OXYGEN

What is pathological supply dependence on oxygen?

The mixed venous oxygen saturation is a measurement of oxygen consumption, made using a pulmonary artery catheter (the measurements are made from the pulmonary artery, and are thus accurate). The SvO₂ (mixed venous oxygen saturation) is proportional to SaO₂ – VO₂/Q x Hb (VO₂ is the venous oxygen content).

This diagram describes oxygen delivery (DO2) and consumption (VO2) in normal and pathological states.

We know that we can go from being completely sedentary to taking high impact exercise without developing tissue hypoxia. This is because we have a physiologic reserve. Under normal conditions, during exercise, if oxygen demand is increased, supply is increased also – by increasing minute ventilation and cardiac output. But what happens if, for example, oxygen delivery starts to fall off (e.g. in a patient who has progressively worsening respiratory or cardiovascular function)? What actually happens, in normal people, is that we compensate for this lower O₂ delivery by making use of our physiologic reserve, we redistribute blood preferentially to the tissues that need them and the amount of oxygen extracted (extraction ratio) increases. Eventually reserve runs out and a critical point (point A on the diagram above) is reached: there just isn’t enough O₂ to match supply, and anaerobic glycolysis takes place.

This is known as “physiological dependence of VO₂ on DO₂”, and can be measured by an increase in arterial lactate concentration.

This plateau in VO₂ is maintained by increasing the extraction ratio for oxygen (O₂ER). Blood flow is redistributed to match local demand for oxygen. The meditors for this process are multiple, the most important of which are the autonomic nervous system and nitric oxide. The critical O₂ER is the point where anaerobic glycolysis takes place. The critical DO₂ in health is about 7 to 10ml/kg/min.

In pathological circumstances, such as systemic sepsis, this whole protective system falls apart: in diseases that affect the microcirculation, there is a loss of O₂ extraction capacity. There is a school of thought that believes that DO₂ needs to be maintained at a higher level that in health, as the tissues are less able to efficiently extract O₂ (1;2) . There is a higher critical DO₂ (to 12ml/kg/min) and pathological dependence of VO₂ on DO₂. A hypothesis was formed that by increasing the DO₂ (supernormalization) by increasing cardiac output and oxygen carriage in sepsis, then oxygen extraction would improve. Randomized controlled trials have been disappointing. We now believe that the inability to extract oxygen occurs on the demand side, due to microcirculatory abnormalities, rather that overall oxygen delivery.

References

   (1)    Appel PL, Shoemaker WC. Relationship of oxygen consumption and oxygen delivery in surgical patients with ARDS. Chest 1992; 102(3):906-911.

   (2)    Shoemaker WC, Appel PL, Kram HB. Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients. Chest 1992; 102(1):208-215.

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