Blood measurements of oxygen transport in clinical practice

Abstract

Human survival depends on its ability to extract O₂ from the atmosphere and to transport it to cells where it is utilized for essential metabolic processes. More than 90% of O₂ consumption is intended for cellular energy production throughout mitochondrial pathways [1]. When O₂ supply is impaired, life-giving energy must be produced by different metabolic pathways, namely the anaerobic processes. However, these processes are not so efficient and capable as oxidative phosphorylation. If a certain hypoxia threshold is exceeded (1) intracellular ATP level and pH drop, (2) cell membrane permeability increases, thereby cytosolic level of Na⁺ and Ca⁺ increases, and (3) mitochondria become uncoupled and lose definitely their ability to produce ATP [1]. A lack of O₂ causes an organ function impairment whose entity depends on severity and time duration of hypoxia. Tissues differ in their ability to withstand anoxia because of different O₂ demand and stores. The most-sensitive cells are the cerebral ones (1–2 min anoxia is sufficient to impair their function), while the muscle is able to withstand hypoxic conditions for about 2 h. Usually cell death is the consequence of a period of anoxia four times the period necessary to cause functional impairment (i.e., 4 min for brain, 25–40 min for heart, liver, and kidney, 8 h for skeletal muscle) [2].