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Hypoxaemic hypoxia (airway obstruction) is more damaging to cells than anaemic or stagnant hypoxia. In order to fully understand the classification of hypoxia, it is useful to consider the example of carbon monoxide poisoning. It is known that hypoxaemic hypoxia is of particular importance in the development of cellular hypoxia and it goes without saying that, in the context of the difficult airway, the principal cause of hypoxaemia is airway obstruction. It is important to understand the mechanisms by which hypoxaemia develops, and the factors which determine the rate of this process. Causes of hypoxaemia occurring during anaesthesia can be divided into the following three categories: problems with O2 supply, problems with O2 delivery from lips to lung, and problems with O2 transfer from lung to blood. Pre-oxygenation aims to increase body O2 stores to their maximum, so that periods of apnoea are tolerated for longer before critical desaturation occurs.
This chapter reviews the roles and distribution of O2 inside the early human gestational sac and its impact on our understanding of the physiology of O2 metabolism by the fetus during the first and early second trimesters of pregnancy. The mammalian fetus is exposed to major fluctuations in O2 concentration from conception to delivery. The first trimester gestational sac has additional barriers to materno-fetal exchange compared to the definitive placenta of the second and third trimesters of pregnancy. Ample dilation of the uteroplacental circulation together with rapid villous angiogenesis are the key factors necessary to adequate placental development and function and subsequent fetal growth. Overall the data have confirmed that the human placenta is not truly hemochorial until the end of the first trimester. Rather it is deciduochorial, being supported by tissue fluids and endometrial secretions.
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