Exposure to intermittent hypoxia and sustained hypercapnia reduces therapeutic CPAP in participants with obstructive sleep apnea

Our purpose was to determine whether exposure to mild intermittent hypoxia leads to a reduction in the therapeutic continuous positive airway pressure required to eliminate breathing events. Ten male participants were treated with twelve 2-min episodes of hypoxia ([Formula: see text] ≈50 mmHg) separated by 2-min intervals of normoxia in the presence of [Formula: see text] that was sustained 3 mmHg above baseline. During recovery from the last episode, the positive airway pressure was reduced in a stepwise fashion until flow limitation was evident. The participants also completed a sham protocol under normocapnic conditions, which mimicked the time frame of the intermittent hypoxia protocol. After exposure to intermittent hypoxia, the therapeutic pressure was significantly reduced (i.e., 5 cmH2O) without evidence of flow limitation (103.4 ± 6.3% of baseline, P = 0.5) or increases in upper airway resistance (95.6 ± 15.0% of baseline, P = 0.6). In contrast, a similar decrease in pressure was accompanied by flow limitation (77.0 ± 1.8% of baseline, P = 0.001) and an increase in upper airway resistance (167.2 ± 17.5% of baseline, P = 0.01) after the sham protocol. Consistent with the initiation of long-term facilitation of upper airway muscle activity, exposure to intermittent hypoxia reduced the therapeutic pressure required to eliminate apneic events that could improve treatment compliance. This possibility, coupled with the potentially beneficial effects of intermittent hypoxia on comorbidities linked to sleep apnea, suggests that mild intermittent hypoxia may have a multipronged therapeutic effect on sleep apnea. NEW & NOTEWORTHY Our new finding is that exposure to mild intermittent hypoxia reduced the therapeutic pressure required to treat sleep apnea. These findings are consistent with previous results, which have shown that long-term facilitation of upper muscle activity can be initiated following exposure to intermittent hypoxia in humans.

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Positive Airway Pressure Prescription and Management for Patients with Obstructive Sleep Apnea

Journal of Rhinology ◽

10.18787/jr.2020.00319 ◽

2020 ◽

Vol 27 (2) ◽

pp. 73-82

Author(s):

Ji Ho Choi

Keyword(s):

Quality Of Life ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Airway Pressure ◽

Positive Airway Pressure ◽

Upper Airway ◽

Background Information ◽

Obstructive Sleep

Obstructive sleep apnea (OSA) is characterized by repeated events of complete or partial upper airway obstruction during sleep and is a chronic sleep disorder that requires long-term comprehensive management. Positive airway pressure (PAP) is recommended for treatment of OSA in adults with excessive daytime sleepiness, decreased sleep-related quality of life, and comorbid hypertension. During PAP therapy, regular follow-up is continuously necessary to evaluate side effects or complications, compliance, and treatment effects such as OSA-related symptoms, quality of life, and consequences. This review provides knowledge about PAP-related background information, indications for PAP prescription including the Korean National Health Insurance criteria, optimal pressure, PAP modes, patient education and support, short-term and long-term management, interpretation of PAP uses, and alternative therapies.

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Long-term facilitation in obstructive sleep apnea patients during NREM sleep

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.6.2751 ◽

2001 ◽

Vol 91 (6) ◽

pp. 2751-2757 ◽

Cited By ~ 59

Author(s):

Salah E. Aboubakr ◽

Amy Taylor ◽

Reason Ford ◽

Sarosh Siddiqi ◽

M. Safwan Badr

Keyword(s):

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Recovery Period ◽

Upper Airway ◽

Flow Limitation ◽

Inspiratory Time ◽

Nasal Cpap ◽

Obstructive Sleep ◽

Long Term Facilitation

Repetitive hypoxia followed by persistently increased ventilatory motor output is referred to as long-term facilitation (LTF). LTF is activated during sleep after repetitive hypoxia in snorers. We hypothesized that LTF is activated in obstructive sleep apnea (OSA) patients. Eleven subjects with OSA (apnea/hypopnea index = 43.6 ± 18.7/h) were included. Every subject had a baseline polysomnographic study on the appropriate continuous positive airway pressure (CPAP). CPAP was retitrated to eliminate apnea/hypopnea but to maintain inspiratory flow limitation (sham night). Each subject was studied on 2 separate nights. These two studies are separated by 1 mo of optimal nasal CPAP treatment for a minimum of 4–6 h/night. The device was capable of covert pressure monitoring. During night 1 (N1), study subjects used nasal CPAP at suboptimal pressure to have significant air flow limitation (>60% breaths) without apneas/hypopneas. After stable sleep was reached, we induced brief isocapnic hypoxia [inspired O2 fraction (Fi O2 ) = 8%] (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 5, 20, and 40 min of recovery for ventilation, timing ( n = 11), and supraglottic pressure ( n = 6). Upper airway resistance (Rua) was calculated at peak inspiratory flow. During the recovery period, there was no change in minute ventilation (99 ± 8% of control), despite decreased Rua to 58 ± 24% of control ( P < 0.05). There was a reduction in the ratio of inspiratory time to total time for a breath (duty cycle) (0.5 to 0.45, P < 0.05) but no effect on inspiratory time. During night 2 (N2), the protocol of N1 was repeated. N2 revealed no changes compared with N1 during the recovery period. In conclusion, 1) reduced Rua in the recovery period indicates LTF of upper airway dilators; 2) lack of hyperpnea in the recovery period suggests that thoracic pump muscles do not demonstrate LTF; 3) we speculate that LTF may temporarily stabilize respiration in OSA patients after repeated apneas/hypopneas; and 4) nasal CPAP did not alter the ability of OSA patients to elicit LTF at the thoracic pump muscle.

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Faculty Opinions recommendation of Long-term effect of continuous positive airway pressure in hypertensive patients with sleep apnea.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.3017956.2697054 ◽

2010 ◽

Author(s):

Rob Basner

Keyword(s):

Sleep Apnea ◽

Continuous Positive Airway Pressure ◽

Airway Pressure ◽

Positive Airway Pressure ◽

Term Effect ◽

Hypertensive Patients ◽

Long Term Effect

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1244 A Curious Case of ASV Failure

SLEEP ◽

10.1093/sleep/zsaa056.1238 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A474-A474

Author(s):

Nishant Chaudhary ◽

Mirna Ayache ◽

John Carter

Keyword(s):

Sleep Apnea ◽

Airway Obstruction ◽

Airway Pressure ◽

Positive Airway Pressure ◽

Central Sleep Apnea ◽

Upper Airway ◽

Upper Airway Obstruction ◽

Neck Extension ◽

Sleep Study ◽

Obstructive Sleep

Abstract Introduction Positive airway pressure-induced upper airway obstruction has been reported with the treatment of obstructive sleep apnea (OSA) using continuous positive airway pressure (CPAP) along with an oronasal interface. Here we describe a case of persistent treatment emergent central sleep apnea (TECSA) inadequately treated with adaptive servo ventilation (ASV), with an airflow pattern suggestive of ASV-induced upper airway obstruction. Report of Case A 32-year-old male, with severe OSA (apnea hypopnea index: 52.4) and no other significant past medical history, was treated with CPAP and required higher pressures during titration sleep studies to alleviate obstructive events, despite a Mallampati Class II airway and a normal body mass index. Drug-Induced Sleep Endoscopy (DISE) showed a complete velopharynx and oropharynx anterior posterior (AP) collapse, long soft palate, which improved with neck extension. CPAP therapy, however, did not result in any symptomatic benefit and compliance reports revealed high residual AHI and persistent TECSA. He underwent an ASV titration sleep study up to a final setting of expiratory positive airway pressure 9 cm H2O, pressure support 6-15 cm H2O (auto-rate), with a full-face mask due to high oral leak associated with the nasal interface. The ASV device detected central apneas and provided mandatory breaths, but did not capture the thorax or abdomen, despite normal mask pressure tracings. Several such apneas occurred, with significant oxyhemoglobin desaturation. Conclusion We postulate that the ASV failure to correct central sleep apnea as evidenced by the absence of thoracoabdominal inspiratory effort, occurred due to ASV-induced upper airway obstruction. Further treatment options for this ASV phenomenon are to pursue an ASV-assisted DISE and determine the effectiveness of adjunctive therapy including neck extension, nasal mask with a mouth closing device and a mandibular assist device.

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