Noninvasive positive pressure therapy of the obesity hypoventilation syndrome
— Obesity Hypoventilation Syndrome (OHS) occurs in obese (body mass index (BMI) >30kg/m 2 ) patients when awake alveolar hypoventilation (PaCO 2 >45 mmHg) can not be attributed to pulmonary parenchymal disease, skeletal restriction, neuromuscular weakness, or pleural pathology .
Most patients with OHS present with chronic hypoventilation, although some may develop acute cardiopulmonary compromise which will be fatal if untreated.
Application of positive airway pressure is that the mainstay of therapy, no matter the presentation.
during this topic review, positive pressure therapy for patients with OHS is discussed.
The pathogenesis, clinical manifestations, diagnosis, and treatment of OHS are discussed separately .)
MODES OF NONINVASIVE POSITIVE PRESSURE THERAPY
— There are two major categories of noninvasive positive pressure therapy that are accustomed treat patients with OHS:
• Continuous positive airway pressure (CPAP)
• Noninvasive positive pressure ventilation (NPPV) Among the available modes of NPPV, there’s bilevel positive airway pressure (BPAP) and volume cycled positive pressure ventilation (VCPPV). Noninvasive positive pressure therapy is often administered during sleep via nasal mask, full mask (covering the nose and mouth), nasal pillows, or hybrid mask (oral mask with nasal pillows). During an episode of acute decompensation, it should be necessary to use NPPV during wakefulness. NPPV may be administered via mouthpiece.
Continuous positive airway pressure
— In patients with coexisting OHS and obstructive apnea (OSA, a disorder characterized by obstructive apneas and hypopneas), nocturnal CPAP may improve alveolar ventilation during sleep while also treating the OSA. Several case reports and prospective series initially reported reduction of awake arterial CO2 tension (PaCO 2 ) after the initiation of chronic nocturnal CPAP ]. Since nocturnal CPAP doesn’t directly augment ventilation aside from by maintaining upper airway patency, the CPAP-related improvement of hypercapnia during both wakefulness and sleep is also thanks to relief of ventilatory muscle fatigue and/or augmentation of central ventilatory drive The latter is also facilitated by relief of nocturnal asphyxia or sleep fragmentation. Nocturnal CPAP therapy doesn’t benefit all patients with OHS Patients who have the benefit of nocturnal CPAP therapy tend to possess a better baseline apnea hypopnea index (AHI), less restrictive physiology on spirometry, and fewer severe oxyhemoglobin desaturation during baseline polysomnography than patients who don’t improve with CPAP and need BPAP. However, these individual patient characteristics aren’t useful determinants of the kind of positive pressure therapy that ought to be initially titrated during nocturnal polysomnography. The failure of CPAP to eliminate nocturnal oxyhemoglobin desaturation remains a frequent indication for NPPV. This was illustrated by a study that matched 23 patients with OSA alone to 23 patients with OHS plus OSA per their BMI, AHI, and spirometry Forty-three percent of the patients with OHS plus OSA continued to spend over 20 percent of their total sleep time with an SpO2 <90 percent even after their CPAP had been titrated to A level that significantly improved the AHI, rapid eye movement (REM) sleep duration, and sleep fragmentation. There are limited clinical data comparing CPAP to NPPV in patients with OHS.
One trial randomly assigned 36 patients with coexisting OHS and OSA, additionally as mild residual hypoventilation on CPAP, to either continue CPAP or begin BPAP The trial defined mild residual hypoventilation as nocturnal oxyhemoglobin desaturation to <80 percent for fewer than ten minutes and nocturnal dioxide retention of but 10 mmHg.
After three months, the patients had similar improvement in their awake PaCO 2 , no matter whether or not they received CPAP or BPAP (although subjective sleep quality and psychomotor vigilance testing improved within the BPAP group).
Nine patients with OHS plus OSA had to be placed directly on BPAP because initial CPAP failed (significant oxyhemoglobin desaturation and/or carbonic acid gas retention), emphasizing the importance of close observation during the initiation of CPAP in patients with OHS. The observations that nocturnal CPAP therapy doesn’t benefit all patients with OHS suggest that some patients with coexisting OHS and OSA probably have abnormal control of breathing and protracted hypoventilation even when the upper airway is patent Moreover, the relative contributions of the underlying pathophysiologic mechanisms that result in chronic hypoventilation probably differ among patients who enjoy CPAP compared to those that don’t reply to CPAP Thus, patients who use nocturnal CPAP should be monitored for evidence that nocturnal hypoventilation still exists despite compliance with therapy.
Clinical symptoms and signs suggestive persistent sleep-related hypercapnia include nocturnal dyspnea, a sensation of smothering in the dead of night, chronic morning headaches, or failure of awake blood gases to enhance.
Any of those findings should prompt investigation of whether the CPAP has been appropriately titrated, applied, and adhered to. Polysomno graphically titrated NPPV should be considered if nocturnal hypoventilation persists despite adequate CPAP therapy for 2 to four months ].
Noninvasive positive pressure ventilation
— NPPV improves nocturnal alveolar ventilation and should also stabilize or improve daytime alveolar ventilation in patients with OHS ].
BPAP and VCPPV are available modes of NPPV, with use of the previous being more common Hybrid modes also exist.
Bilevel positive airway pressure
— During BPAP therapy, an inspiratory positive airway pressure (IPAP) and an expiratory positive airway pressure (EPAP) are independently titrated and set. Tidal volume correlates with the difference between the IPAP and therefore the EPAP. As an example, tidal volume is larger using an IPAP of 15 cm H 2 O and an EPAP of 5 cm H 2 O (difference of 10 cm H 2 O), than an IPAP of 10 cm H 2 O and an EPAP of 5 cm H 2 O (difference of 5 cm H 2 O). Alveolar ventilation is enhanced by a bigger tidal volume, assuming that the vital sign is constant. Nocturnal BPAP therapy usually decreases nocturnal PaCO ], daytime PaCO 2 ], and daytime sleepiness in patients with OHS. it should also improve long-term survival. This was illustrated by a series of 130 patients receiving BPAP for OHS, which found 1-, 2-, 3-, and 5-year survival rates of 98, 93, 88, and 77 percent, respectively These survival rates were better than the 18-month survival rate of 77 percent previously reported for a cohort of patients with OHS, most of whom were untreated Finally, there’s evidence that BPAP maintains normocapnia chronically (probably by improving chemosensitivity and reduces restrictive physiology BPAP probably offers several advantages compared to CPAP. These include active ventilation instead of pneumatic splinting, a lower mean airway pressure (which may cause better tolerance of the therapy), better remainder of the ventilatory muscles, more rapid improvement of acidosis, and a rapid return of normal ventilatory control or chemoreceptor function Well done clinical trials comparing BPAP to other NPPV modalities for the treatment of OHS haven’t been performed. BPAP appears to be effective, even within the presence of atiny low leak at the patient interface, because the inspiratory airflow will continue until the target pressure is reached. This coincides with delivery of the augmented tidal volume, assuming that severe upper airway obstruction and decreased systema respiratorium compliance are absent. If there’s severe upper airway obstruction or decreased system compliance, the target pressure is also reached before delivery of the specified tidal volume, leading to hypoventilation. within the case of severe upper airway obstruction, the EPAP and IPAP are often simultaneously increased. This relieves the upper airway obstruction while maintaining the gradient between the 2 pressures and allowing persistent augmentation of the tidal volume. within the case of decreased system compliance, the IPAP are often further increased once upper airway obstruction is relieved.
Volume cycled ventilation
— In some patients with OHS, upper airway obstruction or decreased system compliance could also be so severe that sufficient alveolar ventilation can’t be achieved with CPAP or BPAP. VCPPV may be considered during this situation. VCPPV insures adequate ventilation by generating pressures high enough to beat the physiologic limitations presented by the patient. Although this modality is also useful during an episode of acute decompensation, the high interface pressures required limit acceptance of this mode as chronic therapy. Short-term nocturnal VCPPV has been reported to boost daytime respiratory failure, with most patients eventually able to return to long-term CPAP or BPAP therapy An improved nocturnal ventilatory drive is that the presumed mechanism. Hybrid modes — Average volume-assured pressure support (AVAPS) may be a hybrid mode of NPPV, with features of ordinary BPAP and VCPPV. during a cross-over study of ten patients with OHS who failed CPAP therapy, BPAP alone was compared to AVAPS [ 21 ]. Both varieties of positive pressure ventilation improved oxygenation, sleep quality, and quality of life. However, AVAPS gave the impression to confer greater improvement in ventilation. Thus, AVAPS could also be a suitable alternative to BPAP and should be useful when rapid improvement of hypercapnia is important to forestall further decompensation of OHS. Further study is critical to further clarify the advantages and role of AVAPS. INITIATING NONINVASIVE POSITIVE PRESSURE THERAPY — Noninvasive positive pressure therapy is indicated for patients with OHS because untreated disease may lead to progressive hypercapnia, hypoxemia, and various adverse effects, including poor neurocognitive function, pulmonary hypertension, and hypertrophy.
Acute decompensated OHS
— Patients who present with an acute decompensation of OHS should have noninvasive positive pressure ventilation (NPPV) initiated expeditiously during a monitored inpatient setting, assuming that they’re acceptable candidates for this therapy (able to cooperate, protect their airway, hemodynamically stable, arterial pH greater than 7.20)
. Bilevel positive airway pressure (BPAP) is that the mode of NPPV that’s generally tried first, with volume cycle positive pressure ventilation (VCPPV) reserved for when sufficient alveolar ventilation can not be achieved with BPAP. Continuous positive airway pressure (CPAP) shouldn’t be employed in this setting. there’s no universal strategy for determining the initial settings:
• For BPAP, one reasonable approach is to start with inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) settings of 4 cm H 2 O and so increase the IPAP every several minutes in increments of two cm H 2 O until the patient appears more leisurely and there’s an appropriate rate of respiration (eg, <30 breaths per minute), oxyhemoglobin saturation (eg, ≥90 percent), pulse (eg, ≤100 beats per minute), and degree of ventilation (eg, pH >7.30 on serial blood gases). The inspired oxygen concentration should be titrated to keep up adequate oxyhemoglobin saturation (eg, ≥90 percent) once the opposite settings are determined. Failure of oxygenation to enhance quickly may require further increases in EPAP. IPAP is mostly increased simultaneously so as to take care of a pressure gradient between EPAP and IPAP that’s sufficient to decrease work of breathing. Frequent blood gases could also be required to verify that improvement in arterial gas exchange is happening.
• For VCPPV, the ventilator mode, rate, tidal volume, inspired oxygen concentration, and end-expiratory pressure must be selected. An assist-control mode is often accustomed fully augment spontaneous respiratory efforts. the biggest tidal volume that consistently maintains an airway pressure but 30 cm H 2 O is mostly chosen, and also the vital sign is then set to attain a moment ventilation of 6 to 10 L/min. The rate are often adjusted as required to attain the ventilatory goals (eg, pH >7.30 on serial blood gases). The inspired oxygen concentration should be titrated to take care of adequate oxyhemoglobin saturation (eg, ≥90 percent) and also the end-expiratory pressure should be like the prior CPAP or EPAP settings. High interface pressures may cause sleep fragmentation, discomfort, intolerance, or an interface leak when VCPPV begins. during this situation, reducing the tidal volume and raising the rate of respiration will decrease the interface pressure while maintaining the specified minute ventilation. in a very retrospective series of patients having an acute ventilatory decompensation of OHS, use of NPPV successfully averted endotracheal intubation all told patients and was related to enhanced survival Chronic compensated OHS — Patients who present with chronic compensated OHS or who are stabilized after an acute decompensation should undergo nocturnal polysomnography. Polysomnography detects coexisting obstructive apnea (OSA), which guides the initial mode of therapy. It also allows the titration of positive airway pressure device settings:
• Patients with both OHS and OSA – Patients with OHS and OSA are often initially treated with nocturnal CPAP Beginning at grade of 4 cm H 2 O, the CPAP is increased in small increments (eg, 2 cm H 2 O) until obstructive events are eliminated . Patients who have persistent alveolar hypoventilation despite the elimination of obstructive events should be converted from CPAP to NPPV. This conversion is mostly done using BPAP because the CPAP settings is used because the place to begin for the titration of BPAP. Beginning with IPAP and EPAP settings similar to the CPAP level at which obstructive events were eliminated, the IPAP is increased in small increments (eg, 2 cm H 2 O) until alveolar ventilation is sufficiently augmented A back-up rate may be set to enhance spontaneous respiratory efforts if necessary. Patients who fail BPAP may try VCPPV, which is initiated as described above.
• Patients with OHS only – Patients with OHS alone should be treated with nocturnal NPPV because CPAP is unlikely to be effective within the absence of OSA. Nocturnal NPPV is usually initiated using the BPAP mode. Beginning with IPAP and EPAP settings of 4 cm H 2 O, the IPAP is increased in increments of two cm H 2 O until alveolar ventilation is sufficiently augmented]. A back-up rate is set to enhance spontaneous respiratory efforts if necessary, although chronic use of this function may cause patient/ventilator asynchrony or Cheyne-Stokes respiration, leading to disrupted sleep continuity or architecture in OHS patients Patients who fail BPAP may try VCPPV, which is initiated as described above irrespective of which mode is employed, clinical decisions are made per whether the alveolar ventilation has been sufficiently augmented. However, this can be difficult to work out. Blood gas analysis is that the gold standard method of assessing alveolar ventilation. However, overnight blood gas analysis requires placement of an indwelling arterial catheter or multiple blood draws, both of which are impractical in most sleep laboratories. The indicator of hypoventilation that’s most ordinarily used is oxyhemoglobin desaturation unrelated to obstructive events. Transcutaneous measurement of arterial CO2 (PaCO 2 ) calibrated respiratory inductance plethysmography, or end tidal CO 2 are alternative techniques, but they’re controversial because their accuracy is uncertain. Follow-up — Once nocturnal positive pressure therapy has been initiated, periodic awake blood gases are useful to verify that alveolar hypoventilation has improved. Repeat polysomnography should be considered within the following situations:
• There are symptoms or signs implicational persistent alveolar hypoventilation (eg, nocturnal dyspnea, a sensation of smothering at the hours of darkness, chronic morning headaches, failure of awake blood gases to improve) despite noninvasive positive pressure therapy. Persistent alveolar hypoventilation suggests that the kind or level of positive pressure therapy may have to be changed.
• Awake blood gases suggest improved alveolar ventilation. the aim of polysomnography during this situation is to see if the extent of positive pressure support will be reduced, since this might improve long-term adherence to therapy. Therapy in some NPPV patients may additionally be ready to be converted to CPAP and nocturnal oxygen supplementation could also be able to be reduced or discontinued
• Factors contributing to the severity of OHS (eg, body mass, hypothyroidism, heavy ethanol consumption, or sedative use) are reduced or eliminated. An associated reduction or elimination of alveolar hypoventilation may permit reduction or elimination of positive pressure therapy. within the case of body mass, weight loss of fifty to 100 pounds is usually required. Supplemental oxygen — Hypoxemia is common in patients with OHS, especially those with coexisting OSA. Supplemental oxygen should be administered whenever 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 are established. Daytime supplemental oxygen are often titrated using oximetry at rest and with exertion. The supplemental oxygen is often added to the respiratory circuit near its connection to the positive airway pressure device. Since the device generates varying degrees of air flow through the tubing that will cause a dilutional effect on the oxygen added to the circuit, the flow of supplemental oxygen may have to be adjusted if the settings are changed. Periodic repeat awake and nocturnal evaluations are necessary to insure that ongoing supplemental oxygen therapy is important and therefore the prescription is correct. the requirement for supplemental oxygen frequently decreases because the patient’s cardiopulmonary status improves with nocturnal positive pressure therapy. Supplemental oxygen alone (without positive pressure therapy) is insufficient therapy for OHS. Although it’s going to improve nocturnal oxyhemoglobin desaturation, it doesn’t relieve upper airway obstruction or augment ventilation, and it should acutely worsen CO2 retention in patients with OHS SUMMARY and suggestions
• Obesity Hypoventilation Syndrome (OHS) exists when there’s obesity and alveolar hypoventilation during wakefulness which can’t be attributed to pulmonary parenchymal or other thoracic pathology.
• There are two major categories of positive pressure therapy that are accustomed treat patients with OHS: continuous positive airway pressure (CPAP) and noninvasive positive pressure ventilation (NPPV). The latter includes bilevel positive airway pressure (BPAP) and volume cycled positive pressure ventilation (VCPPV).
• We recommend that patients with OHS receive nocturnal positive pressure therapy to cut back daytime sleepiness and improve alveolar ventilation ). This recognizes that progressive alveolar hypoventilation may cause hypoxemia that’s sufficient to cause clinically important adverse effects.
• We recommend that supplemental oxygen be administered to patients with OHS if positive pressure therapy alone is insufficient to eliminate hypoxemia ). Supplemental oxygen during sleep are often added to the positive pressure system and titrated after the optimal settings of positive pressure therapy are established. Daytime supplemental oxygen may be titrated using oximetry at rest and with exertion. Supplemental oxygen alone is insufficient therapy for OHS.
• For patients with an acute decompensation of OHS:
• We suggest expeditious initiation of NPPV, instead of CPAP ). NPPV will be administered as BPAP or VCPPV, although BPAP is usually preferred unless it’s insufficient to keep up an open upper airway or to beat the decreased systema respiratorium compliance.
• For patients with chronic compensated OHS:
• A polysomnogram is sometimes performed to detect coexisting obstructive apnea (OSA, a disorder characterized by obstructive apneas and hypopneas) and to guide the titration of the positive airway pressure device settings.
• We suggest that patients with OHS alone be initially treated with nocturnal NPPV, instead of CPAP
• We suggest that patients with OHS plus OSA be initially treated with nocturnal CPAP, instead of NPPV ). These patients should be converted to nocturnal NPPV if they are doing not tolerate CPAP therapy or have persistent alveolar hypoventilation despite CPAP therapy.
• After positive pressure therapy is initiated during sleep, periodic awake blood gases are useful to verify that alveolar hypoventilation has improved. Repeat polysomnography should be considered in special situations.