Abstract

We thank Dr Esquinas [1] for his interesting and constructive comments on our article [2]. We agree that the study has several limitations that should be borne in mind when interpreting the results. As we pointed out in the discussion, we think that variations not only in intrathoracic pressure but also in lung volume may be responsible for the changes observed in inferior vena cava collapse. Previousstudies have consistently reported animmediate reduction in the respiratory rate after initiating high-flow nasal cannula (HFNC) treatment[3-5]. However, one of them[4] alsodescribed a concomitant reduction in the heart rate (HR). Furthermore, this reduction was observed after 6 hours of treatment with HFNC in patients with a mean baseline HR above 100 beats/min. Patients included in those studies were severely hypoxemic and, consequently, may have presented strong sympathetic activation. Several variables may influence HR in severely hypoxemic patients, such as correction of hypoxemia or reduction of upper respiratory resistance and work of breathing. In contrast, we included patients with stable (nondecompensated) heart failure (HF) who were treated with β-blockers and had a median baseline HR value less than 60 beats/min [2]. Thus, in the present study, thesevariablesmayhavelimitedtheinfluenceofsympatheticactivation on the respiratory pattern. The increases reported in end-expiratory lung volume (EELV) [5,6] and the fact that reported values of PaCO2 in previous studies remained invariable before and during HFNC therapy [3,4,7]suggest that the decrease in respiratory rate is due to an increase in tidal volume. Finally, all patients included in our study had a stable respiratory pattern before, during, and after the study. Unfortunately, according to the study design, it is impossible to determine whether the changes observed were due to EELV, endexpiratory positive pressure, or both. We hypothesize that EELV may play amoreimportantrolethanend-expiratorypositivepressureintheresults

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