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.