From a recent study:
Introduction
A high-flow nasal cannula (HFNC) has been used to treat patients with dyspnea. We identified changes in arterial blood gas (ABG) of patients visiting the emergency department (ED) with hypercapnic and nonhypercapnic respiratory failure after use of an HFNC.
Methods
This study was a retrospective chart review of patients with respiratory failure who visited the hospital and used an HFNC in the ED. The study period was July 1, 2011, to December 31, 2013. Patients with Paco2 greater than 45 mm Hg before the HFNC ABG analyses were included in the hypercapnia group; others comprised the nonhypercapnia group...
Results
A total of 173 patients were included after exclusion of 92 according to exclusion criteria. Eighty-one patients (hypercapnia group, 46, and nonhypercapnia group, 35) were included. Paco2 significantly decreased among all patients after use of HFNC (from 54.7 ± 26.4 mm Hg to 51.3 ± 25.8 mm Hg; P = .02), but the reduction was significant only in the hypercapnia group (from 73.2 ± 20.0 to 67.2 ± 23.4; P = .02). Progression to noninvasive or invasive ventilation and mortality rates were similar between the groups.Conclusions
Use of an HFNC in patients with hypercapnia could show a significant trend of decrease in Paco2. Progression to noninvasive or invasive ventilation and mortality rates were similar in patients with and without hypercapnia.
2 comments:
I seem to recall from the 1970s and 80s that it was axiomatic that you did not give high flow nasal 02 to hypercapneic COPD patients because it might depress their ventilatory drive and require mechanical ventilation as their pc02 would elevate. I am reasonably sure I saw that happen on more than one occasion and pulmonary docs preached to their colleagues to use low flow 02.Venti mask etc.Is that something else we were not just wrong about but really very wrong about? Is there an emoticon that expresses puzzlement?
I am sure the original concerns about high fractions of inspired oxygen making hypercapnia worse are correct (though the mechanism has been the subject of debate over the years). We've all seen that enough times. The new high flow cannula technology must have some novel mechanisms that lower CO2, such as washing it out of the dead space or providing some positive pressure. I may need to dive deeper into the physiology in a future post. Then too there's the concern about oxygen toxicity. That's something the pulmonary docs were also preaching about in the 70s and 80s, in the care of patients with ARDS. When newer concerns about volume and pressure related alveolar injury began to take center stage that problem was ignored, though of course it didn't go away. It's a potential unintended consequence someone might want to be thinking about.
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