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).