High-Flow Nasal Cannula versus Noninvasive Ventilation in AECOPD Patients with Respiratory Acidosis: A Retrospective Propensity Score-Matched Study

Wang, Meng; Zhao, Feifan; Sun, Lina; Liang, Ying; Yan, Wei; Sun, Xiaoyan; Zhou, Qingtao; He, Bei

doi:https://doi.org/10.1155/2023/6377441

Canadian Respiratory Journal

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Abstract Introduction Methods Results Discussion Conclusions Data Availability Conflicts of Interest Authors’ Contributions Acknowledgments References Copyright Related Articles

Research Article | Open Access

Volume 2023 | Article ID 6377441 | https://doi.org/10.1155/2023/6377441

High-Flow Nasal Cannula versus Noninvasive Ventilation in AECOPD Patients with Respiratory Acidosis: A Retrospective Propensity Score-Matched Study

Meng Wang,¹Feifan Zhao,¹Lina Sun,¹Ying Liang,¹Wei Yan,¹Xiaoyan Sun,¹Qingtao Zhou,¹and Bei He¹

Academic Editor: Ammara Saleem

Received17 Oct 2022

Revised14 Mar 2023

Accepted30 Mar 2023

Published15 Apr 2023

Abstract

Background. Limited data are available about the clinical outcomes of AECOPD patients with respiratory acidosis treated with HFNC versus NIV. Methods. We conducted a retrospective study to compare the efficacy of HFNC with NIV as initial ventilation support strategy in AECOPD patients with respiratory acidosis. Propensity score matching (PSM) was implemented to increase between-group comparability. Kaplan–Meier analysis was utilized to evaluate differences between the HFNC success, HFNC failure, and NIV groups. Univariate analysis was performed to identify the features that differed significantly between the HFNC success and HFNC failure groups. Results. After screening 2219 hospitalization records, 44 patients from the HFNC group and 44 from the NIV group were successfully matched after PSM. The 30-day mortality (4.5% versus 6.8%, ) and 90-day mortality (4.5% versus 11.4%, ) did not differ between the HFNC and NIV groups. Length of ICU stay (median: 11 versus 18 days, ), length of hospital stay (median: 14 versus 20 days, ), and hospital cost (median: 4392 versus 8403 $USD, ) were significantly lower in the HFNC group compared with NIV group. The treatment failure rate was much higher in the HFNC group than in the NIV group (38.6% versus 11.4%, ). However, patients who experienced HFNC failure and switched to NIV showed similar clinical outcomes to those who first received NIV. Univariate analysis showed that log NT-proBNP was an important factor for HFNC failure (). Conclusions. Compared with NIV, HFNC followed by NIV as rescue therapy may be a viable initial ventilation support strategy for AECOPD patients with respiratory acidosis. NT-proBNP may be an important factor for HFNC failure in these patients. Further well-designed randomized controlled trials are needed for more accurate and reliable results.

1. Introduction

Chronic obstructive pulmonary disease is a common respiratory disease characterized by persistent respiratory symptoms and airflow limitation [1]. Patients may require hospitalization and respiratory support due to acute exacerbations. Noninvasive ventilation (NIV) is the first-line treatment for acute exacerbation of COPD (AECOPD) with respiratory acidosis [2]. However, up to 30% of AECOPD patients do not tolerate NIV due to interface discomfort, sputum retention, impaired communication, and facial skin breakdown [3, 4].

High-flow nasal cannula (HFNC) is a high-flow oxygen delivery system that can provide well-heated and humidified oxygen at continuous high flow rates up to 60 L/min via a large-bore nasal cannula [5]. Previous studies and literature reviews showed that HFNC had many beneficial effects in stable COPD patients, including a constant fraction of inspired oxygen delivery, dead space washout, improved comfort and tolerance, better communication, enhanced secretion clearance, and positive end-expiratory pressure (PEEP) effect, resulting in decreased PaCO₂, reduced inspiratory effort, lower rate of moderate/severe exacerbations, and prolonged duration without exacerbations [6–13]. In AECOPD patients, recent studies also showed that HFNC can reduce PaCO₂ and improve capillary pH as well as the work of breathing and patient comfort [14–16]. However, limited data are available about the clinical outcomes of AECOPD patients with respiratory acidosis using HFNC as initial ventilation support strategy compared with NIV [16–19].

The purpose of this study was to compare the effects of HFNC versus NIV as initiating ventilation support strategy on clinical outcomes in AECOPD patients with respiratory acidosis, as well as to explore the predictors of HFNC failure.

2. Methods

2.1. Study Design and Population

We reviewed all consecutive patients admitted to our 26-bed medical ICU between January 2018 and January 2022 at Peking University Third Hospital, a university-affiliated tertiary hospital in Beijing, China. AECOPD patients with respiratory acidosis were enrolled according to the following criteria: (a) fulfilled the AECOPD criteria [20], (b) had a decreased pH (7.20 < pH < 7.35) with PaCO₂ > 45 mmHg upon admission, and (c) received either NIV or HFNC for initial ventilation support. Schematic of patient selection is shown in Figure 1. This study was approved by the Ethics Committee of Peking University Third Hospital (approval no. M2022265), and due to its observational nature, the requirement for informed consent was waived. All patient records and data were anonymized and deidentified prior to analysis.

2.2. Classification of Patients and Ventilation Settings

All the patients were treated with HFNC and NIV based on our ICU treatment protocol. Patients in the study were classified into two groups based on the ventilation support strategy they received: the HFNC group and the NIV group. The fraction of inspired oxygen was set to keep SpO₂ at 88–92% or PaO₂ at around 60 mmHg in both groups.

Patients in the HFNC group were treated with HFNC as initial ventilation support strategy and switched to NIV when the following criteria was met: (1) intolerance of nasal cannula or high flow rates; (2) worsened pH in conjunction with a rise in PaCO₂ one hour after optimal flow rate settings (highest flow rates tolerated). HFNC was delivered by AIRVO-2™ (Fisher and Paykel Healthcare, Auckland, New Zealand). The initial flow rate was set at 25 L/min and gradually increased to the maximal tolerance of each patient [21]. When arterial blood gas was improved (pH > 7.35 with decreased PaCO₂), the flow rate was gradually decreased (5 L/min each time) and HFNC was discontinued when the flow rate was less than 20 L/min. Treatment failure of HFNC was defined as switching to NIV. When patients in the HFNC group further deteriorated after switching to NIV and met the criteria for intubation, they would be intubated and receive invasive ventilation.

NIV was the initial ventilation support strategy in the NIV group. Noninvasive ventilation was applied with specified NIV ventilator V60 (Philips Respironics, California, United States) via a full-face mask. S/T mode was applied to all patients. Expiratory positive airway pressure (EPAP) was commenced at 4 H₂O and titrated to diminish ineffective inspiratory efforts. Inspiratory positive airway pressure (IPAP) was set at 8 H₂O and gradually increased to achieve a tidal volume of more than 6 mL/kg or to the maximum each patient could tolerate. IPAP was limited to no more than 25 H₂O [22]. NIV was used as long as possible during the first 24 hours, until pH, PaCO₂, and clinical condition improved. When arterial blood gas was improved (pH > 7.35 with decreased PaCO₂), the duration of NIV was gradually decreased until the patient could sustain 24-hour spontaneous breathing without NIV [23]. NIV failure was defined as intubation or death during NIV.

The criteria for intubation in our department were in accordance with published literature, and intubation was left to the discretion of the physician [4, 22, 24]. Major criteria for intubation were (1) cardiac or respiratory arrest; (2) loss of consciousness; and (3) hemodynamic instability. Minor criteria were (1) unable to fit mask; (2) inability to protect the airway; (3) inability to clear secretions; (4) respiratory rate more than 35 breaths per minute; (5) signs of increased work of breathing, accessory muscle use, or abdominal paradox; and (6) worsened pH in conjunction with a rise in PaCO₂ one hour after optimal ventilator settings (highest IPAP tolerated).

2.3. Data Collection

The following data were extracted from electronic medical records for all included patients: demographic information (age, gender, and body mass index), comorbidity severity scores including Charlson Comorbidity Index [25], Simplified Acute Physiology Score (SAPS) II, and Acute Physiology and Chronic Health Evaluation (APACHE) II scores, and outcomes, such as treatment failure, length of ICU stay, length of hospital stay, total ventilation time, and hospital cost. Additionally, clinical, radiological, and laboratory data on admission, such as heart rate, systolic blood pressure, respiratory rate, body temperature, echocardiography results, N-terminal prohormone, brain natriuretic peptide (NT-proBNP), FIO₂, and arterial blood gas results, such as pH, PaO₂, PaCO₂, sodium bicarbonate, and PaO₂-to-FIO₂ ratio, were also collected. Settings of NIV or HFNC during the ICU stay were collected. A propensity score model was used to match patients, and clinical outcomes like 30-day mortality, 90-day mortality, treatment failure rate (defined by switching to NIV in the HFNC group, and intubation or death in the NIV group), length of ICU stay, length of hospital stay, total ventilation time, and hospital cost were compared after propensity score matching (PSM).

2.4. Statistical Analyses

Propensity score matching was applied to reduce the possibility of selection bias and confounding factors. Age, gender, BMI, APACHE II, SAPS II, comorbidities, heart rate, respiratory rate, pH, PaO₂, PaCO2, and PaO₂/FIO₂ were included for propensity score matching. A multivariate logistic regression model was used to estimate patients’ propensity score for receiving HFNC or NIV. A caliper of 0.15 was used for one-to-one nearest neighbor matching.

The consistency test of normal distribution for measurement data was carried out by the Shapiro–Wilk test. According to the distribution, continuous variables were reported as mean ± standard deviation (SD) or median (interquartile range (IQR), from 25^th to 75^th percentiles) and were compared with independent sample t-tests, Mann–Whitney U test, or Kruskal–Wallis test as appropriate. Categorical variables were expressed as percentages and were compared by Fisher’s exact test or chi-square test when appropriate.

Univariate logistic analysis was performed to identify factors related to HFNC failure. Kaplan–Meier curves were drawn to assess the length of ICU stay, length of hospital stay, and total ventilation time, and log-rank tests were used to compare the differences between the HFNC failure, HFNC success, and NIV groups.

All statistical analyses were performed using SPSS 26.0 (IBM Corporation, Armonk, NY, USA). values less than 0.05 were considered significant.

3. Results

3.1. Study Population

There were 2219 ICU admissions between January 2018 and January 2022, and 151 patients were included in this study, with 48 receiving HFNC and 103 receiving NIV. The baseline characteristics of both groups before propensity score matching are presented in Table 1. Compared with the HFNC group, patients in the NIV group exhibited lower GCS scores and a larger proportion of home NIV use, hypertension, and diabetes mellitus. After propensity score matching, there were 44 patients from the HFNC group and 44 patients from the NIV group, with mean ages of 78.4 and 80.2 years, respectively. The baseline characteristics of the two groups were well balanced after propensity score matching (Table 2). The ventilation settings of HFNC and NIV are shown in Table 3.

3.2. Clinical Outcomes

The clinical outcomes of the matched patients are shown in Table 4. The 30-day mortality (4.5% versus 6.8%, ), 90-day mortality (4.5% versus 11.4%, ), and intubation rate (4.5% versus 11.4%, ) did not differ between the HFNC and NIV groups. The treatment failure rate was significantly higher in the HFNC group than in the NIV group (38.6% versus 11.4%, ). However, length of ICU stay (11 (IQR, 7–15) versus 18 (IQR, 11–27) days, ), length of hospital stay (14 (IQR, 9–17) versus 20 (IQR, 16–30) days, ), total ventilation time (7 (IQR, 4–11) versus 13 (IQR, 7–23) days, ), and hospital cost (4392 (IQR, 3450–7889) versus 8403 (IQR, 5738–17469) $USD, ) were significantly lower in the HFNC group compared with NIV group.

We compared the differences in clinical outcomes between the HFNC success, HFNC failure, and NIV groups. Figure 2 shows the Kaplan–Meier curves for length of ICU stay (Figure 2(a)), length of hospital stay (Figure 2(b)), and total ventilation time (Figure 2(c)). There was no significant difference between the HFNC failure group and the NIV group in terms of the length of ICU stay, length of hospital stay, or total ventilation time, while the HFNC success group showed a significantly lower result than the other two groups (Table 5).

(a)

(b)

(c)

In the HFNC group before PSM, 17 of 48 patients experienced treatment failure. We performed univariable logistic regression analyses to identify factors related to treatment failure in the HFNC group (Table 6). Univariate analysis showed that log-transformed NT-proBNP was an important factor for HFNC failure (). However, due to the relative small number of patients who failed HFNC, the events per variable (EPV) were not adequate for multivariate logistic regression.

4. Discussion

The current study examined the impact of HFNC and NIV on clinical outcomes in AECOPD patients with respiratory acidosis admitted to the ICU. After screening and propensity score matching, 44 patients who received HFNC and 44 patients who received NIV were included in our study, with well-balanced baseline characteristics. Our current findings suggested that HFNC followed by NIV as rescue therapy might be a viable initiating ventilation strategy for AECOPD patients with respiratory acidosis, as there was no difference in 30-day mortality and 90-day mortality and significantly shorter length of ICU stay, length of hospital stay, and total ventilation time when compared to NIV therapy, which is the “gold standard” in these patients. In addition, NT-proBNP level upon admission was an important factor for HFNC failure.

The overall short-term mortality rate varies from 1.8% to 20.4% for hospitalized patients with AECOPD [26, 27]. Several clinical trials comparing HFNC with NIV in AECOPD patients with respiratory acidosis have indicated promising clinical outcomes with HFNC. In a prospective observational study, Lee and colleagues found no difference between the HFNC and NIV groups in terms of intubation rate (25% HFNC versus 27.3% NIV, ), 30-day mortality (15.9% HFNC versus 18.2% NIV, ), or device application days (7 HFNC versus 8 NIV, ) in patients with AECOPD and moderate hypercapnic respiratory failure [16]. In another observational cohort trial, Sun and colleagues compared the outcomes of HFNC and NIV in patients with COPD exacerbation and moderate acute hypercapnic respiratory failure (arterial pH between 7.25 and 7.35). Both groups had comparable device failure rates (28.2% HFNC versus 39.5% NIV, ) and 28-day mortality rates (15.4% HFNC versus 14% NIV, ). Neither the length of ICU stay (7 days HFNC versus 8 days NIV, ) nor hospital stay (9 days HFNC versus 10 days NIV, ) differed significantly between the two groups [18]. In a subgroup analysis of 65 patients from a large randomized controlled trial, Doshi and colleagues also found identical failure rates of HFNC and NIV at 72 h (23.5% versus 25.8%, ) [28]. A few randomized controlled trials also revealed similar clinical outcomes between the HFNC and NIV groups. In a randomized clinical trial, forty patients were randomly assigned to the HFNC group and NIV group. There was no difference in the duration of hospitalization (11.5 days HFNC versus 11.0 days NIV, ) or mortality rate (15% HFNC versus 15% NIV, ) between the two groups [19]. In a multicenter noninferiority randomized trial conducted by Cortegiani et al., eighty patients with mild-to-moderate AECOPD (arterial pH: 7.25–7.35, PaCO₂ ≥ 55 mmHg before ventilator support) were randomly allocated to either the HFNC group or the NIV group. In terms of reducing PaCO₂, both treatments showed a significant effect on PaCO₂ reduction over time. After 2 h of treatment, HFNC was not statistically inferior to NIV since the mean difference in PaCO₂ reduction between the two groups was 2.66 mmHg, which was within the noninferiority threshold of 10 mmHg. The length of hospital stay (10 days HFNC versus 13 days NIV, ) and in-hospital mortality (5% HFNC versus 15.4% NIV, ) were comparable across the two groups. In addition, 32% of patients in HFNC group switched to NIV by 6 hours, and 57.5% received NIV during hospitalization [17]. In a more recent large retrospective study of 173 hospitalized COPD patients receiving HFNC, 68 patients (39%) experienced HFNC failure [29].

In the present study, the 30-day and 90-day mortality rates of the overall cohort were 5.7% and 8.0%, respectively, which are consistent with the findings of previous studies [26, 27], reinforcing the external validation of our results. There was no difference in 30-day mortality between the HFNC and NIV groups, which is consistent with previous studies reporting mortality [16–19]. The mortality rate was comparable between one study (5% HFNC versus 15.4% NIV) and ours (4.5% HFNC versus 6.8% NIV) [17]. However, the 30-day mortality rate was significantly higher in the other three studies. In two studies, this may have been due to the overall lower PaO₂/FIO₂ in their studies compared with ours ((134.6 ± 7.4 mmHg versus 200.0 ± 53.4 mmHg) [16] and (139.2 ± 6.7 mmHg versus 200.0 ± 53.4 mmHg) [18]), indicating more severe respiratory failure. In the study conducted by Papachatzakis, the APACHE II scores of the enrolled patients were significantly higher than ours (20.5 versus 16), which represented a higher mortality risk. These factors may explain why our investigations yielded different outcomes.

In contrast to the results of previously mentioned studies [16–19], HFNC was substantially related to shorter length of ICU stay, hospital stay, and total ventilation days than NIV in this study. This result may be attributable to the longer length of ICU stay, hospital stay, and total ventilation days in the NIV group. High arterial PaCO₂ and coexisting morbidities such as diabetes, hypertension, and cancer have been demonstrated to be related to extended ICU and hospital stays [30, 31]. In the present study, the patients enrolled had higher arterial PaCO₂ and more coexisting morbidities, which may partially explain the discrepancy between the current study and earlier studies. Our results also showed that patients who responded well to HFNC may experience a significantly shorter length of total ventilation time, ICU stay, hospital stay, and lower hospital cost. Furthermore, when patients failed HFNC therapy and switched to NIV, clinical outcomes were no worse than NIV therapy alone (Figure 2).

In the present study, univariable logistic analysis showed that the NT-proBNP level upon admission might be an important factor for HFNC failure in AECOPD patients with respiratory acidosis. NT-proBNP is secreted by cardiac myocytes in response to increased arterial and ventricular filling pressure and is widely used for the diagnosis and management of heart failure [32, 33]. In addition to heart failure, NT-proBNP is also elevated in other conditions, including advanced age, renal failure, chronic lung disease, coronary heart disease, pulmonary hypertension, and sepsis [34]. Elevated NT-proBNP levels are also observed in AECOPD patients without primary cardiac abnormalities as a consequence of the release of NT-proBNP from the right ventricle caused by cor pulmonale, pulmonary hypertension, and hypoxemia [35]. Previous studies have shown that elevated NT-proBNP level is associated with worse in-hospital outcomes and is a reliable predictive biomarker of poor prognosis in patients with AECOPD [36, 37]. In a more recent study, Veenstra and colleagues found a significant association between cardiac (myocardial infarction, heart failure, or arrhythmia) (OR = 0.435, ) and vascular (hypertension and peripheral arterial disease) (OR = 0.493, ) comorbidity and a lower likelihood of HFNC success in AECOPD patients [29]. In the present study, our results further indicate that the NT-proBNP level upon admission might be an important factor for HFNC failure in AECOPD patients with respiratory acidosis.

Our study had several limitations. First, it was a retrospective observational study conducted at a single center, and there was a possibility of clinical selection bias regarding the ventilation support patients received. However, HFNC and NIV were both first-line options for these patients in our hospital, which could reduce selection bias. In addition, we used propensity score matching to balance the baseline characteristics between the two groups and evaluated the treatment outcomes based on the matched group, which could further reduce selection bias. Second, due to the relatively high age of patients in our study group, the latest pulmonary function test results were years before admission, which were not suitable to analyze the influence on clinical outcomes. Third, in the present study, we did not rule out patients with comorbid heart failure. As a result, heart failure accounted for 21.6% of the entire study population. NT-proBNP levels in the HFNC and NIV groups were 1251.0 (IQR, 367.0–2437.5) and 1995.0 (IQR, 510.3–3977.5) pg/ml, respectively. Considering the relatively normal LVEF (69.51 ± 6.10%) and high RVSP (38 (IQR, 28–50) mmHg), the elevation in NT-proBNP might be due to the complex interplay of heart failure with preserved ejection with right ventricular dysfunction. We were unable to further investigate the origin based on the retrospective data. Fourth, due to the relatively small number of patients who failed HFNC, the events per variable (EPV) were not adequate for multivariate logistic regression. So we could not further analyze whether NT-proBNP was an independent risk factor for HFNC failure or not. Finally, the sample size was relatively small due to propensity matching, and the results must be interpreted with caution. Large-scale, multicenter, and randomized controlled trials with larger sample sizes are still required to obtain more accurate and reliable results.

5. Conclusions

HFNC followed by NIV as rescue therapy may be a viable initial ventilation support strategy for AECOPD patients with respiratory acidosis, with lower hospital costs, shorter ICU and hospital stays, and similar clinical outcomes compared with NIV. NT-proBNP may be an important factor for HFNC failure in these patients. Further well-designed randomized controlled trials are needed to obtain more accurate and reliable results.

Data Availability

The datasets analyzed during this study are available from the corresponding author upon reasonable request.

Conflicts of Interest

The authors declare that there are no conflicts of interest.

Authors’ Contributions

Meng Wang was responsible for literature search. Meng Wang, Feifan Zhao, Lina Sun, Ying Liang, and Wei Yan collected the data. Meng Wang, Qingtao Zhou, and Bei He designed the study. Meng Wang, Feifan Zhao, Qingtao Zhou, and Xiaoyan Sun analyzed the data. Meng Wang and Qingtao Zhou prepared the manuscript. Meng Wang, Qingtao Zhou, and Bei He reviewed the manuscript. All authors reviewed the results and approved the final version of the manuscript.

Acknowledgments

This study was funded by a clinical cohort construction program of Peking University Third Hospital (no. BYSYDL2021019).

References

D. M. G. Halpin, G. J. Criner, A. Papi et al., “Global initiative for the diagnosis, management, and prevention of chronic obstructive lung disease. The 2020 GOLD science committee report on COVID-19 and chronic obstructive pulmonary disease,” American Journal of Respiratory and Critical Care Medicine, vol. 203, no. 1, pp. 24–36, 2021.
View at: Publisher Site | Google Scholar
B. Rochwerg, L. Brochard, M. W. Elliott et al., “Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure,” European Respiratory Journal, vol. 50, no. 2, Article ID 1602426, 2017.
View at: Publisher Site | Google Scholar
A. Gacouin, S. Jouneau, J. Letheulle et al., “Trends in prevalence and prognosis in subjects with acute chronic respiratory failure treated with noninvasive and/or invasive ventilation,” Respiratory Care, vol. 60, no. 2, pp. 210–218, 2015.
View at: Publisher Site | Google Scholar
E. Ozyilmaz, A. O. Ugurlu, and S. Nava, “Timing of noninvasive ventilation failure: causes, risk factors, and potential remedies,” BMC Pulmonary Medicine, vol. 14, no. 1, p. 19, 2014.
View at: Publisher Site | Google Scholar
M. Nishimura, “High-flow nasal cannula oxygen therapy in adults: physiological benefits, indication, clinical benefits, and adverse effects,” Respiratory Care, vol. 61, no. 4, pp. 529–541, 2016.
View at: Publisher Site | Google Scholar
A. A. Alnajada, B. Blackwood, A. Mobrad, A. Akhtar, I. Pavlov, and M. Shyamsundar, “High flow nasal oxygen for acute type two respiratory failure: a systematic review,” F1000Res, vol. 10, p. 482, 2021.
View at: Publisher Site | Google Scholar
M. E. Yuste, O. Moreno, S. Narbona, F. Acosta, L. Penas, and M. Colmenero, “Efficacy and safety of high-flow nasal cannula oxygen therapy in moderate acute hypercapnic respiratory failure,” Revista Brasileira de Terapia Intensiva, vol. 31, no. 2, pp. 156–163, 2019.
View at: Publisher Site | Google Scholar
L. Pisani, L. Fasano, N. Corcione et al., “Change in pulmonary mechanics and the effect on breathing pattern of high flow oxygen therapy in stable hypercapnic COPD,” Thorax, vol. 72, no. 4, pp. 373–375, 2017.
View at: Publisher Site | Google Scholar
H. Vogelsinger, M. Halank, S. Braun et al., “Efficacy and safety of nasal high-flow oxygen in COPD patients,” BMC Pulmonary Medicine, vol. 17, no. 1, p. 143, 2017.
View at: Publisher Site | Google Scholar
J. Braunlich, M. Kohler, and H. Wirtz, “Nasal highflow improves ventilation in patients with COPD,” International Journal of Chronic Obstructive Pulmonary Disease, vol. 11, pp. 1077–1085, 2016.
View at: Publisher Site | Google Scholar
J. Braunlich, D. Dellweg, A. Bastian et al., “Nasal high-flow versus noninvasive ventilation in patients with chronic hypercapnic COPD,” International Journal of Chronic Obstructive Pulmonary Disease, vol. 14, pp. 1411–1421, 2019.
View at: Publisher Site | Google Scholar
K. Nagata, T. Horie, N. Chohnabayashi et al., “Home high-flow nasal cannula oxygen therapy for stable hypercapnic COPD: a randomized clinical trial,” American Journal of Respiratory and Critical Care Medicine, vol. 206, no. 11, pp. 1326–1335, 2022.
View at: Publisher Site | Google Scholar
J. F. Fraser, A. J. Spooner, K. R. Dunster, C. M. Anstey, and A. Corley, “Nasal high flow oxygen therapy in patients with COPD reduces respiratory rate and tissue carbon dioxide while increasing tidal and end-expiratory lung volumes: a randomised crossover trial,” Thorax, vol. 71, no. 8, pp. 759–761, 2016.
View at: Publisher Site | Google Scholar
J. Braunlich and H. Wirtz, “Nasal high-flow in acute hypercapnic exacerbation of COPD,” International Journal of Chronic Obstructive Pulmonary Disease, vol. 13, pp. 3895–3897, 2018.
View at: Publisher Site | Google Scholar
J. Pilcher, L. Eastlake, M. Richards et al., “Physiological effects of titrated oxygen via nasal high-flow cannulae in COPD exacerbations: a randomized controlled cross-over trial,” Respirology, vol. 22, no. 6, pp. 1149–1155, 2017.
View at: Publisher Site | Google Scholar
M. K. Lee, J. Choi, B. Park et al., “High flow nasal cannulae oxygen therapy in acute-moderate hypercapnic respiratory failure,” The Clinical Researcher J, vol. 12, no. 6, pp. 2046–2056, 2018.
View at: Publisher Site | Google Scholar
A. Cortegiani, F. Longhini, F. Madotto et al., “High flow nasal therapy versus noninvasive ventilation as initial ventilatory strategy in COPD exacerbation: a multicenter non-inferiority randomized trial,” Critical Care, vol. 24, no. 1, p. 692, 2020.
View at: Publisher Site | Google Scholar
J. Sun, Y. Li, B. Ling et al., “High flow nasal cannula oxygen therapy versus non-invasive ventilation for chronic obstructive pulmonary disease with acute-moderate hypercapnic respiratory failure: an observational cohort study,” International Journal of Chronic Obstructive Pulmonary Disease, vol. 14, pp. 1229–1237, 2019.
View at: Publisher Site | Google Scholar
Y. Papachatzakis, P. T. Nikolaidis, S. Kontogiannis, and G. Trakada, “High-flow oxygen through nasal cannula vs. Non-invasive ventilation in hypercapnic respiratory failure: a randomized clinical trial,” International Journal of Environmental Research and Public Health, vol. 17, no. 16, p. 5994, 2020.
View at: Publisher Site | Google Scholar
D. Singh, A. Agusti, A. Anzueto et al., “Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease: the GOLD science committee report 2019,” European Respiratory Journal, vol. 53, no. 5, Article ID 1900164, 2019.
View at: Publisher Site | Google Scholar
J. Xia, S. Gu, W. Lei et al., “High-flow nasal cannula versus conventional oxygen therapy in acute COPD exacerbation with mild hypercapnia: a multicenter randomized controlled trial,” Critical Care, vol. 26, no. 1, p. 109, 2022.
View at: Publisher Site | Google Scholar
L. Fan, Q. Zhao, Y. Liu, L. Zhou, and J. Duan, “Semiquantitative cough strength score and associated outcomes in noninvasive positive pressure ventilation patients with acute exacerbation of chronic obstructive pulmonary disease,” Respiratory Medicine, vol. 108, no. 12, pp. 1801–1807, 2014.
View at: Publisher Site | Google Scholar
J. Duan, X. Tang, S. Huang, J. Jia, and S. Guo, “Protocol-directed versus physician-directed weaning from noninvasive ventilation: the impact in chronic obstructive pulmonary disease patients,” Journal of Trauma and Acute Care Surgery, vol. 72, no. 5, pp. 1271–1275, 2012.
View at: Publisher Site | Google Scholar
J. Phua, K. Kong, K. H. Lee, L. Shen, and T. K. Lim, “Noninvasive ventilation in hypercapnic acute respiratory failure due to chronic obstructive pulmonary disease vs. other conditions: effectiveness and predictors of failure,” Intensive Care Medicine, vol. 31, no. 4, pp. 533–539, 2005.
View at: Publisher Site | Google Scholar
T. M. Koppie, A. M. Serio, A. J. Vickers et al., “Age-adjusted Charlson comorbidity score is associated with treatment decisions and clinical outcomes for patients undergoing radical cystectomy for bladder cancer,” Cancer, vol. 112, no. 11, pp. 2384–2392, 2008.
View at: Publisher Site | Google Scholar
A. Singanayagam, S. Schembri, and J. D. Chalmers, “Predictors of mortality in hospitalized adults with acute exacerbation of chronic obstructive pulmonary disease. A systematic review and meta-analysis,” Annals of the American Thoracic Society, vol. 10, no. 2, pp. 81–89, 2013.
View at: Publisher Site | Google Scholar
J. C. Peng, W. W. Gong, Y. Wu, T. Y. Yan, and X. Y. Jiang, “Development and validation of a prognostic nomogram among patients with acute exacerbation of chronic obstructive pulmonary disease in intensive care unit,” BMC Pulmonary Medicine, vol. 22, no. 1, p. 306, 2022.
View at: Publisher Site | Google Scholar
P. B. Doshi, J. S. Whittle, G. Dungan et al., “The ventilatory effect of high velocity nasal insufflation compared to non-invasive positive-pressure ventilation in the treatment of hypercapneic respiratory failure: a subgroup analysis,” Heart & Lung, vol. 49, no. 5, pp. 610–615, 2020.
View at: Publisher Site | Google Scholar
P. Veenstra, N. Veeger, R. J. H. Koppers, M. L. Duiverman, and W. H. van Geffen, “High-flow nasal cannula oxygen therapy for admitted COPD-patients. A retrospective cohort study,” PLoS One, vol. 17, no. 10, Article ID e0272372, 2022.
View at: Publisher Site | Google Scholar
Y. Wang, K. Stavem, F. A. Dahl, S. Humerfelt, and T. Haugen, “Factors associated with a prolonged length of stay after acute exacerbation of chronic obstructive pulmonary disease (AECOPD),” International Journal of Chronic Obstructive Pulmonary Disease, vol. 9, pp. 99–105, 2014.
View at: Publisher Site | Google Scholar
F. Dong, K. Huang, X. Ren et al., “Factors associated with inpatient length of stay among hospitalised patients with chronic obstructive pulmonary disease, China, 2016-2017: a retrospective study,” BMJ Open, vol. 11, no. 2, Article ID e040560, 2021.
View at: Publisher Site | Google Scholar
M. Oremus, R. McKelvie, A. Don-Wauchope et al., “A systematic review of BNP and NT-proBNP in the management of heart failure: overview and methods,” Heart Failure Reviews, vol. 19, no. 4, pp. 413–419, 2014.
View at: Publisher Site | Google Scholar
J. de Miguel Diez, J. Chancafe Morgan, and R. Jimenez Garcia, “The association between COPD and heart failure risk: a review,” International Journal of Chronic Obstructive Pulmonary Disease, vol. 8, pp. 305–312, 2013.
View at: Publisher Site | Google Scholar
N. M. Hawkins, A. Khosla, S. A. Virani, J. J. McMurray, and J. M. FitzGerald, “B-type natriuretic peptides in chronic obstructive pulmonary disease: a systematic review,” BMC Pulmonary Medicine, vol. 17, no. 1, p. 11, 2017.
View at: Publisher Site | Google Scholar
O. Ediboğlu and C. Kıraklı, “Can NT-pro BNP levels predict prognosis of patients with acute exacerbations of chronic obstructive pulmonary disease in the intensive care unit?” Balkan Medical Journal, vol. 35, no. 6, pp. 422–426, 2018.
View at: Publisher Site | Google Scholar
S. Vallabhajosyula, T. M. Haddad, P. R. Sundaragiri et al., “Role of B-type natriuretic peptide in predicting in-hospital outcomes in acute exacerbation of chronic obstructive pulmonary disease with preserved left ventricular function: a 5-year retrospective analysis,” Journal of Intensive Care Medicine, vol. 33, no. 11, pp. 635–644, 2018.
View at: Publisher Site | Google Scholar
R. Pavasini, G. Tavazzi, S. Biscaglia et al., “Amino terminal pro brain natriuretic peptide predicts all-cause mortality in patients with chronic obstructive pulmonary disease: systematic review and meta-analysis,” Chronic Respiratory Disease, vol. 14, no. 2, pp. 117–126, 2017.
View at: Publisher Site | Google Scholar

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Copyright © 2023 Meng Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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