Perret C, Verdon F, Enrico J F
Bull Physiopathol Respir (Nancy). 1975 Sep-Oct;11(5):613-36.
This review considers functional repercussions of shock state on the different stages of oxygen transport from alveolus to mitochondria. At the pulmonary level, the decrease in perfusion pressure induces disturbances in the distribition of VA/Q ratio, and therefore leads to aerial hypoxaemia. Prolonged ischemia injures the air-blood barrier and reduces the area of exchange. Decrease in oxygen delivery to the tissue is related to a fall in cardiac output (hemorrhagic and cardiogenic shock) or to a primary disturbance in peripheral circulatory distribution (septic shock) or to a primary disturbance in peripheral circulatory distribution (septic shock). The intervention of compensating factors leads to a redistribution of the regional perfusion and probably to an easier oxygen delivery by haemoglobin. However circulatory inhomogeneity by itself produces a progressive deterioration of microcirculation. Decrease in intracapillary circulation. Decrease in intracapillary circulation and impairment in blood rheologic properties contribute to aggregates formation and intravascular coagulation. The result is a decrease in capillary diffusion capacity and in oxygen intracellular transport. When intracellular PO2 reaches a critical level, the functional exclusion of mitochondria involves a metabolic shift to anaerobiosis. The value of hyperlactacidemia as a sign of oxygen debt is discussed.
本综述探讨了休克状态对从肺泡到线粒体的氧运输不同阶段的功能影响。在肺部，灌注压降低会导致通气/血流比值分布紊乱，进而引起低氧血症。长时间缺血会损伤气血屏障并减少交换面积。组织氧输送减少与心输出量下降（失血性和心源性休克）、外周循环分布的原发性紊乱（感染性休克）有关。代偿因素的干预会导致区域灌注重新分布，可能使血红蛋白更容易输送氧气。然而，循环不均匀本身会导致微循环逐渐恶化。毛细血管内循环减少。毛细血管内循环减少和血液流变学性质受损会导致聚集物形成和血管内凝血。结果是毛细血管扩散能力和细胞内氧运输下降。当细胞内氧分压达到临界水平时，线粒体的功能抑制会导致代谢转向无氧代谢。文中讨论了高乳酸血症作为氧债指标的价值。
