In disasters such as fires, landslides, and avalanches, hypoxic conditions caused by oxygen deficiency in victims lead to respiratory failure in the lungs. Hypoxia-induced hypoxia-sensitive factor-1 regulates the expression of hundreds of different cell-type-specific genes at the cellular level. Oxygen deficiency triggers the activation of anaerobic glycolysis. Under hypoxic conditions, insufficient oxygen leads to the inhibition of cytochrome c oxidase, located in complex IV of the oxidative phosphorylation pathway where adenosine triphosphate is produced, resulting in inadequate ATP production and increased production of unwanted reactive oxygen radicals (ROS), which are toxic to cells. Increased anaerobic metabolism also leads to significant increases in the concentrations of metabolites such as lactate and succinate. Increased lactate stabilizes hypoxia-sensitive factor 1α in macrophages, consequently increasing the production of vascular endothelial growth factor (VEGF) in endothelial cells. This shifts the polarization direction of macrophages to repair mode after injury or tissue damage. T cells also lose their sensitivity to chemokines and become trapped in the inflammation area. On the other hand, increased succinate molecules increase glycolysis while also increasing ROS production. Increased ROS inhibit mitochondrial function, reactivating anaerobic glycolysis. Furthermore, succinate inhibits prolyl hydroxylases (PHDs), which are responsible for the hydroxylation and degradation of HIF-1α, thus preventing HIF-1α from being hydroxylated. Therefore, decreased hydroxylation leads to the stabilization of HIF-1α, which in turn causes transcription of genes involved in proliferation, angiogenesis, and metastasis. Unlike lactate, increased succinate polarizes macrophages into fight-or-flight mode. Although oxygen deficiency causes an increase in respiratory rate, it inevitably negatively affects blood pH. In situations where hyperventilation develops, respiratory alkalosis occurs, while in situations where hypoventilation develops, respiratory acidosis occurs. Increased lactate, acetate, or citrate concentrations at the cellular level are the cause of metabolic alkalosis. Both hypoxia and low pH have direct and indirect effects on the immune system and generally produce negative immunosuppressive effects.