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Sleep apnea syndrome and chronic obstructive pulmonary disease or COPD (see Glossary) often coexist in the same person, who is at increased risk of respiratory failure. One investigator found advanced COPD in 11% of sleep apnea patients, probably higher than in the general population. This study proposes to investigate any association between sleep apnea and early-stage COPD, detectable mainly through laboratory testing of forced expiration and forced oscillation of respiration. This presents difficulties in sleep apnea patients because obesity and upper airway obstructrion due to various anatomic abnormalities have both been shown to affect these measures. It has been difficult to separate the effects of obesity from those of sleep apnea because of the frequent correlation in severity of both. The authors proposed to accomplish this by studying only obese snorers without chronic bronchitis, who had either moderately severe or severe sleep apnea. They studies 170 patients (136 males, 34 females) attending the sleep clinic for snoring and a history of restless sleep, none previously evaluated or treated for sleep apnea, none with a history of COPD, asthma, or chronic bronchitis, but all with obesity defined by a body mass index or BMI (see Glossary) greater than 25 but less than 34. All subjects had a standard overnight laboratory polysomnogram, spirometry (see Glossary). and the forced oscillation method of breathing assessment (see Glossary), arterial blood gas analysis, and x-ray cephalometric analysis of the dimensions of the skull and airway. The authors used an Apnea/Hypopnea Index (see Glossary) of 10-30 to define moderate sleep apnea, above 30 to define severe sleep apnea, and below 10 to define an absence of sleep apnea. By these criteria, 62 of their subjects had no sleep apnea (average AHI=4.5), 56 had moderate sleep apnea (average AHI=18.3), and 52 had severe sleep apnea (average AHI=57.2). All three groups had equivalent ages (mid-50's), BMI (28-30), smoking history (25% were nonsmokers, 35% ex-smokers, and 40% current smokers), and neck circumferences. As one might expect the oxygen saturation low was lower in the severe sleep apneics (73.5) but not different in the non-apneics and moderate apneics (88 and 85). Neither degree of obesity nor neck circumference correlated with severity of apnea. On pulmonary function testing, total lung capacity and vital capacity were similar in the three groups, adn all three showed similar decreases in functional residual capacity and expiratory residual volume (see Glossary). Forced expiratory volume decreased significantly as the AHI increased, as did expiratory flow rate. On oscillatory testing, there were significant decrease in respiratory conductance and increase in respiratory resistance associated with increasing AHI. Arterial oxygen saturation decreased and arterial carbon dioxide increased significantly with increasing AHI. There were also associated with increasing AHI significant differences in the cephalometric measures, but I will leave out trying to describe these lest I embark on an anatomy lesson of which I am quite incapable! The authors commented that conventional pulmonary function tests are generally considered unhelpful for the diagnosis of sleep apnea, but there does seem to be an association between chronic obstructive pulmonary disease and sleep apnea. COPD may lead to excessive blood carbon dioxide and pulmonary hypertension during the day. This study, controlling for the adverse effects of obesity on lung function, found significant decreases in expiratory flow rates and specific respiratory conductance associated with increasing severity of sleep apnea. This relationship was independent of obesity and age.

I must begin by admitting that much of the respiratory terminology used in this paper takes me far outside my primary specialty of psychiatry and also outside my familiarity with sleep disorders. Also, the statistics are very detailed and complex. I doubt that any lay readers would pursue this paper to its conclusion, which remains a bit unclear in its clinical significance. All that said, I still find something of general interest here: that sleep apnea is associated with significant impairment of breathing function even during the waking state. This not the stereotypical "Pickwickian syndrome" since these patients had not (yet) developed chronic emphysema and bronchitis. The concern this raises is that their sleep apnea, in addition to their obesity and whatever smoking history they might have, increases their risk of eventual waking respiratory disease, in addition to the already known risks of hypertension, heart attacks, strokes, and accidents. It may or may not interest you that, when I applied for SSDI on the basis of sleep apnea, I was routinely classified as having a "respiratory" disease, which meant that I was referred to a pulmonologist--not necessarily a sleep specialist--for an evaluation to include pulmonary function testing. This, of course, was quite beside the point of diagnosing and assessing the severity of my sleep apnea, but it had to be done because Social Security demanded it. The danger existed that a normal result on an irrelevant test could create a misleading impression of absent disease. Luckily, I was able to redirect my evaluation to a pulmonologist who was quite expert in sleep disorders and recognized the irrelevance of the pulmonary function tests, but did them anyway. My doctor noted that my "sleep apnea is of such severity that he has evidence of chronic carbon dioxide retention with a resting partial pressure of CO2 of 46 on room air." In their study, these authors had found a significant increase in arterial CO2 with AHI, the most severe group averaging 40.4 plus or minus a standard deviation of only 0.7 The usual rule of thumb is that three standard deviations from a mean (in this case, 2.1 + 40.4 = 42.5 puts an individual higher than 95% of all subjects. In the end of my evaluation I was diagnosed with "mild obstructive airway disease" in addition to my apnea. I have never smoked.

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