Alternatives to the hypoxic drive theory

Since 1960, several studies have demonstrated what really happens when CO2 retainers are exposed to supplemental oxygen.  The best explanation comes from John Haldane himself in what is now referred to as the Haldane Effect, and another process we refer to as ventilation/ perfusion (V/Q) mismatching.

1.  The Haldane effect:   This law was created by John Haldane, a pioneer of oxygen therapy.  He proved that as Deoxygenation of the blood increases its ability to carry carbon dioxide.  Thus, the less oxygen on hemoglobin, the more CO2 on hemoglobin.  CO2 attaches to unsaturated hemoglobin molecules. Oxygen is more soluble in water and therefore has a higher affinity for hemoglobin, so if you increase oxygen in the blood by supplemental oxygen, CO2 molecules are forced off hemoglobin and oxygen takes its place.  This causes an increase in CO2 in the blood, or an increased PaCO2.

Most people would simply increase their respiratory rate and blow off this CO2. Yet COPD retainers who are in respiratory distress may not have the capacity to increase their respiratory rate, so their respiratory rate remains the same.  This causes their PaCO2 to rise.

Now consider that this patient may have an elevated hemoglobin level after years of oxygen deprivation, and you're going to have lots of extra CO2 molecules roaming around the blood stream.  This may be on top the patients already elevated CO2 retention.

All these CO2 molecules are transported back to the lungs for ventilation to take place.  Yet because many alveoli are poorly ventilated (V/Q mismatching), and because the patients ability to increase ventilation is tapped out, PaCO2 levels will rise.

The Haldane effect was proven by a study described in 1996 in Critical Care Medicine, "Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease." (1)

2.  V/Q mismatching:  Consider that V = Ventilation and P = Perfusion.  So, generally this is Ventilation/ Perfusion mismatching.  It is caused by increased airway narrowing due to airway remodeling, bronchospasm, and increased sputum production.  Where this occurs, the lungs are perfused but poorly ventilated.  It means that in areas of the lungs where V/Q mismatching occurs do not allow CO2 to enter the lungs, and oxygen to enter.

When an alveoli is poorly ventilated the vasculature around it will constrict so oxygen goes to alveoli that are ventilated well.  This is how that patient's body has made efficient use of his diseased lungs.

Now add 100% oxygen and you screw up this naturally occurring phenomenon.  Now the vasculature around that non-ventilating alveoli dilates, and this causes blood to be sent to the non functioning alveoli.  Now you have even greater V/Q mismatching and more CO2 that doesn't get out of the blood.  The end result, therefore, is an increase in PaCO2.

This theory was proven via a study completed in 1980 and reported in American Review of Respiratory Disorders, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure," (2)

These two theories are far more viable than the hypoxic drive theory, and both have been proven by science.  Regardless, the hypoxic drive theory continues to be the gold standard theory.

References:

1. Hanson, et all, "Causes of hypercapnia with Oxygen Therapy in patients with Chronic Obstructive Pulmonary Disease," Critical Care medicine, 1996, volume 24, pages 23-28 (abstract available by link)  Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218), and reference # 12 (Robinson, ibid, page 1527), and #13 (Dick, C.R., ibid)
2. Aubier, M, et al, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure", American Review of Respiratory Diseases,  1980, Volume 122, pages 747-754 (abstract available by link) Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218)

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