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Rol of high-flow therapy in patients with persistent hypercapnia after an acute COPD exacerbation

In the last issue of BMC Pulmonary Medicine, Pisani et al have published a very interesting study related to the effects of high flow therapy in patients with persistent hypercapnia after an acute COPD exacerbation.

It is well known that a number of observational studies have reported increased mortality associated with chronic hypercapnia in patients with COPD. For this reason, long-term High-Intensity Noninvasive Positive Pressure Ventilation (NIV) has been suggested as a strategy to decrease the PaCO2levels. However, this approach may be not well tolerated in all the patients. More recently, high flow nasal cannula therapy (HFNC) has been proposed as an alternative method to reduce hypercapnia in these patients.

Pisani et al have recently published a promising results related to HFNC in hypercapnic COPD. Fifty COPD patients recovering from an acute exacerbation requiring hospital admission and with persistent hypercapnia, despite having attained a stable pH (i.e. pH > 7,35 and PaCO2 > 45 mmHg on 3 consecutive measurements), were enrolled in an interventional study. It is very important to take into account that documented or highly suspected OSA/COPD overlap syndrome was not considered an exclusion criteria (defined as the presence of 15 or more obstructive respiratory events per hour of sleep, when a previous full night polysomnography (PSG) was available (n.12 patients) or from a positive Epworth questionnaire and a Body Mass Index (BMI) > 25 (n.11 patients). Cardiac decompensation, restrictive thoracic disorders, renal insufficiency, cancer, and neurological disease were considered exclusion criteria.

On day 1 the patients underwent a preliminary trial with HFNC to set the optimal flow, using the AIRVO 2. The patients were asked to breathe while trying to keep their mouth closed at flow rates from 20 L/min up to 40 L/min for a minimum of 15 min, if tolerated, for each trial. At the end of this test, the maximum level tolerated for 15 min was chosen as the flow to be used for the experimental procedure. Temperature was set according to the patient’s tolerance starting from 31 °C, up to 37 °C, while FiO2 was adjusted to maintain an SaO2between 92 and 94%. Between 9 am of day 2 and 9 am of day 5 (72 h period), patients underwent HFNC for at least 8 h/day plus during the nighttime.

Overall, 70% of patients (35/50) received NIV prior to HFNC. As usual, HFNC was well tolerated with a global tolerance score of 4.0 ± 0.9. When patients were separated into groups with or without COPD/OSA overlap syndrome, the “pure” COPD patients showed a statistically significant response in terms of PaCO2 decrease (p = 0.044). In addition, the subset of patients with a lower pH at enrolment were those who responded best in terms of CO2 clearance (score test for trend of odds, p = 0.0038).

In conclusion, what authors have shown us is that in COPD patients recovering from an episode of AHRF, which have reached a normal pH, the use of HFNC is associated with a statistically significant reduction in PaCO2 and respiratory rate. The better response was obtained in the subset of individuals with a lower pH level. However, this was not the case for COPD patients with the overlap syndrome. This fact underlines the importance of a good selection of patients in the studies and the problem to interpret the results when mixing patients with different characteristics.

These results provide more evidence about the efficacy of HFNC in hypercapnic COPD patients, in this case, in patients with persistent hypercapnia after an acute COPD exacerbation. It is always mandatory for the authors to finish the study saying that the results of this study may be useful to determine the sample size and the “ideal” characteristics of patients to include in future RCT.

BMC Pulm Med. 2020; 20: 12.

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