haut de page









mise à jour du
11 novembre 2003
Sleep Med Reviews
2003; 7; 1; 9-33
The upper airway in sleep:
physiology of the pharynx
Indu Ayappa, David Rapaport
Division of Pulmonary and Critical Care Medicine, New York University School of Medicine
Télécharger ce texte au format PDF


Summary :
The upper airway is the primary conduit for passage of air into the lungs. Its physiology has been the subject of intensive study: both passive mechanical and active neural influences contribute to its patency and collapsibility. Different models can be used to explain behavior of the upper airway, including the "balance of forces" (airway suction pressure during inspiration versus upper airway dilator tone) and the Starling resistor mechanical model.
As sleep is the primary state change responsible for sleep disordered breathing (SDB) and the obstructive apnea/hypopnea syndrome (OSAHS), understanding its effects on the upper airway is critical. These include changes in upper airway muscle dilator activity and associated changes in mechanics and reflex activity of the muscles. Currently SDB is thought to result from a combination of anatomical upper airway predisposition and changes in neural activation mechanisms intrinsic to sleep.
Detection of SDB is based on identifying abnormal (high resistance) breaths and events, but the clinical tools used to detect these events and an understanding of their impact on symptoms is still evolving. Outcomes research to define which events are most important, and a better understanding of how events lead to physiologic consequences of the syndrome, including excessive daytime somnolence (EDS), will allow physiologic testing to objectively differentiate between "normal" subjects and those with disease.
Effect of sleep on upper airway resistance/collapsibility

Radiographic measurements have shown that during wakefulness patency of the upper airway is well maintained in different postures, although the reflexes which control this seem to be critical. However, with the onset of sleep there are several modifications that may occur in the factors affecting patency of the upper airway including changes in neuromuscular activation, ventilation, chemical and mechanical load responses.

Significant increases in upper airway resistance associated with sleep have been shown in animals and humans. Supraglottic resistance has been shown to increase from low values (1±2 cm H2O/L/s) to values as high as 5±10 cm H2O/L/s and to 50 cm H2O/L/s in heavy snorers. Less is known about changes in airway caliber, but most studies suggest that it decreases during sleep, with the lateral pharyngeal walls playing an important role in thisnarrowing These changes in mechanics induced by sleep could result in either hypoventilation (loss of the reflex response to increased airway load), or a reflex induced increase in ventilatory output with maintained ventilation and blood gases. Some degree of hypoventilation occurs at sleep onset in normals. That this is a consequence of the mechanics rather than a change in set-point for CO2 has been shown in a study where unloading by CPAP or breathing He/O2 mixtures (characterized by reduced density) returned mildly elevated sleeping PCO2 to awake levels.

Although it is likely that sleep in normals induces increased collapsibility in the airway (decreased tone to the upper airway dilators), the effect on calculations of resistance is confounded by reflex responses (or their absence). Thus it has been shown that sleep has an effect on multiple aspects of upper airway behavior.
Effect of sleep on muscle tone in the upper airway

The change in muscle activity of the upper airway with onset of sleep has been investigated directly by measuring the EMG, by using measured changes in pharyngeal wall compliance or by using derived values of ventilation and airway resistance. Many studies have shown that the phasic inspiratory activity of the genioglossus and geniohyoid are maintained during sleep in normals. Conversely, decreases in both tonic and phasic tone have been shown in the genioglossus, geniohyoid, tensor palatini, levator palatini, palatoglossus and other respiratory muscles at the onset of sleep. These have been shown to be associated with transient decreases in ventilation and increased upper airway resistance. However, in normal subjects these decreases are short lived and parallel those seen in the diaphragm and intercostal muscles, which rise as a response to induced obstructive hypoventilation and mild hypercapnea (1±2 mmHg) seen during sleep.

The role that both tonic and phasic tone play in maintaining airway patency is shown by denervation studies, which in an animal model resulted in collapse of the airway during sleep. In healthy human subjects, dense upper airway anesthesia increases upper airway resistance during sleep and can cause prolongation of apnea. Despite this, the marked decrease in EMG seen in all airway muscles during REM sleep does not result in uniform obstruction.

Some of this last paradox may be due to the protective effect of the reduced inspiratory airway pressures generated during REM sleep, again illustrating the difficulty in using Øow and resistance of the collapsible airway as indices of function during conditions of changing effort.

Effect of sleep on load response

Whereas during wakefulness application of a resistive load to the airway results in increased respiratory drive, this response may be lost or greatly attenuated during sleep. There is debate over whether a similar response to airway loading exists by which the upper airway muscle tone directly increases in response to resistive loading of the system. However, it is difficult to separate this possible direct effect from a non-specific increase in ventilatory drive. Despite numerous studies that have measured upper airway resistance and genioglossal EMG during wakefulness, sleep and with resistive loading, the direct relationship between GGEMG activity and upper airway resistance during sleep is unclear, with conflicting results in multiple studies.

Possible reasons for conflicting observations include the assumption that muscle activity (EMG) is a surrogate of muscle fiber shortening, and the fact that in most experiments muscle activity can only be measured in a few locations/muscles, which do not fully reflect the total airway muscle response.

Effect of CO2 on muscle activity during sleep

In the awake state, elevation of CO2 is a powerful respiratory stimulant. There is a large literature on the effect of sleep on this response, and the consensus is that this may be only minimally affected by sleep, at least in non-REM stages. Less is known about the effect of sleep on CO2 responses of the upper airway muscles, independent of general respiratory stimulation. The results from studies examining changes in GG activation with hypercapnia are variable, and hypercapnia has been shown to decrease collapsibility of the airway similar to tracheal displacement.