Why we avoid O2 in COPD

I'll start by saying we don't

Long story short, if you have a hypoxic patient of any description, they need oxygen, so please don't be afraid of giving them lots of it while you figure out what's going on.

Even in patients with significant COPD, only about 10% will have any trouble with retaining CO2, so don't worry about it in the immediate, emergency situation.

The worst thing you can do is to deny a hypoxic patient from having lifesaving O2 therapy!

But what about COPD?

So here it gets more complicated.

In a patient without significant lung disease, giving oxygen will help to reduce hypoxia, but it shouldn't affect their respiratory drive.

This is because breathing is pretty much entirely driven by Carbon Dioxide, as explained in our video below.

In a patient with COPD, they become desensitised to higher levels of CO2 in the blood, and so they need a higher level of CO2 to generate enough respiratory drive to breathe properly.

This is a problem because as CO2 levels increase, the patient can become narcotised or drowsy by the effects of having higher levels of CO2 in the blood, and this means they have a narrower range of CO2 levels that will produce enough respiratory effort, without becoming drowsy.

Hypoxic drive

At medical school we're taught that patients who retain CO2 rely on their hypoxic drive to breathe.

Hypoxic drive is the respiratory effort generated as a result of low levels of oxygen in the blood, independent of CO2, and it does exist as a concept.

It's very rare for this to be the main driving factor in normal situations, because if the oxygen is low, it's usually due to a lack of ventilation, in which case the CO2 will also be high, and that will be the main driver of breathing.

However in unusual circumstances, such as at altitude, we see it in action. When breathing air at altitude, you can easily exhale enough CO2, but there isn't enough oxygen in the air because the ambient pressure is so low.

You will hyperventilate, despite having normal or low CO2, at least for a while, because of your hypoxic drive, in an attempt to increase your oxygen levels.

We're taught at medical school that this is what is driving respiratory effort in COPD patients, and therefore giving them extra oxygen will reduce their breathing effort.

This is sort of right, but not the whole picture.

So what happens when I give too much oxygen?

Three things happen:

• You reduce hypoxic drive (but this is a tiny proportion of the issue)
• You mess up hypoxic pulmonary vasoconstriction
• You mess up the Haldane effect

What is hypoxic pulmonary vasoconstriction?

To get oxygen into your blood, you need to first ventilate (V), to get the oxygen into the alveoli, then perfuse (Q) blood to the alveoli, to get the oxygen into the blood.

At any one time, different areas of the lung will receive better or worse ventilation, and likewise with perfusion.

If we ventilate an alveolus but don't perfuse it, or vice versa, then oxygen can't get into the blood. This is what we mean by V/Q mismatch.

• An alveolus that is ventilated but not perfused is called dead space
• An alveolus that is perfused but not ventilated is called shunt

To improve this V/Q matching, we have a really powerful reflex in place called hypoxic pulmonary vasoconstriction (HPV).

An alveolus with low oxygen levels will automatically constrict the blood vessel supplying it to divert blood to better ventilated areas of the lung.

This is where our oxygen therapy becomes a problem.

If we have a COPD patient with poorly ventilated areas of lung as a result of emphysema, they will be using HPV to divert blood away to less damaged parts of their lungs.

If we give them lots of oxygen, a small amount of this oxygen will trickle into the diseased areas, and fool the alveolus into thinking it has enough oxygen, so it will relax the blood vessel and start receiving a load of blood.

This then results in two problems:

• Blood is diverted away from the properly-working bits of lung, so the patient gradually becomes more hypoxic
• CO2 builds up in the alveoli that aren't being ventilated, and therefore in the blood

This is the main reason why giving lots of oxygen to a known CO2-retainer is bad news.

The Haldane effect

Kudos for reading this far. You probably don't need to know this bit, but if you're a nerd like us, then please join us.

The Haldane effect is as follows:

• Haemoglobin has a lower affinity for CO2, when there is lots of oxygen about

This is good for two reasons:

• Haemoglobin will pick up CO2 when oxygen is low - i.e. in the peripheral tissues where the CO2 needs to be taken away from
• Haemoglobin will then dump CO2, when oxygen is high - i.e. in the lungs, where we want to get rid of CO2

This is all well and good, until we artificially put a load of oxygen into badly ventilated alveoli.

Not only do we mess up the patient's hypoxic drive, and their hypoxic pulmonary vasoconstriction, but we also mess up their Haldane effect, because the 'falsely' high oxygen levels encourage the haemoglobin to offload CO2, which then gets stuck in the alveolus and re-dissolves back into the blood.

One more thing...

Excessive oxygen induces oxidative damage, as the name might suggest.

This worsens and can even cause airway inflammation, which is particularly an issue in COPD patients.

Oh and one more...

If you fill a badly-ventilated alveolus with pure oxygen, then all of that oxygen is likely to dissolve across into the blood, leaving nothing behind to keep the alveolus open (because there's no nitrogen in pure oxygen), so you get increased atelectasis.

So there you go - the five reasons we avoid lots of oxygen in patient's known to retain CO2

• Hypoxic drive
• Hypoxic pulmonary vasoconstriction
• Haldane effect
• Worsening airway inflammation
• Increased atelectasis

And what we should be doing for patients retaining CO2

• Therapies to remove the cause (antibiotics for infection, nebulisers for secretions)
• Ventilatory support (non-invasive or invasive ventilation)
• Just enough oxygen to stop them being hypoxic, without affecting their respiratory drive, where possible

Here's our summary video for this post: