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Author: Scott Carrington / Codes: ELP1, NeuP3, RP8, SLO1, SLO3 / Published: 09/12/2015

So you’re in the Emergency Department when a medical alert arrives. He’s tachypnoeic, tachycardic and visibly cyanotic with saturations of 75% on room air. You start to reach for the high flow oxygen but there’s a voice in your head saying

“STOP! What about his hypoxic drive”!

I was taught in medical school that humans breathe when carbon dioxide levels within the CSF increase. However in COPD patients, this is no longer sensitive and instead the patient breathes when the oxygen level reduces. I was told that if we give a patient with COPD high flow oxygen, we suppress their hypoxic drive and they reduce their respiratory rate

This just isn’t true. While giving high flow oxygen can lead to a rise in carbon dioxide, the truth lies in a combination of a ventilation/perfusion mismatch and the Haldane effect

Ventilation perfusion mismatching

In a well ventilated and well perfused alveolus, oxygen moves into the alveolus during inspiration, is exchanged for carbon dioxide, which is then removed during exhalation. However in a poorly ventilated alveolus, the capillaries constrict to divert blood away towards a well ventilated alveolus where carbon dioxide can be removed.

Now when we give high flow oxygen, this increases the amount of oxygen within the alveolus causing the capillaries to dilate allowing deoxygenated blood to go past the alveolus. However because this alveolus is not well ventilated, the carbon dioxide isn’t removed from the blood and returns into the circulation, progressively increasing the amount of carbon dioxide within the blood.

Haldane effect

In normal physiology, haemoglobin exchanges oxygen for carbon dioxide in the tissues. Some of this carbon dioxide is bound to the haemoglobin while the majority reacts with water in the red cell to form hydrogen and bicarbonate ions. The hydrogen then binds onto the haemoglobin molecule while the bicarbonate is transported within the plasma.

When the red cell gets to the lungs, oxygen displaces the carbon dioxide and hydrogen from the red cell which then react with the bicarbonate to form water and carbon dioxide which can be breathed out.

Now the more desaturated the haemoglobin, the more carbon dioxide it can carry and the more hydrogen ions it can buffer. So if we provide excessive oxygen, we increase the oxygen content of the venous circulation, saturating the haemoglobin and preventing it from transporting carbon dioxide effectively.

Instead, the carbon dioxide is carried freely in the blood, decreasing the blood pH.

So what’s the bottom line?

The bottom line is that patients die without oxygen.

If your patient is acutely unwell and hypoxic, then give them oxygen, but make sure you review them. We need to give them just the right amount which can be guided by their oxygen saturations from the pulse oximeter.

So if your patient has COPD, titrate their oxygen saturation to between 88 and 92%, and all other patients need oxygen saturations between 94 and 98%.

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