INTRODUCTION — Nocturnal alterations in gas exchange, such as oxygen desaturation and hypercapnia, are an important clinical problem in patients with chronic obstructive pulmonary disease (COPD). Potential forms of treatment include supplemental oxygen, pharmacologic agents, and nocturnal ventilatory support. (See "Sleep-related breathing disorders in COPD".)
The use of nocturnal ventilatory support in the management of patients with stable COPD will be reviewed here. The management of acute exacerbations of COPD and sleep-related breathing disorders in COPD are discussed separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications" and "Sleep-related breathing disorders in COPD".)
RESPIRATORY MUSCLE WEAKNESS IN COPD — In severe COPD, hypercapnia is largely due to poor matching of ventilation and perfusion, known as V/Q mismatch or dead space ventilation, which is a result of lung parenchyma and airway destruction. Some patients are able to partially compensate by increasing their minute ventilation, but others are not, possibly related to respiratory muscle weakness and other issues listed below.
Respiratory muscle weakness in patients with COPD probably results from a number of factors including the following [1]:
●Change in configuration of the diaphragm caused by hyperinflation, which puts the diaphragm at a mechanical disadvantage
●Compromised nutrition, which is commonly encountered in severe COPD (see "Malnutrition in advanced lung disease")
●Presumed "exhaustion" from the excessive resistive load imposed by the underlying disease
The evaluation of respiratory muscle weakness in COPD is described separately. (See "Respiratory muscle training and resting in COPD", section on 'Respiratory muscle resting'.)
Rationale for respiratory muscle rest — It has been hypothesized that nocturnal noninvasive ventilation (NIV) can improve both nocturnal and daytime respiratory function in patients with advanced COPD by providing periods of rest for weakened respiratory muscles. The evidence related to this hypothesis is of limited quality and conflicting, as described below [1-7].
●Pro – The possibility that respiratory muscle rest might improve respiratory muscle function in patients with severe stable COPD was initially examined by having patients sleep in an iron lung, a form of noninvasive negative pressure ventilation [2]. It was noted that the respiratory muscle effort could be markedly reduced over the short term during assisted ventilation, implying respiratory muscle "rest" [2].
In two case series examining the effects of nocturnal NIV, improvement in daytime gas exchange was noted, and this was sustained over long periods of time, sometimes even years [4,5]. A reduction in daytime arterial carbon dioxide tension (PaCO2) appeared to parallel increases in indices of respiratory muscle strength and endurance, supporting the belief that respiratory muscle rest with nocturnal assisted ventilation was responsible for the benefit [5].
Nocturnal muscle rest may also lead to other improvements in daytime respiratory function, such as a decrease in hyperinflation. This was examined in a series of 46 patients with stable hypercapnic COPD who used nocturnal positive pressure NIV. In addition to a significant reduction in hypercapnia, hyperinflation was reduced based on decreases in the ratio of residual volume to total lung capacity (RV/TLC, a measure of air trapping) at 6 and 12 months. Inspiratory capacity (IC), vital capacity (VC), and forced expiratory volume in one second (FEV1) also improved, consistent with a reduction in hyperinflation and a favorable change in diaphragm configuration [6].
●Con – An alternative hypothesis is that, in advanced COPD, the diaphragm spontaneously adapts to the increased respiratory load to avoid fatigue, and that resting the diaphragm muscle may have little impact on function. This is supported by the observation that biopsies of the diaphragm in patients with severe COPD and hyperinflation show an increased proportion of type-I, or slow-twitch fibers, and a decreased proportion of type-II, or fast-twitch fibers, relative to normal controls and individuals with mild airways obstruction [7]. These histopathologic changes are similar to those seen in the limb muscles of athletes undergoing endurance training and make the diaphragm more resistant to fatigue.
PATIENT SELECTION FOR NOCTURNAL NIV
Chronic stable hypercapnia — Nocturnal noninvasive ventilation (NIV) is indicated for a small portion of patients with COPD who have chronic hypercapnia [8]. While guidelines vary, the most common COPD patients for whom nocturnal NIV is used are those with daytime hypercapnia (eg, arterial carbon dioxide tension [PaCO2] ≥52 mmHg), oxygen desaturation during sleep (eg, pulse oxygen saturation [SpO2] ≤88 percent for ≥5 minutes of ≥2 hours of nocturnal sleep oximetry) despite the use of supplemental oxygen at ≥2 L/min, which is required for Medicare reimbursement, and those with an acute exacerbation that necessitated use of continuous NIV during the hospitalization [9-11]. The 2020 American Thoracic Society (ATS) guidelines suggest using a resting PaCO2 >45 mmHg (not during exacerbation) as a threshold for NIV, but this is not supported by randomized trials and does not permit reimbursement by any payers [8].
NIV initiated during exacerbation — Patients with severe, hypercapnic COPD who have a favorable experience with NIV during a hospitalization for an acute-on-chronic hypercapnic COPD exacerbation may be candidates for long-term nocturnal NIV after discharge. The ATS guidelines advise deferring the decision until after resolution of the acute event (approximately two to four weeks) [8], as approximately 20 percent of patients who required NIV in the hospital were no longer hypercapnic two to four weeks after discharge [12]. However, individualized decision-making is reasonable particularly in patients with chronic hypercapnia preceding the hospitalization [8]. For these patients, we typically obtain outpatient polysomnography (PSG) after the patient has stabilized to identify any additional sleep-related breathing disorders. (See "Sleep-related breathing disorders in COPD", section on 'Diagnosis'.)
During post-discharge monitored PSG, preferably with transcutaneous capnometry, NIV pressure and oxygen settings can be titrated, as needed.
Evaluation for other causes of chronic respiratory failure — For stable patients who have persistent hypercapnia when awake with or without oxygen desaturation during sleep, we obtain polysomnography and an echocardiogram before initiating nocturnal NIV.
●Polysomnography to exclude sleep apnea – Nocturnal hypoxemia or hypercapnia may be caused by superimposed or predominant obstructive sleep apnea (OSA), or less commonly central sleep apnea (CSA). For patients with hypercapnic COPD, screening for sleep-related breathing disorders is advisable prior to NIV initiation [8,13]. In-laboratory PSG is preferred over home sleep testing. However, PSG is not required and may not be necessary for the more cachectic COPD patient with little or no clinical evidence for OSA. The management of sleep-disordered breathing in patients with COPD is discussed separately. (See "Sleep-related breathing disorders in COPD", section on 'Obstructive sleep apnea'.)
●Echocardiogram – Heart failure (right and left) and pulmonary hypertension can contribute to nocturnal gas transfer abnormalities and should be evaluated by echocardiogram. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Sleep-disordered breathing in heart failure".)
PRACTICAL ASPECTS — Once the decision is made to proceed with nocturnal noninvasive ventilation (NIV) for chronic respiratory failure due to COPD, the following components are then addressed (table 1).
Location of NIV initiation — Initiation of NIV in patients with hypercapnic COPD must be performed carefully, to ensure that it does not cause respiratory decompensation. When initiation of NIV occurs in the context of a hospitalization for an exacerbation of COPD, the patient is monitored closely (ie, symptoms, continuous heart rate and blood pressure monitoring, pulse oxygen saturation) to ensure that positive airway pressure (PAP) provides supported ventilation without increasing air trapping [14]. Generally, the settings that are effective in the hospital can be used at home after discharge. A detailed discussion of NIV initiation during a COPD exacerbation is provided separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)
For patients who have more gradually progressive symptoms and hypercapnia, nocturnal NIV is typically initiated in a hospital environment or in a sleep laboratory (after excluding other sleep-related breathing disorders), where the patient can be closely monitored for evidence of decompensation [15-18]. Depending on the sleep laboratory, nocturnal NIV may be initiated after several hours of polysomnography (PSG) to exclude obstructive sleep apnea (OSA) and central sleep apnea (CSA).
The ATS guidelines offer a controversial opinion suggesting home NIV initiation rather than initial in-laboratory overnight polysomnography (PSG) to titrate NIV settings in patients with chronic stable hypercapnic COPD, but qualify this advice as conditional and of very low certainty [8]. In contrast, most sleep specialists and this author suggest initiation in a monitored setting such as a sleep laboratory or hospital.
Preliminary evidence in favor of telemonitored home initiation of NIV comes from a trial in which 67 patients with stable COPD and a mean PaCO2 55±6.7 mmHg [7.3 ±0.9 kPa] were randomly assigned to home initiation with telemedicine support or hospital initiation [19]. The telemedicine connection enabled remote monitoring with transcutaneous carbon dioxide measurement and adjustment of ventilator parameters. At three and six-month follow-up visits, the two groups had similar decrements in PaCO2 and improvements in quality of life. Further study of advanced telemonitoring is warranted.
Interface — Selection of an interface is similar to the selection for OSA or nocturnal NIV for other diseases. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Choosing the correct patient-device interface' and "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Patient selection and alternative modes of ventilatory support".)
Several types of nasal and oronasal masks (picture 1 and picture 2) are shown to the patient, and selection is based on fit and comfort. Careful sizing is necessary to ensure absence of leak without creating pressure points on the face. A full face mask is used if the patient is a habitual mouth breather.
PAP selection — For patients whose hypoventilation is due to severe COPD, bilevel PAP (BPAP) is preferred over continuous PAP (CPAP) [13]. In contrast, for those whose symptoms and hypercapnia are largely due to OSA, CPAP may be sufficient. In both instances, the effect of PAP should be formally assessed. Potential alternatives to BPAP devices for nocturnal NIV are the volume and pressure-targeted ventilators. One of these is occasionally necessary in patients with poor synchrony or inadequate ventilation using the BPAP device. (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Patient selection and alternative modes of ventilatory support".)
There are no specific data that support the use of a volume-targeted ventilator over a pressure-targeted one in COPD. However, one study exclusively used a volume-targeted ventilator with good results, although the majority of patients suffered from neuromuscular disease [20].
Protocol for initiation in stable patients — The optimal approach for initiation of BPAP for nocturnal NIV has not been determined. We typically start with an expiratory positive airway pressure (EPAP) level of 5 cm H2O and an inspiratory positive airway pressure (IPAP) of 10 cm H2O and gradually increase. The final IPAP level is urged to be >15 cm H2O guided by patient tolerance (range, 12 to 20 cm H2O) with the EPAP level at least 5 cm H2O lower than the IPAP pressure [8]. Data from two separate European groups [12,21], as described in more detail below, have shown reduced readmissions and most importantly, improved survival with a targeted effort at improving minute ventilation and reducing hypercapnia more aggressively. These studies have suggested an advantage of adding a backup rate, which is not easily reimbursable in the United States.
High intensity NIV aims to decrease arterial carbon dioxide tension (PaCO2) to normal or near-normal levels, through increases in breathing frequency and airway pressures [22-24]. In a series of 73 patients with hypercapnic COPD, high-intensity NIV with breathing frequencies of 21±3 breaths/min and mean inspiratory/expiratory positive airway pressures of 28±5/5±1 cm H2O were used [22]. After one year, PaCO2 decreased 7 mmHg, on average. The two and five year survival rates were 82 percent and 58 percent, respectively. A preliminary randomized trial of 17 hypercapnic patients compared a "low" IPAP (14 to 16 cm H2O) with a "high" IPAP (25 to 30 cm H2O) for six weeks and confirmed that the higher level was better tolerated [23]. Further study is needed to determine the optimal pressures for BPAP in COPD and to assess outcomes such as compliance and quality of life.
When NIV is initiated electively, the patient should be familiarized with interface and other equipment during the day. It is often helpful to see how the patient tolerates PAP at the proposed settings several hours before sleep. When ready for sleep, the patient is reattached to the BPAP device and observed by the nursing and respiratory therapy or sleep laboratory staff periodically during the night. Once good synchrony and stable patient-ventilator interaction and tolerance are observed, supplemental oxygen is adjusted, if needed, to achieve a saturation of 90 to 93 percent (table 1).
Those patients who tolerate at least a short period of assistance are deemed initially successful. A careful review of the necessary documentation for certification is undertaken prior to sending the patient home.
Monitoring — During initiation, monitoring should focus on the patient's acceptance of the device, level of dyspnea, oxygenation, and stability of vital signs. For more severely ill patients, continuous cardiac, blood pressure, and oximetry monitoring may be used as well as transcutaneous capnometry (tcCO2) but this is more expensive and not readily available for most clinicians. (See "Overview of polysomnography in adults", section on 'Measured variables'.)
Arterial blood gases (ABG) are generally not useful while titrating the initial settings in the more stable patients. However, an ABG obtained in the morning after patients return to their spontaneous breathing state may be useful to guide further titration, if tcCO2 monitoring is not available. A reasonable goal is for the PaCO2 to decrease by approximately 5 to 10 mmHg, although the optimal target is not known. As noted above, "high intensity" pressure support aiming to reduce PaCO2 or tcCO2 by >4 mmHg has proven beneficial in two randomized trials from Europe [12,21].
The patient's subjective report of sleep quality and level of dyspnea is also assessed. Formal electroencephalography (EEG) assessment of sleep in the hospital setting is fraught with difficulty, so that we generally rely upon nurses' and therapists' observations to describe the patient response, including apparent quality of sleep and complications such as mask leakage.
Ongoing evaluation after discharge includes assessment of hours of use per night, quality of sleep, and daytime dyspnea, and also periodic overnight oximetry and daytime arterial blood gases [25]. It has become more common to see the patient within the first month after discharge to avoid the costly penalties of the 30 day readmission.
Treatment failure — In our practice, we determine treatment failure based on the following parameters:
●Patient intolerance, as indicated by patient request to discontinue nocturnal assisted ventilation.
●Worsening dyspnea, hemodynamic instability, or unresponsive hypoxemia.
●Signs of respiratory failure. Criteria for respiratory failure include tachypnea (respiratory rate >24/min) and respiratory acidosis (eg, pH <7.35).
If the patient appears to be intolerant of nocturnal assisted ventilation due to the nasal mask, a repeat trial using a full face mask may be attempted (picture 3). (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Adaptation and follow-up after initiation".)
Humidification — Nasal saline and/or heated humidification may enhance comfort by decreasing dryness in the upper airway. However, some patients with COPD are particularly sensitive to changes in humidity of inspired air and may prefer to omit humidification. It is important to avoid excess heating that may lead to water condensation, also called "rainout," in the tubing or mask; reducing the temperature setting of the heated humidifier may help reduce rainout. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)
Adherence — For patients using nocturnal NIV, tolerance and adherence are important issues. A comprehensive education program for the patient and appropriate family members when NIV is initiated may help improve adherence. No clear data help predict compliance with nocturnal NIV among COPD patients, although among patients with OSA, those with the most severe sleep disturbances are the ones most likely to comply with CPAP treatment. Therefore, an empiric trial of nocturnal NIV is often the only alternative. (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)
EFFICACY OF NOCTURNAL NIV — Studies of nocturnal positive pressure noninvasive ventilation (NIV) for COPD have yielded mixed results because of methodologic issues and problems with long-term compliance, but an increasing body of evidence (described in the following sections) suggests that NIV is of benefit in selected patients [8].
While the American Thoracic Society (ATS) guideline suggests use of nocturnal NIV in patients with chronic stable hypercapnia (PaCO2 >45 mmHg) [8], the majority of clinical trials have used a threshold of PaCO2 ≥52 mmHg. Based on current reimbursement restrictions, the lower PaCO2 threshold is not a practical consideration at this time.
Effects on hospitalization and mortality — Data regarding the effect of nocturnal NIV on survival and the rate of hospital admissions in patients with COPD and chronic hypercapnia are conflicting, possibly due to differences in the inspiratory pressures used for NIV [12,21,26-29].
In a meta-analysis of eight trials (837 patients) described in the ATS guideline, mortality risk decreased by 14 percent in the NIV group compared with usual care (RR 0.86; 95% CI 0.58-1.27), although certainty was low; a trend towards a decrease in hospitalizations was noted [8].
The following two trials, which used high inspiratory pressures, found a significant benefit to nocturnal NIV in terms of survival and hospitalization:
●In a randomized trial of 116 patients with COPD and hypercapnia (arterial carbon dioxide tension [PaCO2] >53 mmHg), continuing nocturnal NIV after hospitalization for a COPD exacerbation prolonged the time to readmission or death compared with supplemental oxygen alone [12]. NIV was administered using a "high pressure strategy" [24] with a median inspiratory pressure of 24 cm H2O, a median expiratory pressure of 4 cm H2O, and a back-up rate of 14 breaths/minute, delivered via pressure support ventilator and titrated to reduce the transcutaneous carbon dioxide by ≥4 mmHg (see 'PAP selection' above). Supplemental oxygen was titrated to maintain pulse oxygen saturation >88 percent or arterial oxygen tension (PaO2) >60 mmHg with morning pH ≥7.30. The median time to readmission or death was 4.3 months (interquartile range [IQR] 1.3 to 13.8 months) in the NIV plus oxygen group, compared with 1.4 months (IQR 0.5 to 3.9 months) in the home oxygen alone group. At 12 months, 16 patients had died in the NIV plus oxygen group versus 19 patients in the home oxygen alone group.
●In a randomized trial of 195 patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) IV COPD and a baseline PaCO2 ≥52 mmHg (7 kPa), nocturnal NIV resulted in a one-year mortality of 12 percent, while the control group mortality was 33 percent (hazard ratio 0.24, 95% CI 0.11-0.49) [21]. NIV was titrated to reduce PaCO2 by ≥20 percent or achieve a PaCO2 <48 mmHg (6.5 kPa).
●A randomized trial of nocturnal NIV (known as the Assisted Ventilation in Chronic Airflow Limitation study or AVCAL) was performed in 144 patients with severe COPD and moderate hypercapnia (PaCO2 >46 mmHg) [26]. The effects on survival, lung function, and quality of life of NIV plus long-term oxygen therapy (LTOT) were compared with LTOT alone. NIV plus LTOT improved sleep quality and initial nocturnal hypercapnia, with fair compliance to NIV therapy (mean nightly use [standard deviation (SD)], 4.5 [3.2] hours/night). After a mean follow-up of 2.2 years, the NIV group had an improved survival out to 36 months, but thereafter the survival curves converged. The forced expiratory volume in one second (FEV1) and PaCO2 at 6 and 12 months were not different between the groups. Despite improved initial survival and sleep quality, quality of life was actually lower with NIV.
Trials that did not show a benefit to nocturnal NIV generally used lower NIV pressures include the following:
●A randomized trial examined the quality of life, mortality rate, hospital stay, and intensive care unit (ICU) admissions in 122 stable hypercapnic COPD patients who were assigned to NIV plus LTOT or LTOT alone [27]. After two years, there was no difference in mortality or hospital admissions between the groups. Health-related quality of life was improved in the NIV group. The only significant difference in outcome was that ICU stay was decreased by 75 percent in the NIV patients and 20 percent in those on LTOT alone.
●In a third trial, no benefit was found from domiciliary NIV on the rate of subsequent hospitalizations and mortality in 52 patients with advanced COPD treated for one year [28].
Dyspnea, hypersomnolence, pulmonary function, and PaCO2 — Uncontrolled case series using nocturnal NIV in advanced COPD reported significant improvements in dyspnea, daytime hypersomnolence, and awake PaCO2 [20,30-32]. In contrast, results from randomized trials and systematic reviews of nocturnal NIV in COPD are conflicting regarding these outcomes, although accumulating evidence suggests benefit [8,16-18,33].
As examples:
●The American Thoracic Society guideline describes a meta-analysis of 13 randomized trials in which quality of life, dyspnea, and exercise tolerance were improved with NIV compared to usual care [8]. This is in contrast to a prior systematic review that included seven studies and 245 subjects and found no benefit after at least three months of nocturnal NIV on PaCO2 and PaO2, six-minute walk distance (6MWD), health-related quality of life (HRQoL), pulmonary function, respiratory muscle strength, or sleep efficiency [33]. However, the small sample size of the studies precluded a definitive conclusion.
●In an unblinded, 12 week study, 72 patients with COPD and chronic hypercapnia were randomly assigned to pulmonary rehabilitation (PRehab) plus nocturnal NIV or rehabilitation alone [34]. The NIV group experienced greater improvements in daytime PaCO2 (mean difference -2.5 mmHg [-0.3 kPa]; p<0.01) and daily step count measured by a pedometer (mean difference 1269 steps/day, p<0.01).
●A randomized trial of nocturnal NIV (mean inspiratory positive airway pressure [IPAP] of 18 cm H2O) plus long-term oxygen therapy (LTOT) to LTOT alone was performed in 14 stable, hypercapnic, oxygen-dependent patients with COPD [17]. There was an unusually high compliance rate, which the investigators attributed to their extra efforts while patients spent several days in the hospital for the initiation of therapy. This study found a small but statistically significant reduction in daytime PaCO2 of 3.3 mmHg and an improved quality of life after three months of treatment. The most responsive patients were those with evidence of sleep-related hypoventilation, as indicated by marked nocturnal increases in transcutaneous CO2 tension (figure 1).
Rehabilitation and nocturnal NIV — The potential benefit of combining other therapies with NIV has also been examined [34,35]. As an example, a trial was performed in 72 patients with chronic hypercapnic COPD to determine the effects of nocturnal NIV combined with PRehab on health-related quality of life, functional status, and gas exchange compared with PRehab alone [34]. Patients were randomly assigned to nocturnal NIV/PRehab or PRehab alone for three months. The addition of NIV significantly improved daytime PaCO2. NIV had additional benefits compared with PRehab alone in terms of improved health-related quality of life, functional status, and gas exchange.
Adverse effects — Adverse events related to NIV include discomfort, skin breakdown, and rash. In addition, NIV implementation is resource intensive and requires easy access to medical personnel skilled in NIV with weekly or biweekly telephone calls or office visits. (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Adaptation and follow-up after initiation".)
NEGATIVE PRESSURE VENTILATION — Negative pressure ventilation using devices other than the iron lung (eg, cuirass and "poncho-wrap" ventilators) have not been beneficial in COPD when evaluated in controlled trials [15]. Negative pressure devices are associated with poor patient tolerance due to limitations in patient positioning and movement, and thus, have been replaced by positive pressure noninvasive ventilation (NIV). (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Patient selection and alternative modes of ventilatory support", section on 'Negative pressure ventilators'.)
FUTURE DIRECTIONS — Efforts are in progress to design more powerful pressure-targeted equipment for nocturnal noninvasive ventilation (NIV) to compete with the bilevel positive airway pressure (BPAP) device. Software improvements are being developed to facilitate patient synchrony and improve patient tolerance of nocturnal assisted ventilation. (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Patient selection and alternative modes of ventilatory support".)
Additional studies are needed to clarify which patients with COPD are most likely to benefit from nocturnal NIV and which NIV settings and devices are optimal. In order to better define the population to benefit, it will be important for future studies to resolve criticisms of the "positive" NIV trials [12,21] related to not performing polysomnography (PSG) studies to identify any contribution from obstructive sleep apnea and not ensuring that the patient had achieved a "chronic stable state" after their acute illness.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic obstructive pulmonary disease" and "Society guideline links: Assessment of oxygenation and gas exchange".)
SUMMARY AND RECOMMENDATIONS
●Respiratory muscle weakness may contribute to alterations in gas exchange, such as oxygen desaturation and hypercapnia, in advanced chronic obstructive pulmonary disease (COPD). Hypothetically, nocturnal respiratory muscle rest might improve daytime gas exchange and respiratory function, however clear proof of this is lacking. (See 'Respiratory muscle weakness in COPD' above.)
●In stable patients with COPD and nocturnal desaturation despite the use of supplemental oxygen, assessment for sleep-disordered breathing may identify patients with superimposed or predominant obstructive sleep apnea. (See 'Patient selection for nocturnal NIV' above and "Sleep-related breathing disorders in COPD".)
●For hypercapnic patients with COPD who have recurrent oxygen desaturation during sleep despite the use of supplemental oxygen, we suggest initiating nocturnal noninvasive ventilation (NIV) rather than continuing to use supplemental oxygen alone (Grade 2C). Reasonable thresholds for hypercapnia and oxygen desaturation are a daytime arterial carbon dioxide tension (PaCO2) ≥52 mmHg and oxygen desaturation during sleep (eg, pulse oxygen saturation [SpO2] ≤88 percent for ≥5 minutes of ≥2 hours of nocturnal sleep oximetry) despite supplemental oxygen at ≥2 L/min, respectively. (See 'Patient selection for nocturnal NIV' above.)
●Nocturnal NIV may also be used in patients with COPD who are recovering from an acute exacerbation that necessitated use of continuous NIV. (See 'Patient selection for nocturnal NIV' above.)
●For COPD patients who meet criteria for use of nocturnal NIV, we advise instituting NIV in a hospital or sleep laboratory environment rather than at home, particularly for the more severely ill patients. (See 'Location of NIV initiation' above.)
●Nocturnal NIV is administered via a standard nasal mask, using a bilevel positive airway pressure (BPAP) device. Occasionally, a volume or pressure-cycled ventilator is needed for patients with poor synchrony or inadequate ventilation. (See 'PAP selection' above.)
●Typically, the initial BPAP settings are an expiratory positive airway pressure (EPAP) level of 5 cm H2O and an inspiratory positive airway pressure (IPAP) of 10 cm H2O. These are gradually increased to tolerance or a decrease in PaCO2 of approximately 10 mmHg. The final IPAP level is usually near 15 cm H2O (range 12 to 20 cm H2O) with the EPAP level at least 5 cm H2O lower than the IPAP pressure. Supplemental oxygen is added to obtain an oxygen saturation of 90 to 93 percent. (See 'Protocol for initiation in stable patients' above.)
●Initial monitoring should focus on patient acceptance of the device, level of dyspnea, oxygenation, and stability of vital signs. This may include continuous cardiac, blood pressure, and oxygen saturation monitoring for the first one or two nights, and transcutaneous carbon dioxide (tcCO2) monitoring where available. After the first night of NIV, an arterial blood gas (ABG), obtained before the patient returns to spontaneous breathing, is often useful to guide further titration. (See 'Monitoring' above.)
●Once patients are stable and willing to utilize the equipment when they return home, ongoing evaluation includes assessment of hours of use per night, quality of sleep, and daytime dyspnea, and also periodic overnight oximetry and daytime arterial blood gases. (See 'Monitoring' above.)
●Nocturnal NEGATIVE pressure ventilation is NOT used for patients with advanced COPD due to sleep disruption from the device and lack of demonstrated benefit. (See 'Negative pressure ventilation' above.)
