High FIO2 Deleterious in Acute Asthma

Abstract & Commentary

Synopsis: Adult patients presenting with acute asthma without significant respiratory acidosis who were given 100% oxygen to breathe had slight increases in arterial PCO2 and slight decreases in arterial pH and peak expiratory flow, as compared with patients who received only 28% oxygen.

Source: Rodrigo GJ, et al. Chest. 2003;124(4): 1312-1317.

Supplemental oxygen is a mainstay of the treatment of acute severe asthma, although it has been postulated that breathing too high a concentration might induce or worsen respiratory acidosis. Rodrigo and colleagues conducted this study in 2 hospital emergency departments in Uruguay to investigate this hypothesis. Adult patients presenting with acute asthma uncomplicated by signs of infection or complicating illness were randomized to breathe 2 different concentrations of supplemental oxygen (28% and 100%) via mask prior to initiating bronchodilator therapy. Rodrigo et al assessed the severity of dyspnea, vital signs, arterial blood gases, and peak expiratory flow (PEF) before and after the 20-minute oxygen breathing periods.

Seventy-four patients with acute asthma (mean age, 38; initial PEF 41 ± 12% of predicted) completed the study. Initial values for PaO2 and PaCO2 while the patients breathed room air were 78 ± 13 and 36 ± 4 mm Hg, respectively; no patient had an initial PaO2 < 58 mm Hg or an initial PaCO2 > 46 mm Hg. Heart and respiratory rates did not change with oxygen therapy and were not different in the 2 groups; dyspnea and wheezing scores were similar before treatment and were not presented after oxygen administration.

Mean arterial PCO2 was higher (38.0 vs 35.4 mm Hg; P = 0.03), and arterial pH lower (7.38 vs 7.41; P = 0.01), after 20 minutes of oxygen therapy in the 100% group as compared to the 28% group. Four patients in the 100% oxygen group experienced a rise in PaCO2 from < 50 mm Hg to > 50 mm Hg. Patients receiving 100% oxygen had a slight decrease in PEF (24 L/min; 11%), whereas those receiving 28% oxygen has a slight increase (7.6 L/min; 3%), and this difference was statistically significant (P = 0.001). Based on their findings, Rodrigo et al recommend that supplemental oxygen therapy in acute asthma be titrated to an oxyhemoglobin saturation (measured by pulse oximetry) of 92% or more, rather than administered in some standardized, fixed concentration or liter flow.

Comment by David J. Pierson, MD

This study of patients presenting with acute asthma who had not yet received bronchodilator therapy showed that, on average, patients given 100% oxygen to breathe had slightly higher PaCO2 and slightly lower pH values after 20 minutes than those given 28% oxygen. Arterial PCO2 decreased in about as many patients as it increased, but among those given 100% oxygen, 42% of the patients had increases in PaCO2 of 2-14 mm Hg (mean, 5 mm Hg), and the change for the whole group was statistically significant in comparison with the 28% oxygen group.

It is important to point out several features of this study that could affect clinical practice. Although the study period was brief (less than an hour, counting the various measurements), Rodrigo et al withheld bronchodilator therapy until after it was completed. In clinical practice, aerosol therapy would be begun immediately, and whether the observed differences would have been present under such circumstances cannot be known. Either by design or because of the patient mix seen in the participating emergency departments, the study also included no patients with clinically important acute respiratory acidosis. One might worry that patients with more severe attacks might have even greater changes in PCO2 and pH in response to high FIO2 than those in this study, but that is unknown.

On the other hand, one can wonder whether any of the changes in these values documented in this study were clinically important. Whether administration of 100% oxygen would affect the clinical response to bronchodilator therapy or lead to more patients having to be intubated is unknown. Still, it makes sense, based on these findings, not to give patients with acute asthma any more oxygen than is necessary to adequately saturate their hemoglobin.

Although there was a slight, but statistically significant, fall in PEF among the patients who received 100% oxygen in comparison with values from those who got 28% oxygen, Rodrigo et al make no comment on this other than to correlate it with changes in PaCO2 values, and no possible physiologic explanation is offered. I doubt whether the PEF differences are clinically (as opposed to statistically) significant, but I must confess that I cannot think of a reason why airflow limitation would be increased by a higher concentration of oxygen in the breathing mixture. Perhaps a reader can enlighten me.

David J. Pierson, MD, Pulmonary and Critical Care Medicine, Harborview Medical Center, University of Washington, is Editor of Critical Care Alert.