Oxygen therapy for asthma can elevate CO2

Patients with acute exacerbations of asthma randomised to receive high concentration oxygen therapy showed a greater rise in CO2 than those who received titrated oxygen to keep SpO2 > 93%.
This study has a few weaknesses but raises an interesting challenge to the dogma of high flow oxygen (and oxygen driven nebulisers) for all acute asthma exacerbations.

The suggested main mechanism for the elevation in CO2 is worsening ventilation/perfusion mismatching as a result of the release of hypoxic pulmonary vasoconstriction and a consequent increase in physiological dead space. The authors remind us that this has been demonstrated in other studies on asthma and acute COPD exacerbations. The authors infer that high concentration oxygen therapy may therefore potentially increase the PaCO2 across a range of respiratory conditions with abnormal gas exchange due to ventilation/perfusion mismatching

Some of the weaknesses include lack of blinding, recruiting fewer patients than planned, and changing their primary outcome variable after commencing the study (which the authors are honest about) from absolute CO2 to increase in CO2 (since it was apparent on preliminary analysis of the first few patients that presenting CO2 was the primary determinant of subsequent CO2). Furthermore, the CO2 was measured from a transcutaneous device as opposed to the true ‘gold standard’ of arterial blood gas analysis, although good reasons are given for this.

Despite some of these drawbacks this study provides us with a further reminder that oxygen is a drug with some unwanted effects and therefore its dose needs to be individualised for the patient.

Background The effect on Paco(2) of high concentration oxygen therapy when administered to patients with severe exacerbations of asthma is uncertain.

Methods 106 patients with severe exacerbations of asthma presenting to the Emergency Department were randomised to high concentration oxygen (8 l/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93% and 95%) for 60 min. Patients with chronic obstructive pulmonary disease or disorders associated with hypercapnic respiratory failure were excluded. The transcutaneous partial pressure of carbon dioxide (Ptco(2)) was measured at 0, 20, 40 and 60 min. The primary outcome variable was the proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min.

Results The proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min was significantly higher in the high concentration oxygen group, 22/50 (44%) vs 10/53 (19%), RR 2.3 (95% CI 1.2 to 4.4, p<0.006). The high concentration group had a higher proportion of patients with a rise in Ptco(2) ≥8 mm Hg, 11/50 (22%) vs 3/53 (6%), RR 3.9 (95% CI 1.2 to 13.1, p=0.016). All 10 patients with a final Ptco(2) ≥45 mm Hg received high concentration oxygen therapy, and in five there was an increase in Ptco(2) ≥10 mm Hg.

Conclusion High concentration oxygen therapy causes a clinically significant increase in Ptco(2) in patients presenting with severe exacerbations of asthma. A titrated oxygen regime is recommended in the treatment of severe asthma, in which oxygen is administered only to patients with hypoxaemia, in a dose that relieves hypoxaemia without causing hyperoxaemia.

Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma
Thorax. 2011 Nov;66(11):937-41

2 thoughts on “Oxygen therapy for asthma can elevate CO2”

  1. Dear Dr Reid,

    I think it is definitely an interesting study. However, whether this should change our management of these patients has yet to be proved. This is mainly due to the fact that the paper failed to show any change in patient outcome i.e. mortality, Hospital LOS, or ICU LOS. Hypercapnia, as we know from previous ICU based studies, isn’t necessarily a bad thing, and may in fact, provide a benefit to patient’s due to its possible bronchodilatatory effects.

    An interesting follow on study would be to compare a hypercapnic group to non-hypercapnic asthma patients and to study the outcomes. This may then change clinical management, but for the time being it may actually be dangerous to start the O2 titration in a group of patients who desperately need it!


  2. Interesting results, but I can’t understand how they’re physiologically plausible.

    In terms of V/Q matching, oxygen therapy may lead to pulmonary vasodilation, but in general a low V/Q ratio tends to cause significantly less hypercarbia than a high V/Q ratio, and is more responsive to increasing ventilation.

    Theoretically too, increasing the PAO2 decreases the PACO2 and thus the PaCO2 by increasing the gradient across which CO2 diffuses out.

    Regarding percutaneous monitoring, my understanding is that it correlates badly with PaCO2, but is useful for trends within individual patients. It’s use then in a trial like this is convenient but unreliable. It’s effect may also be skewed – wouldn’t SpO2 affect the readings by causing peripheral vasoconstriction?

    The other issue I have is that by giving O2 you’re preoxygenating a patient who might need an RSI, as well as offering them symptomatic relief by removing one of the drivers of their dyspnoea.

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