Clinical Reviews in Allergy and Immunology @Copyright 1998 by Humana Press Inc. 1080-0549/98/25-54/$15.50
Physiology of the Nose and Paranasal Sinuses philip Cole The Gage Research Institute, 223 College Street, Toronto, Canada M5T 1R4
Special Features Introduction Comparative studies demonstrate the existence of nasal structures and of paranasal sinuses that are common to a wide range of animal species. By contrast with m a n y animals, h u m a n olfactory and turbinate structures and functions are vestigial (Figs. 1-3) (1), but h u m a n paranasal sinuses are relatively well developed. Obviously useful and important functions of olfaction and respiratory air processing can be attributed to the nose, but despite m a n y thoughtful speculations, conclusive evidence of functional importance of the paranasal sinuses has yet to be found. The existence of paranasal sinuses may be unexplained, but their susceptibility to disease is a common source of misery for patients and a focus of attention for clinicians. Similar diseases h a v e been f o u n d in animals. Sinus diseases are prevalent in both acute and chronic form, and, in most cases, they are closely associated with nasal disorders. Indeed, as a common example, paranasal sinus involvement has been demonstrated by imaging studies in a large proportion of patients suffering from coryza (2). It is unlikely that other inflammatory "sinus diseases" are confined to sinus cavities, and usually the term rhinosinusitis is more descriptive. In addition to frequently mistaken self-diagnoses, sinus diseases are c o m m o n globally (33 million cases/yr in the US--National Center for Health Statistics), they are distressing to the sufferer, and progression to vital structures in their proximity can lead to serious complications, but the relatively benign course of acute rhinosinusitis encourages neglect in m a n y cases. In other cases, its severity, chronicity, and extension to associated air passages and air-containing cavities with attendant complications add a major contribution to the heavy morbidity Clinical Reviews in Allergy and Immunology
25
Volume 16, 7998
26
Cole
Fig. 1. Coronal section of the nasal cavity of a seal demonstrating enormous turbinate structure. (Reprinted with permission from Negus [1].)
t
t
V
!
MAN A
B
Single Scroll
C
D
E
F
A
g
C
0
BISON A
B
E
F
Double Scroll C
O
TREE KANGAROO
A
e,
C
O
Foldea
Fig. 2. Comparative anatomical studies of maxilloturbinate turbinates, saggital and coronal views. Note simplicity of human turbinate structure. (Reprinted with permission from Negus [113
burden of respiratory diseases--a burden that is most heavily weighted against the very young, the old, and the underprivileged throughout the world. The incidence and lethal complications of respiratory disClinical Reviews in Allergy and Immunology
Volume
16,
1998
Nose and Paranasal Sinuses
27
B
A
Frontal sinus Ethmoidal
cell Orbit
Ethmoturbinal Maxilloturbinal Maxillary
dy
sinus
Palate
Palate
Fig. 3. Coronal nasal sections comparing turbinates of humans (A) and domestic cat (B). The nasal olfactory area of the cats also exceeds that of humans. (Reprinted with permission from Negus [1].)
eases are many times greater in underdeveloped than in developed countries. Economic consequences of nasal and sinus diseases are substantial. In addition to an incalculable number of cases, it has been estimated that in the US alone, they lead to the loss of at least 200 million days of employment annually. More than $5 billion are spent on medication and much of it is symptomatic, as advertising and the shelves of drug stores affirm. Doctor visits, together with diagnostic and surgical measures, add many millions of dollars more to the economic burden of rhinosinusitis (3). This article is concerned mainly with applied physiology of the human nose and paranasal sinuses, and important features of the region that are discussed in detail in other chapters of Diseases of the Sinuses receive only brief reference here.
Nasal and Sinus Mucosa Apart from the mouth, pharynx, and terminal pulmonary air passages, patency of the respiratory airways and air-containing cul-de-sacs in continuity with them is maintained by relatively inflexible cartilage and by bone. Hygiene and health of these patent passages and cavities are preserved by a specialized ciliated epithelium and a mucociliary defense mechanism which they share in continuity. They also share ubiquitous respiratory tract diseases that are modified by characteristic Clinical Reviews in Allergy and Immunology
Volume
16,
1998
28
Cole
•0•@•--
Mucus (viscoelastic)
~///;i((l(/{/(',~~i~-O;:lci~sr !,?.~rji.ues id ciliarynu
Fig. 4. Mucociliary transport. (Reprinted with permission from Cole [4], p. 24.)
features of the passages and cavities, and, in addition, several diseases are unique to particular sites. Furthermore, failure of defense mechanisms of the upper airways can provide a gateway that allows infectious diseases to enter and disseminate to other regions of the body. Ciliated columnar epithelium that lines the nose and sinuses is b o u n d e d by squamous epithelium of the anterior nose and the pharynx, respectively. In both newborn and laryngectomized subjects, ciliated epithelium occupies a greater proportion of the anterior nose than in other subjects, which suggests that squamous metaplasia of ciliated epithelium is a response to the trauma of environmental exposures. The area of the l u m i n a l surface of the columnar e p i t h e l i u m that lines the r e m a i n d e r of the nose and the sinuses is greatly e x p a n d e d by 200-300 m i c r o v i l l i / c e l l that enhance the potential for exchanges b e t w e e n epithelial cells and the nasal lumen. A large p r o p o r t i o n of these c o l u m n a r cells also bear cilia, several h u n d r e d / c e l l , which beat 1 0 0 0 x / m i n in sequence w i t h those of n e i g h b o r i n g ciliated cells. The m e c h a n i s m s u n d e r l y i n g this o r d e r l y m e t a c h r o n o u s a c t i v i t y are unexplained. When the mucociliary mechanism is functioning normally, the cilia beat in a serous periciliary fluid of low viscosity. This fluid is deep enough to avoid entanglement of cilia with discontinuous islands of viscoelastic mucus that float on its surface. Yet it is not so deep as to prevent tips of the beating cilia from propelling the mucus along wellestablished tracks to the pharynx, where it is swallowed (Fig. 4) (4). The floating masses of mucus contain entrapped and dissolved contaminants from inspired ambient air, and along their course to the pharynx they sweep up cellular debris, microorganisms, and other detritus from the serous surface. It has been estimated that the mucus and its contents cross epithelial cells at a rate of 6-10 cells/s (5), b u t clearance studies demonstrate that although the mucociliary transport rate averages about 6 m m / m i n , it is subject to wide variation and it differs also Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
29
between different sites. Seromucinous glands and epithelial goblet cells secrete the thin pericellular fluid and the thick viscoelastic mucus (6). In addition to physical removal of microorganisms and other noxious materials by mucociliary transport, an important line of defense is provided by the surface fluids that contain macrophages, basophils and mast cells, leukocytes, eosinophils, and antibacterial/antiviral substances that include immunoglobulins, lactoferrin, lysozymes, and interferons. These cells and substances discourage microbial colonization and enhance the protective properties of the nasal and sinus mucosa that guard against infection. Cytoplasm of the cilia contains clearly patterned ultrastructural elements whose function is concerned with flexion and extension of ciliary beating (7). Abnormalities of these ultrastructures can result in dyskinesias, which are inherited in some cases as primary disorders (Kartagener's, Young's, and other less clearly defined autosomal recessive inherited syndromes). Abnormalities of the cilia and their ultrastructure are not c o n f i n e d to the nasal mucosa, they are widely distributed, and have been demonstrated in peripheral respiratory epithelium and in other ciliated cells. Abnormalities of the ciliary bodies are found also as accompaniments of mucosal injury (infective and other forms of irritation). They consist of cytoplasmic extrusions in the form of blebs and outgrowths of the ciliary membrane. Aberrant cilia are commonly found also in electron microscope studies of biopsy specimens obtained from apparently healthy subjects. Except in the rare cases of Kartagener's or even more rare Young's and other less welldefined inherited syndromes, the physiological and clinical significance of the many observed ciliary anomalies is unknown. In health, variations are wide, but abnormalities of metachronal ciliary beat and of secretions and barriers in the course of mucociliary flow can lead to pathological consequences. Ciliary beat frequency and mucus transport rate vary substantially, they are not closely correlated, and each can be modified by quantities and qualities of seromucinous secretions. Cystic fibrosis (mucoviscidosis) is an example of inherited disease of abnormal exocrine secretion, and, more commonly, allergens, infections, and irritants also alter the quantity and the chemical and physical properties of nasal secretion, which can result in impairment of mucociliary function. Mucociliary function is remarkably resistant to climatic extremes, to moderate concentrations of the majority of environmental air pollutants (including tobacco smoke), to particulate loading, to wide variations in pH, and to most prescription nasal medications. However, some preservatives (e.g., benzalkonium chloride) are harmful (8), and medications containing them should be avoided. Hypotonic and detergent aqueous solutions injure cilia, and desiccation of the mucosa is Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Cole
30
disastrous to them. Rhinovirus can destroy not only cilia, but also epithelial cells; their junctions loosen, and they may become detached from the basement membrane. As a consequence, impairment of defensive function leaves the mucosa vulnerable to both spreading and secondary infection. Full recovery of mucociliary function following such infection m a y require several weeks. Normal mucociliary function provides a first line of defense. It is of fundamental importance to health of the airways and associated recesses, but the narrow middle meatal cleft, which provides the main exit for mucociliary flow from the sinuses to the nasal cavities, is susceptible to obstruction. In this ostiomeatal complex, mucosal swelling, polyps, or thickened secretions that result from common nasal inflammatory conditions can create a vicious cycle in which pathological changes become irreversible without therapeutic intervention. Occlusion of an ostial orifice, directly or more remotely by obstruction elsewhere within the narrow confines of the middle meatus, is a primary cause of inflammatory sinus disease. Anterior ethmoid cells are common sites of disease, and ethmoiditis is usually associated with an obstructed infundibulum (9,10). (See also Sinus Air Flow later in this article.)
The Nasal Airways A l t h o u g h m o u t h or t r a c h e o s t o m a l b r e a t h i n g can sustain life indefinitely, the parallel nasal cavities provide preferred breathing passages that are supplemented by the oral airway under demanding conditions of exercise or of severe nasal obstruction, but exclusive oral breathing is rare (11). Patients can become firmly habituated to "mouth" (oronasal) breathing, and it can persist despite relief of obstruction. Thermal and water vapor pressure gradients favoring exchanges between inspiratory air and mucosa are much greater at respiratory portals than elsewhere in the air passages. The portal airway meets major demands in cleansing, heating, and moistening 15 kg of ambient air that is required for p u l m o n a r y ventilation of h u m a n adults every 24 h. The spontaneously positioned labial orifice enables the m o u t h to process ambient air effectively (12) in the short term, but continuous secretion and repeated redistribution of saliva (or the oral intake of other aqueous fluid) are necessary to p r e v e n t localized d r y i n g of mucosa, and to maintain both oral conditioning of ambient air and oropharyngeal comfort. The nose is better equipped than the m o u t h to meet long-term air-conditioning demands, since, by contrast with salivation, supply of moisture is continuous and its wide distribution over the nasal mucosa is aided by the mucociliary mechanism. Moreover, as will be discussed later in this article, the m o u t h is less effective than the nose in recovering moisture (and heat) from the 15 k g / d of expiratory air. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
31
Nevertheless, although exclusive nasal breathing may be preferable, it is clearly less than essential. It is readily abandoned during exercise when inspiratory air-conditioning demands are great, and it is abandoned also during speech and in other less exacting circumstances, such as surprise and preoccupation. Chronic "mouth" breathing can lead not only to oral and pharyngeal discomfort and to gingivitis, but there is much evidence to support the view that it can lead also to abnormalities of facial growth and dentition.
Nasal Air-Flow Sensation Nasal symptoms are very common, but patients' subjective assessments of nasal dyspneas are not closely correlated with objective findings (13). Indeed, physiological nasal air-flow resistive changes resulting from exercise, from recovery following exercise, from postural effects, and from the nasal cycle, although frequent and substantial, are seldom noticed, nor is it unusual for gross structural abnormalities to be found on clinical and rhinomanometric examination of patients without complaints of nasal airway obstruction. On the other hand, neither is it unusual for complaints of obstruction to be unsupported by clinical and objective findings. Sensory interpretations of nasal patency are influenced not only by ambient and pathophysiological conditions, but also by psychological factors. A prominent feature of nasal inspiratory air flow is a sensation of chill within the nasal cavities. Its degree and penetration, which can extend to the pharynx and beyond, are dependent on ambient air conditions of temperature and humidity and on flow velocity. The sensation is absent in expiration, and it is consistent with thermal demands of the air stream. In addition to thermal sensation, auditory sensation accompanies nasal air flow. Its intensity is directly related to air-flow velocity and its consequent flow disturbance, it is present in both inspiratory and expiratory phases, and its presence is a source of great reassurance to parents of sleeping infants. Similar thermal and auditory sensations accompany oral breathing. In addition to cool air and deep nasal inspiration, several aromatic substances, notably L-menthol, enhance the sensations of chill, air flow, and nasal patency (13). By contrast, ambient air with a heavy concentration of tobacco smoke can produce a sensation of nasal stuffiness. Objective measurements of nasal air-flow resistances have demonstrated, however, that in healthy subjects, despite the nasal sensations, patency is unaffected by these exposures. L-Menthol also induces a sensation of chill in the oral mucosa and the skin (menthol lozenges and after-shave preparations). This menthol isomer is thought to exert its enhanced sensory effects by altering calcium transport in neural tissues (13), but mechanisms of the sensaClinical Reviews in Allergy and Immunology
Volume 16, 1998
32
Cole
tion of nasal stuffiness induced by tobacco smoke have not been elucidated. Specific nerve endings for temperature or flow detection have not been identified in nasal mucosa, but nonmyelinated sensory nerve fibers with plexiform endings have been demonstrated terminating in the lamina propria and between epithelial cells (13). In addition to cognition, other sensory neural responses to nasal air flow are widespread. They are reflected in EEG changes (13) and may be of importance to mechanics of breathing in both wakefulness and sleep. Breathing cool (fresh!!) air reduces not only the sensation of dyspnea, but also respiratory contractions of thoracic muscles. These effects are enhanced by increased respiratory air flow (deep breaths!!) and diminished by topical nasal anesthesia (13).
Nasal Resistors The Nasal Valve Nasal resistance to respiratory air flow is of similar magnitude to the sum of the resistances of all the remaining air passages. The major portion of nasal resistance is confined to a narrowed caudal (anterior) segment that is thus the major resistor of the entire respiratory airway system. Beyond the narrowing, the nasal cavum and succeeding airway segments offer comparatively little resistance to inspiratory air flow (Fig. 5) (14). In expiration, the glottis narrows and provides additional resistance to air flow during this phase of breathing (see Respiratory Air Processing later in this article). Descriptions of the narrowed nasal segment, termed the nasal valve, can be confused by an unnecessarily extensive terminology that does not simplify understanding of its dimensions or its function (15). The lumen of the valve extends several millimeters beyond the triangular cleft that is evident on rhinoscopic examination of the vestibule. The apex of this triangle is less acute in Negroid than Caucasian noses, thus enabling the inferior turbinate to be examined without instrumentation in such cases. The cleft is the entrance to a dynamic functional segment of the airway, and it is b o u n d e d by the caudal edge of the compliant upper lateral cartilage and by a line opposite to it on the comparatively rigid cartilaginous septum. Its short base lies across the bony nasal floor. It is obliquely situated between horizontal nostril and vertical piriform aperture. The functional valve extends several millimeters from its triangular entrance to the piriform entrance of the anterior cavum, and it is much shorter and wider ventrally than dorsally. It is bounded laterally by compliant alar tissues and, in the vicinity of the rigid entry to the bony cavum, by erectile tissue at the caudal end of the inferior turbinate. The medial wall of firm septal cartilage supports an extensive Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses 0.5
33
A
0.4
ro 0.3
E .9.o ~..
0.2
0.1
0 . 0 ~
0-2cm
2-4cm
4-6cm
depth in the nose (cm)
o.~
B
0.4
0,2
0.1
0.0
m
T
0-2cm
2..4cm
T 4-6cm
6-8cm
depth in the nose (cm)
Fig. 5. Distribution of resistance in 2-cm segments of the nasal cavities. The resistance is most marked in the anterior nose. The erectile anterior turbinate portion is reduced, and more caudally situated resistance remains after decongestion. (A) Untreated. (B) Decongested. (Reprinted with permission from Hirschberg et al. [14].)
body of erectile tissue in its dorsal portion. This mass of septal erectile tissue, although not readily recognizable on rhinoscopic examination, is demonstrated clearly by tomographic imaging and by cadaver studies (see Figs. 6-9) (4,16-18). Stability of the compliant alar wall is maintained by resistance to deformation of its tissues and by isometric Clinical Reviews in Allergy and Immunology
Volume 16, 1998
34
Cole
Fig. 6. Injected cadaver material. Extensive accumulations of capacitance vessels that constitute erectile tissues of the septum and lateral nasal walls. This is most marked in the anterior nose. (Reprinted with permission from Wustrow [7].)
inspiratory activity of alar muscles. Both oppose inspiratory transmural pressures (4). The nasal valve is a functional complex of compliant and dynamic tissues. Over a distance of several millimeters, its lumen is regulated by lateral and medial erectile mucosa, modulated by the tone of alar muscles, and stabilized by bone and cartilage. As noted above, it is the major resistor of the respiratory airways, and it performs an essential function in ensuring disruption of laminar flow of the inspiratory air stream (see Respiratory Air Processing later in this article).
The Nasal Alae In healthy adult noses, alar movement in response to nasal breathing is insignificant during resting ventilation, but it is often quite marked in young children. Inspiratory nasal alar dilator muscle activity increases with ventilation and opposes transmural pressures. Measurements of alar movement toward the septum induced by inspiratory transmural pressures of exercising adults has been determined by video studies and found to be very small (4), and when exercise is sufficiently Clinical Reviews in Allergy and Immunology
Volume 16, 1998
35
Nose and Paranasal Sinuses
.....
.
,~Jl
url
::~
2;
G2GZ
L
~
Xg
"
C
Fig. 7. Computed X-ray axial and coronal tomograms of the nasal cavities. Effects of vasoactive substances. Note both medial (septal body) and lateral erectile tissues in the anterior nose. (Reprinted with permission from Cole et al. [16].)
severe, vestibular transmural respiratory pressures are reduced by a switch to oronasal breathing. EMG studies show alar dilator muscle activity to accompany each nasal inspiration, and the activity varies directly not only with ventilation, but also with nasal resistance, hypoxia, and hypercapnia. It ceases with mouth or tracheostomal breathing (4). As with other upper-airway-stabilizing muscles, alar dilator muscle activity precedes diaphragmatic contraction. The dilator muscles that stabilize the anterior nasal Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Cole
36
A
CORONAL SECTIONS
NASAL VESTIBULE
NASOPHARYNX
/
Septal
body
'
00
"
Irregular septum
Fig. 8. Magnetic resonance imaging of coronal sections of the nasal airways from nostrils to choana. Note septal body and adaptation of airway to septal irregularity. (MRIs from Cole et al. [18]. Tracings from Cole [4], p. 27. Reprinted with permission.)
airway also increase its patency in demanding and emotional situations, such as severe exercise, air hunger, anger, and fear. As the volume of respiratory air flow is maintained through a nasal segment that becomes narrowed, linear velocity of the air stream increases and elevates transmural pressure, a compressing force, at the site of narrowing (Bernoulli). At a critically elevated inspiratory transmural pressure, the compliant portion of the narrow nasal valve collapses partiaUy or completely, thereby limiting further or occluding the airway (4). The caudal end of the upper lateral cartilage is free from septal attachment and has a flexible fibrous joint with the lower lateral cartiClinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
A
37 AXIAL SECTIONS
B
Fig. 9. Magnetic resonance imaging axial views show medial and lateral erectile tissues. Note erectile tissue in valve area caudal to bony inferior turbinate. (MRIs from Cole et al. [18]. Tracings from Cole [4], p. 29. Reprinted with permission.)
lage. Thus, it is the alar region most disposed to comply with transmural pressures. However, until a critical transmural pressure is achieved, normal alar tissues and dilator muscles provide sufficient rigidity to withstand deformation. Thus, lumen and resistance of the normally functioning valve is little affected by the transmural pressures that are generated by nasal breathing at rest, and, as already noted, the switch to oronasal breathing that accompanies exercise reduces the Clinical Reviews in Allergy and Immunology
Volume 16, 1998
38
Cole
nasal fraction of respiratory air flow and the alar burden of transmural pressure. Alar dilator muscle weakness increases alar compliance with inspiratory air flow pressures and reduces the critical transmural pressure at which collapse of the valve occurs. Under these conditions, nasal obstruction can result from modest inspiratory air flow, as in cases of Bell's and other facial muscle palsies. The tendency toward alar collapse can be increased also by impairment of normal alar skeletal stiffness or by alar deformity. Such defects are congenital, traumatic, or, more commonly, complications of rhinoplasty (4). Inspiratory collapse can occur also with normally robust alae and healthy dilator muscles w h e n transmural pressures are elevated by the Bernoulli effect of excessive narrowing in the valve region. Such narrowing can accompany structural abnormalities of the anterior septum, of the alae themselves, of the mucosa, or combinations of these factors. Wide alar retraction approximately halves air-flow resistance of the healthy Caucasian nose. The remaining resistance is reduced even further by the effect of topical decongestants on erectile mucosa of the cavum, mainly in its anterior segment (Fig. 5) (14). By contrast with alar retraction, since the valve is narrow, slight mucosal or skeletal intrusions on the lumen by displacement of its medial a n d / o r lateral wall can result in a substantial decrease in cross-sectional area, and exponential increase in both air-flow resistance and transmural pressure. Nasal obstruction is caused, most commonly, by mucosal swelling that extends into the valve region, and it is exacerbated by structural e n c r o a c h m e n t on the valve l u m e n of septal or, more rarely, alar deformity (4). Substantial obstruction can occur with comparatively m i n o r aberrations of this nature, whereas only gross deviations or swelling is obstructive in other parts of the nasal cavities (Figs. 10 and 11) (19,20). However, although an entirely regular midline septum in an adult is not the most common finding, septal irregularity is symptomless in most cases (4). A predominance of septal deviations in males suggests a traumatic etiology. There is evidence to sugges t that they result also, in both sexes, from parturition injuries sustained during rotation of the fetal head in the birth canal and, indeed, they are reported to be less frequent in Caesarean than vaginal births (4). R h i n o m a n o m e t r y has confirmed benefits of corrective septal surgery in the anterior nasal segment (21). It is reported also that the more d e m a n d i n g corrective surgery of the alar cartilages can restore and, in cosmetic cases, maintain appropriate patency of this region (21-24). Objective measurements have demonstrated that rapid maxillary expansion, a c o m m o n orthodontic procedure that enlarges the upper dental arch, widens the piriform aperture and results in a marked and Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
39 Bony Cavum Obstructions
Anterior Nasal Obstructions
Dimensions of Obstructions 3O mR
s mm I 5 mm
Fig. 10. Septal deviations simulated by means of plastic foam strips of differing thickness, adherent to the septum and sited in the anterior nose and the cavum. (Reprinted with permission from Chaban et al. [19].)
~
35-
30-
mm
25-
Z o
'=="
20-
,1-
i 15-
10-
5Baseline" Variation 0
t Caudal Septum
I I Upper Piriform Lateral Aperture Cartilage Site of Obstruction in Nasal Cavity
I Bony
Cavum
Fig. 11. Resistive effects of simulated septal deviations. This is most marked in the anterior nose. Large simulated deviations and spurs have little resistive effect in the cavum. (Reprinted with permission from Cole [20].)
lasting increase in nasal patency (4). This method has been employed as one of the alternatives in management of obstructive narrowing in the valve region. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
40
Cole
Several different prosthetic devices are available to support the alae in order to maintain or to increase patency of the anterior nose and to improve the comfort of nasal breathing (e.g., Francis dilators). These devices are usually inserted in the nasal vestibule, but a recent innovation (Breathe Right) consists of a spring-loaded plastic strip that adheres to the vestibular skin and opens the valve. Despite undoubted increased patency and ease of breathing, our attempted therapeutic use of these devices to relieve severe snoring and other breathing disorders in sleep has been disappointing.
Erectile Tissue Erectile tissues of the septum and lateral nasal wall (4) achieve particular prominence in the anterior nose (Figs. 6-9). Injection studies of vascular nasal tissues of cadaver material illustrate the manner in which blood content of the capacitance vessels of erectile tissues can regulate airway lumen and air-flow resistance principally in the narrowed valve segment. In vivo, tomographic imaging, acoustic rhinometry, and air-flow studies have confirmed the distribution of nasal erectile tissues (Fig. 5) that is demonstrated by cadaver injection studies, and have clearly shown the mucosal volume changes that occur in the spontaneous nasal cycle, and in response to vasoactive substances and to postural stimuli. In addition, imaging studies validate the clinical observation that nasal erectile tissues accommodate to structural irregularities (Fig. 8), and they maintain a remarkably constant airway width of 2-3 m m in the more patent nasal cavum despite marked septal deviations. Other injection studies of cadaver tissues show nasal erectile tissue as a venous mat 1-5 m m thick (25) consisting of accumulations of tortuous, irregular, intercommunicating, valveless venous sinuses. These vessels have a rich sympathetic nerve supply (26) and respond by constriction to stimulation of both cz-1 and cz-2 receptors (27). They terminate in muscular "throttle" veins that possibly regulate venous drainage (26). The ability of erectile tissues to maintain an adequate nasal airway can be defeated by moderate structural asymmetries at narrowed sites, with resulting intermittent obstruction by cyclic or postural mucosal swelling. More severe skeletal deviation a n d / o r pathological mucosal swelling lead to more persistent obstruction and, as already noted, resistive effects of structural irregularities or mucosal swelling are critical in the valve region where the cross-sectional area is n o r m a l l y restricted (4). Nasal erectile tissues are not confined to the vascular mucosa of the turbinates. In the congested nose, swelling of erectile tissues covering the bony inferior turbinate is accompanied by swelling of the latClinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
41
eral nasal wall caudal to it. The lateral wall tissues extend several millimeters beyond the bony piriform aperture, and when congested, they intrude on the lumen of the valve. Swelling and shrinking of these tissues, e.g., by topical decongestant, can be detected readily by rhinoscopy and demonstrated clearly by t o m o g r a p h y (Fig. 9), acoustic rhinometry, and air-flow studies. Further substantial intrusions on the valve lumen result from congestion of erectile tissues of the anterior septum (Figs. 6-9). An anterior septal erectile body is well recognized in European rhinological literature, but it is neglected in English language texts. The main mass of septal erectile tissue is located caudal to the middle turbinate and dorsal to the inferior turbinate. It is inconspicuous on rhinoscopic examination, since it is partially masked by the columella and the two sides of the septum cannot be viewed simultaneously. Tomographic imaging that embraces the anterior nose shows the septal body clearly, but routine sinus tomography does not usually include this region. Although the septal body of erectile tissue is seldom a direct target of therapy, it is interesting to consider the possibility that surgical elevation of anterior septal tissues might inadvertently affect it and contribute to the benefits of septoplasty. Inflammation brings about a paresis of capacitance vessel tone (28,29) that allows these vessels, which constitute the nasal erectile tissues, to fill with blood, most markedly in recumbency. The airways may be narrowed further by other accompaniments of inflammation that include accumulation of extravascular fluid, secretion, transudate, and exudate of fluid and macromolecules through permeable epithelial junctions (6,30), but response to decongestant indicates that a major proportion of the swelling is vascular. Blood content of capacitance vessels and blood flow through resistance vessels are controlled by vascular tone, and the two systems function independently, but they respond to many stimuli in a similar manner. Vascular tone is influenced by local metabolic and vasoactive substances, by thermal conditions, and by neurotransmission. In addition to adrenergic and cholinergic neurotransmitters, many other substances concerned with neurotransmission and vasoactivity have been detected in nasal tissues in health and disease. Several of these substances act also on nasal secretory elements, but, in many cases, their precise functions are unknown. They are listed in Table 1.
The Nasal Cycle In health, nasal congestion and decongestion alternate over time in each nasal cavity as an apparently spontaneous resistive cycle, and although unilateral resistances can fluctuate between severe obstruction and optimum patency (Fig. 12) (31,32), healthy subjects are usually Clinical Reviews in Allergy and Immunology
Volume 16, 1998
42
Cole
Table 1 Nonadrenergic, Noncholinergic Neuropeptides and Biochemical Mediators~ Neuropeptides
Mediators Adenosine Bradikinin Chemotaxins Heparin Leukotrienes Prostaglandins Serotinin Trypsin Nitric oxide (?)
Calcitonin gene-related peptide Galinin Gastrin-releasing peptide Neurokinins Neuropeptide Y Peptide histidine isoleucine Somatostatin Substance P
aNonadrenergic and noncholinergic substances found in reactive nasal mucosa affecting blood vessel tone and permeability and seromucinous secretion.
_"]o 24
b D o r s a l l y Recumoent~,~
20-
~
16.
g
12-
rr
8-
Z
4-
i 0900
~ 1300
~
">
~
1700
h
Ib 2100 Hours
?s
1'7 6
01 O0
~I 0500
2~L 0900
Fig. 12. The nasal cycle demonstrated by nasal air-flow resistances. Amplitude increases in recumbency. Left (x) and right (o) resistances reciprocate. Combined resistances (0) show little change throughout the 24-h period of observation. (Reprinted with permission from Cole [31].)
unaware of the changes. The additional p h e n o m e n o n of reciprocity of resistances b e t w e e n sides (as one side congests, the opposite side decongests) minimizes alteration of combined resistances of the paired nasal cavities (4,31,32) (Fig. 12). Reciprocity is irregular in young children, but w h e n present, as in most adults, stabilization of total nasal resistance might diminish awareness of unilateral resistance changes. The resistive homeostasis of the combined nasal cavities is susceptible to disturbance by structural asymmetry or by inflammatory mucosal Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
43
disease. Either can result in symptoms owing to obstruction of the airway (4,33,34). Amplitude and frequency of the resistive nasal cycle are irregular, and the latter parameter is measured in hours (Fig. 12) (4). Minor fluctuations of briefer duration are superimposed on the leisurely progression of the cycle, but reciprocity between sides is fairly consistent and the resulting combined resistance remains fairly stable. Although the constantly changing resistances may not satisfy all criteria of cyclical activity and may be episodic rather than periodic, the term "nasal cycle" is firmly established and widely known. This curious cycle has been recognized for several centuries in yoga literature (35) where it is cited as a sign of good health. Modification of the cyclical phases by pressures exerted in the axillary region (see Posture and Pressure Effects) and by breathing maneuvers plays an important role in the yoga pranayama breathing exercises (4,35,36). The cycle has received attention in Western rhinology literature during the last 100 yr (37). The nasal cycle is reported to be present in about 80% of the adults in whom it has been sought (4), and its absence may be temporary. It has been found also in children and infants (4) in whom, as noted above, frequency and reciprocation between sides are less regular than in adults. A similar resistive cycle has been demonstrated in cats, dogs, pigs, rabbits, and rats, which, like humans, exhibit erectile nasal tissue (4). In humans, the cycle is amplified in recumbency, but it is otherwise unaffected by sleep, nasal occlusion of short duration, or topical anesthesia, but it is partially suppressed by tracheostomal breathing and it returns on resumption of the natural airway (4). Since the cycle is a vascular phenomenon, it is abolished temporarily by topical decongestant and, if the decongestant is applied unilaterally, the cycle continues contralaterally (38). Other cyclical phenomena that demonstrate lateralization synchronous with the nasal cycle have been reported in humans (4). They include electrocortical activity, sweating, pupil size, conjunctival capillary diameter, and even cognitive performance. It seems that the nasal cycle and its modifications (see Posture and Pressure Effects) are sensitive indicators of widely distributed neuroautonomic activity that reciprocates between sides of the body. The cycle provides an interesting source of speculation, but does not necessarily perform a functionally useful role in the nose.
Posture and Pressure Effects Unilateral nasal decongestion results from assumption of contralateral recumbent postures, and to contralateral pressures applied to the body surface in upright subjects, it is accompanied by ipsilateral nasal congestion (Fig. 13) (39). Sweat secretion also responds contraClinical Reviews in Allergy and Immunology
Volume 16, 1998
44
Cole
!i L " /
Fig. 13. Topographical anatomy of the pressure points that alter nasal resistance. (Reprinted with permission from Haight and Cole [39].)
l a t e r a l l y to p o s t u r e a n d b o d y surface p r e s s u r e s (4,39), a n d b o t h nasal a n d sweat responses appear to be m e d i a t e d by a similar sympathetic route. These reciprocal responses of capacitance vessels to pressure stimuli override the s p o n t a n e o u s nasal cycle (4,39) w h o s e mucovascular reciprocity they resemble in minimizing change in air-flow resistance of the combined nasal cavities. As the upper nasal cavity becomes more patent and the lower more resistive on assumption of a lateral recumbent posture, periodic reciprocation of the nasal cycle begins anew if this lateral posture is maintained. However, although reciprocal resistive postural responses occur during brief periods of lateral recumbency, they are temporary, and progression of the cycle does not appear to be affected on return to the dorsal posture. It seems likely that receptors i n v o l v e d in the nasal vascular pressure reflex are deeply situated, since the response to lateral chest wall pressure that takes place despite local anesthesia of the skin could not be elicited following intercostal nerve block in a single subject w h o was otherwise consistently responsive. It is of interest to note also that no similar nasal reflex responses were elicited w h e n superficial heat, cold, or painful stimuli were applied unilaterally to the b o d y surface (4). In standing subjects, amplitude of the cycle is much smaller than in seated or recumbent subjects (4), and it is unaffected by the pressures of weight bearing on one foot or the other. Absence of stimuli Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
45
from gravitational pressures on the trunk region of the body surface or action of the cardiovascular homeostatic reflex of capacitance vessels (40) might account for the amplitude differences. In healthy noses, there is little change in resistance of the combined nasal cavities as a subject assumes dorsal recumbency from an upright position (28), nor are there sleep-related changes of nasal resistance (Miljeteig et al., 1992, unpublished). In recumbency the nasal cycle continues, and vasoactive mucosa of the cyclically decongested side remains little affected. On the congested side, where tone of capacitance vessels is reduced, additional mucosal swelling occurs in response to the increased hydrostatic pressure of recumbency, but the swelling has little effect on resistance of the combined nasal cavities. Even severe unilateral cyclical obstructions that have been noted in recumbent and sleeping subjects do not exert a major effect on total nasal resistance (41). By contrast, in the presence of nasal mucosal inflammation, as most people are aware, congestion increases on assumption of a recumbent posture (28,29), since capacitance vessel tone is decreased and the vessels respond to postural hydrostatic pressures by increased blood content. Even in the upright patient, as already noted, the nasal cycle is modified by nasal mucosal diseases, and stabilizing reciprocal adjustments are disrupted (34). In the presence of cyclical, postural, or inflammatory mucosal swelling, resistive effects of structural abnormalities are exacerbated and moderate structural obstructions m a y become evident only under these circumstances. It has been suggested that the decrease in intranasal pressures that accompanies sniffing may be sufficient, if frequently repeated, to induce distension of capacitance vessels, especially in the presence of inflammation. A vicious cycle, typified by the chronically sniffing patient with nasal obstruction, has been put forward as an example supporting this plausible supposition (42). Effects of physiological and pathological nasal mucosal swelling in the ostiomeatal complex on the paranasal sinuses are discussed in other sections of this article.
Air Flow Nasal Air-Flow Distribution The distribution of inspiratory and expiratory air flow in h u m a n nasal cavities has been studied by many methods. Probably the most definitive results have been obtained by Swift and Proctor (Fig. 14) (43), who used hemi-nasal models obtained as casts from fresh h u m a n cadavers. They determined direction and linear velocity of nasal air streams by means of a micro-Pitot device. A transparent plastic sheet Clinical Reviews in Allergy and Immunology
Volume 16, 1998
46
Cole
/ 9 I Ix./.,".,".--"
,
~
\
Fig. 14. Direction and velocity of the inspiratory air stream during resting breathing. Size of points indicates velocity, which is greatest in the anterior nose. Main airstream flows between superior and inferior turbinates. (Reprinted with permission from Swift and Proctor [43], p. 80.)
substituted for a septum, and a perforation through it enabled the Pitot device to be placed at known nasal sites while air was passed through the model cavity at measured rates. Figure 14 shows linear flow velocities and directions within the model nasal cavity that are attained by ambient air at a flow approximating resting inspiration. Linear velocity of inspiratory air is markedly greater anteriorly in the region of the nasal valve than elsewhere in the nasal cavity. Indeed, in vivo it is greater than elsewhere in the respiratory passages. The mainstream courses between the inferior and superior turbinates with only minimal flow along the nasal floor and roof. Specialized olfactory mucosa is sheltered from the inspiratory mainstream (43) and, thus, avoids exposure to harm from the blast of unmodified ambient air. Air enters the nose through the horizontal nostril, mainly via its ventral portion. It takes a sharp turn and follows a curved course through the main nasal passage to exit to the nasopharynx by the vertical choana, and then takes another sharp turn to the oropharynx. The shape of the nasal vestibular region and its adjustment by alar muscles direct inspiratory air medially to course along the septum where the mainstream proceeds as a ribbon 2-3 mm thick arching between inferior and superior turbinates. By contrast with the inspiratory air stream, well-conditioned expiratory air is dispersed throughout the nasal cavity. It expels olfactants from the olfactory cleft, and gives up heat and water to nasal mucosa that is cooled by inspired ambient air (see Respiratory Air Processing later in this article). Olfactory sniffs, directed by alar positioning, form eddies in the upper nasal cavity (43). Vigorous sniffs assist cilia by propelling mucus toward the nasopharynx, and by dragging mucoelastic secretions from narrow meatal regions and sinus ostia. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
47
Reduction of intranasal pressures by sniffs with partially collapsed alae draws air from the sinuses displacing mucus in proximity with the ostia into the nasal cavity. Snorts dislodge material from the postnasal region to the pharynx, where the nasally produced secretions and their contents are swallowed. Sinus ostia in the middle meatus are sheltered from the nasal mainstream and its noxious contents, but nose blowing, to expel accumulated secretion from the nasal cavities, risks forcing contaminated nasal contents into sinus cavities. Simulations of nasal airways by models obtained from casts, from tomographic imaging, and generated by computer and the use of water with dyes and particles in place of air have advanced understanding of nasal air flow, but they have not accurately reproduced in vivo flow conditions. In addition to the complex structure of the bony and cartilaginous nasal skeleton, dimensions of the nasal lumen are determined by a dynamic mucovascular lining and, as discussed earlier in this article, in the compliant anterior nose by voluntary muscles and transmural respiratory air-flow pressures. Adjustments of the nasal lumen by erectile and alar tissues have not been reproduced in model studies, and normal septal contours, which include the substantial anterior septal body, have been largely ignored. These factors are of importance, since air-flow velocities, pressures, and resistances vary exponentially with cross-sectional areas, and relatively minor dimensional changes, especially in narrowed regions of the nose, can bring about major changes in air-flow parameters. Reproduction of these critical features by model studies has not yet been achieved.
Nasal Air-Flow Characteristics The mode of distribution of air flow through the nasal cavities and its flow characteristics are crucial to effective cleansing, warming, and moistening, and to recovery processes. During nasal breathing, ambient air streams converge as they are drawn into the nasal vestibule by inspiratory effort, and convergence promotes laminar flow through the narrow nasal valve (44). Spontaneous positioning of the labial orifice promotes a similar flow pattern during oral inspiration. If this laminar flow regime persisted through the upper airways where, in many segments, the midstream is several millimeters from the mucosa, an insulating marginal lamina and absence of mixing would impede exchanges of heat, water, and contaminants between air stream and mucosa. Under such conditions, the burden of preparing inspiratory air for gaseous exchanges in the alveoli would fall on bronchial passages of a small cross-section (2-mm diameter in the 4 th to 14 ~ subdivisions), where small dimensions and reduced air-flow velocity enable exchanges between air and mucosa to take place under laminar Clinical Reviews in Allergy and Immunology
Volume 16, 1998
48
Cole
flow conditions. The mucosa of these passages is less well adapted to withstanding hostile environmental exposures than mucosa of the upper air passages. Fortunately, the unfavorable scenario described above does not prevail during nasal or spontaneous oral breathing. Laminar flow cannot persist b e y o n d the nasal valve (or the labial orifice), except m o m e n t a r i l y near the beginning and end of each inspiration. As inspiratory air leaves the narrow valvular region and enters the much larger cross-section of the cavum, its linear velocity, which is as great as 18 m / s in resting subjects, decelerates to 3-4 m / s (43). Deceleration releases kinetic energy (E = kv2where E = energy, k is a constant, and v represents linear velocity), which is dissipated in the generation of inertial disturbances that disrupt the insulating marginal lamina and promote mixing in the air stream. The disturbances are entrained to the bronchi, and are enhanced en route by frictional forces and irregularities of both lumen and flow velocity (45). In addition to mass movement of air parallel with the walls of the respiratory passages, disturbances resulting from orifice flow and from frictional forces induce vigorous movement of air particles. As this movement increases with ventilation, the component of air particle velocities perpendicular to the airway walls increases also, and this component determines the effectiveness of exchanges between air stream and mucosa. Therefore, with increasing ventilation, increased disturbances compensate to some degree for decreased transit time through each airway segment, and nonlaminar flow approaches turbulence as disturbances are augmented by increased ventilation.
Respiratory Air Processing As noted above, effective exchanges between air and mucosa require a disturbed pattern of respiratory air flow. Effectiveness of the exchanges, which include heat, water, and soluble and insoluble ambient air contaminants in both gaseous and particulate form, is dependent on the degree of flow disturbance. Greater penetration of incompletely processed ambient air that accompanies increased ventilation is partially offset, as already described, by increased inertial disturbance, mixing, and mucosal contact. The nose is the principal site of particle deposition and absorption of soluble gaseous contaminants of i n s p i r a t o r y air. Particulates impinge (46) and are entrapped by surface mucus that is transported to the pharynx by ciliary action and swallowed. A portion of dissolved substances is absorbed into the tissues, and the remainder follows a similar route to that followed by insoluble particulates. Smaller particle size and lesser gaseous solubilities increase penetration of air contaminants. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
49
Nose and Paranasal Sinuses Table 2
Inspiratory Air Temperature (~ ~ Nasal b r e a t h i n g Tracheostomal breathing
Portal
Pharynx
Subglottis
Trachea
Carina
20 20
31
33
35 30
36 32
~Warming of inspiratory air ~n its passage to the lungs during resting breathing. Oral inspirations achieve the same temperature at subglottic level as nasal inspirations when lips and mandible are spontaneously positioned. Conditioning of tracheostomal inspirations extend more deeply into the smaller air passages. Respiratory air rapidly achieves and maintains full saturation at all temperatures throughout the air passages.
Cleansing of ambient air and heat and water exchanges are substantial in either nasal or oral breathing passages (45,47). Indeed, they are of similar extent when the mouth and labial orifice are spontaneously positioned, and they extend more deeply into the air passages during tracheostomal breathing (Table 2). However, neither nasal nor oral air conditioning is complete, and disturbed flow and processing continue in the large-diameter airways leading to the lungs. Thermal and aqueous equilibria are approached by the reduced velocity and close contact of the air stream with the enormous mucosal area of the smaller bronchi, and finally, inspiratory air mixes with the large volume of residual air that provides an additional buffer against incomplete conditioning (47). Temperature of the peripheral air passages and of pulmonary blood is unaffected even by great extremes of ambient air temperature (45,47), and thermal damage by these extremes is confined to the proximal airway mucosa. On expiration, orifice flow, resulting from narrowing of the glottis, ensures disturbed flow, and as a consequence, convective exchanges between air and cooled mucosa bring about partial recovery of heat and water. Recovery takes place mainly in the nasal cavities, where the temperature gradient between expired air and cooled mucosa is greater than elsewhere in the respiratory passages, and the recovery process is much less effective in oral expiration. Recovery of heat and water has survival value for many animal species in extreme habitats (45), but it is not of great physiological importance to humans except in severely demanding circumstances, such as vigorous physical activities of polar hunters or high-altitude climbers. Complex turbinate structures with relatively large mucosal surface areas are found in several animal species (1) living in both Arctic and hot desert conditions, and these features are related also to body surface insulation and to sweating (48). Well-insulated and nonsweating animals tend to exhibit relatively large turbinate mucosal areas. Turbinate mucosal area of the seal (Fig. 1) exceeds its skin surClinical Reviews in Allergy and Immunology
Volume 16, 1998
50
Cole
face area, that of the sheep is similarly extensive, and turbinate area of the domestic cat exceeds that of the human adult (1) (Figs. 2 and 3). As in the thermoregulatory regions of the skin of humans and animals (e.g., rabbits' ears), the vascular system of the nasal mucosa (26,27) is rich in arteriovenous shunts. These shunts and their blood flow are concerned with adjustment of skin and nasal mucosal temperature. In circumstances in which it is necessary to lose body heat, elevated blood flow elevates surface temperature. The increased temperature gradient between skin or mucosal surface and adjacent air increases heat (and water) loss. In circumstances in which heat (and water) needs to be retained, blood flow is appropriately decreased, resulting in decreased surface temperature and decreased heat loss. Thus, the nasal mucosa appropriately adjusts retention or release of heat (and water) in expiratory air as it leaves the body. In humans, recovery approximates 30% in temperate conditions, and it increases to about 50% in Arctic conditions. Losses are much greater during oral or tracheostomal breathing, and also by pyrexial patients whose respiratory water loss may assume clinically important proportions. Recovery percentages are increased or decreased to meet the need for loss or retention of heat, and the ranges of these proportions are greatly extended in animals whose body surface insulation and turbinate mucosal areas are greater than in humans and whose ability to lose heat by sweating is less (45,47). There is no evidence to support the suggestion that nasal mucosal blood flow adjusts to rapid changes in the temperature of inspired ambient air as might occur as a subject moves from warm indoors to cold outdoors or the reverse. These circumstances are accommodated by extension of inspiratory air conditioning more or less deeply toward the peripheral airways, where an immense reserve of mucosal area is available to meet incompletely satisfied heat and moisture demands (45).
Sinus Air Flow The paranasal sinuses do not play a significant role in processing respiratory air and, by comparison with the nasal cavities, air flow through them is inconsequential. Sinus ostia in the middle meatus are sheltered from direct exposure to contamination and injury by ambient air. Fluctuations of nasal respiratory air flow pressures at resting ventilation approximate <+100 Pa (+1.0 cm H20) and displace air through patent ostia with each breath. This minute volume is supplemented by diffusion and the pumping effect of pulse wave pressures (49,50). Greater pressures generated by increased ventilation, by nose blowing, and by vigorous sniffs against collapsed alae enhance exchanges of air between nasal and paranasal cavities, and also increase the risk of introducing noxious material. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose and Paranasal Sinuses
51
There is exchange also between the air content of a sinus and its surface fluid by movement of gas molecules along vapor pressure gradients (49,50). In the presence of obstructed ostia, gas diffusion can affect intrasinus pressures and result in a sensation of fullness, discomfort, or even pain. Benefits of "aeration" of a diseased sinus by surgical creation of an artificial or an enlarged ostium probably result from equilibration of pressures between nasal and paranasal cavities, and improved drainage rather than from increased flow of air. It is of interest to note, however, that despite the creation of an artificial opening into the nose, patterns of mucociliary flow persist within the maxillary sinus, and trails of red cells tracking toward the natural ostium can be seen on sinus endoscopy. Patency of the ostia is essential to the health of the paranasal sinuses, and the dangers of obstruction in the region of an ostium, e.g., by inflammatory disease of the nose or sinus, have been mentioned earlier in this article. Recent investigations have shown that in health, despite marked physiological congestion of the nasal mucosa, by lateral recumbent postures, sinus ostia remain patent. Experiments with an intubated antrum (Haight and Cole, 1992, unpublished) showed ostial resistance to air flow to increase as a subject assumed ipsilateral recumbency from an upright position, and the resistance was decreased by assumption of the contralateral posture (see also Posture and Pressure Effects, earlier in this article). However, recording of antral air pressures demonstrated that they reflected freely the respiratory pressures in the nose in all postures, i n d i c a t i n g that despite resistive mucosal changes, the maxillary ostium remained patent. It was undetermined whether the site of resistance changes was in the immediate ostial tissues or in adjacent tissues of the middle meatus.
Conclusions The Nasal and Paranasal Sinus Cavities A secretory mucosa and unobstructed mucociliary transport are essential to respiratory and olfactory functions of the nose, a n d to health of the nasal cavities and the paranasal sinuses. The ostiomeatal complex w i t h i n the n a r r o w cleft of the m i d d l e meatus is susceptible to obstructions of mucociliary flow from the sinuses. Mucosal swelling, polyps, and altered properties of secretion that result from comm o n nasal disorders can i m p a i r m u c o c i l i a r y clearance, a n d sinus disease is a c o m m o n consequence. I m a g i n g studies h a v e d e m o n strated that i n f l a m m a t o r y nasal disease is f r e q u e n t l y a c c o m p a n i e d by sinusitis, and the converse has been verified in a large proportion of cases. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
52
Cole
Nonlaminar characteristics of inspiratory air flow are induced by the constricted lumen of the nasal valve and entrained through the airways leading to the lungs. These characteristics are of essential physiological importance in that they promote cleansing and conditioning of ambient air, and thereby protect peripheral pulmonary air passages and their terminations from injury by ambient air. In addition, the human nose exhibits vestiges of a process of recovery of heat and water from expiratory air that is much more extensive and of survival value in animal species adapted to extreme environments. The paranasal sinuses do not make a significant contribution to the respiratory air processing that takes place in the nasal cavities.
References* 1. Negus VE. The comparative anatomy and physiology of the nose and paranasal sinuses. London: Livingstone, 1958. 2. Gwaltney JM Jr, Phillips D, Miller RD, Riker DK. Computed tomographic study of the common cold. N Engl J Med 1994;330:25-30. 3. Kimmelman CP. The problem of nasal obstruction. Otolaryngol Clin N Am 1989;22(2):253-264. 4. Cole P. The respiratory role of the upper airways. St. Louis, MO: Mosby-Year Book 1993; pp. 1-59. 5. Proetz AW. Air currents in the upper respiratory tract and their clinical importance. Ann Otol Rhinol Laryngol 1951;60:439-467. 6. McCaffrey TV. The nose and sinus mucosa and mucous. Curr Opinion Otolaryngol Head Neck Surg 1994;2:10-15. 7. Jorissen M, Cassiman J-J. Relevance of the ciliary ultrastructure in primary and secondary dyskinesia: a review. Am J Rhinol 1991;5(3):91-101. 8. Deitmer T, Scheffler R. The effects of different preparations of nasal decongestants on ciliary beat frequency in vitro. Rhinology 1993;31:151-153. 9. Stammberger H. Endoscopic endonasal surgery--concepts in treatment of recurring rhinosinusitis. Part 1. Anatomic and pathophysiolgic considerations. Otolaryngol Head Neck Surg 1986;94(2)143-147. 10. Messerklinger W. Diagnosis and endoscopic surgery of the nose and its adjoining structures. Acta Otolaryngol (Belg) 1980;34(2):170-176. 11. Cole P. The mouth and throat. In: The Respiratory Role of the Upper Airways. St. Louis, MO: Mosby-Year Book, 1993; pp. 61-90. 12. Cole P, Forsyth R, Haight JSJ. Respiratory resistance of the oral airway. Am Rev Respir Dis 1982;125:363-365. 13. Cole P. Assessment of the upper airways. In: The Respiratory Role of the Upper Airways. St. Louis, MO: Mosby-Year Book, 1993; pp. 125-158. 14. Rhinology 1995;33:10-13. 15. Kasperbauer JL, Kern EB. Nasal valve physiology implications in nasal surgery. Otolaryngol Clin N Am 1987;20(4):699-719. 16. Cole P, Haight JSJ, Cooper PW, Kassel EE. A computed tomographic study of nasal mucosa: effects of vasoactive substances. J Otolaryngol 1983;12(1):58. *Several references in this list have been chosen for their own extensive reference lists which may be useful for readers who wish to refer to original work on which this chapter is based. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
Nose a n d Paranasal Sinuses
53
17. Wustrow F. Schwellkorper am Septum nasi. Z Anat Entwicklung 1951; 116:139. 18. Cole P, Haight JSJ, Naito K, Kucharczyk W. Magnetic resonance imaging of the nasal airways. Am J Rhinol 1989;3(2):63. 19. Chaban R, Cole P, Naito K. Simulated septal deviations. Arch Otolaryngol Head Neck Surg 1988;114:413. 20. Cole P, Chaban R, Naito K, Oprysk D. The obstructive nasal septum: effect of simulated deviations on nasal airflow resistance. Arch Otolaryngol Head Neck Surg 1988;114:410. 21. Mertz JS, McCaffrey TV, Kern EB. Objective evaluation of anterior septal surgical reconstruction. Otolaryngol Head Neck Surg 1984;92(3):308-311. 22. Briant TDR. Management of severe septal deformities. J Otolaryngo11985;14(2): 120-124. 23. Sulsenti G, Palma P. The nasal valve area: structure, function, clinics and treatment. Acta Otolaryngol Ital 1989;(Suppl 22):3-25. 24. Adamson P, Smith O, Cole P. The effect of cosmetic rhinoplasty on nasal patency. Laryngoscope 1990;100:357-359. 25. Batson OV. The venous networks of the nasal mucosa. Ann Otol Rhinol Laryngol 1954;63(3):571-580. 26. Cauna N. Blood and nerve supply of the nasal lining. In: Proctor DF, Andersen IB, eds., The Nose: Upper Airway Physiology and the Atmospheric Environment. Amsterdam: Elsevier Biomedical, 1982; pp. 45-69. 27. Bende M. The physiologic importance of the nasal mucosal vascular bed: a review. Am J Rhinol 1990;5:189-191. 28. Rundcrantz H. Postural variations of nasal patency. Acta Otolaryngol (Stockh) 1969;68:435-443. 29. Hasegawa M, Saito Y. Postural variations in nasal resistance and symptomatology in allergic rhinitis. Acta Otolaryngol 1979;88:268-272. 30. Erjefalt I, Persson CGA. Inflammatory passage of plasma macromolecules into airway wall and lumen. Pulmon Pharmacol 1989;2(2):93-102. 31. Cole P, Haight JSJ. Posture and the nasal cycle. Ann Otol Rhinol Laryngol 1986;95:233. 32. Stocksted P. Rhinometric measurements for determination of the nasal cycle. Acta Otolaryngol (Stockh) 1953;(Suppl 109):159-175. 33. Arbour P, Kern EB. Paradoxical nasal obstruction. Can J Otolaryngo11975;4(2):333-338. 34. Ogura JH, Stocksted P. Rhinomanometry in some rhinologic diseases. Laryngoscope 1958;68:2001-2014. 35. Singh B, Chhina GA. Some reflections on ancient Indian physiology. In: Keswani NH, Manchandra SK, eds., The Science of Medicine and Physiological Concepts in Ancient and Mediaeval India. 264 International Congress of Physiological Sciences, New Delhi, 1974. 36. Shannahoff-Khalsa D. Lateralized rhythms of the central and autonomic nervous systems. Intern J Psychophysiol 1991;11(3):225-251. 37. Kayser R. Die exacta Messung der Luftdurchgangigkeit der Nase. Arch Laryngol Rhinol 1895;3:101-120. 38. Principato JJ, Ozenberger JM. Cyclical changes in nasal resistance. Arch Otolaryngol 1970;91:71-77. 39. Haight JSJ, Cole P. Unilateral nasal resistance and asymmetrical body pressures. J Otolaryngol 1986;Suppl 16:1-31. 40. Rothe CF. Reflex control of veins and vascular capacitance. Physiol Rev 1983;63(4):1281-1342. 41. Hudgel DW, Robertson DW. Nasal resistance during wakefulness and sleep in normal man. Acta Otolaryngol (Stockh) 1984;98:130-135. Clinical Reviews in Allergy and Immunology
Volume 16, 1998
54
Cole
42. Brown EA. Measurement of resistance of the nasal passages 1-3. Rev Allerg 1967;21:472-857. 43. Swift DL, Proctor DF. Access of air to the respiratory tract. In: Brain D, Proctor DF, Reid LM, eds., Respiratory Defense Mechanisms. New York: Marcel Dekker, 1977; pp. 63-93. 44. Swift DL. Physical principles of airflow and transport phenomena influencing air modification. In: Proctor DF, Andersen I, eds., The Nose: Upper Airway Physiology and the Atmospheric Environment. Amsterdam: Elsevier Biomedical, 1982;337-348. 45. Cole P. Cleansing and conditioning. In: The Respiratory Role of the Upper Airways. St. Louis, MO: Mosby-Year Book, 1993; pp. 91-123. 46. Leopold DA. Pollution: The nose and sinuses. Otolaryngol Head Neck Surg 1992;106:713-719. 47. Cole P. Modification of inspired air. In: Mathew OP, Sant'Ambrogio G, eds., Respiratory Function of the Upper Airway. New York: Marcel Dekker, 1988. 48. Scott JH. Heat regulating function of the nasal mucous membrane. J Laryngol 1953;87:461,462. 49. Aust R, Falck B, Svanholm H. The intrinsic functions of the paranasal sinuses in health and inflammation. Rhinology 1984;22:105-107. 50. Drettner B. The maxillary ostium in sinusitis. Eye, Ear, Nose, Throat Monthly 1966;45:66-70.
Clinical Reviews in Allergy and Immunology
Volume 16, 1998