Upper Digestive Tract

Anatomy and Physiology

The upper aerodigestive tract is a single conduit that must integrate and
separate two very different vital functional systems: breathing and swallowing. In the
healthy state, the anatomic structures and their neural substrates exquisitely
coordinate each function through sensory-motor integration. The ability to swallow
safely is critical for nutrition, hydration, and quality of life; however, its significance
is often taken for granted when the physiology and pathophysiology are not fully
appreciated. Understanding the anatomy and physiology of deglutition is not only
required to properly evaluate and treat patients with dysphagia but also necessary to
maximize functional outcomes after surgical interventions for head and neck cancer.
Dysphagia is not a disease, but rather a symptom or a collection of symptoms
that broadly describe difficulty swallowing. Under the umbrella term dysphagia, finer
distinctions are made that refer to the phase of swallowing where impairments exist.
For

example,

patients

may

have

oral,

pharyngeal,

oropharyngeal,

pharyngoesophageal, or esophageal dysphagia. Dysphagia can also vary in terms of

severity from mild to severe. However, it is unknown how much aspiration in a
particular patient will result in pneumonia. Some patients can only tolerate a minimal
amount of aspiration, while others tolerate larger amounts. The end point of
dysphagia is pneumonia or airway obstruction. Unfortunately, to date, there is no
universally accepted, standardized system that can be used to objectively define
severity levels. In addition, the evaluation and treatment of dysphagia are often
complicated by the fact that some patients are acutely aware of difficulty swallowing,
while others may not perceive its presence or recognize the symptoms.
The swallowing difficulty can develop gradually from neurologic or
respiratory disease, or be acquired suddenly as a result of injury or surgery. The
multitude of different etiologies for dysphagia can often be delineated with a
thorough history and physical examination. Instrumental assessments of swallowing

function provide additional information that will further characterize swallowing

function so that treatment can be planned. Effective therapeutic interventions are
based upon each patient's specific physiology. Swallowing exercises can increase
muscle strength and range of motion of swallowing structures. Skill training can
instruct patients to use swallowing maneuvers such as breath-holding before drinking.
Compensatory strategies such as changing head position can also be used to alter
swallowing biomechanics. Diet alterations can be instituted so that unsafe food
consistencies are eliminated. Surgical interventions, such as vocal fold augmentation
or esophageal dilatation, may be required as the primary treatment, or in addition to
swallowing therapy.
The ability to eat and drink safely and efficiently is fundamental to our quality
of life. The wide variety of food and liquid that we enjoy throughout each day
requires precise management because of the shared function of the upper
aerodigestive tract. Indeed, modern research has shown that the pharyngeal swallow
is not a stereotypic reflex as it was first described; rather, it is a patterned motor
response to sensory input. As such, pharyngeal muscle force and contraction duration
must rapidly and consistently adjust depending upon what is to be swallowed (1,2).
To accomplish this feat, separate and overlapping phases of swallowing use sensorymotor integration Swallowing dysfunction can occur in each phase individually or
collectively across them.
Anticipatory Phase
The anticipatory phase is often considered the first true step in swallowing
because visual information, olfactory stimulation, and experience interact to form the
initial motor plan (3). A common statement in the culinary profession is, "we eat with
our eyes first." The adult has a well-developed motor plan for swallowing different
types of food and drink that is based upon appearance (visual processing),
consistency (tactile processing), taste (chemical processing), and bolus size
(proprioceptive processing). Most have experienced a sudden awareness that an item
placed in the mouth did not match what was expected. This observation can be
viewed as practical evidence that a plan had been violated. Another example that

illustrates this concept can be seen when we perceive a liquid to be very hot or a food
is suspected of being very spicy. When experience indicates these possibilities, a
slower presentation to the mouth will follow and care will be taken to ensure a
smaller bolus size because of the anticipated negative effects.
It is also at the anticipator) level where distinctions between food and nonfood
items are made and where palatability is determined. Oral intake may be avoided as a
result of the information perceived and processed during this phase. If an individual is
forced to eat or drink an item that he or she has predetermined (anticipated) is unsafe
or undesirable, then gagging, coughing, and dysphagic symptoms may be observed. It
is important to note that these are not behaviors that can be controlled; rather, they are
in response to sensory stimulation. The anticipatory phase provides the initial sensory
input to cortical swallowing structures. In patients with dementia or other cognitive
impairments, the sensory processing of visual, olfactory, and experiential information
can be altered. As such, the motor plan implemented to swallow may not match that
of the bolus itself, putting the patient at risk for dysphagia.
Oral Preparatory Phase
Once solid and semisolid food is placed in the mouth, it must first be prepared
for the pharyngeal phase. The combination of mastication and saliva production is
considered to be the first step in digestion. Saliva from the submental, sublingual, and
parotid glands flows into the oral cavity to mix with the bolus and begin the chemical
process of food breakdown. The mandible closes to crush solid food and the rotatory
motion of mastication enables the molars to shear and shred the food. The muscles of
mastication are the masseter, temporalis, medial pterygoid, and lateral pterygoid
muscles (Table 56.1). The masseter, temporalis, and medial pterygoid muscles elevate
the mandible,

Summary Chart Of Peripheral Sensory And Motor Components Of Deglutition

Swallowing Phase Action
Oral preparatory

Pharyngeal

Esophageal

Labial closure
Mastication

Muscle

Orbicularis oris
Masseter
Temporalis
Medial pterygoid
Lateral pterygoid
Buccinator
Bolus formation
Genioglossus
Hypoglossus
Styloglossus
Palatoglossus
Tongue sensation
Anterior two-third
Posterior one-third
Tongue taste
Anterior two-third
Posterior one-third
Soft palate depression
Palatoglossus
Velopharyngeal closure
Levator veli palatini
Tensor veli palatini
Palatoglossus
Superior constrictors
Vocal fold closure
Lateral cricoarytenoid
Interarytenoid
Thyroarytenoid
Laryngeal elevation
Mylohyoid
Anterior belly, digastric
Stylohyoid
Posterior belly, digastric
Geniohyoid
Thyrohyoid
Upper esophageal segment Cricopharyngeus
relaxation

Nerve
Facial nerve (CN VII)
Mandibular nerve (CN V3)
Mandibular nerve (CN V3)
Mandibular nerve (CN V3)
Mandibular nerve (CN V3)
Facial nerve (CN VII)
Hypoglossal nerve (CN XII)
Hypoglossal nerve (CN XII)
Hypoglossal nerve (CN XII)
Pharyngeal branch (CN X)
Lingual nerve (CN V3)
Glossopharyngeal nerve (CN IX)
Chorda tympani nerve (CN VII)
Glossopharyngeal nerve (CN IX)
Pharyngeal branch (CN X)
Pharyngeal plexus (CN X)
Trigeminal nerve (CN V3)
Pharyngeal branch (CN X)
Pharyngeal plexus (CN X)
Recurrent laryngeal nerve (CN X)
Recurrent laryngeai nerve (CN X)
Recurrent laryngeai nerve (CN X)
Trigeminal nerve (CN V3)
Trigeminal nerve (CN V3)
Facial nerve (CN VII)
Facial nerve (CN VII)
Cervical 1 (CI)
Cervical 1 (CI) via hypoglossal nerve (CNXII)
Pharyngeal plexus, recurrent laryngeal nerve (CN X)

while the lateral pterygoid depresses the mandible, thereby opening the mouth.
Contraction of the masseter and medial pterygoid muscles also results in lateral
mandible movements required for the rotary motions. Sensory and motor innervation
to the muscles of mastication and salivary glands is provided by several branches of
the trigeminal nerve. The cyclic motion of the mandible and motions of the tongue
are mediated, in part, by a cortical central pattern generator (CPG). A CPG is
essentially neural circuitry that generates rhythmic movement. It is important to
remember that during this phase, the airway is open and active breathing continues.
During mastication, respirator) rate becomes more rapid and irregular when compared
to tidal breathing (4). If the bolus is not well controlled, solid food may fall into the
open airway resulting in aspiration or asphyxiation. Also during mastication, the
circular fibers of the orbicularis oris muscle work to actively close the lips and

maintain the food or liquid within the oral cavity. An incompetent oral sphincter will
result in drooling of saliva or loss of food and liquid out of the mouth. This
circumstance is very embarrassing for patients and severely impacts the social aspects
of meals. Neurologic diseases and surgical resections that prevent labial closure or
impair sensation can cause anterior oral loss of food or liquid.
During mastication, the complex motions of the tongue move and guide
prandial material by placing it between the molars, shifting food from side to side,
and ultimately collecting it to form a single, cohesive, prepared bolus. Tongue motion
is highly complex because it is composed of several intrinsic and extrinsic muscles
that are oriented in multiple directions. The intrinsic lingual muscles are the superior
and inferior longitudinal muscles, the transverse muscle (transverse lingualis), and the
vertical muscle (vertical lingualis). Extrinsic lingual muscles are the genioglossus
muscle that protrudes the tongue, the hypoglossus muscle to depress the tongue, and
the styloglossus muscle that elevates and retracts the tongue. All of these muscles are
innervated by the hypoglossal nerve (cranial nerve [CN] XII). The palatoglossus
muscle is innervated by the pharyngeal branch of the vagus nerve (CN X) and
elevates the back of the tongue to prevent premature spillage into the pharynx. In
addition to muscle strength and coordination, adequate sensory input is necessary for
safe swallowing.
Sensor processing by the tongue and oral cavity is required to adequately
prepare the bolus and maintain its cohesion. Tactile sensation to the anterior twothirds tongue is mediated by the lingual nerve (CN V3) and taste sensation is
provided to this region by the chorda tympani nerve (CN VII). The glossopharyngeal
nerve (CN IX) provides both sensory and taste to the posterior one-third of the
tongue. Oral sensation is also basic to proprioception because the oral structures and
changing bolus characteristics must continually interact until the bolus is perceived to
be fully prepared to swallow.
Oral preparation through mastication essentially places everyone on a
"pureed" diet, since humans do not swallow solid food whole. Difficulty swallowing
pills can be attributed to both the anticipatory phase where fear and anxiety affect
swallowing function in addition to volitional inhibition of mastication. Maintaining

bolus cohesion and control is aiso needed for liquids and puree consistencies so that
the next phase of swallowing can be accomplished.
Oral Transfer Phase
Once the bolus is prepared, it must be collected into a cohesive unit and moved to the
posterior oral cavity. Oral transfer is accomplished by containing the bolus within the
center of the tongue while the tongue tip contacts the alveolar ridge and pushes the
bolus back across the hard palate using a wave-like propulsive force. During both the
preparatory and transfer phases, sensor)' information is gathered in relation to bolus
size and texture. Although it is not understood how humans have an intrinsic
knowledge in relation to swallowing safety, the bolus will be subdivided if it is
determined to be too large. Once the bolus reaches the posterior oral cavity, the lateral
portions of the tongue press on the anterior facial pillars (innervated by CN IX) to
terminate the oral phase and subsequently trigger the pharyngeal phase. Throughout
the oral preparatory and transfer phases, the soft palate is pulled down and forward by
the palatoglossus muscle (innervated by the pharyngeal branch, CN X) to maintain
contact with the posterior tongue, thus sealing the oral cavity from the
nasopharyngeal airway (Table 56.1). This mechanism allows maintenance of the
bolus within the oral cavity while continuing to breathe through the nose (Fig. 56.1).
Oral dysphagia is present when the bolus is inadequately prepared or
controlled. Poor dentition can lead to an inadequately prepared solid bolus that may
have the potential to block the airway if aspirated. Failure to clear the oral cavity after
a primary or secondary swallow can also result in aspiration after o; between
swallows. Reduced posterior oral control and/or weak velar depression may produce
premature loss or "premature spillage" of a bolus into the pharynx or larynx before
the pharyngeal phase of swallowing is "triggered." If the bolus cannot be controlled
or transferred, gavage feedings may be necessary in order to bypass the oral cavity. A
significant delay or failure to elicit the pharyngeal phase is classified as oral
dysphagia, regardless of bolus location, since it is the oral tongue that must trigger the
pharyngeal response. Impaired cognitive function or poor sensation can cause patients
to "forget" to elicit the pharyngeal swallow. Significantly reduced lingual range of

motion, as a result of surgery or neurologic disease, can impair tongue strength or

prevent the posterior tongue from reaching the facial arches to trigger the swallow.
Oral dysphagia can occur in isolation or concomitant with pharyngeal dysphagia. It is
important to always keep in mind that the airway remains open during the oral
preparatory and transfer phases because the patient is breathing; therefore, prandial
aspiration can occur both before and after the swallow.

Figure 56.1 Posterior oral containment of the bolus. Note velar depression and
airway continuity from the nasal passages to the trachea (dotted line). B, bolus; V,
velum; M, mandible; H, hyoid; A, arytenoid; P, posterior pharyngeal wall, *, UES; T,
trachea.

Pharyngeal Phase
The pharyngeal phase begins with elevation of the soft palate to seal the nasopharynx
from the oropharynx (Table 56.1). Mediated by the sensory and motor fibers that are
primarily contained in the pharyngeal plexus, velopharyngeal closure is the result of
elevation and tensing of soft palate and contraction of the palatopharyngeal muscles,
combined with anterior motion of the posterior pharyngeal wall (Passavant ridge,
superior pharyngeal constrictor muscle). 'I he adenoid pad and uvula may also aid in
velopharyngeal closure. If the patient has velopharyngeal incompetence, they can
experience nasal regurgitation during the swallow. Within milliseconds of velar
elevation,

Figure 56.2 Elevation of the velum with subsequent closure of the nasopharynx. The
hyoid and larynx are elevating. The arytenoids are about to approximate the petiole of
the epiglottis to close the laryngeal aditus. B, bolus; V, velum; M, mandible; H,
hyoid; A, arytenoid; P, posterior pharyngeal wall; *, UES; T, trachea.

the posterior tongue lowers to enable the bolus to enter the oropharynx (Fig. 56.2).
The base of tongue retracts and exerts the primary propulsive force on the bolus. The
upright epiglottis protects the airway by dividing the bolus and directing it into the
lateral channels of the pharynx toward the hypopharynx. The larynx begins to elevate,
moving in a superior and anterior trajectory. Activation of the thyrohyoid muscle
(innervated by the first cervical nerve via the hypoglossus nerve) and the suprahyoid
musculature (mylohyoid, anterior and posterior digastrics, stylohyoid, and geniohyoid
muscles) results in the superior and anterior thrust of the hyoid bone to the mandible.
During laryngeal elevation, the true and false vocal folds adduct (lateral
cricoarytenoid, interarytenoid, and thyroarytenoid muscles, all innervated by the
recurrent laryngeal nerve, CN X) as the arytenoid cartilages are drawn forward (5).
Vocal

Figure 56.3 The hyolaryngeal complex elevated, with complete closure of the airway.
The bolus is about to enter the UES. B, bolus; V, velum; M, mandible; H, hyoid; P,
posterior pharyngeal wall; *, UES; T, trachea.

fold paralysis or severe vocal fold atrophy often results in glottic incompetence,
which can result in aspiration during the swallow. The complex combination of base
of tongue retraction, laryngeal elevation, and contraction of the aryepiglottic muscles
creates contact between the arytenoids and the epiglottic petiole (Pig. 5G.3). This
mechanism closes the laryngeal vestibule during pharyngeal bolus transit. Strong
closure of the laryngeal entrance (aditus) can prevent aspiration and compensate for
reduced glottal closure.
A common misconception is that the epiglottis inverts to protect the airway
(6,7). In fact, the epiglottis has no motor innervation and cannot actively move An
upright epiglottis protects the airway by capturing and containing material within the
valleculae. Epiglottic inversion is then biomechanically created by the combination of
the tongue

Figure 56.4 The inverted epiglottis within the bolus stream. The opaque circle is a
coin, which is used to correct for magnification. B, bolus; M, mandible; H, hyoid; E,
epiglottis; T, trachea; C, coin.

base retraction, hyolaryngeal elevation, and the weight of the bolus (Fig. 56.4). The
inverted epiglottis can enter the upper esophageal sphincter (UES) and may help to
direct the bolus into the esophagus. When epiglottic inversion does not occur, it
suggests the presence of base of tongue weakness and/or is often associated with
reduced hyolaryngeal elevation. Sometimes, all that is needed to promote epiglottic
inversion is to increase bolus size or to alter the biomechanics by having the patient
tuck the chin toward their chest during the swallow.
For the bolus to enter the esophagus, the tonic muscle fibers of the UES must
relax to allow the bolus to enter the esophagus. The superior and anterior motion of
the hyoid and larynx during the pharyngeal phase creates a traction force that opens
the lumen. Hyolaryngeal elevation must be of sufficient height and duration to allow
the entire bolus to pass through to the upper esophagus (Fig. 56.5). If the LIES
opening is limited in width and/or duration, truncation of the bolus and resultant
residue in the post-cricoid region and/or pyriform sinuses (hypopharynx) can result.
Aspiration of this residue can then occur alter the swallow when the airway reopens
for breathing.
Following the tail of the bolus by several milliseconds is a sequential
contraction of the pharyngeal muscles starting with the superior constrictor, followed
by the middle constrictor and then the inferior constrictor. The wavelike motion of the
pharyngeal constrictors is often mistaken for peristalsis; however, peristalsis can only
be present in a circumferential "tube." The function of the sequential motion of the
pharyngeal constrictors is to maintain a closed system within the pharynx during
bolus transit (by contacting the tongue base) and to provide a "clearing wave" to
assure that the entire bolus leaves the pharynx in anticipation of

Figure 56.5 A relaxed UES, with the opening into the esophagus maintained by
hyolaryngeal elevation. B, bolus; V, velum; M, mandible; H, hyoid; P, posterior
pharyngeal wall; T, trachea.
airway opening. Patients who have had chemoradiation lor the treatment of cancer in
this region often have inadequate clearing of material due to weakness and reduced
range of motion of these muscles, putting them at risk for dysphagia. The pharyngeal
phase of swallowing transpires in approximately 1 second or less. This rapid
sequence of events is controlled by bilateral CPGs located within the brainstem.
Esophageal Phase
Active closure of the UES prevents air from entering the esophagus during breathing
and also protects the airway from invasion by refluxate from the esophagus and/or
stomach. The primary muscle of the UES is the cricopha-ryngeal (CP) muscle within
the inferior constrictor muscles, with dual innervations from the glossopharyngeal
nerve (CN IX) via the pharyngeal plexus and the recurrent laryngeal nerve (CN X)

(Table 56.1). Once the bolus enters the esophagus, the circular and longitudinal
muscles enable peristalsis to transport the bolus until it reaches the lower esophageal
sphincter (LES) at the distal esophagus. The LES is a single muscle that, like the
LIES, is tonic at rest. The EES relaxes with swallowing, enabling prandial material to
enter the stomach. Esophageal dysphagia is present when either of the sphincter
muscles (UES or LES) fails to open during deglutition (achalasia). Achalasia can be
caused by a neurologic failure within the enteric nervous system scarring from
radiation, or possibly repeated acid reflux.
A CP "bar" is a common finding on fluoroscopic swallowing studies but is not
always a source of dysphagia unless it impedes bolus flow (Eig. 56.6). This finding
can be due to hypertonicity and/or fibrosis of the muscle. This finding can also be the
result of compensation to provide laryngeal protection in the face of esophageal
dysmotility (esophageal-phalangeal rellux). High-resolution esophageal manometry
may be helpful in characterizing different types of esophageal dysphagia.

Figure 56.6 A CP bar. Although the fibers have not relaxed fully, the bar diverts but
does not obstruct bolus flow. B, bolus; T, trachea; CP, cricopharyngeal muscle.

Breathing And Swallowing

The dual nature of the upper aerodigeslive tract necessitates central inhibition of
respiratory muscles during each swallow. Cessation of breathing, combined with
airway closure is called deglutitive apnea. Another common misconception is that
babies can simultaneously breathe and swallow; nonetheless, vocal fold adduction
and deglutitive apnea are also present in infants (8,9).
Several investigators have identified a preferred coordination between
breathing and swallowing, finding that most swallows are timed to occur during mid
to early exhalation (10,11). Exhalation has been reported to occur almost exclusively
following every swallow, even those that occur during the inhalation phase. A target
lung volume was recorded in healthy subjects who were found to consistently
swallow between 51% and 56% of their vital capacity, irrespective of respiratory'
pattern (12). hung volumes above functional residual capacity are associated with
positive subglottic air pressures that are generated during each swallow (13,14).
Lung-thoracic unit recoil creates the positive pressure by compressing the closed
respiratory system during deglutitive apnea. Spontaneous changes in pharyngeal
swallowing function have been measured in healthy adults when swallows are timed
to occur at extremes in lung volume. Changes in lung volume are associated with
changes in the amount of subglottic pressure that is generated, indicating that respi
ratory signaling is also integrated into the sensory portion of each swallow. Emerging
research points to the sensor)' receptors in the subglottis as the most likely structure
that communicates the status of the respiratory system to the swallowing CPG (1518). Due to the link between the respirator)' system and swallowing, pulmonary
disease such as chronic obstructive pulmonary disease is considered to be a primary
risk factor for dysphagia because of the additional demands that deglutition places on
the respirator)'system (16,17)
Summary
Oropharyngeal swallowing is a multifactorial process that requires precise
coordination of multiple muscles and nerves. The wide variety of consistencies that
are consumed necessitates a high degree of sensor)' input to assure that the motor

output will provide the safest and most efficient swallow. Sensory processing begins
before food is placed in the mouth and continues in the oral and pharyngeal cavity. A
portion of sensory input is also received from the respiratory system. Dysphagia can
develop when there is a disruption at any level of sensory-motor integration.
Therefore, knowledge of the anatomy and physiology of the upper aerodigestive tract
in relation to swallowing is critical for the optimal care of patients.
Highlight

Swallowing is not a stereotypic reflex, but rather a patterned motor response

based upon the type of liquid or food to be swallowed.

Diseases and treatments of the head and neck, such as cancer, can alter die ability

to swallow, and therefore a high index of suspicion is necessary for these patients.
Termination of the oral phase and triggering of the pharyngeal phase is created by
the tongue contacting the facial pillars. Therefore, reduced tongue motion/strength

could impair this transition to the next swallowing phase.

The epiglottis does not move independently but radier is moved by other
structures. An upright epiglottis splits the bolus around the larynx into the
pyriform sinuses. With base of tongue motion, hyolaryngeal elevation, and the
weight of the bolus, the epiglottis inverts. The lack of epiglottic inversion points

to a deficiency in one or more of the factors that lead to its movement.

Glottal incompetence can result in aspiration during the swallow. Strong closure
of the laryngeal aditus superior to the level of the true vocal folds provides a layer

of airway protection in this case.

The superior-anterior motion of the larynx creates opening of the LIES.
Deficiencies in this movement due to surgery (such as suprahyoid release),
scarring (such as chemoradiation), or neurologic deficiencies, will result in a
shorting opening phase of the LIES, despite normal relaxation of the cricopharyngeus muscle itself. This increases the possibility of postcricoid residue, which

may be at risk of aspiration after the swallow is completed.

Proper coordination of breathing and swallowing can improve the strength, and
therefore efficiency, of the swallow.

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