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During the course on a single obstructive sleep apnea event, the amount of effort exerted to resume breathing increases. The magnitude of this effort may be important to arousals. It may also be relevant to blood pressure increases associated with an acute apnea. Therefore the authors investigated factors which might determine differences in the magnitude of this effort within and between individuals. The latter is especially difficult to assess in the usual studies involving small numbers of subjects, so the authors gathered a large sample of 116 patients with Obstructive Sleep Apnea (OSA).
The authors studied these patients with measurement of esophageal pressures (Pes); higher Pes represents more respiratory effort. Pes measured for the three breaths prior to each apnea were averaged to yield a "preapneic Pes". During the apnea, Pes recorded during the first three obstructed breaths were examined for the lowest pressure swing, termed the minimal initial pressure (PesMin). Likewise, from the largest pressure swing during the last three obstructed breaths the highest pressure swing was termed the maximal final pressure (PesMax), which was taken as a measure of the maximal respiratory effort during the apnea. The difference between PesMin and PesMax (deltaPes) was considered to measure the increase in respiratory effort during the apnea. To adjust this for the duration of the apnea, this measure (deltaPes) was divided by the the apnea duration to yield a ratio measure (RPes) In order to yield data usable according to these analyses, only apneas lasting 20 seconds or more were used (the usual threshold duration for apneas is 10 seconds) and all apneas preceded by fewer than three unobstructed breaths were discarded.
(WARNING: all the italics and bold-face expressions above are intended to help the reader understand a rather complicated set of expressions for different ways of analyzing esophageal pressure data. However, I am not at all sure that they succeed. Further summary of this article will attempt to minimize reference to these abbreviations and use equivalent expanded terms instead.)
The patients were initially referred to the center for symptoms suggestive of OSA. Only those patients were included in the study whose initial polysomnography showed an Apnea Index greater than 20/hr, a total sleep time greater than 3 hr, and a proportion of obstructive and mixed apneas greater than 80% of all apneas. Besides standard diagnostic polysomnography, they had esophageal pressure measured with a 10-cm balloon placed in the esophagus. Esophageal pressure measurements were done on 30 randomly selective apneas during NREM sleep and on all apneas during REM sleep. Mixed and central apneas were excluded. Pulmonary function and blood gas testing was also performed.
The sample consisted of 113 men and 3 women, averaging in age 52 years (SD=+/-0.9, range 22-77). The group was subdivided by a median split into a Younger Group of 58 patients, of average age 44 (SD=+/-0.9) and an Older Group (also 58 in number) of average age 60 (SD=+/-0.7). For the group as a whole, Body Mass Index (BMI) was 33 (SD=+/-0.6). Younger and Older Groups did not differ significantly on BMI (34 vs. 31). The group as a whole had moderate to severe OSA with mean Apnea/Hypopnea Index (AHI) of 89 (SD=+/-2) and mean Apnea Index (AI) of 76 (SD=+/-2). Younger and Older groups did not differ significantly on these measures, though the means for the Older group were a bit lower (AHI for Younger=92, Older=86). Mean duration of apneas was 25 secs (SD=+/-1), without any significant difference between Younger (24) and Older (26). Hypoxemia varied widely, with a range of lowest blood oxygen saturation from 39 to 92%. The Younger and Older groups differed in that the Older subjects had slightly but significantly higher average lowest oxygen saturations (87 vs. 83) and a minimum oxygen saturations (68 vs. 62). Thus, the Older group had somewhat less hypoxia.
Waking blood gases (oxygen=73 and carbon dioxide=40) were within normal limits for the subjects as a whole, without significant differences between Younger and Older Subjects. However, 28 subjects had low waking blood oxygen (65 or less) and 15 had high waking blood carbon dioxide (45 or above), suggestive of chronic obstructive pulmonary disease. Older patients had lower lung volumes than Younger patients, reflected in lower Forced Expiratory Volume (FEV) and Vital Capacity (VC), but this was of the magnitude expected from normal aging.
As expected in OSA, sleep efficiency was reduced, with reduced percentages of REM and slow-wave sleep. Compared to the Younger group, the Older patients had more light NREM sleep (stages 1 & 2) and fewer short awakenings of less than 20 secs but more longer awakenings, so that Older patients had longer wake time after sleep onset but an equal degree of sleep fragmentation.
Although apneas in REM were longer and associated with more desaturation, PesMax was less, indicating about half the respiratory effort in REM vs NREM apneas.
During NREM sleep, Pes increased progressively throughout the apnea though with a wide range of variability, while oxygen saturation decreased an average of 12%, with less variability. All indices of respiratory effort in NREM sleep were lower in Older than in Younger patients. Besides age, PesMax correlated with BMI, apnea index, apnea duration, lowest oxygen saturation, and fall in oxygen saturation. Age was the single most important contributor.
During REM sleep, changes in Pes during apneas were less regular and more erratic. They showed similar correlations as NREM apneic respiratory efforts though fewer factors reached significance, probably due to smaller sample size. Decrease in oxygen saturation, apnea duration, and age independently contributed to the variation of PesMax.
The authors note that the "novelty in our data is the demonstration of a lower respiratory effort during apneas with increasing age" which suggests that "aging causes respiratory effort during apneas to decrease." They noted the exception that their data may not apply to patients whose apneas are extremely brief, since they studied only apneas lasting 20 secs or longer. The measures of respiratory effort they used were all highly intercorrelated, as one might expect.
They offer varied explanations for their results, of which the most convincing (to me) were that aging is associated with a reduced respiratory drive or performance involving the diaphragm and chest wall musculature, and/or that older subjects have reduced ventilatory response to hypoxia, and less response of ventilatory drive during waking, sleep, and conditions of high carbon dioxide.
These considerations may help explain the unexpected spontaneous improvement with age in severity of sleep apnea recently reported in untreated OSA patients. Less respiratory effort would result in lower suction pressure and therefore in less tendency to collapse the upper airway.
Indices of respiratory effort were correlated with the apnea index, which likewise reflects increased tendency to collapse the upper airway with increased pressure. The awake Pes being correlated with the maximal end-apneic Pes suggests that patients with increased pulmonary resistance during waking develop more respiratory effort during waking which will continue into sleep.
The authors found it interesting that all indices of respiratory effort were lower in REM than in NREM sleep. There was also associated with REM sleep a prolongation of apnea duration. There are some studies suggesting decreased ventilation in REM sleep and decreased ventilatory response to hypoxia and high blood carbon dioxide in REM as well. In contrast to normal subjects, OSA patients do not awaken faster from REM sleep than NREM sleep in response to demand for increased respiratory effort, again suggesting a lesser response to upper airway occlusion in REM sleep associated with OSA. These considerations may help us understand the special relationship of obstructive apneas to REM sleep, even though on the face of this data one might expect less obstructive apneas, if anything, during REM sleep. The determinants of level of repiratory effort in REM were similar to those in NREM but with fewer independent contributors and less systematic changes.
Thus, the main conclusions of this study are that respiratory effort to resume breathing in OSA decreaes in REM vs. NREM sleep and also descreases with increasing age.
This is one of those studies where the findings, by themselves, seem well-founded and credible enough--once you get past the complicated statistical terminology. However, it leaves me looking for points of relevance to the clinical situation of patients like ourselves.
To me, it was news that OSA could "burn out" or at least improve in frequency of respiratory-related arousals as OSA patients get older. Of course, these are different subjects in the Younger and Older groups and ideally one would like to see a long-term follow-along study of many OSA patients to determine the "natural course" of the disease. Generally, I have thought of OSA as a chronic disease which worsens with age. But the authors' finding of decreased respiratory effort in older patients does suggest a way that OSA might improve: the older patients exert less occlusive pressure on the upper airway. This does not seem to make for longer or more frequent apneas or hypopneas, or more hypoxia. It makes me wonder whether the average CPAP pressures needed by older patients is lower than that needed by younger patients; this information should be easily obtained from the records of sleep clinics.
On the other hand, there seems something wrong about the idea that one way to alleviate obstruct sleep apnea is to exert less effort to breathe. If this were so, respiratory depressant medications like benzodiazepines might be therapeutic for OSA, which seems contrary to common wisdom. The sleep of the older patients was shorter, lighter, less effficient, and more interrupted than that of younger patients, so one might posit other mechanisms, such as the upper airway resistance syndrome, to disrupt sleep continuity in the older OSA patients. It also seems probable that in old patients, perhaps substantially older than the present sample, diurnal patterns of sleep and waking start to decay, so that prolonged napping during the day is usual, and may disorganize sleep patterns. Perhaps a generally lighter sleep is the penalty paid for reduced respiratory responses to increased resistance to breathing.
The authors did not include measures of daytime napping and viligance to assess whether the overall impact of the different sleep and breathing pattern of older subjects might be more negative on their alertness and cognitive function but this might require additional control groups of normal subjects for the effects of age on neuropsychological function.
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