Hypoxia hypoxemia

Yan, S.R, Mackman, N., Kisiel, W., Stern, D.M., and Pinsky, D.,J. Hypoxia/hypoxemia-induced activation of the procoagulant pathways and the pathogenesis of ischemia-assodated thrombosis, Arterioscler. Thromb. Vase. Biol, 19, 2029, 1999. 

Chemoreceptor response to decreased arterial P02. Hypoxia has a direct depressant effect on central chemoreceptors as well as on the medullary respiratory center. In fact, hypoxia tends to inhibit activity in all regions of the brain. Therefore, the ventilatory response to hypoxemia is elicited only by the peripheral chemoreceptors. 

Arterial PO2 must be sufficiently high ( 90mmHg) to create a diffusion gradient from the arterial blood to the tissue ceEs. Low arterial PO2 (hypoxemia) results in tissue hypoxia O2 starvation). 

In contrast, hypnotic doses of benzodiazepines may worsen sleep-related breathing disorders by adversely affecting control of the upper airway muscles or by decreasing the ventilatory response to CO2. The latter effect may cause hypoventilation and hypoxemia in some patients with severe COPD, although benzodiazepines may improve sleep and sleep structure in some instances. In patients with obstructive sleep apnea (OSA), hypnotic doses of benzodiazepines may exaggerate the impact of apneic episodes on alveolar hypoxia, pulmonary hypertension, and cardiac ventricular load. Caution should be exercised with patients who snore regularly partial airway obstruction may be converted to OSA under the influence of these drugs. 

NO. A dose-response curve for inhaling 5-80 ppm was described, and full reversal of hypoxia-induced PAH was also reported in this paper. No dilatory effects were observed on the systemic circulation. Others confirmed (Girard et al., 1992) and extended (Fratacci et al., 1991) these findings in animal experiments with hypoxia- and thromboxane-induced pulmonary hypertension. These experimental observations initiated a new field of research activity examining the clinical and experimental effects of inhaled NO in states of pulmonary hypertension of varied etiology with or without concomitant hypoxemia. We review here some of this research. The field has grown so rapidly, however, that only original contributions are cited. 

In late gestation, fetal mean arterial pressure responses to hypoxia can be variable. In 1974, Cohn and colleagues reported that there was no significant change in fetal mean arterial pressure with isocapnic hypoxemia, but that mean pressure increased when the fetus became acidemic during the insult (15). Subsequently, other authors have described a significant increase in mean arterial pressure with maternal inhalation hypoxia (27), umbilical cord occlusion (24,25,32,33), and... 

Numerous physiological and clinical conditions are associated with hypoxemia, ranging from acute episodes of hypoxia (asthma) to chronic sustained hypoxia (ascent to high altitude, COPD) or chronic intermittent hypoxia (OSA). During these episodes of hypoxia, activation of both peripheral and central sites likely occurs, with the net response refiecting a coordination of these drives by the pattern-generating network. 

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