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The first author herself kindly provided extensive feedback on the article summary and comments, and some of this has been incorporated into changes in the original test. However, I felt that her own explanation of the process under study showed a remarkable lucidity and deserves quoting here more or less in full:
The patency of the upper airway results from a complex balance of forces which act in opposite directions: the suction pressure, generated by the activity of the diaphragm, causes the upper airway (the collapsible part of the upper airway, i.e., the pharynx) to collapse. To oppose this collapsing force is the tone of the pharyngeal wall, which mainly depends on the activity of the pharyngeal dilating muscles. The ability to oppose the collapsing forces is best measured by the compliance (ratio of change in volume to change in pressure) of the pharyngeal walls. A highly compliant pharynx will collapse even with very small suction pressures. The problem is that the activity of the diaphragm and that of the upper airway (UAW) dilating muscles are in part independent. The phasic (during inspiration) activity of both the diaphragm and the UAW muscles are dependent on the activity of the respiratory center (the respiratory drive), but the tonic activity of the UAW muscles is mainly dependent on the regulation of posture, whereas the diaphragm is largely independent of postural control.
Dr. Krieger's explanation is so clear, and my own summary of her article so abstruse, that I have trouble relating and reconciling the two--but I trust Dr. Krieger's picture is the more accurate. For example, it came as a surprise to me to learn that the musculature of the upper airway and that of the diaphragm differed in that the former changes tone considerably with posture whereas the latter does not. Of course, one thinks of the mechanical forces of tissues pressing on the upper airway in a reclining position, but one could also imagine a postural effect of an obese abdomen pressing down on the diaphragm when the patient lies down.
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AUDIENCE (AND AUTHOR) COMMENTS
Therefore, during REM sleep, when postural muscle tone is abolished, the UAW is highly collapsible (floppy) and will collapse, even with very low suction pressure (respiratory effort or esophageal pressure).
Increasing respiratory effort will not reestablish ventilation, if the UAW muscle tone is not increased more than the suction pressure increases (that is, becomes more negative). Therefore, the response of the respiratory system to a UAW occlusion during sleep is inadequate: increasing respiratory effort will increase suction pressure, and worsen UAW collapse. Only an arousal, restoring UAW muscle tone, will allow breathing resumption (but will also cause sleep fragmentation).
The point of CPAP needed by older/younger patients is well taken. Indeed, in the sample reported the average CPAP was 10.4 cm H2O in the older group, and 11.4 cm H2O in the younger group. We had shown in an earlier paper that the amount of respiratory effort during the apneas is a predictor of the level of CPAP needed to normalize breathing during sleep.
Finally, benzodiazepines would be therapeutic if they decreased suction pressure more than they decrease UAW muscle activity, which is not the case.
MY RESPONSE
I commend Dr. Krieger's account above to anyone interested in getting a clearer picture of the realtionship between pressure and muscular changes in sleep apnea.
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