Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4473_Библиотеки_им_академика_М_И_Перельмана
.pdf
24 Pathophysiology ofObstructive Sleep Apnea
https://t.me/medicina_free
303
upper airway patency during sleep. OSA develops in the presence of both elevated mechanical
loads on the upper airway and defects in compensatory neuromuscular responses.
A sleep history and physical examination is
important in identication of patients and appropriate referral for polysomnography.
Understanding nuances in the spectrum of presenting complaints and polysomnography correlates are important for diagnostic and therapeutic
approaches. Knowledge of common patterns of
OSA may help identify patients and guide
therapy.
Although obesity is a major risk factor for
OSA, roughly 30% of patients with OSA are not
obese, emphasizing the need for a high index of
suspicion in clinical practice. Further, the prevalence of OSA is 2–3 times greater in men than in
women and in older compared to middle-aged
individuals. Menopause is a well-established risk
factor for OSA in women. OSA can yield major
neurocognitive manifestations, including excessive daytime sleepiness/fatigue, impaired cognition, reduced quality of life, and an up to
sevenfold increased risk of road trafc accidents.
Treatment of OSA leads to improvements in
many of these outcome measures. There is evolving evidence to support the role of OSA as an
independent risk factor for adverse cardiovascular sequelae. Although some argue that OSA was
simply a marker of an unt patient group, rigorous recent studies have shown that OSA is causally linked to a number of important sequelae.
OSA is now a well-established risk factor for
hypertension (both incident and prevalent), stroke
and probably myocardial infarction, congestive
heart failure, and death. OSA has been causally
linked to the development of hypertension based
on large rigorous cross-sectional and longitudinal
epidemiological studies, mechanistic animal
studies, and most recently interventional trials
[56]. The underlying causes of OSA vary considerably between aficted individuals. Important
components likely include pharyngeal anatomy,
pharyngeal dilator muscle responsiveness to
respiratory challenges during sleep, the arousal
threshold, and the instability of the negative feedback control system regulating ventilation (loop
gain).
The pathophysiology of OSA is complex and
incompletely understood. A narrowed upper airway is very common among OSA patients, and is
usually in adults due to nonspecic factors such
as fat deposition in the neck, or abnormal bony
morphology of the upper airway. Functional
impairment of the upper airway dilating muscles
is particularly important in the development of
OSA, and patients have a reduction both in tonic
and phasic contraction of these muscles during
sleep when compared to normals. A variety of
defective respiratory control mechanisms are
found in OSA, including impaired chemical
drive, defective inspiratory load responses, and
abnormal upper airway protective reexes. These
defects may play an important role in the abnormal upper airway muscle responses found among
patients with OSA.Local upper airway reexes
mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect.
A better understanding of the integrated
pathophysiology of OSA should help in the
proper management of this important multi-facet
disorder and the development of new therapeutic
techniques.
References
1. Hesiod, Cadwell RS.Hesiod’s Thegony. Newburyport:
Focus Classical Library; 1987. p.52.
2. Rechtschaffen A.The single mindedness and isolation
of dreams. Sleep. 1978;1:97–109.
3. Lavie P. Restless nights: understanding snoring and
sleep Apnea. New Haven, CT: Yale Univercity Press;
2003.
4. Gastaut H, Tassinari CA, Duron B. Polygraphic
study of the episodic diurnal and nocturnal (hypnic
and respiratory) manifestations of the Pickwick syndrome. Brain Res. 1967;1:167–86.
5. Guilleminault C, Eldridge FL, Dement WC.Insomnia
with sleep apnea: a new syndrome. Science.
1973;181:856–8.
6. Benjaeld AV, Ayas NT, Eastwood PR, Heinzer R, Ip
MSM, etal. Estimation of the global prevalence and
burden of obstructive sleep apnoea: a literature-based
analysis. Lancet Respir Med. 2019;7(8):687–98.
7. Pham LV, Schwartz AR.The pathogenesis of obstructive sleep apnea. J Thorac Dis. 2015;7:1348–72.
8. Hou H, Zhao Y, Yu W, Dong H, Xue X, Ding J, etal.
Association of obstructive sleep apnea with hypertension: a systematic review and meta-analysis. J Glob
Health. 2018;8:010405.
304
https://t.me/medicina_free
K. Gunhan
9. Sateia MJ. International classication of sleep
disorders- third edition: highlights and modications.
Chest. 2014;146(5):1387–94.
10. Olaithe M, Bucks RS, Hillman DR, Eastwood
PR. Cognitive decits in obstructive sleep apnea:
insights form a meta-review and comparison with deficits observed in COPD, İnsomnia, and sleep deprivation. Sleep Med Rev. 2018;38:39–49.
11. Eckert DJ.Phenotypic approaches to obstructive sleep
apnoea—new pathways for targeted therapy. Sleep
Med Rev. 2018;37:45–59.
12. Orem J, Lovering AT, Dunin-Barkowski W, Vidruk
EH.Tonic activity in the respiratory system in wakefulness. Sleep. 2002;25:488–96.
13. Venner A, Todd WD, Fraigne J, Bowrey H, EbanRothschild A, etal. Newly identied sleep-wake and
circadian circuits as potential therapeutic targets.
Sleep. 2019;42:1–14.
14. Eckert DJ, Jordan AS, Merchia P. Central sleep
apnea: pathophysiology and treatment. Chest.
2007;131:595–607.
15. Tepedino M, Illuzzi G, Laurenziello M, Perillo
L, Taurino AM, et al. Craniofacial morphology
in patients with obstructive sleep apnea: cephalometric evaluation. Braz J Otorhinolaryngol.
2020;18:921–9.
16. Bassiouny A, Nasr S, Mashaly M, Ayad E, Qotb M,
etal. Electron microscopy study of peripheral nerves
in the uvulae of snorers and obstructive sleep apnoea
patients. J Laryngol Otol. 2009;123:203–7.
17. Baudouin R, Blumen M, Chaufton C, Chabolle
F. Adult sleep apnea and tonsil hypertrophy: should
pharyngoplasty be associated with tonsillectomy?
Sleep Breath. 2019;23:917–23.
18. Schwab RJ, Kuna ST, Remmers JE. Anatomy and
physiology of upper airway obstruction. In: Kryger
MH, Roth J, Dement WC, editors. Principles and practice of sleep medicine. Philadelphia, PA: Saunders;
2005.
19. Lu D, Tan L, Wu Y, Cao C, Deng Z.Leptin and leptin
receptor gene polymorphisms in obstructive sleep
apnea: a HuGE review and meta-analysis. Sleep
Breath. 2015;19:1073–8.
20. Flores-Mir C, Korayem M, Heo G, Withmans M,
Major MP, etal. Craniofacial morphological characteristics in children with obstructive sleep apnea syndrome: a systematic review and meta-analysis. J Am
Dent Assoc. 2013;144:269–77.
21. Ruehland WR, Rochford PD, Pierce RJ, Rhinder J,
Jordan AS, etal. Genioglossus muscle responses to
resistive loads in severe OSA patients and healthy
control subjects. J Appl Physiol. 2019;127:1586–98.
22. Cammaroto G, Stringa LM, Iannella G, Meccariello
G, Zhang H, etal. Manipulation of lateral pharyngeal
wall muscles in sleep surgery: a review of the literature. Int J Environ Res Public Health. 2020;17:5315.
23. Brennick MJ, Pack AI, Ko K, Kim E, Pickup S, etal.
Altered upper airway and soft tissue structures in the
New Zealand obese mouse. Am J Respir Crit Care
Med. 2009;179:158–69.
24. Winck AD, Heinzmann-Filho JP, Soares RB, da Silva
JS, Woszezenki CT, etal. Effects of obesity on lung
volume and capacity in children and adolescents: a
systematic review. Rev Paul Pediatr. 2016;34:510–7.
25. Kirkness JP, Madronio M, Stavrinou R, Wheatley JR,
Amis TC.Surface tension of upper airway mucosal
lining liquid in obstructive sleep apnea/hypopnea syndrome. Sleep. 2005;28:457–63.
26. Berry RB, Randall M.Abnormal upper airway sensation in OSA– cause or effect? Sleep. 2005;28:542–4.
27. Turnbull CD, Wang SH, Manuel AR, Keenan BT,
McIntyre AG, eta al. Relationships between MRI fat
distributions and sleep apnea and obesity hypoventilation syndrome in very obese patients. Sleep Breath.
2018;22:673–81.
28. Schwartz AR, Patil SP, Laffan AM, Polotsky V,
Schneider H, Smith PL. Obesity and obstructive
sleep apnea: pathogenic mechanisms and therapeutic
approaches. Proc Am Thorac Soc. 2008;5:185–92.
29. Caballero-Eraso C, Shin MK, Pho H, Kim LJ, Pichard
LE, etal. Leptin acts in the carotid bodies to increase
minute ventilation during wakefulness and sleep and
augment the hypoxic ventilatory response. J Physiol.
2019;597:151–72.
30. Carberry JC, Jordan AS, White DP, Wellman A,
Eckert DJ. Upper airway collapsibility (Pcrit) and
pharyngeal dilator muscle activity are sleep stage
dependent. Sleep. 2016;39:511–21.
31. Matsuda M, Ogawa T, Sitalaksmi RM, Miyashita M,
Ito T, et al. Effect of mandibular position achieved
using an oral appliance on genioglossus activity in healthy adults during sleep. Head Face Med.
2019;15:26–33.
32. Chen KS, Zu M, Zhang Z, Chang WC, Gaj T, etal. A
hypothalamic switch for REM and non-REM sleep.
Neuron. 2018;97:1168–76.
33. Trinder J, Jordan AS, Nicholas CL.Discharge properties of upper airway motor units during wakefulness
and sleep. Prog Brain Res. 2014;212:59–75.
34. Gold AR, Marcus CL, Dipalo F, etal. Upper airway
collapsibility during sleep in upper airway resistance
syndrome. Chest. 2002;121:1531–40.
35. Perri RA, Kairaitis K, Cistulli P, Wheatley JR, Amis
TC.Surface cephalometric and anthropometric variables is OSA patients: statistical models for the OSA
phenotype. Sleep Breath. 2014;18:39–52.
36. Perri RA, Kairaitis K, Wheatley JR, Amis
TC. Anthropometric and craniofacial sexual dimorphism in obstructive sleep apnea patient: is there
male-female phenotypical convergence? J Sleep Res.
2015;24:82–91.
37. Walsh JH, Leigh MS, Paduch A, Maddison KJ,
Philippe DL, et al. Evaluation of pharyngeal shape
and size using anatomical optical coherence tomography in individuals with and without obstructive sleep
apnoea. J Sleep Res. 2008;17:230–8.
38. Tanizawa L, Chin K. Genetic factors in sleepdisordered breathing. Respir Investig. 2018;56:111–9.
39. Fogel RB, Trinder J, White DP. The effect of sleep
onset on upper airway muscle activity in patients
24 Pathophysiology ofObstructive Sleep Apnea
https://t.me/medicina_free
305
with sleep apnoea versus controls. J Physiol.
2005;564:549–62.
40. Tom C, Roy B, Vig R, Kang DW, Aysola RS, et al.
Correlations between waist and neck circumferences
and obstructive sleep apnea characteristics. Sleep
Vigil. 2018;2:111–8.
41. Nieman GF, Satalin J, Kollisch-Singule M, Andrews
P, Aiash H, et al. Physiology in medicine: understanding dynamic alveolar physiology to minimize
ventilator-induced lung injury. J Appl Physiol.
2017;122:1516–22.
42. Heinzer RC, Stanchina ML, Malhotra A. Effect of
increased lung volume on sleep disordered breathing
in sleep apnoea patients. Thorax. 2006;61:435–9.
43. Heinzer RC, Stanchina ML, Malhotra A. Lung volume and continuous positive airway pressure requirements in obstructive sleep apnea. Am J Respir Crit
Care Med. 2005;172:114–7.
44. Patil SP, Schneider H, Marx JJ. Neuromechanical
control of upper airway patency during sleep. J Appl
Physiol. 2007;102:547–56.
45. Remmers JE, deGroot WJ, Sauerland
EK. Pathogenesis of upper airway occlusion during
sleep. J Appl Physiol Respir Environ Exerc Physiol.
1978;44:931–8.
46. Zhao D, Li Y, Xian J, Qu Y, Zhang J, et al.
Relationship of genioglossus muscle activation and
severity of obstructive sleep apnea and hypopnea
syndrome among Chinese patients. Acta Otolaryngol.
2016;136:819–25.
47. Kubin L.Neural control of the upper airway: respiratory and state-dependent mechanisms. Compr
Physiol. 2016;15:1801–50.
48. Ehsan Z, Mahmoud M, Shott SR, Amin RS, Ishman
SL. The effects of anesthesia and opioids on the
upper airway: a systematic review. Laryngoscope.
2016;126:270–84.
49. Faizal WM, Ghazali NNN, Khor CY, Badruddin IA,
Zainon MZ, et al. Computational uid dynamics
modeling of human upper airway: a review. Comput
Methods Programs Biomed. 2020;296:105627.
50. Pal T, Dutta PK, Maka S. Modulation-demodulation
hypothesis of periodic breathing in human respiration.
Respir Physiol Neurobiol. 2018;252:28–37.
51. Orr JE, Malnotra A, Sands SA. Pathogenesis of
central and complex sleep apnoea. Respirology.
2017;22:43–52.
52. Wellman A, Jordan AS, Malhotra A.Ventilatory control and airway anatomy in obstructive sleep apnea.
Am J Respir Crit Care Med. 2004;170:1225–32.
53. Ceratl V, Silva H, Carvalho C, Costa-Pereira A,
Azevedo I, et al. Model for prediction of pediatric OSA: proposal for a clinical decision rule.
Laryngoscope. 2015;12:2823–7.
54. Younes M. Contributions of upper airway mechanics and control mechanisms to severity of obstructive
apnea. Am J Respir Crit Care Med. 2003;168:645–58.
55. Lin H, Wang C, Zhang H, Ziong H, Li Z, et al.
Threshold of the upper airway cross-section for
hypopnea onset during sleep and its identication
under waking condition. Respir Res. 2019;20:280–9.
56. Morgan TD, Remmers JE. Phylogeny and animal
models: an uninhibited survey. In: Kushida CA, editor. Obstructive Sleep Apnea. New York: Informa
Healthcare; 2007.
Rhinomanometry
https://t.me/medicina_free
ZeynepOnerciAltunay
25
Core Messages
• Rhinomanometry allows objective assessment
of nasal resistance, the ratio of transnasal
pressure over transnasal airow measured
during nasal respiration.
• Many aspects of the study of nasal physiology have been studied with the aid of
rhinomanometry.
• Rhinomanometry assesses the overall effect of
nasal airway dimension and shape on the passage of air through the nose.
25.1 Introduction
Rhinomanometry is the simultaneous measurement of airow through the nose and pressure
across the nose during breathing. Figure 25.1
shows plots of transnasal pressure and ow during respiration. As the patient inspires, the curves
go downward showing a decrease in pressure and
the corresponding movement of air in the direction of the lungs. As the patient changes to expiration, the curves move upward, corresponding to
pressure increasing and causing the movement of
air out of the nose. Dividing the maximum pressure reached during normal inspiration by the
highest ow gives a nasal resistance value that
correlates with the symptom of nasal obstruction
in symptomatic patients. This objective test has
been crucial in increasing understanding in many
areas of nasal physiology. While the extent of its
use varies in different parts of the world, it is still
used in research and in clinical assessment of
nasal function.
Resistance calculated at the maximum pressure
and ow correlates with the symptom of nasal
obstruction.
This chapter will provide a framework to put
the role of rhinomanometry in context among the
other tools used to objectively assess nasal function. The methods of rhinomanometry will be
described. The research role that rhinomanometry has played in discoveries in nasal physiology
will be covered, including the nasal cycle,
changes with growth, posture, and exercise;
changes to the downside of the nose when a
patient is lying down; and resistance in the normal nose and the nose with disturbed breathing
function. The chapter ends with a summary of the
clinical applications for which rhinomanometry
has been used.
Z. O. Altunay (*)
Department of Otorhinolaryngology, Head and Neck
Surgery, University of Health Sciences Haseki
Training and Research Hospital, İstanbul, Turkey
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
Ö. Ö. Celebi, T. M. Önerci (eds.), Nasal Physiology and Pathophysiology of Nasal Disorders,
https://doi.org/10.1007/978-3-031-12386-3_25
307
308
Expiration
PressureFlow
https://t.me/medicina_free
Fig. 25.1 The plot of
pressure and ow during
respiration. As the
patient inspires, the
curves go downward
showing a decrease in
pressure and the
corresponding
movement of air in the
direction of the lungs.
As the patient changes
to expiration, the curves
move upward
corresponding to
pressure increasing and
the movement of air out
of the nose
∆P
Z. O. Altunay
Inspiration
Expiration
•
V
Inspiration
CMAYO
2012
25.2 The Context
ofRhinomanometry
inAssessing Nasal
Respiratory Function
25.2.1 What Are theFunctions
Associated withNasal
Respiration?
mizes the above functions. Rhinomanometry
assesses the overall effect of nasal airway dimension and shape on the passage of air through the
nose.
Comfortable nasal breathing corresponds with a
dimension and shape of the nasal airway that in
general optimizes the multiple functions of the
nose.
The movement of the diaphragm and lungs
results in the movement of air through the nose.
The passage of air through the nose is benecial
for the lungs because of the warming, humidi-
25.2.2 What Anatomic Elements are
Encountered During Nasal
Respiration?
cation, and protective functions of the nose. The
mucous layer in the nose can trap particulates,
allowing the cilia to sweep them away. In addition, elements of the immune system are able to
have contact with antigens, stimulating protective responses. Furthermore, air is delivered to
the olfactory area providing the enhancement of
taste and the protective function of detecting
potentially harmful substances or organisms. The
measurement of some of the important physiologic components of nasal respiration, warming,
humidication, mucociliary clearance, and olfaction is covered in other chapters in this book as
noted above.
As air passes through the nose, comfortable
nasal breathing corresponds with a dimension
and shape of the nasal airway that in general opti-
Measurement of the nasal airway assesses the
nasal airstream which may be variably affected
by the physical dimension of the components of
the nasal airway, including the vestibule, valve
area, turbinates, and sinus openings. The presentation of these anatomic elements as air is
inspired through the nose is different than the
shape of the presenting surfaces as air is expired.
This may reect different functions of the two
phases.
The rst part of inspiration is the passage of
air through the vestibule in a curve rst superiorly and then toward the nasal valve area. The
airstream then passes through a narrower area
referred to as the internal valve. This corresponds
to the area under the caudal end of the upper lat-
25 Rhinomanometry
https://t.me/medicina_free
309
Fig. 25.2 Volume rendering of the nasal airway. Using
3D image analysis software and CT scans, the nasal airway is portrayed. This gives the same image early anato-
eral cartilages and is clearly seen on casts or volume renderings of the nasal airway (Fig.25.2).
As the airstream leaves the valve area, it is dispersed in a wider distribution, thus providing
contact with more surface area of the turbinates
than if the airstream had passed unimpeded. The
turbinates provide the working surface of the
nose. By having protuberant curved surfaces,
they act as anges in the airstream providing
increased surface areas on which to contact the
air for humidication, warming, and ltering.
The air then passes on to the choana and turns
again, this time in the direction of the larynx and
tracheobronchial tree.
As the inspired airstream passes the uncinate,
the natural os of the maxillary sinus is protected
from exposure to the passing airstream. Openings
from the frontal sinus, anterior ethmoid cells, and
posterior ethmoid cells are similarly sheltered by
presenting bafes though maxillary sinus accessory openings and postsurgical openings can present additional openings to the inspired air.
Computational uid dynamics (CFD) studies have
suggested only minimal, if any, effect of single
maxillary sinus openings on the respiratory airstream in a typical (unoperated) nose, whereas the
presence of an accessory os can result in some airow into the maxillary sinus [1, 2].
mists accomplished with wax castings. Note the narrow
part of the airway at the valve area
When considering any possible impact of the
nasal passage during expiration, retention of heat
is usually mentioned. This may be facilitated by
having the air pass over the turbinates before
encountering the restriction of the valve area. The
bafes that sheltered the ostia in the inspiratory
direction now may function to catch the expired
air. Some associate this phenomenon with nitric
oxide from the maxillary sinus serving a regulatory function in respiration. Computational uid
dynamics (CFD; see below) in 3D models showed
an increase in maxillary sinus airow rate with
high expiratory ow rates simulating nose blowing [2].
As the airstream leaves the valve area, it is dis-
persed in a broader distribution, thus providing
contact with more surface area of the turbinates
than if the airstream had passed unimpeded.
25.2.3 Objective Measurement
ofNasal Respiratory Function
Of the various anatomic elements present, measurements of the airstream are primarily inuenced
by the dimension of the valve and turbinates, by the
relative thickness of the mucosal lining, and, at
times, by the respiratory effort of the patient.
310
https://t.me/medicina_free
Z. O. Altunay
The objective methods of assessing the nasal
respiratory passages include (a) measurement of
the dimension of the airway, (b) measurement of
the nasal airow alone, and (c) rhinomanometry,
the simultaneous measurement of the transnasal
pressure and airow.
25.2.3.1 Measurement
oftheDimension
oftheAirway
The assessments of the dimensions of the nasal
airway are not measurements of the airow
through the nose during respiration. Imaging
with CT or MRI and then doing a 3D reconstruction of the airway will demonstrate the airway dimensions in different parts of the nose.
This can be helpful especially when used in
conjunction with computational uid dynamics
(CFD).
Acoustic rhinometry also measures the airway
dimension by calculations done on sound waves
reected back by intranasal structures. While this
is not an assessment of the ow of air through the
nose, it can be useful for measuring relative airway dimensions as well as changes with time,
treatment, or various interventions [3].
Computational uid dynamics (CFD) uses
imaging, typically a CT scan done at one point
in time, to generate a 3D model of the airway
and then apply uid dynamic modeling to that
airway [4]. By using different transnasal pressures representing a respiratory cycle, the software can calculate the relative ow velocity in
a number of anatomic sites in the nasal airway
for various points in time during respiration.
This capability offers exciting possibilities for
the future study of the impact of various anatomic variations or pathology on the airstream.
Those studying nasal physiology will be faced
with the task of nding the meaning of the
plethora of different ow vectors that result
from CFD analysis of the nasal airway. To identify the meaningful parameters derived from
the large amount of data is a tantalizing possibility for future study that will be facilitated by
ever increasing computer processing speed and
data handling.
25.2.3.2 Measurement oftheNasal
Airow Alone (Peak Flow
Measurement)
Measuring only nasal airow is popular especially with physicians who already use similar
equipment to monitor their asthmatic patients by
measuring peak lower airway ows. While this
has the limitations of some dependence on patient
effort, it has been relatively popular because of its
simplicity and the ready availability of the equipment [5]. It has been demonstrated that physicians would like to have a simple tool for
objective assessment of results in allergic rhinitis
[6]. Since the rate of ow changes throughout the
respiratory cycle, taking the measurement at
some constant point can help decrease the variability of results and provide a standard for comparison. In this case, the “constant” point is the
“peak” airow reached with maximal effort. Peak
nasal inspiratory ow can be measured by modifying the peak ow device for nasal inspiration.
The measurements can be affected by valve collapse occurring at higher airows that may not
occur at normal physiologic ows [7].
Nonetheless, this method has been popular, and
normative values have been collected [8–11].
Both peak nasal inspiratory ow (PNIF) and
peak nasal expiratory ow (PNEF) measurements have been used. There is some debate
about the variability of results [12, 13], but the
tests have been shown to be useful, particularly
for challenge testing in patients with allergic rhinitis [14].
25.2.3.3 Rhinomanometry:
TheSimultaneous
Measurement
oftheTransnasal Pressure
andAirow
Collecting simultaneous pressure and ow values allows the calculation of nasal resistance or
conductance. Calculation of the ratio of pressure to ow could be done at any one of many
simultaneous pressure-ow values along the
continuously changing curve during respiration
(Fig. 25.3). Using a specic airow value at
which to measure the pressure-ow values is an
25 Rhinomanometry
https://t.me/medicina_free
311
Fig. 25.3 The plot of pressure versus ow. Each point
represents the simultaneous measurement of pressure and
the corresponding ow value. Pressure values are on the
x-axis and ow values on the y-axis. The sigmoid shape of
the curve shows that in general there is a gradual increase
in the pressure to ow ratio as one goes further out the
curve toward the maximum values reached in normal respiration. Thus, for a given patient, the resistance value
reported can vary depending on the point on the curve that
is selected for calculating the result
important element allowing consistent comparisons. Viewing the entire sigmoid pressure-ow
curve also allows the observation of the position
and amount of curvature that reects the amount
of ow the patient is generating for the range of
pressures occurring in the course of their nasal
breathing. Rhinomanometry is used (except in
rare studies) to assess the pressure and ow
across the entire nasal airway, from nasal
entrance to nasopharynx.
The use of CFD analyses done from CT
images inspires thoughts of using microsensors
to unobtrusively detect the pressure and ow
changes during respiration for multiple sites in
the nasal airway. Just as Lindemann [15] had
actual measurements using tiny thermocouples to
validate the corresponding CFD calculations they
did for temperature at many sites in the nose,
multiple localized pressure and ow measurements could verify the results of CFD analyses
that yield multiple differing ow vectors at different anatomic sites in the nasal airway. Such
Fig. 25.4 The sigmoid pressure-ow curves for two different patients. The curve that is closer to the x-axis (pressure) represents the more obstructed nasal airway with
higher resistance values
validation of CFD, if combined with actual pressure measurements for a given patient, could
move it out of the category of assessing airway
dimensions to the category of yielding measured
information about nasal airow.
The plot of pressure and ow during inspiration
and expiration yields a sigmoid curve that is closer
to the x-axis (pressure axis) when nasal obstruction
is greater.
25.2.4 Rhinomanometry
forMeasurement ofNasal
Respiratory Function
As noted in the introduction, when rhinomanometry is performed, continuous measurement of
transnasal pressure shows a rising and falling
curve in the positive and then negative direction
throughout each respiratory cycle (Fig.25.1). As
the changing pressure drives an accelerating and
then decelerating ow of air, a plot of airow
shows a similar positive and negative excursion.
Plotting pressure (x-axis) versus ow (y-axis)
during inspiration and expiration yields a sigmoid curve that is closer to the x-axis when
obstruction is greater (Figs.25.3 and 25.4). Vogt
312
PressureFlow
•
Insp
https://t.me/medicina_free
Z. O. Altunay
C
∆P
Insp
A
B
CMAYO
2012
Exp
Insp
•
V
Fig. 25.5 The path of the pressure-ow curve away from
the origin during inspiration (the accelerating limb, A)
does not follow the same curve on the path back to the
D
Exp
pointed out that the path of the pressure-ow
curve away from the origin during inspiration
(the accelerating limb) often does not follow the
exact same curve on the path back to the origin
(decelerating phase). The same is true for the
expiratory limb (Fig.25.5).
V
n
o
i
t
a
r
e
l
e
C
c
c
A
Exp
origin (decelerating phase, B). The same is true for the
expiratory limb (C, D)
n
o
i
t
D
a
r
e
l
e
c
e
D
ration would cause an error in unilateral pressure
assessment. Anterior rhinomanometry thus is not
used in patients with nasal septal perforations.
Since the total airway is not measured when the
anterior method is used, it is necessary to derive
the total airway values by adding the right and
n
o
i
t
a
r
e
l
A
e
c
c
A
n
o
i
t
B
a
r
e
l
e
c
e
D
∆P
left ow values for each corresponding pressure
value along the pressure-ow curve (Fig.25.6).
25.3 How Is theMeasurement
Done
withRhinomanometry?
25.3.2 Transnasal Flow
Measurement: Anterior or
25.3.1 Dierent Techniques: Most
Posterior Method
Common Method
Flow through the nasal airway is most commonly
The most commonly employed method of doing
rhinomanometry is called anterior masked rhinomanometry. The different methods of rhinomanometry are distinguished by the location of
the pressure detection and the apparatus for ow
measurement. Table25.1 lists the different types
(methods) of rhinomanometry and the methods
of pressure and ow detection that dene them.
For measurement of the nasal airway of a
measured by attaching a owmeter at the outlet
of the mask which is sealed tightly on the patient’s
face. The usual owmeter consists of pressure
detection on either side of a resistive element.
Originally nozzles were used to measure the ow
through each nostril. When using a mask (or
body plethysmograph), unilateral measurements
can be done by occluding the opposite nostril
with tape.
patient with a nasal septal perforation, only the
total airway is measured because the septal perfo-
Since the total airway is not measured when the
anterior method is used, it is necessary to derive
25 Rhinomanometry
https://t.me/medicina_free
Table 25.1 The different types of rhinomanometry
Type of
rhinomanometry Flow detection Pressure detection
Anterior masked with
full face mask
Anterior masked with
partial face mask
Anterior with nozzle Device connected to
Posterior with full face
mask
Posterior with partial
face mask
Body plethysmograph Movement of chest inside
Anterior masked rhinomanometry is the type most commonly employed
Device on outlet of full
face mask
Device on outlet of partial
face mask
nozzle held to nostril
opening
Device on outlet of full
face mask
Device on outlet of partial
face mask
body plethysmograph
Catheter with sealed connection to
non-measured nostril
Catheter with sealed connection to
non-measured nostril
Nozzle held to non-measured nostril Unilateral
Catheter by nasopharynx—either transoral
or transnasal
Catheter by nasopharynx—either transoral
or transnasal
Posterior catheter by nasopharynx—either
transoral or transnasal or anterior catheter
to non-measured nostril
patient is wearing a mask by measuring the pressure inside the mask. Measurement in the nasopharynx can be done in several ways. As shown
in Table 25.1, in anterior rhinomanometry, the
nasopharyngeal pressure is detected using a tube
sealed over the opposite nostril, turning the
unmeasured nasal passage into an extension of
the tube (Fig.25.7). In posterior rhinomanometry, the nasopharyngeal pressure is measured by a
catheter that is held in the back of the oropharynx
with the lips sealed or by a tube passed to the
nasopharynx along the oor of the nose
(Fig.25.8). The rst of these methods can take
Fig. 25.6 For a given pressure value, the total ow is
equal to the right-sided ow plus the left-sided ow, both
measured at that pressure value. Flows are only additive if
measured at the same pressure. This is analogous to two
electrical currents being additive at the same voltages
the total airway values by adding the right and left
ow values for each corresponding pressure value
along the pressure-ow curve (Fig.25.6).
extra time to learn for some patients.
It is also possible to measure a segment of
transnasal pressure using a double catheter with
the two openings on each side of the segment to
be measured or by passing a catheter only partially along the oor of the nose. This methodology has only been employed in research but
could potentially assess resistance at particular
areas of the anatomic dimension of the airway,
e.g., at a site suspected to be causing the symp-
25.3.3 Transnasal Pressure
Measurement forPosterior
Rhinomanometry
tom of nasal obstruction. This calculation uses
the approximation of assuming a constant ow
along the length of the nasal airway. Haight and
Cole passed a catheter progressively further
Measurement of transnasal pressure requires
pressure detection in two sites, outside the nose
and in the nasopharynx. Measurement of pressure outside the nose is easily done when the
along the nasal airway while measuring the pres-
sure at its tip and found that the greatest change
in pressure and resistance occurred at the nasal
valve [16].
313
Side(s) that can
be directly
measured
Unilateral
Unilateral
Total or unilateral
Total or unilateral
Total or unilateral
Соседние файлы в папке Библиотека им академика М.И. Перельмана