbon dioxide. Respiratory rate does not change, so the minute ventilation rises by a similar amount. This overbreathing also begins before conception; the PC02 is lowest in early gestation. Progesterone also increases erythrocyte [carbonic anhydrase], which will also lower PC02. Carbon dioxide production rises sharply during the third trimester, as fetal metabolism increases. The fall in maternal PC02 allows more efficient placental transfer of carbon dioxide from the fetus, which has a PC02 of around 55 mmHg (7.3 kPa). The fall in Pco2 results in a fall in plasma bicarbonate concentration (to ~ 18-22 mmol/l by comparison with 24-28 mmol/l) which contributes to the fall in plasma osmolality; the peripheral venous pH rises slightly (Table 2.2; Fig. 2.4).

The increased alveolar ventilation results in a much smaller proportional rise in P02, from around 96.7 to 101.8 mmHg (12.9-13.6 kPa). This increase is offset by the rightward shift of the maternal oxy-haemoglobin dissociation curve caused by an increase in 2,3-diphosphoglycerate (2,3-DPG) in the erythrocytes. This facilitates oxygen unloading to the fetus, which has both a much lower P02 (25-30 mmHg; 3.3-4.0 kPa) and a marked leftwards shift of the oxyhaemoglobin dissociation curve, due to the lower sensitivity of fetal haemoglobin to 2,3-DPG.

There is an increase of ~16% in oxygen consumption by term, due to increasing maternal and fetal demands. Since the increase in oxygen-carrying capacity of the blood (see 'Haematology', p. 12) is ~18%, there is actually a

Vital Tidal Inspiratory capacity volume capacity

Non-pregnant Pregnant

Functional residual capacity

Vital Tidal Inspiratory capacity volume capacity

Functional residual capacity

Functional Residual Capacity

Non-pregnant Pregnant

Fig. 2.3 Alterations in lung volumes associated with normal human pregnancy. In general terms, inspiratory reserve and tidal volumes increase at the expense of expiratory reserve and residual volumes.

Table 2.2 The influence of pregnancy on some respiratory variables

Non-pregnant Pregnant - term

O2 consumption ml/min 200 250

Venous pH 7.35 7.38

Table 2.3 Although the increases in resting cardiac output and minute ventilation are of the same order of magnitude in pregnancy, there is less spare capacity for increases in cardiac output on moderate exercise than for increases in respiration



Cardiac output

Minute +40% 7.5-10.5 l/min +1000% (up to ~80 l/min) ventilation



Chemoreceptor sensitization


[hco3 jr

Plasma osmolality]

Fig. 2.4 Flow chart of the effects of over-breathing. HCO3, bicarbonate; Na, sodium; Pc02, carbon dioxide tension; PROG, progesterone.

fall in arterio-venous oxygen difference. Pulmonary blood flow, of course, rises in parallel with cardiac output and enhances gas transfer.

Pregnancy places greater demands on the cardiovascular than the respiratory system [7]. This is shown in the response to moderate exercise (Table 2.3).

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