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(Chest. 2005;128:657-662.)
© 2005 American College of Chest Physicians

Outcome of Patients With Stable COPD Receiving Controlled Noninvasive Positive Pressure Ventilation Aimed at a Maximal Reduction of PaCO2*

Wolfram Windisch, MD; Sergej Kostic, MD; Michael Dreher, MD; Johann Christian Virchow, Jr, MD, FCCP and Stephan Sorichter, MD

* From the Department of Pneumology (Drs. Windisch and Sorichter, Mr. Kostic, and Mr. Dreher), University Hospital Freiburg, Freiburg; and Department of Pneumology (Professor Dr. Virchow), University Hospital Rostock, Rostock, Germany.

Correspondence to: Wolfram Windisch, MD, Department of Pneumology, University Hospital Freiburg, Killianstrasse 5, D - 79106 Freiburg, Germany; e-mail: windisch{at}med1.ukl.uni-freiburg.de


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Study objectives: The role of noninvasive positive pressure ventilation (NPPV) has been well established in the treatment of acute hypercapnic respiratory failure due to COPD. However, evidence for a sustained improvement in blood gas levels and survival in patients with stable hypercapnic COPD following NPPV is still lacking. There is concern that this might be due to low inspiratory pressures of < 18 cm H2O used in previous studies, which thereby did not achieve a reduction of PaCO2. Therefore, the 2-year survival and changes in lung function and blood gas levels were analyzed in patients with stable hypercapnic COPD in whom controlled pressure-limited NPPV was titrated to achieve a maximal improvement in PaCO2.

Design: Retrospective study between March 1997 and September 2003.

Setting: General ward of a university hospital.

Patients: Thirty-four consecutive patients with stable (mean pH 7.40 ± 0.03) hypercapnic COPD (mean age, 63.4 ± 9.7 years [± SD]; mean body mass index, 28.3 ± 7.3 kg/m2).

Measurements and results: Daytime PaCO2 during spontaneous breathing decreased by 6.9 ± 8.0 (95% confidence interval, – 9.9 to – 3.9), from 53.3 ± 4.8 to 46.4 ± 7.0 mm Hg (p < 0.001); while daytime PaO2 increased by 5.8 ± 9.4 (95% confidence interval, 2.3 to 9.3), from 51.7 ± 8.8 to 57.5 ± 9.3 mm Hg (p = 0.002); and FEV1 increased by 0.14 ± 0.16 (95% confidence interval, 0.08 to 0.20), from 1.03 ± 0.54 to 1.17 ± 0.59 L (p < 0.001) after 2 months of NPPV. This was achieved with mean inspiratory pressures of 27.7 ± 5.9 cm H2O (range, 17 to 40 cm H2O) at a mean respiratory rate of 20.8 ± 2.5 breaths/min (range, 14 to 24 breaths/min). The 2-year survival rate was 86%.

Conclusions: Controlled NPPV using a mean inspiratory pressure of 28 cm H2O is well tolerated over longer periods and can improve blood gas levels and lung function. Prospective, randomized controlled trials of high-intensity NPPV are required to evaluate its role in patients with stable hypercapnic COPD.

Key Words: blood gases • chronic respiratory failure • COPD • hypercapnic respiratory failure • lung function • noninvasive positive pressure ventilation • noninvasive ventilation • outcome • survival • ventilator settings


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Noninvasive positive pressure ventilation (NPPV) delivered by a nasal or a full-face mask is a well-established and increasingly used therapeutic option for patients with hypercapnic respiratory failure (HRF) due to COPD.123 Several randomized controlled trials (RCTs)23456 have established the role of NPPV as first-line intervention in the management of acute exacerbation of COPD with HRF. In this setting, NPPV can reduce the need for intubation and improve the outcome by lowering the rate of complications and mortality as well as shortening hospitalization.

In contrast, as has recently been reviewed there is no conclusive evidence of whether NPPV should be provided routinely to patients with stable hypercapnic COPD.7 A metaanalysis8 of RCTs in patients with stable COPD concluded that pulmonary function, gas exchange, and sleep efficiency did not improve following 3 months of nocturnal NPPV in this group. In addition, a 1-year RCT9 and a 2-year RCT10 have indicated that NPPV used for home mechanical ventilation (HMV) did not improve survival when added to long-term oxygen therapy.

All published RCTs used either inspiratory pressures from 10 to 18 cm H2O or/and a spontaneous mode of ventilatory support for NPPV that achieved only modest reductions in PaCO2. There is increasing concern that inspiratory pressures of < 18 cm H2O might have been insufficient to reduce the PaCO2 sufficiently during spontaneous breathing in order to provide a clinical benefit for the patient.1112 However, there is increasing evidence that chronic hypercapnia is a poor prognostic sign in patients with COPD.1314 In addition, long-term survivors of patients with chronic HRF due to COPD have been shown to have higher reductions in mean PaCO2 during the first 2 years following initiation of NPPV.15 Accordingly, indirect evidence supporting the hypothesis that more aggressive ventilation aimed at maximally decreasing PaCO2 could provide beneficial effects for patients with stable hypercapnic COPD has been published.15 Nevertheless, RCTs have not been undertaken to investigate this.

It has been shown that controlled pressure-limited NPPV using inspiratory pressures of up to 30 cm H2O in COPD with stable severe hypercapnia was well tolerated over 6 months and led to a decrease of PaCO2 toward normocapnia.12 The objective of the present study, therefore, was to assess changes in blood gas levels and long-term outcome in a larger group of patients with COPD and chronic HRF who were treated by controlled NPPV aimed at achieving maximal improvement of PaCO2.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Patients
All patients with COPD who were stable and hypercapnic, and who presented with typical symptoms of HRF such as fatigue, dyspnea, and morning headache despite supplemental oxygen and administration of bronchodilators were offered NPPV. There were no predefined criteria to decide which patients were not to receive NPPV. Patients who were established on NPPV between March 1997 and September 2003 were included in the analysis. All patients were treated on the general ward at the Department of Pneumology, University Hospital Freiburg, Germany. Only patients in whom COPD was the leading cause of HRF were analyzed. Patients with other leading causes of chronic HRF such as neuromuscular disorders or chest wall deformities were excluded.

Only patients with stable disease when adapted to NPPV were included. Patients who were established on NPPV during acute HRF (breathing frequency > 30 breaths/min or pH < 7.35), those who were planned for weaning from invasive ventilation, and those who had undergone intubation or tracheotomy during the last 3 months were excluded.

NPPV
Patients were established on pressure-limited NPPV (PV401/PV403; Breas Medical AB; Moelnlycke, Sweden) in the assist/control mode. Commercially available nasal masks (Contour Nasal Mask; Respironics; Murrysville, PA) or individually built nasal masks were used, but no full-face masks were used. A one-way circuit with an expiratory valve was used in all patients. Passive humidification using a heat and moisture exchanger (Hygrovent S; Medisize bv; Hillegom, the Netherlands) was provided if patients had dryness of the mucosa both in the hospital and at home. NPPV was titrated to achieve passive ventilation with a maximal decrease in PaCO2 by gradually increasing ventilator settings as previously described.12 Accordingly, inspiratory pressures were increased step by step until a further increase was not tolerated by the patient. Specific target values of PaCO2 were not used. This approach is standard care in our hospital and was applied in all patients following a standardized protocol. As the majority of patients were receiving long-term oxygen therapy prior to NPPV treatment, supplemental oxygen was also added to NPPV in order to maintain a arterial oxygen saturation > 95% while receiving NPPV.

All patients were carefully instructed in the use of the ventilator. Patients were discharged when a maximal reduction in PaCO2 was achieved and maintained for at least 2 days with inspiratory pressures set to the individually tolerated maximum. At that time, improvements in blood gas levels during nocturnal NPPV were verified by blood gas measurements at night while patients were receiving NPPV. In addition, patients were discharged with NPPV only if they were comfortable with their NPPV therapy and if they were able to tolerate NPPV during night, reporting subjectively improved sleep quality.

After discharge, NPPV was predominantly used during the night. However, patients were also instructed to use their ventilator for up to 4 h during daytime if necessary in order to control hypercapnia and symptoms. A first control visit was carried out regularly 2 months after establishment of NPPV in order to care for patients who had problems at home with the ventilator or the mask despite trouble-free adaptation to NPPV in the hospital. At that occasion, ventilator settings were also slightly adapted to further optimize subjective comfort during NPPV. In addition, further adjustments on ventilator settings were tested if patients were still hypercapnic during night while receiving NPPV to achieve a further reduction in PaCO2 after acclimatization at home. Further control visits were carried at least once in a year. Earlier readmission occurred during acute exacerbation or if needed to resolve problems with NPPV.

Measurements and Data Collection
All patients who successfully adapt to NPPV are registered in a hospital database. Patients who were considered eligible for NPPV, but refused NPPV at the initial visit due to either intolerance or inconvenience were not registered. The following data were entered for analysis: predominant underlying cause of HRF, and further diseases contributing to comorbidity; arterial blood gas analysis while breathing room air; arterial blood gas analysis during nocturnal NPPV after satisfactory establishment; lung function parameters using body plethysmography; inspiratory mouth occlusion pressures; type of ventilator; ventilator settings; ventilator mode; duration of hospital stay; and time of death. Patients or their relatives or their general practitioners were contacted and interviewed about the patient’s current status by telephone if the patient had not been seen at a control visit during the last month.

All blood gases were obtained at rest from the arterialized earlobe (AVL OMNI; Roche Diagnostics; Graz, Austria). Lung function parameters were assessed (Masterlab-Compact Labor; Jaeger; Hochberg, Germany). Inspiratory mouth occlusion pressures (ZAN100; ZAN Gerätetechnik; Oberthulba, Germany) were measured both during quiet breathing (mouth occlusion pressure 100 ms after the onset of inspiration during quiet breathing) and during maximal inspiratory mouth pressure (PImax). For PImax, the peak pressure was obtained as previously described.16

Statistical Analysis
Statistical analysis was performed using statistical software (Sigma-Stat, Version 2.03; SPSS; Chicago, IL). Data are presented as mean ± SD after testing for normal distribution (Kolmogorov-Smirnov test). Comparison of measurements at different dates was performed using the paired t test after testing for normal distribution with the presentation of the 95% confidence interval for difference of means. If the test for normal distribution failed, the median values were given, and the Wilcoxon signed-rank test was performed and indicated. Group comparisons were performed using the unpaired t test. Statistical significance was assumed with a p value < 0.05. Two-year survival was assessed by Kaplan-Meier actuarial curve analysis.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Forty-eight patients were identified from the registry, in whom COPD was diagnosed as the leading cause of chronic HRF and who received NPPV for HMV (Fig 1 ). Fourteen patients did not qualify for further analysis: 5 patients were established on pressure-limited NPPV during unstable disease; 6 patients received volume-limited ventilation during unstable disease; data of 3 patients were not available: 1 patient moved to another area; 1 patient discontinued NPPV due to long-term normalization of PaCO2; and 1 patient withdrew after 1 month due to noncompliance.



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  		Figure 1.. Patients with HRF due to COPD who were established on HMV during March 1997 and September 2003: recruitment of patients for analysis.

 
The mean age of the remaining 34 patients (7 women and 27 men) was 63.4 ± 9.7 years (range, 43 to 77 years). The mean body mass index was 28.3 ± 7.3 kg/m2 (range, 17.3 to 49.3). The mean cumulative smoking history was 40.3 ± 23.4 pack-years (range, 0 to 100 pack-years), and one patient with no smoking history had homozygous {alpha}1-anti- trypsin deficiency (type PI ZZ). The majority of patients had significant comorbidities: 16 patients had chronic arterial hypertension; 13 patients were obese (body mass index > 30 kg/m2); 6 patients had diabetes mellitus type II; 6 patients had congestive heart failure; 5 patients had stable coronary heart disease; 5 patients had stable chronic renal failure; 2 patients had chronic atrial fibrillation; and 1 patient had gastric cancer.

The mean ventilator settings after establishment of NPPV were as follows: mean inspiratory pressure, 27.7 ± 5.9 cm H2O (range, 17 to 40 cm H2O); mean respiratory rate, 20.8 ± 2.5 breaths/min (range, 14 to 24 breaths/min); inspiratory time, 1.0 ± 0.2 s (range, 0.7 to 1.5 s); trigger setting, – 0.3 ± 0.4 cm H2O (range, – 1.0 to 1.1 cm H2O), although patients received passive ventilation most of the time. Supplemental oxygen was administered with a mean flow of 2.0 ± 1.3 L/min (range, 0 to 6 L/min).

All patients were able to tolerate nocturnal NPPV prior to discharge without discomfort or relevant side effects. Hypercapnia improved significantly during nocturnal NPPV: the mean pH was 7.44 ± 0.05, the mean PaCO2 was 45.9 ± 5.6 mm Hg, the mean PaO2 (while receiving supplemental oxygen) was 83.9 ± 13.6 mm Hg, and mean HCO–3 was 31.9 ± 4.3 mmol/L. A mean of 13.0 ± 6.9 hospital days was necessary to achieve optimal adjustment of the patient to the ventilator.

Blood gas levels during spontaneous breathing and lung function improved significantly following 2 months of NPPV (Table 1 ). Obese patients were not different compared to nonobese patients in terms of PaCO2 prior to NPPV (52.0 ± 4.7 mm Hg vs 54.2 ± 4.8 mm Hg, p = 0.217) and drop of PaCO2 following NPPV (8.4 ± 6.1 mm Hg vs 6.0 ± 8.5 mm Hg, p = 0.407). The PImax, which was lower than the 5% percentiles of age-matched healthy subjects,16 did not increase despite improvements of blood gas levels (Table 1). Ventilator settings were only slightly changed during further individually planned control visits in order to optimize subjective comfort and to maintain decreased levels of PaCO2. The 2-year survival rate was 86%.


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  		Table 1.. Blood Gas Levels, Lung Function Parameters, and Mouth Occlusion Pressures Prior to NPPV and 2 Months After Establishment of NPPV in Patients With Chronic HRF Due to COPD*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
In the present analysis, controlled NPPV using relatively high inspiratory pressures with a mean of 28 cm H2O has been shown to significantly improve lung function and blood gas levels during spontaneous breathing in patients with stable hypercapnic COPD. Thereby, FEV1 increased by a mean of 0.14 L, PaCO2 could be decreased by a mean of nearly 7 mm Hg, and PaO2 could be increased by nearly 6 mm Hg following 2 months of predominantly nocturnally applied NPPV. This is in contrast to a 8 of four RCTs evaluating 3 months of NPPV in patients with stable COPD in which NPPV did not significantly improve blood gas levels or lung function. However, bilevel pressure ventilation was applied in all studies, and low mean inspiratory pressures from 10 to 18 cm H2O were chosen.9171819 Interestingly, the study with the strongest decrease in PaCO2 did also use the highest inspiratory pressures ranging from 16 to 22 cm H2O.18 We would therefore argue that any conclusion suggesting that NPPV has no effect on lung function and blood gas levels in patients with stable COPD is premature and most likely related to insufficient inspiratory pressures used in previous studies. In contrast to bilevel pressure ventilation with relatively low inspiratory pressures of < 18 cmH2O, which did not improve blood gases in a clinically relevant order of magnitude, the present analysis gives (uncontrolled) evidence that NPPV using higher inspiratory pressures can indeed improve blood gas levels in patients with chronic HRF due to COPD for a prolonged period of time.

This is important, since the improvement of blood gas levels is one major goal when NPPV is applied for HMV. Accordingly, PaCO2 was the primary end point that informed the power calculation in the most recent RCT10 on NPPV in patients with stable hypercapnic COPD. However, the reduction of diurnal PaCO2 was only modest in this study10 when bilevel pressure ventilation was used in the spontaneous/timed mode with mean inspiratory and expiratory pressures of 14 cm H2O and 2 cm H2O, respectively. In an editorial to this study, Elliott11 emphasized that hypercapnia is a poor prognostic sign in COPD, and that more aggressive ventilation might have resulted in a larger decrease in PaCO2 and other end points. In addition, there is evidence that long-term survivors of stable COPD had a significant decrease of PaCO2 during the first and second year following the institution of NPPV compared to patients who died earlier.15 Thus, there is more evidence favoring aggressive NPPV aimed at improving blood gas levels in order to achieve clinically relevant benefits in stable COPD. Accordingly our study is in agreement with previous data from our group12 that controlled NPPV with mean inspiratory pressures up to 30 cm H2O can improve blood gas levels in stable COPD.

In the present study, patients with obesity or different comorbidities were not excluded in order to present the real-life spectrum of COPD. Polysomnography was not performed, and it cannot be excluded that successful treatment of coexisting obstructive sleep apnea has contributed to the benefit gained by NPPV independently from the COPD status. However, the drop of PaCO2 was comparable between obese and nonobese patients, indicating that obesity was not a major determinant for the improvement of PaCO2 during spontaneous breathing, and this is comparable to previous observations.20

Clinical experience strongly suggests that adaptation to NPPV requires close and prolonged instruction and practice, and it has been suggested that establishing NPPV in inpatients under close supervision will enhance the success rate of NPPV.1121 In the present analysis, NPPV was carefully adapted in hospitalized patients (13 days) and a regular control visit was carried out 2 months after establishment of NPPV. This might be the reason why only 1 of 37 patients dropped out due to noncompliance after NPPV was successfully initiated.

The 2-year survival rate of 86% is encouraging compared to former observations,152122 including both stable and unstable patients,1522 which confines a further comparison. In addition, two RCTs910 failed to show that NPPV using bilevel pressure ventilation with inspiratory pressures < 14 cm H2O plus supplemental oxygen is superior to oxygen alone regarding survival. However, controlled NPPV aimed at maximally improving blood gas levels can also be maintained over a longer period of time and might improve survival in COPD with chronic HRF.

There are certainly limitations of the present study. First, the presented results need to be verified by prospective RCTs. Secondly, we do not provide validated data on health-related quality of life, sleep quality, and exacerbation rates. There is indirect evidence, however, that these parameters did improve, as suggested by the low number of patients who withdrew, the significant improvement in blood gas levels, and the subjectively reported improvement of sleep quality. However, this needs to be addressed in a more quantitative fashion in further studies including the assessment of the influence of coexisting obstructive sleep apnea on the success of NPPV. Third, the group of patients who found entry in our registry is somewhat selected, and we cannot provide data on how many patients were offered NPPV, but who did either not tolerate or refused NPPV while in the hospital. It has previously been shown that a significant amount of patients with COPD (20%) discontinued NPPV during the initiation process.23 Therefore, our results cannot be generalized to all patients with chronic HRF due to COPD. In addition, we cannot demonstrate how further adjustments on ventilator settings at the first control visit have influenced the gas exchange during the further course. This needs to be addressed in further studies.

Despite these limitations, the present study suggests that the technique of NPPV application might be a major factor determining success of NPPV treatment in patients with stable COPD. Accordingly, the results of the several RCTs910171924 in which bilevel pressure ventilation with low inspiratory pressures was used need to be viewed with caution; therefore, there is a need to investigate other modified techniques of NPPV that might have more beneficial effect on outcomes in patients with stable COPD.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
Controlled NPPV using a high mean inspiratory pressure of 28 cm H2O is well tolerated over a prolonged period by patients with stable HRF due to COPD after careful adaptation to NPPV in the hospital. This treatment can lead to a significant improvement in lung function and blood gas levels during spontaneous breathing. Further RCTs using NPPV with higher inspiratory pressures are needed to verify the benefits of NPPV on outcome in these patients.


   Footnotes
 
Abbreviations: HMV = home mechanical ventilation; HRF = hypercapnic respiratory failure; NPPV = noninvasive positive pressure ventilation; PImax = maximal inspiratory mouth pressure; RCT = randomized controlled trial

Received for publication August 11, 2004. Accepted for publication December 22, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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