Con: Can Physiological Risk Factors for Obstructive Sleep Apnea be Determined by Analysis of Data Obtained from Routine Polysomnography?

The following argument was prepared in response to the question without the knowledge of the contents of the opposing argument. The answer is CLEARLY NO. The mechanisms of ventilatory instability in obstructive sleep apnea (OSA) are complex [1, 2], and defining them with confidence requires interventions that are not practical in routine polysomnography [3–5]. If it is not possible to measure instability traits from routine polysomnograms (PSGs), how is it that since 2015 papers and reviews are being published at an impressive rate in top-rated journals using an approach that claims to estimate all the stability factors from standard clinical PSGs? All these papers are based on a method proposed by Terrill et al. in 2015 to measure loop gain (LG) [6], and subsequently “improved” to provide more and more traits [7]. The basic approach is to measure ventilation in the hyperpneic phase between obstructive events (Vdrive). Without arousal, Vdrive is assumed to reflect chemical drive at the end of apnea. Arousal, if present, is assumed to contribute a fraction of Vdrive. A model with four variables (LG, time constant of chemical responses, circulatory delay, and the arousal contribution) is used to partition Vdrive into the components related to arousal (a constant predicted from the model; Varousal) and that related to the chemical drive (Vchem). The model is then used to estimate the time course of the chemical drive during the obstructed phase. From this LG, the chemical drive preceding arousal (arousal threshold), airway collapsibility, and pharyngeal muscle compensation are derived [8]. In our view, this model is based on untenable assumptions and does not identify the traits that are truly relevant to ventilatory instability in OSA: