Blood measurements of oxygen transport in clinical practice

  • M. Girardis
  • L. Rinaldi
  • S. Busani
Conference paper


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].


Adult Respiratory Distress Syndrome Blunt Chest Trauma Mixed Venous Blood Cellular Energy Production Cell Membrane Permeability Increase 
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Copyright information

© Springer-Verlag Italia 2003

Authors and Affiliations

  • M. Girardis
  • L. Rinaldi
  • S. Busani

There are no affiliations available

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