Changes in cardiovascular physiology in pregnancy and implications for women with heart disease
The most striking cardiovascular change in early pregnancy is a marked decrease in peripheral resistance, which falls by up to 30% of its prepregnancy value (1). This is most likely due to the changes in maternal hormone levels (particularly progesterone, relaxin, prostacyclin, and prolactin) brought about by the developing conceptus, stimulated in part by its secretion of human chorionic gonadotropin (similar in structure to luteinizing hormone), although exactly how these hormones act to do this remains uncertain (2).
It is probably mediated in part by the increases in nitric oxide production in the endothelium (3), and by increased resistance to the effects of angiotensin II and norepinephrine (noradrenaline). As pregnancy progresses, the placental circulation is established, and its blood flow of up to 700 mL per minute by the third trimester (about 10% of cardiac output) acts as a low resistance shunt which contributes to the loss of peripheral resistance (4). These changes would produce a marked decrease in blood pressure if their effect was not counteracted by the increase in circulating blood volume of up to 50% (there is a large increase in plasma volume and a somewhat smaller increase in the circulating red cell mass, resulting in a decrease in haemoglobin concentration—the ‘physiological anaemia of pregnancy'). This increase occurs because the decrease in blood pressure stimulates the production of renin in the kidney leading to the formation of angiotensinogen and angiotensin I, which is then converted into angiotensin II by a converting enzyme (2). This would normally produce vasoconstriction, but this action is blocked by the hormone changes described earlier. However, its effects on the adrenal cortex and kidney are not blocked, resulting in a three- to fourfold increase in aldosterone levels, causing cumulative sodium and water retention which expands the circulating volume and restores cardiac preload. The overall net change is an up to 50% increase in resting cardiac output, which peaks between 26 and 36 weeks of pregnancy, and which represents a considerable challenge to anyone with impaired cardiac function.Clinically, these changes are manifested by a small (about 10 mmHg) decrease in blood pressure as pregnancy progresses, reaching a nadir between 26 and 34 weeks of gestation, and then rising slowly thereafter back to the prepregnancy level by about 40 weeks (5). Resting heart rate increases by about 15-20 beats per minute (bpm) by the early third trimester; a resting heart rate of 90-100 bpm is common but rates higher than this should be investigated. Both cardiac output and blood pressure can decrease in pregnant women who are allowed to lie on their back in late pregnancy, because the weight of the uterus compresses the inferior vena cava and obstructs venous return. This can cause the woman to feel faint and may if prolonged lead to a reduction in placental perfusion and fetal hypoxia; the supine position should therefore be avoided in late pregnancy and labour, especially if the mother has an epidural anaesthetic (which also encourages venous pooling in the legs).
The stress and pain of labour also places an increased demand on the heart (6), which can largely be avoided by the use of regional anaesthetic for pain relief. Because rapid onset of sympathetic blockade can decrease blood pressure acutely, it is usual to administer such a blockade very slowly with careful monitoring.