Blood flow and oxygen delivery to fetal organs and tissues during sustained hypoxemia

Abstract

To examine the fetal cardiovascular responses to a sustained reduction in O2 delivery (DO2), studies were conducted on 13 chronically instrumented fetal lambs (128-138 days gestation) made hypoxemic for 7.9 +/- 0.5 h by lowering maternal inspired O2 concentration to 9-10%. Fetal descending aortic PO2 fell initially from 18.0 +/- 1.0 to 10.7 +/- 0.6 mmHg, whereas pH decreased progressively from 7.326 +/- 0.006 to 6.843 +/- 0.023. Blood flow to the cerebral hemispheres, myocardium, and adrenal glands rose maximally by 110.2 +/- 22.5, 253.7 +/- 41.1, and 338.7 +/- 55.0%. Cerebral hemispheric DO2 fell progressively, whereas DO2 to the myocardium and adrenal was maintained until 7.9 h, when it fell significantly. There was also a rise in blood flow to brown adipose tissue. Blood flow to the gut and skeletal muscle was maintained, whereas flow to the spleen and kidney fell. DO2 to all these tissues fell markedly because of the progressive decline in blood O2 content. It is concluded that fetal cardiovascular function was well maintained in the face of severe hypoxemia and marked acidemia.

Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat

“…This is due to diffusion of oxygen through the walls of perfusion tubings (which have to be small and thin for the rat placenta) and other surfaces. Breathing hypoxic mixtures (9 -15% O 2 ) by the mother reduces fetal arterial PO 2 in vivo by 25-50% (1,2,28,34,(52)(53)(54). In our experiments, the hypoxic challenges reduced PO 2 by 30%.…”

Fetal growth restriction: adaptations and consequences

“…During acute hypoxaemia, blood flow to the brain, heart and adrenal glands is increased and blood flow to the gastrointestinal, renal and peripheral vascular beds decreases (Jensen et al, 1987a,b;Yaffe et al, 1987;Jansen et al, 1989;Giussani et al, 1993). This redistribution of fetal cardiac output is also maintained with prolonged hypoxaemia in pregnancy, presumably as a consequence of the action of vasoactive hormones (Bocking et al, 1988;Rurak et al, 1990).…”

Are we (mis)guided by current guidelines on intrapartum fetal heart rate monitoring? Case for a more physiological approach to interpretation

“…If the hypoxic insult is slow and persistent the fetus has ample time to make metabolic adjustments and exhibit different FHR patterns. 38,39 In the absence of metabolic acidaemia fetal sheep at least can sustain these protective cardiovascular adaptations virtually indefinitely, [40][41][42] but they begin to fail with the development of acidaemia, with substantial falls in fetal and cerebral oxygen consumption at pH <7.0.…”