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LETTER TO THE EDITOR

High Intensity Positive Pressure Ventilation and Long Term Pulmonary Function Responses in Severe Stable COPD. A Delicate and Difficult Balance

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Pages 359-360 | Published online: 15 May 2014

Abstract

Method to improve minute ventilation (MV) during spontaneous breathing (SB) in stable severe chronic obstructive pulmonary disease (COPD) have a great clinical relevant in long term outcome. In this scenario, recommendations of early use of high-Intensity non-invasive Positive pressure Ventilation (HI-NPPV) or intelligent Volume Assured Pressure (iVAP) Support in Hypercapnic COPD have been proposed by safe therapeutics options. We analyze in this letter, Ekkernkamp et al. study that described the effect of HI-NPPV compared with SB on MV in patients receiving long-term treatment. We consider that interpretation of relationships between ABG, functional parameters, and respiratory mechanics reported need clarifications. Further prospective large clinical trials identifying the best mode of ventilation according to the characteristics in severe stable COPD are necessary to balance an effective approach and response on clinical symptoms and long-term effects.

Dear Editor,

Methods to improve minute ventilation (MV) during spontaneous breathing in stable COPD have significant clinical relevance. Recommendations for early use of high-intensity non-invasive positive pressure ventilation (HI-NPPV) and intelligent volume assured pressure support (iVAPS) in hypercapnic COPD have been proposed (Citation1).

In their study, Ekkernkamp et al. (Citation2) report that long-term HI-NPPV increases MV by an average of 26% compared with spontaneous breathing. Similar increase in MV was also observed with iVAPS. We would like to address some aspects of this study that would facilitate a proper clinical extrapolation of the information.

First, the relationships between arterial blood gases, functional parameters, and respiratory mechanics require further clarification. We know that in COPD, improvement of these parameters is dependent on decreasing lung hyperinflation, reducing inspiratory load, influencing ventilatory pattern and dyspnoea (Citation3–5). However, in Ekkernkamp's study the residual volume (% = from 159 to 160) and the total lung capacity (% = from 85 to 95) have increased. This is not in line with reduction of hyperinflation. Interestingly, there was only limited data for differences between obese and non-obese patients. It is known that functional response on auto-PEEP and inspiratory capacity especially for non-obese COPD could be different (Citation3,Citation5).

Second, in obese patients the mass of obesity reduces chest wall compliance and lung volumes, including the functional residual capacity. Decreased pulmonary compliance and increased upper airway resistance can in turn increase the load on inspiratory muscles. As a result, in obese patients, higher levels of ventilatory drive are required to maintain normocapnia, despite a progressive decline in chemosensitivity due to hypercapnea. Could this possibly explain the difference in respiratory rate in obese and non-obese COPD?

During HI-NPPV, breathing pattern and respiratory rate are relevant because any increment in MV could influence excessive auto-PEEP levels, oxygen cost, work of breathing, and an ineffective trigger, especially in non-obese COPD (Citation6).

Third, a definition of leaks as percentage difference between inspiratory and expiratory tidal volume is controversial, and this couldn't take into account mask leakages.

Fourth, the values of PaCO2 before HI-NPPV are directly proportional to the achieved results, as reported by several studies (Citation3–5). Comparing efficacy HI-NPPV and iVAPS in reducing PaCO2; it is interesting to note that during iVAPS, non-obese COPD fails to achieve a good reduction of PaCO2 with a lower respiratory rate and MV when compared to obese COPD. This difference is not observable during HI-NPPV (Citation2).

Fifth, some authors suggest that difference of respiratory rate and MV in non-obese COPD during iVAPS is due to a greater difficulty in triggering, given these patients develop greater hyperinflation and greater total lung capacity than obese ones (Citation2). However, it seems more likely that restrictive component in obese COPD correlates with a higher respiratory rate and MV during iVAPS. In addition, trigger sensitivity can play a significant role in determining respiratory rate.

Finally, daytime versus night ventilatory measurements could be different, even if it is controversial because sleep efficacy (Citation7), and inflation has not yet been evaluated in detail (Citation8). Relevant aspects to consider are the long-term effects such as mortality, and variations in nutritional status (Citation4), dyspnoea, health-related quality of life, and dynamic hyperinflation.

Declaration of Interest Statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

References

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  • Díaz O, Bégin P, Torrealba B, Effects of noninvasive ventilation on lung hyperinflation in stable hypercapnic COPD. Eur Respir J 2002;20(6):1490–1498.

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