Arterial oxygen tension

Neufeld, 0. Smith, J. R. and Goldman, S. L. Arterial Oxygen Tension in Relation to Age in Hospital Patients. 

Flower, R.W. and Patz, A. (1971). Oxygen studies in retrolental fibroplasia. IX. The effects of elevated arterial oxygen tension on retinal vascular dynamics in the kitten. Arch. Ophthamol. 85, 197-208. 

MRSE MethiciUin-resistant Staphylococcus epidermitis Pao2 Arterial oxygen tension... 

Certain Investigators, however, have expressed interest in the matter recently. The possibility that a history of asthma may increase the probability of an acute byssinotic reaction to cotton dust is suggested by a paper by Hamilton et al. ( ). The senior author of this paper had had asthma as a child. Promptly after exposure to the air in a dusty part of a cotton mill he exhibited pronounced shortness of breath with tightness in the chest and accompanying major temporary decreases in FEVi and arterial oxygen tension. The episode is described as "byssinosis". The authors remark It is unlikely that many textile workers with an initial response to cotton dust such as the one described here would remain working in dusty areas." Although the authors state that "It is not possible from the present study to conclude that a prior history of atopy confers sensitivity to cotton dust", the present writers were left with the impression that the authors suspect that such may be the case. 

In all of these studies, some subjects acutely exhibited mild arterial hypoxemia, increases in alveolar-arterial oxygen tension... 

Complicated pneumoconiosis (PMF) is associated with a reduction in ventilatory capacity, low diffusing capacity, abnormalities of gas exchange, low arterial oxygen tension, pulmonary hypertension, and premature death ... 

Patients with severe COPD can have a low arterial oxygen tension (Pa02 45 to 60 mm Hg) and an elevated arterial carbon dioxide tension (PaC02 50 to 60 mm Hg). Hypoxemia results from hypoventilation (V) of lung tissue relative to perfusion (Q) of the area. The low V Q ratio progresses over several years, resulting in a consistent decline in the Pa02. 

As the symptoms progress, patients may develop frank pulmonary edema, manifested by progressive dyspnea, diffuse crackles on chest auscultation and cyanosis (34). In phosgene-exposed patients, chest X-rays may indicate pulmonary edema before development of these symptoms and physical findings (34). Pulmonary arterial pressure remains normal. However, as arterial oxygen tensions decrease, patients may develop ischemic changes on EKG. Some patients may develop a fever up to 40°C (104°E). Erequently, patients will develop copious amounts of frothy, protein-rich sputum and tracheal secretions. 24-30h after phosgene exposure, patients may die due to asphyxiation and cardiac failure secondary to pulmonary edema (34). 

Investigation of those overexposed to screening smokes should include, at least, chest radiograph, pulmonary function tests, arterial oxygen tension measurement, blood clinical chemistry, sputum culture, ophthalmic examination with slit-lamp biomicroscopy, and possibly measurement of intraocular pressure. If available, CT scan may be used to assess the severity of lung injury (Hsu et al., 2005). With some smokes, notably white phosphorus, there may be skin contamination with severe irritation and penetrating bums the management of white phosphoms skin burns is discussed in detail in Section VI.A.2. 

The quantity of oxygen transported per unit of time by convection to the brain is determined by the blood flow rate, the oxygen capacity, the oxygen affinity of blood, and the arterial oxygen tension. Under normal conditions the mean overall blood flow rate in cerebral tissue of dogs, monkeys, and humans ranges between 50 and 65 ml/100 g-min (8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18). Specific measured mean values of 80 to 110 ml/100 g-min were determined for cerebral cortex (18,19, 20, 21, 22, 23, 24, 25, 26, 27), and 15 to 25 ml/100 g-min were measured for white matter (20, 23, 26). 

Respiratory Acidosis. Under conditions of respiratory acidosis with carbon dioxide tensions between 50 and 60 mm Hg the 02-dependent elevation of cerebral blood flow is activated after reduction of cerebral venous oxygen tension to 35 mm Hg. Critical conditions of oxygen supply result from a further reduction of arterial oxygen tension when the cerebral venous oxygen tension falls below 30 mm Hg. With a cerebral... 

Figure I. Effect of progressively decreasing arterial oxygen tension on cerebral blood flow and cerebral oxygen uptake under conditions of respiratory acidosis.

When—under comparable conditions—the arterial oxygen tension was lowered to such an extent that values of oxygen tension below 30 mm Hg occurred in the cerebral venous blood, a decrease in arterial blood flow and in oxygen uptake was registered, whereas the glucose uptake of the cerebral tissue and the lactate-pyruvate ratio of cerebral venous blood continued to increase. In these experiments the return to initial... 

Under the conditions of cerebral edema and nonrespiratory acidosis, the cerebral blood flow rate did not increase as soon as the oxygen tension in cerebral venous blood decreased below the reaction threshold. During edema, a decrease of oxygen tension below the threshold value led to a slight decrease in cerebral blood flow and cerebral oxygen uptake however, glucose uptake of the cerebral tissue and the lactate-pyruvate ratio of the cerebral venous blood increased. When arterial oxygen tensions were returned to normal, the cerebral blood flow and the cerebral... 

Effects of Varying Maternal Arterial Oxygen Tension. Oxygen, air, and various N2-air mixtures were administered randomly to four ewes for 3-10-min intervals (47). The inspired gases achieved maternal arterial 02 tensions ranging from 30-350 mm Hg. During this interval the isolated... 

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