Hypoxia kills. Hypercapnia happens.

“Steady on his O2 there. He’s a COPD patient; we don’t want him to stop breathing.”

A 73 year old man with COPD not on home oxygen and usually well-controlled had come in with an exacerbation. His ABG showed a clear type I respiratory failure with a normal base excess, and predominantly emphysematous changes on the xray. His saturations were 93% on 60% oxygen. I overheard doctors and nurses worried that he was on 60% oxygen, and they moved him down to 35% oxygen. They were concerned that he would stop breathing.

The hypoxic drive theory as it is taught is debunked  yet its legacy remains. The BTS states this – search their article for “hypoxic drive” and see for yourself. That’s not to say that if you give oxygen to a COPD patient, you wouldn’t increase the PCO2. This can and does happen. The reason behind this has nothing to do with decreased respiratory drive. Let’s dive into the physiology of COPD.

Our respiratory drive comes about 85% from chemoreceptors in the medulla and 15% from chemoreceptors in the carotids and aorta. The ones in the medulla sense the pH of the CSF, which is a surrogate for CO2 levels. That’s why any metabolic acidosis can also generate an increased respiratory rate despite normal pO2 and pCO2.

The peripheral chemoreceptors are more interested in oxygen. If oxygen levels drop below 60 mm Hg, then they get excited in most people. When high flow oxygen is given, it is true that this drive may be reduced so much as to be virtually switched off. However, most of the respiratory drive comes from the central chemoreceptors, so even if this were switched off, the patient should still breathe. In fact, if the patient were at all ‘dependent on the hypoxic drive’ and this was switched off, the lack of ventilation and subsequent CO2 rise (as pCO2 and ventilation are inversely proportional) should switch the medulla chemoreceptors into overdrive. Studies have also shown that the minute ventilation is not decreased in COPD patients given high flow oxygen. So why does the pCO2 rise?

There are two changes that occur when high flow oxygen is given to a COPD patient:

1. V/Q mismatch worsens

Hypoxic vasoconstriction is nature’s way of identifying poorly performing alveoli and not wasting valuable blood on them. Suppose an alveolus is underventilating for whatever reason. As oxygen levels in the alveolus drop, the smooth muscle of the pulmonary capillaries around that alveolus constrict, reducing the flow to the underperforming alveolus. This means that the blood is free to seek out better performing/ventilated alveoli, leading to better ventilation perfusion matching.

It’s like the UK government cutting funding to sports in which Team GB failed to get a medal during the Olympics. The resources (blood) could be used for greater effect if spent on sports where we have real medal chances (well ventilated alveoli).

Suppose now that high flow oxygen is given. Suddenly, no alveolus is so hypoxic that it can’t get any blood. In fact, the blood now finds its way to all the alveoli, and is not necessarily directed to the crème de la crème.

It’s like the UK government saying that any sport that gets a copper medal gets funding, then introducing a copper medal at the Olympics for anyone who finishes in the top 8 positions.  Whilst this may seem great for the diversity of sports represented (more alveoli getting blood), it means that the funding for the top performing sport has to be drastically reduced, which is not the most effective use of resources.

The remaining alveoli with actually decent ventilation are no longer getting the most blood, and poorly ventilated alveoli are now being used to try and get rid of CO2. And that won’t work.

2. The Haldane effect

As pO2 increases, this decreases the affinity of Hb for CO2. This means less CO2 is bound to Hb, leading to an increase in the partial pressure of CO2 (without an increase in the total CO2 content of the blood).

Both these effects would also happen if Mo Farah were given high flow oxygen. The reason he doesn’t go into Type 2 respiratory failure is firstly because he probably has better ventilated alveoli than the typical COPD patient and secondly because he would compensate for any increase in the pCO2 by increasing his minute ventilation, which would rapidly normalise his pCO2. It is the very fact that he can compensate for any rise in pCO2 that makes him safe to have high flow oxygen. In any patient with a reduced ability to increase the work of breathing/ventilation rate, high flow oxygen could potentially lead to dangerously raised pCO2 levels. Note how this does not just mean the select group of COPD patients who retain CO2, but also those with any possible ventilation problem e.g. chest wall deformities, neuromuscular problems and the morbidly obese. The BTS guidance reflect this:

“For most patients with known chronic obstructive pulmonary disease (COPD) or other known risk factors for hypercapnic respiratory failure (eg, morbid obesity, chest wall deformities or neuromuscular disorders), a target saturation range of 88–92% is suggested pending the availability of blood gas results.”

So, giving high flow oxygen does not lead to apnea, although high oxygen flow rates can lead to a rise in CO2. A rising pCO2 can be looked for with both blood gases and clinical assessment of the patient (drowsiness, jitters and twitches, bounding pulse and raised blood pressure etc.).  There will nearly always be some rise in the pCO2 in a COPD patient as more oxygen is given, for the two reasons given above. Even if the pCO is rising, this in itself is not an indication for NIV or invasive ventilation. It is only when the pH drops below 7.35 that ventilation is indicated. (See page vi8 of the BTS guidance).

The warning signs of raised pCO2 will generally happen slowly, and a rising pCO2 leading to acidosis can be managed by NIV or intubation as necessary. A patient who has died of hypoxia cannot be managed.

Bottom line: make giving enough oxygen your first and foremost priority in any acutely unwell and/or hypoxic patient, no matter what.


6 thoughts on “Hypoxia kills. Hypercapnia happens.

  1. I wish you had treated my elderly Father who sadly passed away, he was left at home following a failed discharge with CAP curb score of 3 ,( copd and fibrosis). At 2.30 he was drowsy falling asleep and hadnt used his 02 since 9 am . At 8 30 am his sats were recorded at 86-88 and at 2′ 30 his sats were 78% .His target was 88-92 . Initially on discharge he was prescribed short burst oxygen therapy at 2 hrs a day when he had been on continuous 3 litres O2 for 48 hrs . He was seen by a resp nurse who left him at home to further deteriorate I had him readmitted as soon as i knew what his sats were and 3 days later he sadly passed away with resp acidosis, tragic end to a special man.

  2. also his d dimer came back at 11.92 he was on tinzaparin can you explain this result ? is it a definate indicator if on anti coagulants?
    Thanks if you can add any light? 🙂

  3. Susan,

    I’m really sorry to hear about your father. I cannot imagine the cocktail of emotions you would have felt at the time and maybe still do. I do hope things are getting more bearable with time.

    For the d-dimer result, was this 11.92 or 1,192 µg/L? If it was 1,192 then this was a positive result. It sounds like he had an infection at the time, which can raise d-dimer without there necessarily being a significant clot. The d-dimer can also be raised despite being on anticoagulants if there is high clot turnover i.e. continued clot formation and breakdown despite the anticoagulant. I have emailed you a presentation I gave on d-dimer and hope this is helpful.

    Thank you for your kind comments on my blog and I hope to hear more from you.

    1. Thank you for your reply d dimer as of your comment…… im really just trying to breakdown all events in my head as to what led to his death… i now understand ABG’s and as a Specialist nurse myself its great ! Keep sharing your knowledge !

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