TABLE 3.

Physiological changes of pregnancy that make pregnant women more susceptible to infection 2 (Soma-Pillay et al., 2016; Förger and Villiger, 2020).

Respiratory	• Increase in oxygen demand due to ∼15% increase in the metabolic rate and ∼20% increased consumption of oxygen. • 40–50% increase in minute ventilation due to an increase in tidal volume. • Arterial pO2 increases and arterial pCO2 decreases with a compensatory reduction in serum bicarbonate concentrations to 18–22 mmol/l. • Mild fully compensated respiratory alkalosis, arterial pH 7.4. • Decreased functional residual capacity. • Inspiratory reserve volume is reduced during early pregnancy, but increases in the third trimester, as a result of reduced functional residual capacity. • Subjective feeling of breathlessness without hypoxia.
Cardiovascular	• Cardiac output increases ∼20% by 8 weeks gestation mostly due to peripheral vasodilation which is mediated by endothelium-dependent factors. • A total of 25–30% fall in systemic vascular resistance in the first trimester, but increases to 40% by 20–28 weeks gestation. • Increase in stroke volume which is possibly due to the early increase in ventricular wall muscle mass and end-diastolic volume. • Heart is physiologically dilated, and myocardial contractility is increased. • Blood pressure decreases in the first and second trimesters but increases to pre-pregnancy levels in the third trimester. • Pulmonary vascular resistance (PVR) decreases significantly. • Serum colloid osmotic pressure is reduced by 10–15%. The colloid osmotic pressure/pulmonary capillary wedge pressure gradient is reduced by about 30%, making pregnant women particularly susceptible to pulmonary edema. • Changes may include a bounding or collapsing pulse and an ejection systolic murmur in ∼90% of pregnant women.
Immune	• A pro-inflammatory microenvironment which is crucial for normal implantation and parturition. • Monocyte activity in peripheral blood is higher during pregnancy than post-partum, and a tolerogenic subset of innate cells is at work in the placenta during pregnancy. • A downregulation of effector T cell activity and an expansion of regulatory T cells after delivery, the immunomodulatory effects mediated by fetal antigens and pregnancy hormones disappear, giving rise to T cell activity and persisting monocyte activity.