Sleep physiology / 03

The airway closes, and three signals find out about it at different times.

Between the back of the nose and the top of the larynx there is no bone and no cartilage — only a muscular tube that has to stay open on muscle tone alone. Sleep turns that tone down. Watch what happens to the air moving, to the effort spent trying to move it, and to the oxygen in the blood, when the tube gives way.

Why the tube closes at all

Everywhere else the airway is held open by something rigid. The nose has bone; the larynx and the trachea have cartilage rings, drawn at the bottom of the figure. The stretch in between — the pharynx — has neither, and it cannot, because it has to be able to collapse: that is how swallowing and speech work. It is held open instead by around twenty small muscles, the genioglossus chief among them, pulling the tongue and the pharyngeal walls forward against the suction of each breath in.

Awake, this is effortless and invisible. A reflex senses the negative pressure of each inspiration and stiffens the airway a fraction of a second before that pressure peaks. Sleep switches the reflex off. Tone drops at sleep onset and drops again in REM, and from then on the pharynx is defended only by whatever background activity is left. Whether that is enough depends on how much closing pressure the anatomy generates: a set-back jaw, a large tongue, tonsils, fat in the neck, fluid that has shifted out of the legs since the person last stood up. Pushing the collapsibility slider is pushing that closing pressure past what sleeping tone can resist.

Reading the three traces

Airflow fails first, and it fails in a particular shape. Before anything is scored at all, the top of each inspiration flattens into a plateau. The airway has become a Starling resistor — a floppy tube whose maximum flow is fixed by its own closing pressure — and past that ceiling, pulling harder achieves nothing whatsoever. That flattened contour is flow limitation, and it is the earliest sign on the page. Set collapsibility to about halfway and it is all you get: narrowing, snoring, no scored events.

Effort is the trace that decides what the event is called. Through a complete obstructive apnea the chest goes on moving, and moves more: carbon dioxide is accumulating, drive is climbing, and each attempt is bigger than the last. That crescendo against a closed airway is the signature of obstruction. A central apnea looks identical on the flow channel and flat on this one — nothing is blocked, the brain has simply stopped asking. The effort belt is how the two are told apart, and it is the main reason an oximeter alone cannot do it.

Oxygen arrives late and leaves late. There is a lung full of air to get through first, then eight or nine seconds for blood to travel from lung to fingertip, then the oximeter's own averaging window on top. So the desaturation belonging to an event usually reaches its lowest point after that event has ended: the airway is open again, the sleeper is breathing hard, and the number on the screen is still falling. Drag the playhead to the end of an apnea and watch how far the oximeter still has to go.

The saturation curve does not fall in a straight line either, and that is the oxyhemoglobin dissociation curve doing its work. From 97% down to about 92% the fall is gentle; past 90% it steepens sharply. Two apneas of identical length can cost four points or fourteen depending on where on that curve they begin — part of why the same airway is a more serious problem at altitude, or with lung disease, or in REM.

What ends the event

Nothing on the traces reopens the airway. What reopens it is an arousal: a few seconds of cortical activation that restores dilator tone the way waking would, without the sleeper ever knowing. The airway snaps open, there is a snort, breathing overshoots, carbon dioxide is blown off below where it started — and with the stimulus gone, tone falls and the tube closes again. Left alone this cycles every thirty to fifty seconds, for hours.

That is why the arousal threshold slider changes the illness rather than just the numbers. Set it low and the sleeper is rescued early: events are short, oxygen barely moves, the oximetry looks almost reassuring — and there are a great many arousals, so the night is shredded. That is the person with no dramatic desaturations who is nonetheless exhausted. Set it high and you get the opposite: long events, deep desaturation, an alarming-looking oximetry trace, and comparatively intact sleep. The same airway, two different illnesses, and they do not respond to the same things.

The last two controls behave the way the clinic does. Move from NREM to REM and events lengthen without the anatomy changing at all, because REM withdraws most of the tone the airway was relying on. Roll from the back onto the side and the gravitational load comes off the tongue and the soft palate; at moderate collapsibility that alone takes a montage full of apneas down to a little snoring, which is the entire premise of positional therapy. Set the state to Awake and everything stops — which is the part people find hardest to believe about their own airway. It is perfectly competent all day.

A model, not a recording. The oscillation is not scripted: it emerges from a negative-feedback loop with a transport delay in it, in which collapse reduces ventilation, carbon dioxide rises, chemical drive raises both dilator tone and respiratory effort, an arousal fires once effort crosses the threshold, the airway opens, ventilation overshoots, and drive falls back below what the airway needed. Patency follows the Starling-resistor account of Gold and Schwartz, with a critical closing pressure set by the collapsibility control, dilator tone set by state, and hysteresis added so that reopening a closed pharynx takes more than keeping an open one open. The four controls correspond loosely to the trait framework of Eckert and colleagues (2013), in which anatomy, muscle responsiveness, arousal threshold and loop gain vary independently between people carrying the same apnea–hypopnea index. Oxygen is carried through a single alveolar compartment and a Hill dissociation curve with P₅₀ 26.6 mmHg and n 2.8, then delayed eight seconds for circulation and smoothed to mimic an oximeter's averaging. Events are scored against a moving flow envelope on the AASM duration and amplitude criteria, although a real scorer also requires a desaturation or an arousal before calling a hypopnea, and no one would read an index off two and a half minutes of recording — the rate shown is what this stretch would imply if a whole night ran the same way, which no night does. The numbers are illustrative and internally consistent rather than calibrated against any patient population, and the anatomy is schematic and not to scale. Nothing here diagnoses anything.