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.
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