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Olivier Contal, PhD, PT; Daniel Rodenstein, MD; Jean-Louis Pépin, MD, PhD; Jean-Paul Janssens, MD
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From the Division of Pulmonary Diseases (Drs Contal and Janssens), Geneva University Hospitals; the Service de pneumologie et Centre de médecine du sommeil (Dr Rodenstein), Cliniques Universitaires Saint Luc, Université Catholique de Louvain; and INSERM (Dr Pépin), U 1042, University Hospital, Grenoble.

Correspondence to: Olivier Contal, PhD, PT, Division of Pulmonary Diseases, Geneva University Hospitals, Rue Gabrielle-Perret-Gentil, 6, 1211 Geneva 14, Switzerland; e-mail: olivier.contal@hcuge.ch


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(4):1183-1184. doi:10.1378/chest.12-2694
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Published online
To the Editor:

We would like to submit the following answers to the comments made by Dr Esquinas on our study1 on backup respiratory rate (BURR) in subjects with obesity hypoventilation syndrome (OHS).

  • 1. The population under evaluation was indeed not naive to noninvasive positive pressure ventilation (NPPV). This was a deliberate choice, as we wished to analyze the impact of changes in BURR in subjects with OHS under noninvasive ventilation with as few other changes as possible. Thus, studying a population of patients familiar with NPPV certainly had a favorable impact on their acceptance of the protocol. This is a study limitation stated in the “Discussion” section. Performing the same study in subjects naive to NPPV would have generated other methodologic problems, related to adapting to NPPV, and would have made it more difficult to isolate the effect of changes in BURR.

  • 2. Patients had a high BMI, but this had no effect on the efficacy of NPPV: Patients were normocapnic during daytime, with an appropriate correction of average nocturnal transcutaneous CO2 monitoring (PtcCO2) and oxygen saturation as measured by pulse oximetry under NPPV. Apnea-hypopnea indices obtained under NPPV were in fact quite acceptable for patients with such a high BMI. The majority of the studies in the field reported BMIs >40 kg/m2 both in the United States and in Europe.2-4

  • 3. It is widely accepted that 90% of patients with OHS have upper airway obstruction, and, thus, we cannot accept that the potential effects of upper airway obstruction were not considered in patients. Average expiratory positive airway pressure values were 9.2±1.8 cm H2O (ie, far above what is used in ventilated obstructive or restrictive patients without associated obstructive sleep apnea syndrome); this clearly shows that upper airway obstruction was taken into account. Pressure settings were in agreement with available publications on long-term NPPV in patients with OHS and similar BMI.5-7 However, all patients in this study were put under noninvasive ventilation after an acute episode of hypercapnic respiratory failure and not electively. Polysomnograms performed during our study show a residual obstructive apnea-hypopnea index of 8.6/h under high BURR, vs higher values under low or no BURR, which shows to what extent BURR per se can be an important factor for stabilizing the upper airway.

  • 4. We agree that these patients were stabilized, and, thus, daytime PaCO2 was normalized, which is one of the main goals of NPPV. One can assume that to some extent ventilator drive and ventilator response to CO2 were improved when compared with baseline. Therefore, the same study in subjects naive to NPPV may have been associated with more important changes in nocturnal PtcCO2, although this remains to be documented.

  • 5. There is no evidence to support this hypothesis: Neither total ventilation nor tidal volume significantly decreased under spontaneous (S) mode (in fact, they were slightly higher than under both S/T modes). PtcCO2 clearly shows that there was no hypoventilation under S mode; in all modes, in spite of high BMI values, correction of alveolar hypoventilation was satisfactory.

  • 6. Patient/ventilator asynchrony has been an interest of our group for several years5 and was specifically looked for in this study. We did not find significant patient/ventilator asynchrony on polysomnogram tracings in this study, whatever mode was considered.

In conclusion, we have clearly shown that an S mode is associated with more frequent central and obstructive respiratory events when compared with S/T modes with low or high BURR in severe OHS and high BMI. This shows that BURR settings per se can have an important influence on the quality of NPPV. The impact of BURR must be further assessed in naive subjects with OHS and in other patient groups (ie, COPD, neuromuscular diseases) to better understand its importance in these clinical settings.

References

Contal O, Adler D, Borel J-C, et al Impact of different backup respiratory rates on the efficacy of noninvasive positive pressure ventilation in obesity hypoventilation syndrome: a randomized trial. Chest. 2013;143(1):37-46. [PubMed]
 
Borel J-C, Tamisier R, Gonzalez-Bermejo J, et al Noninvasive ventilation in mild obesity hypoventilation syndrome: a randomized controlled trial. Chest. 2012;141(3):692-702. [CrossRef] [PubMed]
 
Mokhlesi B Obesity hypoventilation syndrome: a state-of-the-art review. Respir Care. 2010;55(10):1347-1362. [PubMed]
 
Priou P, Hamel JF, Person C, et al. Long-term outcome of noninvasive positive pressure ventilation for obesity hypoventilation syndrome Chest. 2010;138(1):84-90. [PubMed]
 
Guo YF, Sforza E, Janssens JP Respiratory patterns during sleep in obesity-hypoventilation patients treated with nocturnal pressure support: a preliminary report. Chest. 2007;131(4):1090-1099. [CrossRef] [PubMed]
 
Pérez de Llano LA, Golpe R, Ortiz Piquer M, et al Short-term and long-term effects of nasal intermittent positive pressure ventilation in patients with obesity-hypoventilation syndrome. Chest. 2005;128(2):587-594. [CrossRef] [PubMed]
 
Storre JH, Seuthe B, Fiechter R, et al Average volume-assured pressure support in obesity hypoventilation: a randomized crossover trial. Chest. 2006;130(3):815-821. [CrossRef] [PubMed]
 

Figures

Tables

References

Contal O, Adler D, Borel J-C, et al Impact of different backup respiratory rates on the efficacy of noninvasive positive pressure ventilation in obesity hypoventilation syndrome: a randomized trial. Chest. 2013;143(1):37-46. [PubMed]
 
Borel J-C, Tamisier R, Gonzalez-Bermejo J, et al Noninvasive ventilation in mild obesity hypoventilation syndrome: a randomized controlled trial. Chest. 2012;141(3):692-702. [CrossRef] [PubMed]
 
Mokhlesi B Obesity hypoventilation syndrome: a state-of-the-art review. Respir Care. 2010;55(10):1347-1362. [PubMed]
 
Priou P, Hamel JF, Person C, et al. Long-term outcome of noninvasive positive pressure ventilation for obesity hypoventilation syndrome Chest. 2010;138(1):84-90. [PubMed]
 
Guo YF, Sforza E, Janssens JP Respiratory patterns during sleep in obesity-hypoventilation patients treated with nocturnal pressure support: a preliminary report. Chest. 2007;131(4):1090-1099. [CrossRef] [PubMed]
 
Pérez de Llano LA, Golpe R, Ortiz Piquer M, et al Short-term and long-term effects of nasal intermittent positive pressure ventilation in patients with obesity-hypoventilation syndrome. Chest. 2005;128(2):587-594. [CrossRef] [PubMed]
 
Storre JH, Seuthe B, Fiechter R, et al Average volume-assured pressure support in obesity hypoventilation: a randomized crossover trial. Chest. 2006;130(3):815-821. [CrossRef] [PubMed]
 
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