CLASSES OF TISSUE HYPOXIA

We identify eight causes of tissue hypoxia, failing into three classes , A, B, and C, depending upon the effect on the critical mixed venous pO(2) and the optimal oxygen consumption rate. The critical mixed veno us pO(2) is the value above which the oxygen consumption rate is optim al and independent of the mixed venous pO(2) and below which the oxyge n consumption rate decreases towards zero. Class A hypoxia: primary de crease in mixed venous pO(2). Causes: 1) ischaemic hypoxia (decrease i n cardiac output), 2) low-extractivity hypoxia (decrease in oxygen ext raction tension, p(x)). Class B hypoxia: primary increase in critical mixed venous pO(2). Causes: 1) shunt hypoxia (increased a-v shunting), 2) dysperfusion hypoxia (increased diffusion length from erythrocytes to mitochondria and/or decreased total capillary endothelial diffusio n area, e.g., tissue oedema, microembolism), 3) histotoxic hypoxia (in hibition of the cytochrome chain). Class C hypoxia: primary increase i n optimal oxygen consumption rare, Causes: 1) uncoupling hypoxia (unco upling of the ATP formation associated with O-2 reduction), 2) hyperme tabolic hypoxia (increased energy metabolism, e.g., due to hyperthermi a).