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Sleep Journal Club

(Click on title to be directed to posting, most recent listed first)

January 2013 Sleep Journal Club
December 2012 Sleep Journal Club
November 2012 Sleep Journal Club
March 2012 Sleep Journal Club
December 2011 Pulmonary/Sleep Journal Club 
July, 2011 Sleep Journal Club
February 2011 Sleep Journal Club
January 2011 Sleep Journal Club
October 2010 Sleep Journal Club


The Phoenix Good Samaritan/VA pulmonary and critical care fellows have a periodic sleep journal club in which current or classic sleep articles are reviewed and discussed. A brief summary is written of each discussion describing the article and the strengths and weaknesses of each article.



January 2013 Sleep Journal Club

Jilwan FN, Escourrou P, Garcia G, Jaïs X, Humbert M, Roisman G. High occurrence of hypoxemic sleep respiratory disorders in precapillary pulmonary hypertension and mechanisms. CHEST. 2013;143(1):47-55. Abstract

This is an important study that highlights the interaction of pulmonary hypertension (PH) and hypoxemia with complications of sleep disordered breathing.  The study intent was to delineate the mechanism of the hypoxemia.  There is a well- known association between hypoxemia at night and pulmonary hypertension but the prevalence in studies has been variable. Sleep disordered breathing is also associated with PH but is generally thought to contribute little to the pathogenesis of the PH.

Methods:  47 patients were entered into the study with 2/3 of patients having idiopathic PH and 1/3 chronic thromboembolic PH. All the chronic thromboembolic PH patients had undergone thromboendarterctomy or had lesions that were inoperable.  Most of the patients were in NYHA class 2 or 3 and were stable on appropriate PH therapy. All patients had the usual evaluations of patients with PH with all receiving overnight attended polysomnograms.


  1. Nocturnal hypoxemia was observed in 82.6 % of the patients. 
  2. The major reason cited for the hypoxemia was ventilation perfusion mismatch.
  3. Sleep Apnea was found in 89% of the studied group. This included both obstructive and central sleep apnea. Of interest is the finding that 67% had a moderately elevated apnea-hypopnea index (AHI, > 15) with 1/3 having a severely elevated AHI (> 30).

Discussion:  The authors conclude that sleep related hypoxemia in PH is quite common.  Since sleep apnea was so prevalent in this study a home or in lab polysomnography should be considered in most patients with PH.

Kuna ST, Gurubhagavatula I, Maislin G, Hin S, Hartwig KC, McCloskey S, Hachadoorian R, Hurley S, Gupta R, Staley B, Atwood CW. Noninferiority of functional outcome in ambulatory management of obstructive sleep apnea. Am J Respir Crit Care Med. 2011;183(9):1238-44. Full Text

This VA sponsored study done at several different sleep centers was undertaken several years ago because of the high demand for sleep testing. The research question addressed was: Is diagnostic home testing followed by autotitraing continuous positive airway pressure (CPAP) inferior in terms of compliance and patient satisfaction with testing and CPAP titration done in an attended setting? 

Methods: Veterans with suspected OSA were randomized to either home testing or standard in-laboratory testing. Home testing consisted of a portable monitor recording followed by at least three nights using an automatically adjusting positive airway apparatus. Participants diagnosed with OSA were treated with CPAP for 3 months. The authors measured the change in Functional Outcomes of Sleep Questionnaire score and the mean daily hours of objectively measured CPAP adherence

Measurements and Main Results: Of the 296 subjects enrolled, 260 (88%) were diagnosed with OSA, and 213 (75%) were initiated on CPAP. Functional outcome score improved both in the home group and in the in-laboratory group but the improvement did not differ. Similarly, daily CPAP adherence was 3.5 ± 2.5 hours/day in the home group and 2.9 ± 2.3 hours/day in the in-laboratory group (P = 0.08).

Conclusions: Functional outcome and treatment adherence in patients evaluated according to a home testing algorithm is not clinically inferior to that in patients receiving standard in-laboratory polysomnography.

John D. Roehrs, MD

Associate Editor

Sleep Journal Club

Reference as: Roehrs JD. January 2013 sleep journal club. Southwest J Pulm Crit Care 2013;6(1):53-4. PDF


December 2012 Sleep Journal Club

Fitzgibbons SC, Chen J, Jagsi R, Weinstein D. Long-term follow-up on the educational impact of ACGME duty hour limits: a pre-post survey study. Ann Surg 2012;256:1108-12. Abstract

The Accreditation Council for Graduate Medical Education (ACGME) responded to political pressure by restricting resident duty hours in 2003. The assumption was made that limiting work hours would address the problem of resident sleep deprivation. The authors evaluated the long-term impact of the duty hour limits on orthopedic residents’ sleep and perception of education at a single institution using a yearly survey. There was no significant change in the average reported hours of sleep (34.6 hours per week in 2003 vs. 33.7 hours per week between 2004 and 2009) despite a decrease in the mean reported number of work hours (74.5 hours in 2003 vs. 66.2  hours in 2009; P = 0.046). However, a decrease in perceived fatigue and its negative impact on patient safety and quality of care was noted. The perceived sufficiency of direct clinical experience, the number of hours spent performing major procedures, and the overall satisfaction with education also decreased. Finally, the residents’ sense of clinical preparedness diminished after the work hour limits were in place. The work hour restrictions resulted in the hiring of 16 additional physician extenders to absorb the work which resulted from the decrease in resident hours. Not studied is whether resident performance changed.

This study suggests that the resident work hour restrictions have been ineffectual in increasing resident sleep; have harmed medical education; and increased medical costs. The ACGME needs to gather further data on resident work hour restriction, and if these results are representative of a consistent trend, develop a different solution to the problem of resident sleep deprivation.

Richard A. Robbins, MD

Reference as: Robbins RA. December 2012 sleep journal club. Southwest J Pulm Crit Care 2012;5:301. PDF


November 2012 Sleep Journal Club

Crawford MR, Bartlett DJ, Coughlin SR, et al. The effect of continuous positive airway pressure usage on sleepiness in obstructive sleep apnoea: real effects or expectation of benefit? Thorax. 2012;67:920-4. Abstract

With continuous positive airway pressure (CPAP) treatment of obstructive sleep apnea, greater hours of CPAP use are associated with reduced sleepiness. However, these open-label studies have not controlled for patient expectation of benefit. The authors performed a meta-analysis combining data on sleepiness measured by the Epworth Sleepiness Scale from three randomized placebo-controlled crossover trials including use of low dose CPAP. High use of CPAP reduced sleepiness more than placebo and more than low use. The authors calculated that 29% of the effect of high usage of CPAP was explained by the expectation of benefit with CPAP.

In retrospect it should not be surprising that there was a significant placebo effect. The primary end point used, improvement in the Epworth Sleepiness Scale, measures the subject’s subjective daytime sleepiness using a short questionnaire. Measuring a subjective benefit with a subjective measure seems likely to amplify any placebo effect. Some might argue that whether the benefit is a placebo effect or not makes little difference.  The important thing is that CPAP does make a difference.

At the right of the abstract is the question “What is the bottom line?” It goes on to say “High use of CPAP does confer real benefits but about 29% of the benefit felt by highly adherent patients in regular clinical care is due to expectation of benefit”. This statement is misleading. It assumes that the only benefit from CPAP is improvement in sleepiness. However, other benefits may occur. For example, a recent article in the American Journal of Respiratory and Critical Care Medicine reported an improved cardiovascular mortality in elderly patients who use CPAP (1). This would seem to be an important benefit.

Richard A. Robbins, MD


1. Martínez-García MA, Campos-Rodríguez F, Catalán-Serra P, et al.Cardiovascular mortality in obstructive sleep apnea in the elderly: role of long-term continuous positive airway pressure treatment: a prospective observational study. Am J Respir Crit Care Med 2012;186:909-16.

Reference as: Robbins RA. November 2012 sleep journal club. Southwest J Pulm Crit Care 2012;5:269. PDF


March 2012 Sleep Journal Club

Kripke DF, Langer RD, Kline LE. Hypnotics’ association with mortality or cancer: a matched cohort study. BMJ Open2012;2:e000850.doi:10.1136/bmjopen-2012-000850.  (Click here for the abstract of the manuscript)

Hypnotic use is estimated at 6-10% in the adult US population.  This study expands previous work that has been done associating hypnotics with increased risk of death.  Using an electronic medical record data base, a matched cohort survival analysis was performed.  This study suggests that use of hypnotics at any dose is associated with an increased risk of death.   Hazard ratios for death or cancer were found to be between 3.6 for low use (< 18 doses of hypnotic / year) and up to 5.32 for frequent use of hypnotics (> 132 doses / year).

This study provides a matched cohort analysis over 2.5 years for hypnotic use in a large population in Pennsylvania. The study raises important questions about hypnotic use and safety in patients.   Unfortunately the study makes broad generalizations that are sometimes not based on strongly supported data other than the author’s previous research or beliefs.  This suggests the research may have a conformational bias.

Several limitations are present when reviewing this paper. The study suggests that hypnotic use is associated with death or development of cancer, however since the report is a cohort study, it cannot imply causality.  Another major limitation of this study is that the cause of death is not reported.  A third limitation is that 38% of the hypnotic users also consumed alcohol.  This is a known contraindication to hypnotic use.  Since the cause of death is not reported there may be an unknown bias towards patients that took hypnotics, used alcohol and had significant cardiovascular co-morbidities including asthma and obstructive sleep apnea.

An additional limitation is how the development of cancer in hypnotic users is reported. The study states in one section that the matched cohorts were adjusted for prior cancers, however in another section they state that patients with prior cancers (other than non-melanoma skin cancers) were excluded from the study.  This study also compares hypnotic use for only 2.5 years but suggests that there is causality between hypnotic use and the development of some cancers specifically lung, prostate, and colon.  Since cancers in these organs take longer than 2.5 years to develop it is unlikely that the hypnotics were the cause of the cancer.

This study does point out the benefits of treatment of insomnia with non –drug therapy (cognitive behavior therapy).  However, since this study was reported in the lay press (LA Times, Feb. 28; Arizona Republic, Feb. 29 and multiple other references) the authors have a responsibility to the public to discuss all the risks and benefits of hypnotic therapy without making broad generalizations that are based primarily on their previous research.    

Tonya Whiting, D.O.

David Baratz, M.D., Associate Editor Sleep, Southwest Journal of Pulmonary and Critical Care

Reference as: Whiting T, Baratz D. March 2012 Sleep Journal Club. Southwest Journal of Pulmonary and Critical Care 2012;4:53. (Click here for a PDF version of the journal club)


December 2011 Pulmonary/Sleep Journal Club

Reference as: Mathew M. December 2011 pulmonary/sleep journal club. Soutwest J Pulm Crit Care 2011;3:171. (Click here for PDF version of the journal club)

Cano-Pumarega I, Durán-Cantolla J, Aizpuru F, Miranda-Serrano E, Rubio R, Martínez-Null C, de Miguel J, Egea C, Cancelo L, Alvarez A, Fernández-Bolaños M, Barbé F. Obstructive sleep apnea and systemic hypertension: longitudinal study in the general population: the vitoria sleep cohort. Am J Respir Crit Care Med 2011;184:1299-304. (Click here for abstract)

Obstructive Sleep Apnea (OSA) is a disorder characterized by intermittent episodes of apnea/hypopnea in which there are periodic oxygen desaturations. These episodes may also result in tachycardia, bradycardia and other EKG abnormalities. The prevalence of OSA per the Wisconsin cohort Study is reported as 4-9% for women and 9-24% for men. There is also an increased prevalence in age groups > 65.  Prior observational studies have shown increased cardiovascular mortality from acute MI, stroke and sudden cardiac death from untreated severe OSA. The link between OSA and the development systemic hypertension has also been postulated. Prior Observational Studies (Wisconsin Sleep Cohort Study, Sleep Heart Health Study) demonstrated discordant results with a positive association seen only in the Wisconsin Sleep Cohort Study. This study was done to see if the diagnosis of OSA serves as an independent risk factor in the development of systemic hypertension.

This study was an observational cohort study done in Spain over 2 phases. Patients were excluded if they were on CPAP, had a known diagnosis of systemic hypertension or had undergone an uvulopalatopharyngoplasty.  2148 pts were eligible for the study and a total of 1557 pts completed the study. The patients with a diagnosis of OSA and no prior diagnosis of systemic hypertension were followed over 7-8 years. The results did not show an increased incidence of systemic hypertension in patients with OSA when other variables such as age, gender, fitness level, BMI, and neck circumference were accounted for.

The study was well done and supported the results of The Sleep Heart Health Study.  The strengths of the study were its large sample size and its design. Although there may not be a causal relationship between OSA leading to systemic hypertension, we can not deny the prevalence of hypertension in patients with OSA. From a clinical standpoint I would like to have another question answered.....should patients with newly diagnosed hypertension or multiple drug resistant hypertension undergo screening for obstructive sleep apnea?

Manoj Mathew, MD MCCM, FCCP

Associate Editor

Pulmonary Journal Club