INTRODUCTION — Obesity hypoventilation syndrome (OHS) is diagnosed in patients with obesity (ie, body mass index [BMI] >30 kg/m2) when awake alveolar hypoventilation (partial pressure of arterial carbon dioxide >45 mmHg) cannot be attributed to other causes (eg, neuromuscular diseases) . Noninvasive positive airway pressure (PAP) is first-line treatment for patients with OHS, although the effect on survival is unclear.
In this topic review, PAP therapy for patients with OHS is discussed. The pathogenesis, clinical manifestations, diagnosis, and other treatments for OHS are discussed separately. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome" and "Treatment and prognosis of the obesity hypoventilation syndrome" and "Epidemiology and pathogenesis of obesity hypoventilation syndrome".)
CHOOSING A MODE OF NONINVASIVE POSITIVE PRESSURE THERAPY — For patients with OHS, we recommend noninvasive positive airway pressure (PAP) therapy during sleep rather than lifestyle modifications alone in order to improve symptoms and parameters of awake ventilation (ie, arterial partial pressure of carbon dioxide [PaCO2]). This recommendation is based upon the rationale that OHS will progress if not treated with PAP and improvement is dependent upon optimal compliance with therapy. Mode selection for initial PAP therapy is determined by the presence or absence of comorbid obstructive sleep apnea (OSA) based on the results of in-laboratory polysomnography (PSG). These recommendations are consistent with those of the American Thoracic Society and the American Academy Sleep Medicine [2,3]. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome", section on 'Identify coexistent sleep disordered breathing'.):
●Approximately 90 percent of patients with OHS have coexisting obstructive sleep apnea (OSA), in which case continuous positive airway pressure (CPAP) is the initial mode of choice. (See 'Continuous positive airway pressure' below.)
●For patients with OHS and sleep-related hypoventilation (ie, few obstructive events during sleep), and patients with acutely decompensated OHS, bilevel positive airway pressure (BPAP) is usually the initial mode of choice. Patients with OHS and OSA who fail or do not tolerate CPAP are also treated with BPAP. For those who fail or do not tolerate BPAP, a hybrid mode (average volume-assured pressure support) or, less commonly, volume-cycled ventilation may be chosen. (See 'Bilevel positive airway pressure' below and 'Volume-cycled ventilation' below.)
During sleep, noninvasive PAP therapy is typically administered via nasal mask, full face mask (covering the nose and mouth), nasal pillows, or hybrid mask (oral mask with nasal pillows). Although noninvasive PAP can be delivered via mouthpiece, this is impractical for use during sleep and is only feasible for treating awake hypoventilation. Helmet interfaces are also available, but there is limited information on their use in treating patients with OHS, and therefore they cannot be recommended. While PAP is mostly administered during sleep, similar principles apply when PAP is administered during wakefulness when patients present with acute decompensation of OHS. Detailed information on interfaces and devices are discussed separately. (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".)
OBESITY HYPOVENTILATION AND OBSTRUCTIVE SLEEP APNEA
Continuous positive airway pressure — The majority (90 percent) of patients with OHS have coexisting obstructive sleep apnea (OSA), a disorder characterized by obstructive apneas and hypopneas. Continuous positive airway pressure ventilation (CPAP) during sleep is the first line mode used in this population.
CPAP delivers a constant pressure throughout the respiratory cycle. In OSA, the main effect of CPAP is the maintenance of upper airway patency, thereby preventing obstructive and hypopneic events and allowing oxygenation and ventilation to continue throughout the respiratory cycle.
Initial settings — In patients with OHS and OSA, initial settings for fixed CPAP during sleep are similar to those in patients with OSA without coexisting OHS. Typically, titration is performed in a laboratory setting with polysomnographic monitoring. Auto-adjusting CPAP should not be used, as the limited information available on its use suggests that it improves hypercapnia in only half of in patients with OHS . Details regarding initiation and titration of CPAP in patients with OSA are discussed separately. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Auto-titrating continuous positive airway pressure (APAP)'.)
Efficacy — Data report reduction of sleep-related and awake arterial carbon dioxide tension (PaCO2) as well as quality of life improvements after the initiation of CPAP [5-11], although normalization of PaCO2 is not universal [4,12]. Since CPAP does not directly augment ventilation other than by maintaining upper airway patency, the CPAP-related improvement of hypercapnia during both wakefulness and sleep may be due to relief of respiratory muscle fatigue and/or augmentation of central ventilatory drive . Similarly, CPAP may not universally eliminate nocturnal oxyhemoglobin desaturation, which is a signal of persistent nocturnal hypoventilation. One study reported that forty-three percent of the patients with OHS plus OSA continued to spend more than 20 percent of their total sleep time with a peripheral oxygen saturation (SpO2) <90 percent despite adequate treatment of OSA with CPAP . (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Obstructive sleep apnea: Overview of management in adults".)
No study has demonstrated that CPAP is superior to bilevel PAP (BPAP) in patients with OHS and OSA [3,15-17]. Best illustrating this is a randomized trial of 215 patients that reported that among patients with OHS and OSA (apnea hypopnea index >30 events per hour), BPAP and CPAP resulted in a similar number of hospitalization days over a five-year period . In addition, no difference was seen in other outcomes including weight loss, lung function, arterial blood gas (ABG) improvement, need for supplemental oxygen, and health-related quality of life. Subsequent subgroup analysis of the two treatment groups based upon the pretreatment level of PaCO2 (45 to 49.9 or >50 mmHg) demonstrated no difference in subsequent awake PaCO2 or PaO2 over three years of follow-up between those patients treated with CPAP or BPAP , suggesting that the degree of hypercapnia at baseline should not be the sole reason to choose BPAP over CPAP. Although the event rate was low in the initial analysis of this group of patients , which could potentially minimize a meaningful difference in the outcomes, these results are consistent with those of smaller and older randomized studies which have also demonstrated similar outcomes with the two therapies (eg, awake PaCO2, hospital admission, persistent or worsening ventilatory failure, nonadherence; sleepiness, quality of life, or need for supplemental oxygen) [15,16]. There are no controlled studies examining the impact of CPAP on survival in OHS plus OSA. The impact of CPAP in patients with OSA alone is discussed separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Efficacy'.)
Predictors of a response to CPAP in patients with OHS are unclear [19,20]. However, patients who benefit from nocturnal CPAP therapy tend to have a higher baseline apnea hypopnea index (AHI), less restrictive physiology on spirometry, and less severe oxyhemoglobin desaturation during baseline polysomnography than patients who do not improve with CPAP. However, these features are not specific and should not deter the clinician from initially choosing CPAP in this population.
Assessing treatment response — Noninvasive positive airway pressure (PAP) therapy is generally provided in conjunction with other therapies for OHS, including weight loss and supportive therapies (eg, avoidance of alcohol and sedatives). (See "Treatment and prognosis of the obesity hypoventilation syndrome".)
Specific follow-up for noninvasive PAP is discussed in this section.
Goals — The major therapeutic goals for patients with OHS who receive noninvasive positive pressure ventilation include :
●Normalization of the arterial carbon dioxide tension (PaCO2) during wakefulness and sleep (ie, PaCO2 <45 mmHg)
●Elimination of oxyhemoglobin desaturation during wakefulness and sleep
●Relief of the symptoms of OHS (typically daytime hypersomnolence)
●Prevention of complications including erythrocytosis, pulmonary hypertension, and right heart failure
●Treatment of underlying OSA (ie, elimination of obstructive and hypopnea events) and/or sleep-related hypoventilation (ie, nonobstructive events)
●Improvement of sleep architecture and quality
Assess symptoms — Within one month of therapy, patients who are prescribed noninvasive PAP should be assessed for their adherence to PAP therapy and for symptoms and signs of persistent sleep-related hypoventilation, including nocturnal dyspnea, a sensation of smothering at night, chronic morning headaches, and hypersomnolence. Any of these findings should prompt investigation of whether the PAP has been appropriately titrated, applied, and adhered to. (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)
Assess indicators of alveolar hypoventilation — Regardless of which mode of PAP is used or whether OSA is present or not, a goal of therapy for OHS is to augment alveolar ventilation during sleep, which, however, is difficult to measure. ABG analysis is the gold standard method of assessing alveolar ventilation. However, overnight ABG analysis requires placement of an indwelling arterial catheter or multiple arterial blood draws, both of which are impractical in most sleep laboratories. Typical indicators include:
●Awake ABG – Periodic (eg, within one to three months) awake ABGs are useful early after PAP titration to verify that alveolar hypoventilation has improved. One retrospective cohort study of 75 treated OHS patients (mostly with CPAP) reported correlations between the hours of daily use and the reduction in daytime PaCO2 and the increase in PaO2  such that failure to improve awake hypercapnia should prompt a review of a patient's settings and adherence with PAP.
●Oxyhemoglobin desaturation during sleep – Residual oxyhemoglobin desaturation during sleep on PAP therapy typically necessitates polysomnography to assess for residual obstructive events or persistent nocturnal hypoventilation.
●Transcutaneous measurement of arterial carbon dioxide [15,23], calibrated respiratory inductance plethysmography, or end tidal CO2 (capnography) are alternative techniques. These are performed in a sleep laboratory, but they are controversial because their accuracy is uncertain .
Repeat in laboratory polysomnography should be considered in the following situations:
●Clinical manifestations of persistent alveolar hypoventilation (eg, nocturnal dyspnea, a sensation of smothering at night, chronic morning headaches, failure of awake blood gases to improve) despite documented adherence with noninvasive PAP. Persistent alveolar hypoventilation suggests that the type or level of PAP may need to be changed. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome", section on 'Clinical manifestations'.)
●Factors contributing to the severity of OHS (eg, body mass, hypothyroidism, heavy ethanol consumption, or sedative use) have been reduced, corrected, or worsened. An associated improvement in alveolar hypoventilation may permit reduction of PAP therapy, while worsening of alveolar ventilation may prompt increasing PAP support. (See "Treatment and prognosis of the obesity hypoventilation syndrome", section on 'Follow-up'.)
●Awake ABGs indicate improved alveolar ventilation. Some experts repeat polysomnography in this situation if it determined that a reduction in high PAP pressures, switching to continuous positive airway pressure (CPAP) from bilevel positive airway pressure (BPAP), or further titration of nocturnal oxygen supplementation may be feasible [19,22,25,26]. However, it is not routinely done by the authors of this topic.
Second line therapies — Patients with OHS who fail or do not tolerate continuous positive airway pressure (CPAP) should be treated with bilevel positive airway pressure (BPAP) [8,11,25,27-29]. Patients in this category include those who, despite adherence to adequate CPAP therapy, fail to normalize daytime partial arterial pressure of carbon dioxide (PaCO2; assuming hypercapnia is OHS-related), have more than several minutes of sleep-related oxyhemoglobin desaturation to <88 percent that is suggestive of residual hypoventilation, or are intolerant of CPAP despite troubleshooting maneuvers. When CPAP is applied during polysomnography, changing to BPAP should be considered when, despite relief of obstructive apneic and hypopneic events, residual oxyhemoglobin desaturation (SaO2 remains <88 percent) suggests persistent hypoventilation that requires additional inspiratory pressure support. Optimization of settings and addressing adherence are discussed separately. (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Choosing the correct patient-device interface' and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)
Bilevel positive airway pressure
Initial settings — During BPAP therapy, an inspiratory positive airway pressure (IPAP) and an expiratory positive airway pressure (EPAP) are independently titrated and set. EPAP is adjusted to overcome upper airway occlusion, and IPAP is increased to augment ventilation further. Tidal volume correlates with the difference between the IPAP and the EPAP. As an example, tidal volume is greater using an IPAP of 15 cm H2O and an EPAP of 5 cm H2O (difference or "delta" of 10 cm H2O), than an IPAP of 10 cm H2O and an EPAP of 5 cm H2O (difference or "delta" of 5 cm H2O). Alveolar ventilation is enhanced by a larger tidal volume, assuming that the respiratory rate is constant.
In patients who have failed CPAP, the predetermined therapeutic CPAP settings can be used if they are available as the starting point for the titration of BPAP. Beginning with IPAP and EPAP settings identical to the CPAP level at which obstructive events were eliminated, the IPAP is increased in small increments (eg, 1 to 2 cm H2O) every five minutes until a sustained oxyhemoglobin saturation >90 percent is achieved or the patient becomes intolerant of the inspiratory pressure (IPAP) .
In cases where OHS and OSA has not been treated with CPAP, initial IPAP and EPAP are usually started at 8 and 4 cm H2O, respectively and incrementally increased until airway obstruction is resolved and hypoventilation is eliminated (maximum IPAP is typically 20 to 30 cm H2O for adults) . Further details on BPAP titration are provided separately. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)
A backup respiratory rate (ie, spontaneous/timed mode) set below the baseline sleep-related respiratory rate is usually provided to augment spontaneous respiratory efforts should central apneas or a low respiratory rate complicate BPAP therapy . However, judicious use of this mode is necessary to prevent patient/ventilator asynchrony or periodic breathing, which may result in sleep fragmentation that limits improvement of OHS related hypersomnia .
Efficacy — Data have shown that BPAP decreases sleep-related and awake PaCO2 [11,15,22,25,29,32,33]. As an example, in a randomized trial of 35 patients with mild OHS, one month of BPAP therapy during sleep compared with lifestyle counseling resulted in decreased awake PaCO2 (-6.2 versus -3.5 mmHg) and also increased PaO2, reduced the apnea hypopnea index, and restored sleep architecture . A meta-analysis of seven studies also confirmed that BPAP, when compared with lifestyle counselling, was superior in improving the PaCO2 (-2.9 mmHg; 95% CI -4.28 to -1.52 mmHg), PaO2 (2.89 mmHg, 95% CI 0.33 to 5.6 mmHg), and bicarbonate level (-2.55 mmol/L, 95% CI -3.28 to -0.88 mmol/L) . However, no differences were reported when BPAP was compared with other forms of positive pressure therapy. A network meta-analysis also reported that BPAP was more effective than other modes of NIV at reducing the PaCO2 .
Data regarding the clinical efficacy of BPAP therapy are somewhat limited. Uncontrolled observational series suggest that improved laboratory measures are also associated with reduced hypersomnolence [27,29,36]. These benefits appear to be maintained long term and correlate with adherence to therapy [8,22,25,29,32,33].
An impact on mortality is less certain. Observational studies estimate one, two- and five-year survival rates of 97 to 98 percent, 92 to 93 percent and 70 to 77 percent, respectively [29,37]. This compares favorably with the lower survival, 77 percent at 18 months, in one series of mostly untreated patients with OHS.
The data comparing CPAP to BPAP in patients with OHS is discussed above. (See 'Efficacy' above.)
●Active ventilation (provides inspiratory pressure support)
●A lower mean airway pressure when treating OSA, which may lead to better tolerance of the therapy
●Better respiratory muscle rest
●More rapid improvement of respiratory acidosis
●Compensation for minor air leaks
Disadvantages compared with CPAP include [30,31,39]:
●Potential for patient-ventilator asynchrony and associated ineffective ventilation. Ineffective triggering due to the failure of the BPAP device to detect inspiratory efforts is generally managed by raising EPAP to ensure airway patency.
●Potential for persistent hypoventilation due to development of central apneas, ineffective triggering of IPAP, or tidal volume limitation due to severe residual upper airway obstruction (ie, obstructive apneas/hypopneas) or decreased respiratory system compliance.
To address the problem of central apnea development, many experts use BPAP in a spontaneous/timed (S/T) mode with a backup rate. One study of 10 patients with stable OHS reported that compared with BPAP using the S/T modes, use of the spontaneous mode resulted in significantly more central and mixed respiratory events and related oxyhemoglobin desaturation .
In the case of severe upper airway obstruction, the EPAP and IPAP can be simultaneously increased. This relieves the upper airway obstruction while maintaining the gradient between the two pressures and allowing persistent augmentation of the tidal volume. In the case of decreased respiratory system compliance, the IPAP can be further increased once upper airway obstruction is relieved.
●BPAP devices are more expensive.
Other noninvasive ventilation modes
Average volume-assured pressure support — Average volume-assured pressure support (AVAPS) is a hybrid mode of PAP with features of standard BPAP and volume-cycled positive pressure ventilation (VCPPV). In the AVAPS mode, the IPAP varies between respiratory cycles in order to achieve a preset tidal volume, which is usually set at 7 to 10 mL per kg of ideal body weight (calculator 1). (See 'Bilevel positive airway pressure' above and 'Volume-cycled ventilation' below.)
AVAPS is an option in patients with OHS who fail or cannot tolerate continuous or bilevel positive airway pressure (CPAP, BPAP, respectively) despite optimal settings and adherence. Patients who fail may include those with residual upper airway obstruction or a reduction in respiratory system compliance which is so severe that sufficient alveolar ventilation cannot be achieved with CPAP or BPAP despite optimization of settings (eg, increasing inspiratory positive airway pressure [IPAP] or increasing the differential between IPAP and expiratory PAP [EPAP]).
While initial studies reported that AVAPS was associated with improved nocturnal ventilation parameters compared with BPAP or CPAP [41,42], subsequent small randomized controlled trials of patients with OHS and OSA have found that daytime PaCO2 at 2 to 3 months is similarly improved regardless of ventilatory mode (AVAPS, BPAP or CPAP).
Volume cycled positive pressure — Although volume cycled positive pressure ventilation is a short-term option for ventilation during sleep in patients with severe OSA, the high pressures that are required often limit its acceptance as chronic therapy; however, it can be used to transition patients to CPAP or BPAP after a few days or weeks (sometimes longer) of use.
OBESITY HYPOVENTILATION AND SLEEP-RELATED HYPOVENTILATION — A small minority (about 10 percent) of patients with OHS have sleep-related hypoventilation (few obstructive events) for which bilevel positive airway pressure (BPAP) is typically the first treatment of choice. An alternative is volume-targeted pressure support ventilation. Continuous positive airway pressure (CPAP) is not effective in these patients since this form of sleep disordered breathing is not associated with obstructive events.
Bilevel positive airway pressure — BPAP initiation is similar to that in patients with obstructive sleep apnea (OSA) who have not been previously titrated on PAP. However, it is critical that a backup respiratory rate be set using the spontaneous/timed mode in this population.
Data supporting BPAP in this population are limited. While most trials demonstrating efficacy of BPAP include mixed populations of OHS patients (ie, both with and without OSA), in the one study that included only patients with OHS without severe OSA , BPAP resulted in improved arterial carbon dioxide tension (PaCO2) and serum bicarbonate over two months of follow-up as compared to lifestyle modification. As an extension of this trial five-year outcomes in OHS patients without severe OSA who were treated with BPAP were compared with control patients who were prescribed lifestyle modification . Due to the duration of this trial, determinations of treatment group differences were limited by both losses to follow-up and abandonment of the randomized treatment arm for the opposite treatment arm. Nonetheless, BPAP therapy was associated with significant improvements in PaCO2, pH, serum bicarbonate, quality of life and daytime sleepiness compared with patients treated with lifestyle modification only. Subgroup analysis suggested that the group of BPAP patients with higher adherence (>4 hours of use per day) had beneficial outcomes related to hospital admissions, emergency department visits, and mortality as compared to those with lower adherence.
BPAP initiation and efficacy are discussed separately. (See 'Bilevel positive airway pressure' above.)
Should patients fail BPAP, average volume-assured pressure support or volume-cycled modes may be options. (See 'Volume cycled positive pressure' above and 'Average volume-assured pressure support' above.)
PATIENTS WITH ACUTE HYPERCAPNIC RESPIRATORY FAILURE AND OHS — Patients who present with an acute decompensation of OHS (ie, acute on chronic hypercapnic respiratory failure) should have noninvasive positive airway pressure (PAP) ventilation initiated expeditiously in a monitored inpatient setting, assuming that they are acceptable candidates for this therapy (eg, able to cooperate, can protect their own airway, are hemodynamically stable (table 2)). In this setting, timely institution of noninvasive ventilation (NIV) successfully averts endotracheal intubation in over 90 percent of patients .
Patients who are not candidates for NIV or who fail this therapy (table 3) should be considered for urgent endotracheal intubation with mechanical ventilation. Contraindications to noninvasive PAP therapy in the acute setting are discussed separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Contraindications'.)
Bilevel positive airway pressure (BPAP) is the mode that is generally tried first, with volume-cycled positive pressure ventilation (VCPPV) reserved for situations when sufficient alveolar ventilation cannot be achieved with BPAP. Continuous positive airway pressure (CPAP) should not be used in this setting. In cases where the diagnosis of OHS is presumed and the patient has not received PAP therapy in the chronic setting, these modes are used until the patient is sufficiently stable to undergo polysomnography with formal titration of PAP settings (ideally within the next two to three months). In those already receiving CPAP, switching to BPAP is appropriate and in those already on BPAP, inspiratory PAP (IPAP) may be cautiously increased above its chronic setting with most patients eventually able to return to long-term CPAP or BPAP therapy .
All patients hospitalized with acute decompensation of OHS should be discharged home on PAP. A systematic review of hospitalized patients with decompensated OHS demonstrated that in-hospital application of empiric PAP (over 90 percent NIV) and discharging patients home on this therapy markedly reduced three-month mortality (relative risk 0.12) when compared with those patients discharged without PAP .
BPAP was the mode of NIV used in most studies and demonstrated consistent and significant decreases in the partial arterial pressure of carbon dioxide (PaCO2) and increases in pH (ie, indices of improved ventilation) during hospitalization [25,47,48]:
Bilevel positive airway ventilation — Bilevel positive airway pressure (BPAP) is the mode that is generally tried first in this setting. Most studies utilize increasing levels of pressure as tolerated by awake patients with no universal strategy for determining the initial BPAP settings in either the awake or sleeping patient with acutely decompensated OHS. We suggest the following:
●If PAP naïve, we typically begin with inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) settings of 4 cm H2O and then increase the IPAP every several minutes in increments of 2 cm H2O until the patient appears more comfortable and there is an acceptable respiratory rate (eg, <30 breaths per minute), oxyhemoglobin saturation (eg, ≥90 percent), heart rate (eg, ≤100 beats per minute), and degree of ventilation (eg, pH >7.30 on serial arterial blood gases 1 to 2 hours later). The inspired oxygen concentration should be titrated to maintain adequate oxyhemoglobin saturation (eg, ≥90 percent). Failure of oxygenation to improve quickly may require further increases in EPAP. IPAP is generally increased simultaneously in order to maintain a pressure difference between EPAP and IPAP that is sufficient to decrease work of breathing and adequately ventilate the patient.
●For those chronically on CPAP, a similar approach can be used, beginning with the baseline CPAP settings as the initial EPAP and IPAP settings and then adjust them rapidly as above.
●For those chronically on BPAP, the IPAP may be increased similarly to that described for a PAP naïve patient.
Volume-cycled ventilation — Volume-cycled positive pressure ventilation (VCPPV) is reserved for situations when sufficient alveolar ventilation cannot be achieved with BPAP. VCPPV delivers a set tidal volume. VCPPV ensures adequate ventilation by generating pressures high enough to overcome the physiologic limitations (upper airway obstruction and reduced respiratory compliance) presented by the patient with OHS. This mode may be tried when BPAP fails in a patient with acute decompensation of OHS. Short-term VCPPV during sleep has been reported to improve daytime hypercapnia, with many patients eventually able to return to long-term CPAP or BPAP therapy [26,45].
For VCPPV, the ventilator mode, respiratory rate, tidal volume, inspired oxygen concentration, and positive end-expiratory pressure (PEEP) must be selected (similarly to invasive mechanical ventilator settings). An assist-control mode is typically used to fully augment spontaneous respiratory efforts (ie, the patient receives an assisted breath with each spontaneous breath). The largest tidal volume that consistently maintains an airway pressure less than 30 cm H2O is generally chosen (generally 7 to 10 mL/Kg of ideal body weight), and the respiratory rate is then set to achieve a minute ventilation of 6 to 10 L/min. The respiratory rate or tidal volume can be adjusted as needed to achieve the acute ventilatory goals (eg, pH >7.30 on serial arterial blood gases). The inspired oxygen concentration should be titrated to maintain adequate oxyhemoglobin saturation (eg, ≥90 percent). If the patient is PAP naïve or their prior CPAP or BPAP settings are unknown, a starting PEEP of 10 cm H2O pressure is recommended with careful clinical monitoring in order to detect patient inspiratory efforts not sensed by the ventilator that would require further increases in PEEP to overcome upper airway occlusion. Should the home CPAP or EPAP settings be known, PEEP should be adjusted with this information taken into consideration.
High interface pressures may cause sleep fragmentation, discomfort, intolerance, or an interface leak when VCPPV begins. In this situation, reducing the tidal volume and raising the respiratory rate will decrease the interface pressure while maintaining the desired minute ventilation. However, these features make this mode of ventilation unsuitable for chronic use.
Invasive mechanical ventilation — Patients who are not candidates for noninvasive ventilation or who fail this therapy (table 3) should be considered for urgent endotracheal intubation with mechanical ventilation. Indications for intubation and invasive mechanical ventilation are similar to those in the general population, although intubation may be challenging due to body habitus. These issues are discussed separately. (See "Direct laryngoscopy and endotracheal intubation in adults" and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit" and "Approach to the difficult airway in adults for emergency medicine and critical care".)
SUPPLEMENTAL OXYGEN DURING POSITIVE AIRWAY PRESSURE VENTILATION — Hypoxemia (sleep-related and awake) is common in patients with OHS, especially in those with coexisting obstructive sleep apnea (OSA). Supplemental oxygen should only be administered when positive pressure therapy alone is insufficient to eliminate hypoxemia. Supplemental oxygen during sleep is titrated during polysomnography to eliminate hypoxemia or severe oxyhemoglobin desaturation after the optimal settings of positive pressure therapy have been established. Supplemental oxygen while awake can be titrated using oximetry at rest and with exertion. (See "Long-term supplemental oxygen therapy".)
Supplemental oxygen is typically added to the respiratory circuit via a specific device connector, either a port located in the mask or to an adaptor positioned in the tubing close to the mask. It should be titrated to the lowest flow that maintains a oxyhemoglobin saturation of >90 percent. Occasionally for intractable hypoxemia, a nasal cannula can be placed underneath the mask.
If the pressure settings are subsequently changed, the flow of supplemental oxygen may need to be adjusted since the change may eliminate the need for supplementation. In addition, pressure changes generate varying degrees of air flow through the tubing and exhalation ports that may cause a dilutional effect on the oxygen added to the circuit. Periodic repeat awake and nocturnal evaluations are also necessary after the initial titration to ensure that ongoing supplemental oxygen therapy continues to be necessary and that the prescription is correct. The need for supplemental oxygen frequently decreases as the patient's cardiopulmonary status improves with nocturnal PAP therapy [22,25,26]. After one to three months of stabilization on PAP, if an awake arterial blood gas verifies resolution of hypercapnia and a concomitant improvement of awake oxygenation without the need for daytime oxygen supplementation, nocturnal oxyhemoglobin saturation testing while on PAP with either a reduced flow of or no supplemental oxygen should be performed.
Supplemental oxygen alone (without positive pressure therapy) is inadequate therapy for OHS. Although it may improve nocturnal oxyhemoglobin desaturation, it does not relieve upper airway obstruction or augment ventilation, and it may acutely worsen carbon dioxide retention even in stable patients with OHS . (See "Mechanisms, causes, and effects of hypercapnia", section on 'Oxygen-induced hypercapnia' and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Titration of oxygen'.)
SUMMARY AND RECOMMENDATIONS
●Obesity hypoventilation syndrome (OHS) exists in patients with obesity who have awake alveolar hypoventilation that cannot be attributed to other causes. (See 'Introduction' above.)
●For patients with OHS, we recommend noninvasive positive airway pressure (PAP) therapy during sleep rather than lifestyle modifications alone in order to improve symptoms and parameters of awake ventilation (ie, arterial partial pressure of carbon dioxide [PaCO2]) (Grade 1B). This recommendation is based upon the rationale that OHS will progress if not treated with PAP and improvement is dependent upon optimal compliance with therapy. (See 'Choosing a mode of noninvasive positive pressure therapy' above.)
●For patients with OHS who have coexisting obstructive sleep apnea (OSA), which is approximately 90 percent of OHS patients, we suggest continuous positive airway pressure (CPAP) rather than bilevel PAP (BPAP) as the first line of treatment (Grade 2C). (See 'Obesity hypoventilation and obstructive sleep apnea' above and 'Continuous positive airway pressure' above.)
●A few weeks after PAP therapy is initiated (eg, within the first month), patients should be monitored for adherence and for symptoms and signs of persistent sleep-related hypercapnia. Periodic awake arterial blood gases (ABGs; eg, first one to three months) should be drawn to assess for residual alveolar hypoventilation. Repeat polysomnography should be performed when features of alveolar hypoventilation persist or when factors contributing to the severity of OHS (eg, body mass, hypothyroidism, heavy ethanol consumption, or sedative use) have changed. Repeat polysomnography is performed by some experts when awake ABGs demonstrate improved alveolar ventilation and a reduction or change in PAP therapy is feasible, although this approach is not validated. (See 'Assessing treatment response' above.)
●For patients with OHS and OSA who fail or do not tolerate CPAP and for patients with OHS and sleep-related hypoventilation (ie, few obstructive events during sleep), we suggest BPAP rather than CPAP (Grade 2C). For those who fail BPAP, hybrid modes (average volume-assured pressure support) or, less commonly, volume-cycled modes may be chosen. (See 'Second line therapies' above and 'Obesity hypoventilation and sleep-related hypoventilation' above and 'Other noninvasive ventilation modes' above.)
For patients with acutely decompensated OHS, BPAP is usually the initial mode of choice provided there are no contraindications and there is no indication for immediate intubation and mechanical ventilation. For those who fail or do not tolerate BPAP, a trial of volume-cycled positive pressure ventilation may be chosen. These patients should be discharged home on PAP (typically BPAP) even if formal polysomnography is pending. (See 'Patients with acute hypercapnic respiratory failure and OHS' above.)
●Hypoxemia (sleep-related and awake) is common in patients with OHS, especially in those with coexisting obstructive sleep apnea (OSA). Supplemental oxygen should only be administered when positive pressure therapy alone is insufficient to eliminate hypoxemia. Supplemental oxygen alone (without positive pressure therapy) is inadequate therapy for OHS. (See 'Supplemental oxygen during positive airway pressure ventilation' above.)
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