The oxygen cascade is a series of steps in the diffusion of the partial pressure of oxygen from atmospheric air down to the mitochondria where it is utilized. The cascade starts with dry air that is inspired into the lungs. We know the atmospheric pressure at sea level is approximately 760 mm Hg and the oxygen content is 21 percent and so inspired air pO2 is reliably calculated, 21 per cent of 760 = 160 mmHg. The only point in the series of steps where the partial pressure of oxygen is easily and commonly measured is in arterial blood where it typically would be 90 mmHg. The other intermediate steps as described are either calculated, extrapolated or theoretical. The pO2 at the mitochondrial level is estimated at 5 mmHg where the oxygen is utilized to produce energy in the form of ATP. Much of the estimated values of PO2 especially below the value measured in the arterial blood is theoretical. Below the arterial blood there are two levels of estimated but not measured oxygen tension, that of the tissue and below that at the mitochondrial level. The description of the oxygen cascade is useful in describing the delivery of oxygen to the mitochondria. The demand for oxygen by the mitochondria is dependent on the metabolism of the tissue and particularly with muscle tissue the activity level. When the demand for oxygen in the mitochondria exceeds the supply, anaerobic metabolism begins to produce lactic acid.
Diseases of the pulmonary system, the lungs and airways affect the oxygen cascade down to where the arterial PaO2 is measured. Generally the only place where oxygen tension is measured is arterial blood. Below this level there may be diseases that affect the cascade of oxygen down to the mitochondria but these would not be diseases of the pulmonary system. Below the arterial supply the diffusion of oxygen depends primarily on the flow of blood from the arterioles into the capillaries, tissue and subsequently into the mitochondria. We can describe but not measure this flow at least in vivo in humans. We know that it is dependent on the resistance in the arterioles. When it is impaired we describe this as stagnant tissue hypoxia. We only know that the blood is stagnant when the tissue develops anaerobic metabolism and produces lactic acid from the lack of oxygen in the mitochondria. We can’t generally measure flow at this level nor measure the oxygen content.