Asthma and sleep-disordered breathing in children and adults
Dr Kristie Ross
University Hospitals
CWRU School of Medicine
UH Rainbow Babies and Children's Hospital
11100 Euclid Ave
OH44106 Cleveland
UNITED STATES OF AMERICA
[email protected]
AIMS: To review the ongoing clinical studies and recent publications that describe the
interaction between asthma and sleep-related breathing disorders; to give an overview of the
epidemiology of asthma and sleep-disordered breathing in adults and children; to discussthe
shared risk factors and inflammatory pathophysiology of sleep-disordered breathing and
asthma, and the evidence that suggests that upper-airway obstruction influences asthma
severity and response to therapy; to discuss the evidence showing that treating sleep disorders,
including insufficient sleep and sleep-disordered breathing, improves asthma outcomes; and
to describe novel methods to measure asthma and sleep-related breathing disorders in the
home-setting.
TARGET AUDIENCE: Allergologist, Allied health professional, Anaesthesiologist, Clinician,
Fellow, General practitioner, Immunologist, Junior member, Nurse, Paediatrician,
Physiologist, Pulmonologist, Researcher, Resident, Respiratory physician, Scientist, Sleep
specialist/technologist, Student
AIMS



State the epidemiology the bidirectional epidemiologic relationship between the asthma and
sleep disordered breathing.
Describe the proposed mechanisms linking asthma and sleep disordered breathing.
Apply evidence to personalize management of paediatric and adult patients with both
conditions.
SUMMARY
Epidemiology
Asthma and obstructive sleep disordered breathing (SDB) are both prevalent conditions in children and
adults, with mounting evidence that a bidirectional relationship exists between the two disorders. They
share risk factors for development, severity, and response to treatment. A number of pathophysiologic
pathways have been implicated in the relationship between these two common disorders, many of which
may have treatment implications.
Asthma
Estimates of the global prevalence of asthma ranges from 1 to 18% [1], with variation attributable to
the difficulties defining asthma given its heterogeneity, variation in global health care resources, and
true variation in susceptibility. Asthma is likely under-recognized in some populations, but may be over
diagnosed and over treated in others. Risk factors are complex and vary with age and population
studied, but include genetic background, pre-natal and early life infections and exposures, race, sex,
diet, occupational exposures, indoor and outdoor pollution exposure, and co-morbid conditions (atopy,
GERD, obesity).
SDB
Obstructive SDB prevalence is estimated to be 2-4% in adults [2,3] and 1-4% [4] in children using
polysomnographic criteria along with clinical symptoms. Risk factors vary by age. In adults, obesity
and male sex are the strongest risk factors for obstructive SDB [2]. While obesity is increasingly
recognized as a risk factor for obstructive SDB in adolescents and children [5], this relationship may be
stronger in adolescents and older children than younger children [6]. In young children, adenotonsillar
hypertrophy is the strongest risk factor for obstructive SDB, and there are similar prevalence rates in
boys and girls [7,8].
Any discussion about these two disorders must acknowledge that both asthma and obstructive SDB are
heterogeneous conditions, complicating attempts to understand and study how they interact with each
other. This heterogeneity makes this area ideal for discussion of personalized approaches to care,
although there are clear gaps between the concept of disease phenotypes and translation in to precision
medicine.
Epidemiologic interactions between Asthma and SDB
The interaction between obstructive SDB and chronic obstructive pulmonary disease (COPD) has been
recognized as the “Overlap Syndrome” for some time, with greater morbidity and mortality observed in
those with both conditions than either alone [9]. There is accumulating evidence that there are
interactions between asthma and SDB as well.
Cross-sectional studies in adults [10- 13]and children [5, 14-16] with asthma have consistently found
an increased risk for obstructive SDB when compared with either control or reference populations, with
most studies describing an approximate 2 fold increase. The relationship appears to be stronger in more
severe or refractory asthma [17, 18], with co-morbid GERD [10], in women [10, 19], with use of inhaled
corticosteroids [10], and with co-morbid obesity [5, 16]. One prospective study also found a dose
dependent relationship between the duration of asthma and the development of incident OSA [20].
There are less consistent data about the prevalence of asthma in populations of adults with obstructive
SDB, with reports ranging from no increase [21] to a 2 fold increase [22, 23] to a 7 fold increase in a
single study [24]. Asthma prevalence was approximately 30% (3-4 fold higher than comparable
populations without SDB) in a large retrospective study of children undergoing adenotonsillectomy for
SDB [25] and in the only randomized controlled trial of adenotonsillectomy for childhood obstructive
SDB [26].
Evidence that the Asthma-Obstructive SDB phenotype has treatment implications
Beyond evidence that each condition appears to increase the risk for finding the other, it is important to
examine whether there is an interaction between the two conditions in a way that affects disease severity
or response to treatment. In our cohort of children followed in a tertiary care asthma program, the
presence of obstructive SDB was associated with a 3.62 fold increase (95% CI 1.26-10.40) in the risk
of being classified as severe asthma using a composite measure after treatment with guidelines based
care during a one year prospective period independent of race, sex, and obesity. [27] In another cohort
of several hundred adults in which OSA risk was defined using a validated questionnaire, high OSA
risk was associated with a similar increased risk (OR 2.87, 95% CI 1.54-5.32) of poor asthma control
after controlling for demographic factors, obesity, and GERD [28]. In the well characterized Severe
Asthma Research Program cohort, participants with high OSA risk had more day and night symptoms,
as well as higher neutrophil counts in induced sputum samples [29]. OSA was more common (OR 3.4,
95% CI 1.2-10.4) in those with an exacerbation prone phenotype in a difficult to treat asthma program
[30]. The mechanisms discussed below may allow for the development of more personalized strategies
in the future.
Putative Mechanisms for Interactions
Physiologic mechanisms that might link asthma and obstructive SBD include effects on the tracheal tug
phenomenon [31], the interdependence of expiratory and inspiratory flow resistance [32],
bronchosconstrictive effects of upper airway obstruction via vagal stimulation [33], increased resistance
load on the lower airways [34], and exacerbation of normal physiologic reduction of functional residual
capacity during sleep leading to increased resistance [35].
Shared local and systemic inflammation may explain the interaction between the two disorders, with
evidence that obstructive SDB is associated with T cell [36] and neutrophil [37] inflammatory cell
infiltration in the upper airway, and increased cysteinyl leukotriene receptor expression [38] and NFB expression [39]. Most studies investigating the relationship between obstructive SDB and systemic
inflammation have found low grade chronic inflammation, with elevations in CRP, IL-6, NF-B, and
TNF- [39, 40] Oxidative stress due to intermittent hypoxemia has been linked to neutrophilic
inflammation, induction of vascular growth factors, and may trigger bronchoconstriction via vagal
stimulation [41-43].
Other than the effects on cysteinyl leukotriene expression, the nuetrophilic and non-TH2 type
inflammation that characterizes the inflammatory and oxidative consequences of obstructive SDB are
not likely to be as responsive to the inhaled corticosteroids typically used to treat asthma. While much
of the focus in understanding the inflammatory relationship between SDB and asthma has focused on
how SDB can worsen inflammation making asthma more severe or difficult to treat, chronic low-grade
inflammation may also adversely affect the force generation properties of the upper airway muscles
[44], linking asthma back to obstructive sleep disordered breathing in a bidirectional manner.
Shared comorbidities (rhinitis, obesity, GERD) may explain the link between obstructive SDB and
asthma. Allergic or non-allergic rhinosinusitis may lead to upper airway obstruction as well as trigger
lower airway inflammation and reactivity. The interaction between obesity and asthma has been well
studied, although not always with consideration of how obstructive SDB may either confound or
mediate observed relationships, possibly explaining some of the disparate findings in the literature.
Treatment effects may explain some of the observed associations. Some researchers have proposed that
the relationship between more severe asthma and obstructive SDB is driven by use of high dose inhaled
steroids or oral steroids. [10, 45] Proposed mechanisms include deposition of fat into the airways and
steroid induced myopathy affecting upper airway muscles.
Sleep fragmentation has also been proposed to play a role in a bidirectional manner. Sleep apnea induced
sleep fragmentation may impair cognitive functioning needed to manage asthma, or may have direct
impacts on airway resistance. [46] Conversely, sleep fragmentation due to asthma may worsen upper
airway collapsibility. [47]
Impact of treatment of obstructive SDB on asthma outcomes
CPAP use in patients with asthma was first reported in 1988 by two groups. In a series of 15 subjects
with uncontrolled asthma despite oral corticosteroids, treatment of mild to moderate OSA with CPAP
over a 2-week period was associated with improved peak flow, reduced day and night symptoms, and
reduced bronchodilator use. Symptoms worsened when CPAP use was stopped. [48] In a second series
of 10 adult and 5 adolescent males, use of CPAP was associated with a reduction in nocturnal asthma
attacks. [49] In another uncontrolled study of 43 adults with nocturnal asthma despite optimized medical
management, treatment with CPAP in those found to have obstructive SDB resulted in improvement in
nocturnal symptoms in the majority of those who were adherent to CPAP use. [50] In a study of 33
participants with well controlled asthma and newly diagnosed obstructive SDB, CPAP use was
associated with improved asthma and sleep related quality of life. [51] In a large retrospective study,
CPAP use abrogated an association with OSA and daytime asthma symptoms. [52] Lung function was
either not measured or found to be unchanged with CPAP treatment in these studies, but Bonay et al
found that treatment with CPAP for one year resulted in improvement in lung function in those with
obstructive lung disease but small yet statistically significant worsening in those without a history of
obstructive lung disease. [53] Others have shown improvement in chronic cough when CPAP is used,
even in the absence of a formal asthma diagnosis. [54]
Adenotonsillectomy is first line treatment for obstructive SDB in children who are surgical candidates.
Similar to the evidence that CPAP treatment may improve asthma outcomes in adults, there are studies
suggesting AT may be associated with improved asthma outcomes in children but no randomized
clinical trials addressing this question. Kheirandish-Gozal et al reported on their practice in a difficult
to treat asthma clinic, in which 43% of children who had a PSG were found to have obstructive SDB.
[56] Among those who underwent adentonsillectomy, there was significant improvement in lung
function, exacerbation rates, and use of quick relief medications. Findings from this study must be
interpreted in light of significant attrition of eligible children. Researchers used data from a large US
insurance database to study children with asthma who underwent adenotonsillectomy and compared
them with matched cases who did not have the procedure. The children undergoing adenotonsillectomy
had a significant reduction in acute exacerbation rates during one year of follow up post procedure, with
no change in the control group. [57] The database used for this study did not include higher risk patients
with public insurance, somewhat limiting the generalizability of the findings. A retrospective database
study in Belguim found using a similar case control design also found reduced respiratory medication
use in children undergoing tonsillectomy compared with controls. [58] In both of these studies, there
appeared to be a larger effect size in younger children than older children and adolescents.
Summary
Asthma and obstructive SDB are prevalent conditions in both children and adults. While the
heterogeneity of each disorder complicated efforts to study their interactions, there is mounting evidence
that there these disorders may influence each other in terms of risk of development, severity, and
response to treatment. Putative pathways by which this bidirectional interaction occurs include
physiologic changes, inflammatory and oxidative derangements, shared co-morbidites, and treatment
effects. There is some uncontrolled evidence that treatment of obstructive SDB improves asthma
outcomes. Further work may help direct personalized strategies that consider the phenotype of both
upper and lower airway disease in making diagnostic and treatment decisions.
REFERENCES
1. Masoli M, Fabian D, Holt S, Beasley R. The global burden of asthma: Executive summary of the
GINA Dissemination Committee Report. Allergy Eur J Allergy Clin Immunol. 2004;59(5):469478.
2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered
breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-1235.
3. Kapur VK. Obstructive sleep apnea: diagnosis, epidemiology, and economics. Respir Care.
2010;55(9):1155-1167.
4. Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc.
2008;5(2):242-252.
5. Redline S, Tishler P V, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleepdisordered breathing in children. Associations with obesity, race, and respiratory problems. Am J
Respir Crit Care Med. 1999;159(5 Pt 1):1527-1532. d
6. Spilsbury JC, Storfer-Isser A, Rosen CL, Redline S. Remission and incidence of obstructive sleep
apnea from middle childhood to late adolescence. Sleep. 2015;38(1):23-29.
7. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr.
1982;100(1):31-40.
8. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apnea and its therapy: clinical
and polysomnographic manifestations. Pediatrics. 1983;71(5):737-742.
9. Owens RL, Malhotra A. Sleep-disordered breathing and COPD: the overlap syndrome. Respir
Care. 2010;55(10):1333-1344.
10. Teodorescu M, Consens FB, Bria WF, et al. Predictors of Habitual Snoring and Obstructive Sleep
Apnea Risk in Patients With Asthma. Chest. 2009;135(5):1125-1132.
11. Li L, Xu Z, Jin X, et al. Sleep-disordered breathing and asthma: evidence from a large multicentric
epidemiological study in China. Respir Res. 2015;16:56.
12. Shen T-C, Lin C-L, Wei C-C, et al. Risk of Obstructive Sleep Apnea in Adult Patients with Asthma:
A Population-Based Cohort Study in Taiwan. PLoS One. 2015;10(6):e0128461.
13. Jonassen TM, Eagan TM, Bjorvatn B, Lehmann S. Associations between obstructive lung disease
and symptoms of obstructive sleep apnoea in a general population. Clin Respir J. March 2016.
14. Ross KR, Hart MA, Storfer-Isser A, et al. Obesity and obesity related co-morbidities in a referral
population of children with asthma. Pediatr Pulmonol. 2009;44(9):877-884.
15. Brockmann PE, Bertrand P, Castro-Rodriguez JA. Influence of asthma on sleep disordered
breathing in children: a systematic review. Sleep Med Rev. 2014;18(5):393-397.
16. Sulit LG, Storfer-Isser A, Rosen CL, Kirchner HL, Redline S. Associations of obesity, sleepdisordered breathing, and wheezing in children. Am J Respir Crit Care Med. 2005;171(6):659-664.
17. Byun MK, Park SC, Chang YS, et al. Associations of moderate to severe asthma with obstructive
sleep apnea. Yonsei Med J. 2013;54(4):942-948.
18. Guven SF, Dursun AB, Ciftci B, Erkekol FO, Kurt OK. The prevalence of obstructive sleep apnea
in patients with difficult-to-treat asthma. Asian Pac J Allergy Immunol. 2014;32(2):153-159.
19. Greenberg-Dotan S, Reuveni H, Simon-Tuval T, Oksenberg A, Tarasiuk A. Gender differences in
morbidity and health care utilization among adult obstructive sleep apnea patients. Sleep.
2007;30(9):1173-1180.
20. Teodorescu M, Barnet JH, Hagen EW, Palta M, Young TB, Peppard PE. Association between
asthma and risk of developing obstructive sleep apnea. JAMA. 2015;313(2):156-164.
21. Pinto JA, Ribeiro DK, Cavallini AF da S, Duarte C, Freitas GS. Comorbidities Associated with
Obstructive Sleep Apnea: a Retrospective Study. Int Arch Otorhinolaryngol. 2016;20(2):145-150.
22. Greenberg-Dotan S, Reuveni H, Tal A, et al. Increased prevalence of obstructive lung disease in
patients with obstructive sleep apnea. Sleep Breath. 2014;18(1):69-75.
23. Bhattacharyya N, Kepnes LJ. Ambulatory office visits and medical comorbidities associated with
obstructive sleep apnea. Otolaryngol Head Neck Surg. 2012;147(6):1154-1157.
24. Alharbi M, Almutairi A, Alotaibi D, Alotaibi A, Shaikh S, Bahammam AS. The prevalence of
asthma in patients with obstructive sleep apnoea. Prim Care Respir J. 2009;18(4):328-330.
25. Bhattacharjee R, Kheirandish-Gozal L, Spruyt K, et al. Adenotonsillectomy outcomes in treatment
of obstructive sleep apnea in children: a multicenter retrospective study. Am J Respir Crit Care
Med. 2010;182(5):676-683.
26. Marcus CL, Moore RH, Rosen CL, et al. A randomized trial of adenotonsillectomy for childhood
sleep apnea. N Engl J Med. 2013;368(25):2366-2376.
27. Ross KR, Storfer-Isser A, Hart MA, et al. Sleep-disordered breathing is associated with asthma
severity in children. J Pediatr. 2012;160(5):736-742.
28. Teodorescu M, Polomis DA, Hall S V, et al. Association of obstructive sleep apnea risk with
asthma control in adults. Chest. 2010;138(3):543-550. doi:10.1378/chest.09-3066.
29. Teodorescu M, Broytman O, Curran-Everett D, et al. Obstructive Sleep Apnea Risk, Asthma
Burden, and Lower Airway Inflammation in Adults in the Severe Asthma Research Program
(SARP) II. J allergy Clin Immunol Pract. 3(4):566-575.e1. doi:10.1016/j.jaip.2015.04.002.
30. ten Brinke A, Sterk PJ, Masclee AAM, et al. Risk factors of frequent exacerbations in difficult-totreat asthma. Eur Respir J. 2005;26(5):812-818. doi:10.1183/09031936.05.00037905.
31. Van de Graaff WB. Thoracic influence on upper airway patency. J Appl Physiol. 1988;65(5):21242131. http://www.ncbi.nlm.nih.gov/pubmed/3209556. Accessed June 27, 2016.
32. Tamisier R, Pepin JL, Wuyam B, Deschaux C, Levy P. Expiratory changes in pressure: flow ratio
during sleep in patients with sleep-disordered breathing. Sleep. 2004;27(2):240-248.
33. Guilleminault C, Quera-Salva MA, Powell N, et al. Nocturnal asthma: snoring, small pharynx and
nasal CPAP. Eur Respir J. 1988;1(10):902-907.
34. Bijaoui EL, Champagne V, Baconnier PF, Kimoff RJ, Bates JHT. Mechanical properties of the
lung and upper airways in patients with sleep-disordered breathing. Am J Respir Crit Care Med.
2002;165(8):1055-1061.
35. Ballard RD, Irvin CG, Martin RJ, Pak J, Pandey R, White DP. Influence of sleep on lung volume
in asthmatic patients and normal subjects. J Appl Physiol. 1990;68(5):2034-2041.
36. Boyd JH, Petrof BJ, Hamid Q, Fraser R, Kimoff RJ. Upper airway muscle inflammation and
denervation changes in obstructive sleep apnea. Am J Respir Crit Care Med. 2004;170(5):541-546.
37. Salerno FG, Carpagnano E, Guido P, et al. Airway inflammation in patients affected by obstructive
sleep apnea syndrome. Respir Med. 2004;98(1):25-28.
38. Goldbart AD, Goldman JL, Li RC, Brittian KR, Tauman R, Gozal D. Differential expression of
cysteinyl leukotriene receptors 1 and 2 in tonsils of children with obstructive sleep apnea syndrome
or recurrent infection. Chest. 2004;126(1):13-18.
39. Israel LP, Benharoch D, Gopas J, Goldbart AD. A pro-inflammatory role for nuclear factor kappa
B in childhood obstructive sleep apnea syndrome. Sleep. 2013;36(12):1947-1955.
40. Nadeem R, Molnar J, Madbouly EM, et al. Serum inflammatory markers in obstructive sleep apnea:
a meta-analysis. J Clin Sleep Med. 2013;9(10):1003-1012.
41. Dewan NA, Nieto FJ, Somers VK. Intermittent Hypoxemia and OSA: Implications for
Comorbidities. Chest. 2015;147(1):266-274.
42. Denjean A, Canet E, Praud JP, Gaultier C, Bureau M. Hypoxia-induced bronchial responsiveness
in awake sheep: role of carotid chemoreceptors. Respir Physiol. 1991;83(2):201-210.
43. Denjean A, Roux C, Herve P, et al. Mild isocapnic hypoxia enhances the bronchial response to
methacholine in asthmatic subjects. Am Rev Respir Dis. 1988;138(4):789-793.
44. Reid MB, Lännergren J, Westerblad H. Respiratory and limb muscle weakness induced by tumor
necrosis factor-alpha: involvement of muscle myofilaments. Am J Respir Crit Care Med.
2002;166(4):479-484.
45. Yigla M, Tov N, Solomonov A, Rubin A-HE, Harlev D. Difficult-to-control asthma and obstructive
sleep apnea. J Asthma. 2003;40(8):865-871.
46. Ballard RD, Irvin CG, Martin RJ, Pak J, Pandey R, White DP. Influence of sleep on lung volume
in asthmatic patients and normal subjects. J Appl Physiol. 1990;68(5):2034-2041.
47. Leiter JC, Knuth SL, Bartlett D. The effect of sleep deprivation on activity of the genioglossus
muscle. Am Rev Respir Dis. 1985;132(6):1242-1245.
48. Chan CS, Woolcock AJ, Sullivan CE. Nocturnal asthma: role of snoring and obstructive sleep
apnea. Am Rev Respir Dis. 1988;137(6):1502-1504.
49. Guilleminault C, Quera-Salva MA, Powell N, et al. Nocturnal asthma: snoring, small pharynx and
nasal CPAP. Eur Respir J. 1988;1(10):902-907.
50. Ciftci TU, Ciftci B, Guven SF, Kokturk O, Turktas H. Effect of nasal continuous positive airway
pressure in uncontrolled nocturnal asthmatic patients with obstructive sleep apnea syndrome.
Respir Med. 2005;99(5):529-534.
51. Lafond C, Series F, Lemiere C. Impact of CPAP on asthmatic patients with obstructive sleep
apnoea. Eur Respir J. 2007;29(2):307-311.
52. Teodorescu M, Polomis DA, Teodorescu MC, et al. Association of obstructive sleep apnea risk or
diagnosis with daytime asthma in adults. J Asthma. 2012;49(6):620-628.
53. Bonay M, Nitenberg A, Maillard D. Should flow-volume loop be monitored in sleep apnea patients
treated with continuous positive airway pressure? Respir Med. 2003;97(7):830-834.
54. Sundar KM, Daly SE, Pearce MJ, Alward WT. Chronic cough and obstructive sleep apnea in a
community-based pulmonary practice. Cough. 2010;6(1):2.
55. Sundar KM, Daly SE, Willis AM. A longitudinal study of CPAP therapy for patients with chronic
cough and obstructive sleep apnoea. Cough. 2013;9(1):19.
56. Kheirandish-Gozal L, Dayyat EA, Eid NS, Morton RL, Gozal D. Obstructive sleep apnea in poorly
controlled asthmatic children: effect of adenotonsillectomy. Pediatr Pulmonol. 2011;46(9):913918.
57. Bhattacharjee R, Choi BH, Gozal D, Mokhlesi B. Association of adenotonsillectomy with asthma
outcomes in children: a longitudinal database analysis. PLoS Med. 2014;11(11):e1001753.
58. Piessens P, Hens G, Lemkens N, Schrooten W, Debruyne F, Lemkens P. Effect of
adenotonsillectomy on the use of respiratory medication. Int J Pediatr Otorhinolaryngol.
2012;76(6):906-910.
FACULTY DISCLOSURES
Dr Kristie Ross has no relevant commercial disclosure to this presentation. I have grant funding from
the National Institutes of Health to study the impact of adentonsillecomy on children, including the
impact on asthma outcomes.
EVALUATION
1. Which of the following is true about the epidemiologic evidence linking asthma and obstructive
sleep disordered breathing?
a. Most studies examining the rates of obstructive sleep disordered breathing in children and adults
with asthma find there is an approximate 2 fold increase in risk compared to populations without
asthma.
b. There is a clear and consistent relationship between asthma severity and risk of obstructive
SDB, such that most studies show children and adults with more severe asthma are at higher
risk for obstructive SDB than those with less severe asthma.
c. In the only randomized controlled study of children with obstructive SDB undergoing
adentonsillectomy, asthma rates were lower than would be predicted in a similar US population.
d. A and B
2. Studies examining putative inflammatory mechanisms that link asthma and obstructive SDB have
found
a. Consistent TH2 or type 2 inflammation (airway and systemic) in obstructive SDB, similar to
classic asthma inflammation
b. Neutrophilic predominant inflammation thought to be due in part to oxidative stress in
obstructive SDB, suggesting treatment with standard asthma therapies that target allergic
inflammation may not be as effective
c. No evidence that there is chronic airway or systemic inflammation in obstructive SDB
d. No evidence that intermittent hypoxemia affects airway inflammation
3. Theoretical physiologic mechanisms that link asthma and obstructive SDB include all of the
following EXCEPT:
a. Tracheal tug phenomenon
b. Increased respiratory load during attempts to open an occluded airway
c. Obstructive events triggering vagal mediated broncoconstriction
d. Sleep fragmentation leading to bronchodilation
4. Adenotonsillectomy in children with obstructive SDB has been shown to:
a. Reduce asthma exacerbations in a randomized controlled trial study design
b. Be associated with reduced asthma exacerbations in a retrospective study using an insurance
database
c. Be associated with reduced respiratory medication use in a retrospective study using an
insurance database
d. B and C
5. CPAP use in those with asthma and obstructive SDB has been shown to:
a. Consistently improve lung function across most studies
b. Consistently worsen lung function by causing air trapping
c. Improve some asthma related outcomes including quality of life and daytime and night-time
symptoms in uncontrolled studies
d. Improve asthma outcomes in randomized controlled trials