Article

Central sleep apnea.

Pulmonary and Critical Care Division, Wayne State University School of Medicine, Harper University Hospital, 3-Hudson, 3990 John R. Street, Detroit, MI 48201, USA.
Primary Care Clinics in Office Practice (Impact Factor: 0.83). 07/2005; 32(2):361-74, vi. DOI: 10.1016/j.pop.2005.02.003
Source: PubMed

ABSTRACT Central sleep apnea (CSA) is characterized by the periodic occurrence of apnea caused by loss of ventilatory motor output. CSA is often discussed as a minor variant of obstructive sleep apnea.However, this view obscures the critical contribution of CSA as an important manifestation of breathing instability in a variety of conditions with diverse causes. Central apnea can also be a physiologic phenomenon in healthy people during sleep onset. Conversely, patients who have obstructive apnea may also develop episodes of apparent central apnea, and apneas that begin as central may become obstructive as respiratory effort is restored ("mixed apneas"). Thus, there is a significant overlap between obstructive and central apnea. This article addresses the pathophysiology, clinical features, and management of normocapnic and hypercapnic CSA.

0 Bookmarks
 · 
103 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sleep-disordered Breathing (SDB) is highly prevalent in patients with spinal cord injury (SCI); the exact mechanism(s) or the predictors of disease are unknown. We hypothesized that patients with cervical (C-SCI) are more susceptible to central apnea than patients with thoracic (T-SCI) or able-bodied controls. Methods: Sixteen patients with chronic SCI, level T6 or above, (8 C-SCI, 8 T-SCI) (age 42.5±15.5 years; BMI 25.9±4.9 kg/m(2)) and 16 matched controls were studied. The hypocapnic apneic threshold and CO2 reserve were determined using non-invasive ventilation (NIV). For participants with spontaneous central apnea, CO2 was administered until central apnea was abolished and CO2 reserve was measured as the difference in end-tidal CO2 (PETCO2) before and after. Steady-state plant gain (PG) was calculated from PETCO2 and VE ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in VE between control and hypopnea or apnea to the Δ PETCO2. Results: Central SDB was more common in C-SCI than T-SCI (63% vs. 13%, respectively; p<0.05). Mean CO2 reserve for all participants was narrower in C-SCI than in T- SCI or control group (-0.4±2.9 vs. -2.9±3.3 vs. -3.0±1.2 L/min/mmHg, respectively; p<0.05). PG was higher in C-SCI than in T-SCI or control groups (10.5±2.4 vs. 5.9±2.4 vs. 6.3±1.6 mmHg/L/min, respectively; p<0.05) and CG was not significantly different. The CO2 reserve was an independent predictor of AHI. Conclusion: C-SCI had higher rates of central SDB, indicating that tetraplegia is a risk factor for central sleep apnea. Sleep-related hypoventilation may play a significant role in the mechanism of SDB in higher SCI levels.
    Journal of Applied Physiology 10/2013; · 3.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Spinal cord injury (SCI) is associated with 2-5 times greater prevalence of sleep disordered breathing (SDB) than the general population. The contribution of SCI on sleep and breathing at different levels of injury using two scoring methods has not been assessed. The objectives of this study were to characterize the sleep disturbances in the SCI population and the associated physiological abnormalities using quantitative polysomnography and to determine the contribution of SCI level on the SDB mechanism. We studied 26 consecutive patients with SCI (8 females; age 42.5 ± 15.5 years; BMI 25.9 ± 4.9 kg/m(2); 15 cervical and 11 thoracic levels) by spirometry, a battery of questionnaires and by attended polysomnography with flow and pharyngeal pressure measurements. Inclusion criteria for SCI: chronic SCI (> 6 months post injury), level T6 and above and not on mechanical ventilation. Ventilation, end-tidal CO2 (PETCO2), variability in minute ventilation (VI-CV) and upper airway resistance (RUA) were monitored during wakefulness and NREM sleep in all subjects. Each subject completed brief history and exam, Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Berlin questionnaire (BQ) and fatigue severity scale (FSS). Sleep studies were scored twice, first using standard 2007 American Academy of Sleep Medicine (AASM) criteria and second using new 2012 recommended AASM criteria. Mean PSQI was increased to 10.3 ± 3.7 in SCI patients and 92% had poor sleep quality. Mean ESS was increased 10.4 ± 4.4 in SCI patients and excessive daytime sleepiness (ESS ≥ 10) was present in 59% of the patients. Daytime fatigue (FSS > 20) was reported in 96% of SCI, while only 46% had high-risk score of SDB on BQ. Forced vital capacity (FVC) in SCI was reduced to 70.5% predicted in supine compared to 78.5% predicted in upright positions (p < 0.05). Likewise forced expiratory volume in first second (FEV1) was 64.9% predicted in supine compared to 74.7% predicted in upright positions (p < 0.05). Mean AHI in SCI patients was 29.3 ± 25.0 vs. 20.0 ± 22.8 events/h using the new and conventional AASM scoring criteria, respectively (p < 0.001). SCI patients had SDB (AHI > 5 events/h) in 77% of the cases using the new AASM scoring criteria compared to 65% using standard conventional criteria (p < 0.05). In cervical SCI, VI decreased from 7.2 ± 1.6 to 5.5 ± 1.3 L/min, whereas PETCO2 and VI-CV, increased during sleep compared to thoracic SCI. The majority of SCI survivors have symptomatic SDB and poor sleep that may be missed if not carefully assessed. Decreased VI and increased PETCO2 during sleep in patients with cervical SCI relative to thoracic SCI suggests that sleep related hypoventilation may contribute to the pathogenesis SDB in patients with chronic cervical SCI. Sankari A; Bascom A; Oomman S; Badr MS. Sleep disordered breathing in chronic spinal cord injury. J Clin Sleep Med 2014;10(1):65-72.
    Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 01/2014; 10(1):65-72. · 2.93 Impact Factor
  • The Journal of Urology 04/2011; 185(4). · 3.75 Impact Factor

Full-text (2 Sources)

Download
90 Downloads
Available from
Jun 11, 2014