The maternal cardiovascular system undergoes profound physiological changes during pregnancy (Williams, 2003). Blood flow to each maternal organ changes at different stages and by different amounts (Figure 4.4). Ultimately, the aim of these gestational changes is to ensure that the mother can meet the metabolic demands of the growing conceptus. The mechanisms of these widespread and variable cardiovascular changes are incompletely understood.
One of the earliest manifestations of this adaptive response is a fall in peripheral vascular resistance. Peripheral vasodilatation is evident from as early as 5 weeks gestation and is almost complete by 16 weeks (Robson et al., 1989). By the end of the first trimester, peripheral vascular resistance has fallen by 40% compared with non-pregnant women. By 24 weeks gestation, cardiac output will have increased by 45% above non-pregnant levels due to an increase in stroke volume and heart rate, and a fall in systemic vascular resistance (Easterling et al., 1987; Robson et al., 1989). Consequently, blood supply to several maternal organs increases dramatically. By 24 weeks, renal perfusion increases by 80% (Davison, 1984), and by term, blood flow to the skin of the hands and feet will have increased by over 200% and uterine artery blood flow by 1000%. Conversely, hepatic and cerebral blood flow remains virtually unaltered (Figure 4.3).
Studies in pregnant baboons (Phippard et al., 1986) and pregnant women (Chapman et al., 1998) suggest that despite this increase in renal blood flow, the relatively under-filled peripheral and renal vasculature stimulates the renin-angiotensin-aldosterone system, which leads to a rise in plasma volume of 1.2-1.5 L (Brown and Gallery, 1994). Stroke volume plateaus at 16 weeks whilst heart rate continues to rise gradually until 32 weeks (Robson etal., 1989). Despite the increase in intravascular volume, the fall in systemic vascular resistance leads to a fall in diastolic blood pressure, which reaches its lowest level at 22-24 weeks gestation, then rises to reach pre-pregnancy levels by term. Systolic blood pressure is not significantly altered during healthy pregnancy (Halligan etal., 1993).
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