Changes in maternal physiology during pregnancy

Cardiovascular and haematological changes begin as early as 4 weeks’gestation and are progressive. During pregnancy the plasma volume increases by 45%. This increase is mediated by a direct action of progesterone and oestrogen on the kidney causing the release of renin and thus an activation of the aldosterone renin-angiotensin mechanism. This leads to renal sodium retention and an increase in total body water. Through an increase in renal erythropoietin production, red cell mass increases by 20%. As the increase in red cell mass is relatively smaller than that of plasma volume, the haemoglobin falls from 150 g litre pre-pregnancy to 120 g litre during the third trimester (Fig. 1). This is termed the physiological anaemia of pregnancy. At two weeks’ post partum, the blood volume has returned to pre-pregnancy levels. The increased circulating volume offers protection for mother and fetus from the effects of haemorrhage at delivery but it can delay the onset of the classical signs and symptoms of hypovolaemia. The white cell count rises throughout pregnancy and peaks after delivery, making diagnosis of infection more difficult. Increased levels of circulating oestrogen and progesterone cause vasodilatation and a consequent fall in peripheral vascular resistance by 20%. As a result, systolic and diastolic blood pressure fall and there is a reflex increase in heart rate of 25%. Stroke volume is increased by 25% and together with that in heart rate, increases cardiac output by 50% by the third trimester. During labour, cardiac output may increase by up to a further 45%. Left ventricular hypertrophy and dilatation facilitate this change in cardiac output but contractility remains unchanged. The enlarging uterus can compress both the inferior vena cava and descending aorta in the supine position. Compression of the vena cava reduces venous return and results in decreased cardiac output, blood pressure and hence placental perfusion. Compression of the descending aorta also leads to a reduction in uterine blood flow. This may cause fetal distress. Aortocaval compression typically occurs after 20 weeks’ gestation but must be considered as a cause of maternal hypotension from the end of the first trimester onwards. To compensate for the effects of aortocaval compression, there is firstly an increase in sympathetic tone causing vasoconstriction and tachycardia. Secondly, Changes in maternal physiology during pregnancy