I.
Introduction
Sleep apnoea is common, underdiagnosed and, left untreated, significantly
increases mortality (He,
Kryger, Zorick, Conway, & Roth, 1988). This report describes upper airway anatomy and nocturnal
respiratory physiology. Pathogenesis of central and obstructive sleep apnoea is
discussed, along with medical and psychosocial sequelae. Reflection concludes
the document.
II.
The pharynx and
upper airway
The pharynx is a fibromuscular tube from the skull’s base to
the level of C6, and is common to the gastrointestinal and respiratory tracts.
The nasopharynx runs between the sphenoid bone and uvula’s
tip. The oropharynx runs from the uvula’s tip to the superior limit of the
epiglottis. The laryngopharynx runs from the epiglottis to the level of the cricoid
cartilage (Last, 1999).
A.
Nasal cavity/nasopharynx
Figure 1 shows the nasal cavity
laterally. In Figure 2, conchae are removed.
The nasal cavity’s pseudostratified columnar epithelium (with
goblet cells) has cilia and mucus to trap/remove particles, vasculature and
serous secretions to warm/humidify air. Superiorly, olfactory receptors detect
smells, transmitting information to the olfactory nerve and bulb (Last, 1999).
The cavity communicates with paranasal sinuses, middle ear (via Eustachian
tube) and nasopharynx (via choanae) (Figure 3) (Williams, Warwick,_Dyson,_&_Bannister, 1989).
Figure 3 shows components of the velopharyngeal sphincter, consisting
of tensor and levator veli palatini, musculus uvulae, palatoglossus,
palatopharyngeus and superior constrictor (Table 1). These assist maintenance
of airway patency (Phillipson,
1993).
B.
Tongue and mouth
The mouth lies between the lips and palatoglossal arches. It
consists of a vestibule (between cheeks/lips and gingivae/teeth), and oral
cavity proper (posteriorly). Superiorly, it is bounded by the hard and soft
palates (Table 1).
The tongue consists of skeletal muscle running longitudinally,
transversely and vertically (Table 2). Genioglossus protrudes the tongue,
widening the oropharyngeal (airway) lumen. On the posterior third of the tongue
is the lingual tonsil (Figure 4). The lingual, palatine, tubal and pharyngeal
tonsils comprise Waldeyer’s ring: lymphoid tissue immunologically protecting
the upper openings of the respiratory and gastrointestinal tracts. Tonsillitis can
therefore occlude the airway (Last, 1999).
C.
Pharyngeal
musculature
The pharynx consists of telescoped superior, middle and inferior
pharyngeal constrictors and a pharyngobasilar fascia. The constrictors attach posteriorly
at the pharyngeal raphe (Figures 5 and 6)(Last, 1999).
III.
Respiratory
physiology during sleep
A.
Airway patency
maintenance
Neurological control of pharyngeal dilator muscles (including
genioglossus, levator palitini) maintains nocturnal airway patency.
Sauerland & Harper (1976) demonstrated tonic activity of
the genioglossi during quiet sleep. In REM sleep, phasic contractions of
genioglossi coincide with inspiration (Figure 7).
Genioglossus activity is stimulated by:
1.
Negative airway
pressure, which activates laryngeal mechanoreceptors, stimulating genioglossus via
hypoglossal nerve (Horner, Innes,
Murphy, & Guz, 1991).
2.
Medullary respiratory
pattern generating neurons (White, 2005).
3.
Neurons moderating
arousal (Fogel et al., 2003).
Nocturnally, responses #1 and #2 are reduced, and #3 is unchanged:
overall predisposing to collapse in susceptible people (White, 2005).
B.
Nocturnal ventilation
control
White (2005) defines respiratory stability by “loop gain”. Apnoea
causes high blood carbon dioxide, which, detected by chemoreceptors, causes hyperpnoea.
Loop gain is the ratio of the response (hyperpnoea) to the disturbance
(apnoea). If loop gain is less than 1, the feedback response will stabilise
respiration. If loop gain exceeds 1, compensatory hyperpnoea causes enough
decrease in blood carbon dioxide to suppress respiratory drive and cause
repeated apnoea (Figure 8).
Loop gain depends on controller and plant gain.
Controller gain represents chemoreceptor sensitivity. Plant
gain represents the size of blood carbon dioxide decrease due to a given
increase in ventilation (White, 2005).
Figure 9 shows alveolar ventilation versus alveolar carbon dioxide.
Broken lines represent responses to falling carbon dioxide: where they meet the
axis represents apnoea.
The slope of the broken lines represents controller gain. Due
to the curve’s shape, a given change in ventilation has a larger impact on
carbon dioxide levels in hypercapnic individuals (Figure 9A). Thus hypercapnia
causes elevated plant gain.
Figure 9B demonstrates how high controller gain (steeper
lines) results in apnoea due to smaller carbon dioxide decrements.
IV.
Sleep apnoea
A.
Definition
Sleep apnoea may be obstructive (84%), central (0.4%) or
mixed (a combination of the two, 15%). An apnoea is a pause in breathing lasting ≥10s
(Morgenthaler, Kagramanov, Hanak, & Decker, 2006).
Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is the
commonest form. In hypopnoea, ventilation is reduced by ≥50% for ≥10s (though
breathing continues). OSAHS is defined as the combination of a) ≥5 occurrences
of apnoea or hypopnoea per sleeping hour and b) inexplicable daytime sleepiness.
It involves upper airway obstruction. Central sleep apnoea (CSA) is
characterised by pauses in nocturnal ventilation resulting from lack of respiratory
drive (Fauci et al., 2008).
B.
Epidemiology
OSAHS is twice as common in men as in women, with 1-4% of
adult males (aged 40-65) affected. 26% of Australian adult males have a respiratory disturbance
index (RDI) above 5[1]
(Bearpark et al., 1995).
Young (2004) and Fauci et al. (2008) describe OSAHS risk
factors:
·
Obesity
·
Hypertension
·
Middle age (40-65)
·
Male gender
·
Upper airway/craniofacial
abnormalities (e.g. acromegaly)
·
Hypothyroidism
·
Myotonic dystrophy
·
Ehlers-Danlos
syndrome
Childhood-specific factors include enlarged adenoids/tonsils,
during rapid tonsillar proliferation (Arens et al., 2001).
Suspected risk factors include smoking, alcohol and genetics
(Young, 2004).
Isolated CSA is a rare condition, and usually appears in
combination with OSAHS (Table 3). Dugdale & Hadjiliadis (2011) describe CSA risk factors:
·
Arthritis of
cervical spine
·
Surgical
complications
·
Encephalitis
·
Poliomyelitis
·
Obesity
·
Stroke
·
Narcotic use
·
Radiation
·
Neurodegenerative
diseases
Childhood-specific risk factors include congenital neurological disorders
(e.g. primary alveolar hypoventilation).
C.
Pathophysiology
1.
OSAHS
Apnoea is caused by nocturnal airway closure. Airway patency
consists of a balance of: 1) Dilation: via contraction of pharyngeal dilators
and 2) Collapse: via negative pressure in inspiration, and airway compression
by adiposity or small bony architecture. In OSAHS, nocturnal relaxation of
dilators causes occlusion, reducing ventilation and causing
hypercapnia/hypoxia. Chemoreceptors respond, causing arousal and return of muscle
tone until sleep resumes (Fauci
et al., 2008).
Negative pressure during inspiration alone cannot cause
airway collapse.
Occlusion in OSAHS patients is due to positive extraluminal pressure (due to
fat deposition or small mandible), which exerts undue force on the airway (Figure
10) (Schwartz, Smith, Wise, Bankman, & Permutt, 1989).
Airway occlusion by enlarged adenoids or tonsils can cause
OSAHS (Figure 11). This commonly occurs in age 2-6 years, due to tonsillitis and
lymphoid proliferation (Arens et al., 2001).
a)
Mechanism for mechanical obstruction
A posteriorly situated maxilla/mandible reduce space for the
airway, competing with the actions of the velopharyngeal sphincter and
genioglossus to maintain patency. OSAHS upper airway diameters are about 66% those
of controls. The size of the soft palate
is also increased, reducing luminal diameter. The smaller intermaxillary space
in these patients displaces the tongue posteriorly, and with their relatively
larger tongue size, tends to occlude the airway (Johal, Patel, & Battagel, 2007). Together, these factors predispose
to nocturnal airway closure by the soft palate and tongue.
2.
CSA
CSA is due to high loop gain in respiratory feedback.
Examples include:
·
Transient CSA in
high altitude (increased controller gain due to hypoxia) (Fauci et al., 2008).
·
Idiopathic CSA due to
innately high controller gain (White, 2005).
·
Congestive heart
failure, due to increased controller gain (chemoreceptor sensitivity) and
slower circulation (Leung & Bradley,
2001).
·
Hypercapnia (obesity
hypoventilation syndrome, central alveolar hypoventilation) causing high plant
gain and respiratory drive reduction (Mellins, Balfour, Turino, & Winters,
1970).
CSA can cause pharyngeal muscle tone reduction and collapse
(OSAHS), producing mixed sleep apnoea (Badr, Roiber, Skatrud, & Dempsey, 1995).
Infantile CSA can be fatal and apnoea-like neurorespiratory
patterns are associated with sudden infant death syndrome (Katz, 2005).
D.
Clinical
manifestation
Table 4 summarises the clinical manifestations of sleep
apnoea variants.
E.
Diagnosis
>80% of OSAHS cases remain undiagnosed (Kapur et al., 1999).
Sleep history is obtained from the patient and their partner
(Epworth Sleepiness Score, Table 5). Examination includes assessing jaw and
upper airway anatomy, obesity, blood pressure and other risk factors.
Diagnostic investigation includes polysomnography (Fauci et al., 2008).
Below we present the diagnostic procedure used in Sydney Children’s Hospital.
F.
Psychosocial
impact
Kales
et al. (1985) showed 66% of sleep apnoea patients report damaged interpersonal
relationships and marriages. Loss of libido and impotence also occur. Patients
report reduced occupational productivity and resignation. Affected students nap
in class and report reduced grades.
Sleep apnoea is known to produce abnormalities of brain
anatomy, causing cognitive deficits (Morrell, 2003).
Psychiatric impacts
of these deficits are measurable (Table 6), and predispose to depression and
damaged relationships (Bixler et al., 2005). Therefore the disease has
significant adverse social effects on patients.
Patients with sleep apnoea are also financially affected.
Figure 12 shows the relationship between apnoea-hypopnoea index (AHI)[2] and annual medical expenditure.
G.
Complications
and outcome
Sleep apnoea patients report more illnesses/hospitalisations
than controls, and are more likely to be undergoing some medical treatment
(Kales et al., 1985). Figure 13 shows apnoea index (AI)[3]
versus patient mortality.
Complications include:
1.
Increased
cardiovascular risk
OSAHS increases the risk of
cardiovascular events (Marin, Carrizo, Vicente, & Agusti, 2005). OSAHS raises mean blood pressure,
increasing the risks of stroke and myocardial infarction (Fauci et al., 2008).
CSA is predisposes to atrial
fibrillation (Leung et al., 2005).
2.
Hepatic disease
OSAHS increases liver steatosis/fibrosis, and upregulates
liver enzymes (Tanné et al., 2005).
3.
Diabetes
mellitus
OSAHS is a risk factor for insulin resistance, independent of
obesity (Ip et al., 2002).
4.
Anaesthesia
complications
Both OSAHS and CSA increase risk of respiratory arrest associated
with anaesthesia, and a restricted upper airway complicates intubation (Benumof, 2004).
5.
Developmental
abnormalities
In the infant, sleep apnoea can cause failure to thrive,
learning/memory and emotional difficulties (von Hofsten, 2004).
V.
Conclusion
Sleep apnoea is a common disorder with serious medical/psychosocial
implications. Its aetiology and sequelae differ between child and adult.
Despite its importance, sleep apnoea often goes undiagnosed. Further research
into public health strategies to more effectively identify and treat this
disease seems prudent.
Nice review! Are you thinking about publishing this as well? If not you should!
ReplyDeleteThanks, glad you liked it.
DeleteI'm not sure, don't know if I can be bothered when the info is all easily available to those who are curious.
Food for thought!