Physiological transition
Cardiovascular
During pregnancy, a woman's cardiac output increases by up to 40% with the maximum increase attained by the beginning of the third trimester. This is brought about by an increase in stroke volume and heart rate, and there is an accompanying increase in left ventricular wall thickness and end-diastolic chamber size.
Accompanying this change is an increase in the maternal blood volume and relative dilutional anaemia as the plasma volume expands by almost 50% while the red cell volume increases by only about 20%. During labour, the cardiac output increases to levels approximately 50% greater than those prior to labour as a result of higher heart rate and stroke volume. By late pregnancy, the uterine blood flow increases to almost 700 mL/minute, accounting for about 12% of total cardiac output (11). With delivery, the uterus empties and contracts, increasing resistance and markedly reducing its blood flow and thus diverting the additional blood volume into the general circulation. Maternal cardiac output remains elevated for about 24 hours after birth, then falls steadily over 1-2 weeks (12). Blood pressure tends to fall for about 2 days after delivery then return to levels found at the end of pregnancy. Pregnancy-related changes in stroke volume, heart rate, and thus cardiac output return to prepregnancy levels by about 6 weeks (13). The increased plasma volume falls rapidly with studies suggesting a reduction of between 10% and 20% within a day of birth, partly as a result of diuresis, and partly from either bleeding or accumulation of peripheral oedema. The red cell mass falls quite quickly after birth, perhaps to non-pregnant levels within 1 or 2 days (1). The fall in plasma volume takes longer, leading to a physiological haemodilution. Accompanying these changes is a transient fall in haemoglobin concentration, reaching a nadir about 4 days after birth but thereafter increasing steadily to reach prepregnancy levels about 1 month later.Thrombosis and coagulation
Delivery of the placenta has the potential to be associated with blood loss greater than the normal physiological bleeding, and as well as the mechanical effect of the contracting uterus occluding the vessels of the placental bed there are changes in haemostasis. Levels of tissue plasminogen activator, released from the placenta, fall abruptly after delivery allowing increased fibrinolysis across the placental bed and release of fibrin degradation products. Although there is consumption of platelets and fibrin, with up to 10% of the body's supplies of both used at the placental site, the fall is very transient and there is a marked rise within a day or two of delivery contributing to an increased risk of thrombosis at this time (1).
Other physiological transitions
With the withdrawal of progesterone after birth, the tidal volume and respiratory rate fall rapidly, however the reduction in diaphragmatic excursion caused by the uterus is relieved allowing normalization of the residual volume and functional residual capacity. The airways also have a reversal of the oedema and vascularity associated with pregnancy. These changes are complete within 2 or 3 weeks. During pregnancy, renal function has been different with an increased glomerular filtration rate, but there is a marked diuresis during the first postpartum week. Changes in the physiological dilatation of the renal pelves and ureters gradually return to normal by 6 weeks. The mechanical effects on the gastrointestinal system are rapidly reversed after birth, with gastric emptying and reflux returning to normal quickly. Other changes that are associated with pregnancy, such as gallbladder emptying and bowel transit time, tend to improve gradually over the puerperium.
Ovarian function
Where breastfeeding is initiated and lactation continues, the normal pulsatile release of gonadotropin-releasing hormone is interrupted and although low levels of follicle-stimulating hormone are secreted and there is some follicular development, the absence of luteinizing hormone leads to inadequate oestradiol secretion and ovulation does not occur (14). This physiological state can persist for long periods, and until lactation ceases women will have few periods or may remain amenorrhoeic. Where breastfeeding is not established, ovulation may occur within a month or two of birth. Only a small proportion of lactating women, perhaps less than 5%, will ovulate during the first 6 months following birth (9). It is likely that increased levels of prolactin play a role in lactational amenorrhoea, but this is transient as prolactin levels may return to normal within 2 months of birth in lactating women.