Physiology of Airway Protection
The pharynx, epiglottis, and vocal cords play a role in protecting
the lower airway from aspiration of foreign bodies and secretions. Although the
epiglottis covers the laryngeal inlet, it is not absolutely essential for airway
protection. Most vital in this protective function is the glottic closure reflex,
which produces protective laryngeal closure during deglutition. The physiologic
exaggeration of this reflex, laryngospasm, is counterproductive to respiration.
Laryngospasm consists of prolonged intense glottic closure in response to direct
glottic or supraglottic stimulation from inhaled agents, secretions, or foreign bodies.
Stimulation from the periosteum or celiac plexus or dilation of the rectum may also
precipitate the problem on a reflex basis.
Various degrees of laryngospasm produce sounds that range from
a high-pitched squeaky sound to total absence of sound. The latter indicates complete
closure of the cords and must be diagnosed and treated immediately. Treatment of
severe spasm may require the use of muscle relaxants such as succinylcholine. However,
forward displacement of the mandible together with oxygen administered by a mask
under pressure is often effective. Strong intermittent pressure applied manually
to a bag full of oxygen can force gas effectively through the upper airway and the
adducted cords. The traditional concerns about limiting airway pressure to avoid
pulmonary barotrauma are not important in this case. However, the stomach contour
should be watched closely in case an inordinate amount of air is forced into the
esophagus. When laryngospasm is less severe, slight amounts of positive pressure
often alleviate the difficulty. In any case, the physician should use these simple
maneuvers before resorting to tracheal intubation.
An indispensable mechanism for expelling secretions and foreign
bodies from the lower respiratory tract is the act of coughing. The major stages
of a cough are characterized by three events. First, there is a deep inspiration
to attain a high lung volume, which allows attainment of maximum expiratory flow
rates. Second, a tight closure of glottis occurs along with contraction of the expiratory
muscles. Intrapleural pressure rises to above 100 cm H2
O such that during
the third (expiratory) phase, a sudden expulsion of air occurs as the glottis opens.
Glottic opening at the onset of the phase is associated with oscillation of tissue
and gas that results in the characteristic noise of a cough
Various physiologic aspects of cough have been observed with radiologic
and endoscopic techniques. None is more important than the dramatic narrowing of
the airway lumen. The physiologic significance of this reduced airway caliber is
the fact that the decreased cross-sectional area increases linear velocity of gas
flow and improves cough effectiveness. Various estimates suggest that this dynamic
compression decreases the cross-sectional area of the trachea and main bronchi to
about 40% of their caliber during normal breathing and increases linear velocity
2.5 times.
Neuromuscular weakness may decrease cough flow rates by limiting
the inspired volume before cough if inspiratory muscles are weakened. Expiratory
weakness does not appreciably diminish flow rates.[3]
The major effect appears to be a reduction in cough-induced dynamic airway compression,
which results in decreased linear velocity of flow.
Glottic closure is the one phase of cough that differentiates
it from other forced expiratory maneuvers and that allows for greater development
of pressures. Closure of the glottis is not crucial, however, to the development
of high pressures and flow rates of a normal cough. This is
well illustrated in tracheotomized and intubated patients. The presence of the endotracheal
tube, for example, does not lessen the buildup of peak pressure during coughing.
However, by preventing normal glottic closure, the tube allows flow to begin as
soon as pressure begins to increase, and in most cases, the tube allows flow to continue
between cough bursts.[4]
The normal timing of pressure
and flow is altered such that cough resembles a normal forced expiration. Because
the tube is noncollapsible, it does not permit the high velocities through the tracheal
segment that it occupies. Secretions therefore are likely to accumulate in the area
at the end of the tube unless subsequent coughs are begun from high lung volumes
to allow high flow rates to be achieved.
