Prescription of high flow oxygen with subsequent increase of SpO2 above 92% without investigation of PaCO2 levels, has become a policy in many hospitals, especially in the ER. Is there any evidence supporting high FiO2 resulting in SpO2 higher than 92% in patients with hypercapnia?
It is important question.My observation which patients with mechanic ventilation, is high and higher FİO2 has made slower respiratory center output, in spite of MV.Because of then, PaCO2 changes hypercapnic state.
I havn`t seen any studies to support this high O2-flow theory! All other arguments against are well known since years
Use of high flow of oxygen does not necessarily mean use of high FiO2, because they are two different parameters (L / min of gaseous mixture versus O2% in the gaseous mixture). In any case, I believe that the target of 88-92% of SO2 in hypercapnic patients should always be respected.
Thank you all for your answers. By high flow O2 I mean the general rule of prescribing O2 at 15L/min when SpO2 drops significantly, which is practically achieved by the use of non rebreathe mask, resulting in high FiO2 indeed. You see, clinicians supporting the aforementioned theory, put forward that a patient in the ER may die because of hypoxemia but not because of hypercapnia. In my point of view though, hypoventilation caused by high FiO2 in such patients can deteriorate hypoxemia.
I believe this question should be addressed according to both the etiology of acute respiratory failure (ARF) and the monitoring of the treatment.
In the type of ARF due to compromised gas exchange, without impairment of ventilation (i.e. expanded pneumonia), high FiO2 and the target SpO2> 92% are definitely beneficial and without significant risk of hypercapnia. In addition, monitoring not only SpO2, but also pO2 and pCO2 with ABG after 30-60 minutes of treatment allows recognizing promptly any tendency to the raising of pCO2.
I attach two recent papers on the subject.
One has to be cautious particularly in home oxygen users about increasing FIO2
in the face of mild to moderate hypercapnia. It is best to have a target SPO2 of 90-92% , and caregivers have to be cautioned against knee jerk reaction in raising O2
levels. Perhaps COPD patients on bileel ventilation are somewhat safer in this regard.
The latest study you may be interested in is by Carly Ann Hollier, et al and is titled "Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study." Published in Thorax. 2014 Apr;69(4):346-53. The author provided a contact e-mail in the article.
The key question of there study was "What are the effects of moderate concentrations of supplemental oxygen on CO2, pH, ventilation and physiological dead space to tidal volume ratio (VD/VT) in people with obesity hypoventilation syndrome (OHS)?"
And the bottom line was that "In OHS, breathing moderate concentration supplemental oxygen for 20 min worsened hypercapnia and induced acidaemia due to hypoventilation and a worsening of VD/VT."
The participants of the study breathed oxygen concentrations (FiO2) of 0.28 and 0.50, each for 20 min, separated by a 45 min washout period. Arterialised-venous PCO2 (PavCO2) and pH, VE and VD/VT were measured at baseline, then every 5 min.
The conclusion of the study reported that "Commonly used oxygen concentrations caused hypoventilation, PavCO2 rises and acidaemia among people with stable OHS. This highlights the potential dangers of this common intervention in this group."
Good luck with your work.
-mh
Not recent, but I was very impressed by the findings of this study:
Article Effect of high flow oxygen on mortality in chronic obstructi...
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