The Pharyngeal Critical Pressure
1996; Elsevier BV; Volume: 110; Issue: 4 Linguagem: Inglês
10.1378/chest.110.4.1077
ISSN1931-3543
AutoresAvram R. Gold, Alan R. Schwartz,
Tópico(s)Tracheal and airway disorders
Resumoapnea/hypopnea index continuous positive airway pressure nonrapid eye movement critical pressure pressure downstream to the collapsible segment esophageal pressure pressure within the segment nasal mask pressure pressure outside collapsible segment pressure upstream to the collapsible segment resistance of portion of tube upstream to site of collapse upper airway resistance syndrome uvulopalatopharyngoplasty maximal inspiratory flow maximal flow Obstructive sleep apnea is a disorder characterized by pharyngeal collapse and occlusion during sleep. The disorder affects between 2% and 5% of the middle-aged population1Young T Palta M Dempsey J et al.Occurrence of sleep disordered breathing among middle-aged adults.N Engl J Med. 1993; 328: 1230-1235Crossref PubMed Scopus (8337) Google Scholar and is associated with significant morbidity and mortality.2Guilleminault C Stoohs R Partinen M et al.Mortality and morbidity of obstructive sleep apnea syndrome: prospective studies on retrospective cohorts.in: Saunders NA Sullivan CE 2nd ed. Sleep and breathing. Marcel Dekker, New York1994: 557-574Google Scholar The mechanism responsible for pharyngeal collapse during sleep remains uncertain. Investigators have identified both anatomic factors3Haponik EF Smith PL Bohlman ME et al.Computerized tomography in obstructive sleep apnea: correlation of airway size with physiology during sleep and wakefulness.Am Rev Respir Dis. 1983; 127: 221-226PubMed Google Scholar, 4Bradley TD Brown IG Grossman RF et al.Pharyngeal size of snorers, non-snorers, and patients with obstructive sleep apnea.N Engl J Med. 1986; 315: 1327-1331Crossref PubMed Scopus (233) Google Scholar, 5Schwab RJ Gefter WB Hoffman EA et al.Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing.Am Rev Respir Dis. 1993; 148: 1385-1400Crossref PubMed Scopus (406) Google Scholar, 6Shelton KE Woodson H Gay S et al.Pharyngeal fat in obstructive sleep apnea.Am Rev Respir Dis. 1993; 148: 462-466Crossref PubMed Scopus (354) Google Scholar and neuromuscular control factors7Remmers JE DeGroot WJ Sauerland EK et al.Pathogenesis of upper airway occlusion during sleep.J Appl Physiol. 1978; 44: 931-938Crossref PubMed Scopus (1396) Google Scholar, 8Anch AM Remmers JE Sauerland EK et al.Oropharyngeal patency during waking and sleep in the pickwickian syndrome: electromyographic activity of the tensor veli palatini.Electromyogr Clin Neurophysiol. 1981; 21: 317-330PubMed Google Scholar, 9Jeffries B Brouillette RT Hunt CE. Electromyographic study of some accessory muscles of respiration in children with obstructive sleep apnea.Am Rev Respir Dis. 1984; 129: 696-702Crossref PubMed Scopus (54) Google Scholar, 10Suratt PM McTier R Wilhoit SC. Alae nasi electromyographic activity and timing in obstructive sleep apnea.J Appl Physiol. 1985; 58: 1252-1256Crossref PubMed Scopus (19) Google Scholar that may lead to increased pharyngeal collapsibility during sleep in patients with obstructive sleep apnea.Although our understanding of the factors responsible for pharyngeal collapse during sleep is limited, treatments have been developed to oppose pharyngeal collapse during sleep in patients with obstructive sleep apnea. One such treatment, nasal continuous positive airway pressure (nasal CPAP), is often prescribed to offset the increase in pharyngeal collapsibility during sleep.11Sullivan CE Issa FG Berthon-Jones M et al.Reversal of obstructive sleep apnoea by continuous positive pressure applied through the nares.Lancet. 1981; 1: 862-865Abstract PubMed Scopus (2024) Google Scholar,12Sullivan CE Issa FG Berthon-Jones M et al.Home treatment of obstructive sleep apnoea with continuous positive pressure applied through a nose-mask.Bull Eur Physiopathol Respir. 1984; 20: 49-54PubMed Google Scholar When an appropriate level of nasal CPAP is prescribed, this treatment is highly effective at opening the pharynx during sleep regardless of the mechanism for elevated pharyngeal collapsibility. Patient compliance with nasal CPAP, however, is variable. Up to 35% of patients receiving nasal CPAP discontinue its use, and those who continue treatment do not use it consistently.13Rolfe I Olson LG Saunders NA. Long-term acceptance of continuous positive airway pressure in obstructive sleep apnea.Am Rev Respir Dis. 1991; 144: 1130-1133Crossref PubMed Scopus (172) Google Scholar, 14Kribbs NB Pack AI Kline LR et al.Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea.Am Rev Respir Dis. 1993; 147: 887-895Crossref PubMed Scopus (1071) Google Scholar, 15Reeves-Hoche MK Meck R Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance.Am J Respir Crit Care Med. 1994; 149: 149-154Crossref PubMed Scopus (331) Google Scholar Therefore, other effective treatments are needed for obstructive sleep apnea to complement or replace nasal CPAP in patients who do not tolerate its use.Many treatments are known to improve the severity of obstructive sleep apnea. These treatments include the following: weight loss,16Harman EM Wynne JW Block AJ. The effect of weight loss on sleep disordered breathing and oxygen desaturation in morbidly obese men.Chest. 1982; 82: 291-294Crossref PubMed Scopus (128) Google Scholar, 17Smith PL Gold AR Meyers DA et al.Weight loss in moderately obese patients with obstructive sleep apnea.Ann Intern Med. 1985; 103: 850-855Crossref PubMed Scopus (354) Google Scholar, 18Suratt PM McTier ME Findley LJ et al.Changes in breathing and the pharynx after weight loss in obstructive sleep apnea.Chest. 1987; 92: 631-637Crossref PubMed Scopus (111) Google Scholar protriptyline,19Brownell LG West P Sweathman P et al.Protriptylene in obstructive sleep apnea: a double blind trial.N Engl J Med. 1982; 307: 1037-1042Crossref PubMed Scopus (168) Google Scholar,20Smith PL Haponik EF Allen RP et al.The effects of protriptylene in sleep disordered breathing.Am Rev Resp Dis. 1983; 127: 8-13Crossref PubMed Scopus (107) Google Scholar uvulopalatopharyngoplasty,21Fujita S Conway W Zorick F et al.Surgical correction of upper airway abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty.Otolaryngol Head Neck Surg. 1981; 89: 923-934Crossref PubMed Scopus (967) Google Scholar, 22Simmons FB Guilleminault C Silvestri R. Snoring and some obstructive sleep apnea can be cured by oropharyngeal surgery.Arch Otolaryngol. 1983; 109: 503-507Crossref PubMed Scopus (146) Google Scholar, 23Katsantonis G. Uvulpalatopharyngoplasty for obstructive sleep apnea and snoring.Op Tech Otolaryngol Head Neck Surg. 1991; 2: 100-103Abstract Full Text PDF Scopus (5) Google Scholar tongue-retaining devices,24Cartwright R Samelson C. The effects of a nonsurgical treatment for obstructive sleep apnea: the tongue retaining device.JAMA. 1982; 248: 705-709Crossref PubMed Scopus (182) Google Scholar,25Cartwright R. Predicting response to the tongue retaining device for sleep apnea syndrome.Arch Otolaryngol. 1985; 111: 385-388Crossref PubMed Scopus (74) Google Scholar mandibular advancement devices26Clark GT Arand D Chung E et al.Effect of anterior mandibular positioning on obstructive sleep apnea.Am Rev Respir Dis. 1993; 147: 624-629Crossref PubMed Scopus (173) Google Scholar,27Eveloff SE Rosenberg CL Carlisle CC et al.Efficacy of a Herbst mandibular advancement device in obstructive sleep apnea.Am J Respir Crit Care Med. 1994; 149: 905-909Crossref PubMed Scopus (182) Google Scholar and surgery,28Riley R Powell N Guilleminault C. Maxillofacial surgery and obstructive sleep apnea: a review of 80 patients.Otolaryngol Head Neck Surg. 1989; 101: 353-361Crossref PubMed Scopus (89) Google Scholar and electrical stimulation of the pharyngeal muscles.29Miki H Hida W Chonan T et al.Effects of submental electrical stimulation during sleep on upper airway patency in patients with obstructive sleep apnea.Am Rev Respir Dis. 1989; 140: 1285-1289Crossref PubMed Scopus (114) Google Scholar,30Podszus T Peter JH Hochban W et al.Electrical hypoglossal nerve stimulation in obstructive sleep apnea [abstract].Am Rev Respir Dis. 1995; 151: A538Google Scholar While each of these treatments offsets an increase in pharyngeal collapsibility during sleep, none of these treatments is universally effective in the manner of nasal CPAP. Furthermore, we are often unable to predict the effect of a treatment on the severity of obstructive sleep apnea in a specific patient. The development of a practical method for predicting the effect of a treatment on the severity of obstructive sleep apnea in a specific patient might guide the clinician's choice from the various alternatives to nasal CPAP.To guide the clinician in selecting treatment for obstructive sleep apnea, we consider the relationship between obstructive sleep apnea and pharyngeal collapsibility. Current evidence suggests that pharyngeal collapsibility varies along a continuum from health (low collapsibility) to disease (high collapsibility). A primary goal of any therapy, therefore, is to decrease pharyngeal collapsibility to levels known to be associated with normal breathing patterns during sleep. Our approach will be to establish a quantitative basis for treating sleep apnea depending on both the degree to which pharyngeal collapsibility is elevated in a patient and the amount by which it is reduced with a specific treatment. To accomplish this, a physiologic basis for measuring pharyngeal collapsibility will be provided; the pharyngeal collapsibility of individuals with varying levels of pharyngeal airway obstruction during sleep will be examined; and the relationship between changes in pharyngeal collapsibility and changes in the severity of obstructive sleep apnea will be elucidated. From this analysis, we will develop a method to treat obstructive sleep apnea by reducing pharyngeal collapsibility “quantitatively.” Throughout the discussion, we will attempt to identify deficits in our knowledge and to suggest potentially fruitful opportunities for clinical investigation. Finally, we will demonstrate how pharyngeal collapsibility can be measured in a clinical sleep laboratory using nasal CPAP.Flow Through Collapsible Tubes: The ModelThe study of pharyngeal collapsibility in obstructive sleep apnea has benefited from earlier research on other systems of collapsible biological tubes. Collapsible tubes are important biological conduits and their function modulates many physiologic events in man. Well-recognized examples include collapse of central veins entering the right atrium,31Holt JP. The collapse factor in the measurement of venous pressure: the flow of fluid through collapsible tubes.Am J Physiol. 1941; 134: 292-299Google Scholar collapse of intrathoracic airways on forced exhalation,32Pride NB Permutt S Riley RL et al.Determinants of maximal expiratory flow from the lungs.J Appl Physiol. 1967; 23: 646-662Crossref PubMed Scopus (248) Google Scholar,33Mead J Turner JM Macklem PT et al.Significance of the relationship between lung recoil and maximum expiratory flow.J Appl Physiol. 1967; 22: 95-108Crossref PubMed Scopus (624) Google Scholar collapse of the nasal alae at high inspiratory airflows,34Bridger GP Proctor DF. Maximum nasal inspiratory flow and nasal resistance.Ann Otol Rhinol Laryngol. 1970; 79: 481-486Crossref PubMed Scopus (139) Google Scholar collapse of pulmonary capillaries in lung zones 1 and 2,35West JB Dollery CT Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures.J Appl Physiol. 1964; 19: 713-724Crossref PubMed Google Scholar and collapse of subendocardial capillaries at high levels of left ventricular end-diastolic pressure.36Downey JM Kirk ES. Inhibition of coronary blood flow by a vascular waterfall mechanism.Circ Res. 1975; 36: 753-760Crossref PubMed Scopus (233) Google Scholar Explanations of the behavior of these varied biological conduits have been proposed using a simple model of flow through collapsible tubes. In recent years, this model has also been applied to the pharyngeal airway. Using the model, investigators have quantified differences in pharyngeal collapsibility during sleep among normal subjects, snorers, and patients with obstructive sleep hypopnea and apnea. Moreover, the model has been used to study the relationship between changes in pharyngeal collapsibility and changes in the severity of obstructive sleep apnea. The simplicity of the model makes it a potentially useful clinical tool for improving utilization of the many treatment alternatives to nasal CPAP.The subject of flow through collapsible tubes has been discussed in a clearly written review by Green.37Green JF. Fundamental cardiovascular and pulmonary physiology: and integrated approach for medicine. Lea & Febiger, Philadelphia1982: 9-16Google Scholar In this discussion of the subject, we have adapted his approach to the purpose of describing the pharyngeal airway as a collapsible tube. The model (Fig 1A) consists of a tube passing through a sealed box. The tube is characterized by two rigid segments with a collapsible segment interposed between, within the box. The pressure in the box outside the collapsible segment is constant (Pout). In this discussion, we will assume that the segment within the box is so collapsible that whenever the pressure within the segment (Pin) falls below Pout, the segment collapses. Conversely, whenever the Pin exceeds the Pout, the segment opens. Thus, the Pin at the moment of collapse (Pin') is equal to the Pout. The Pin' is also known as the critical pressure (Pcrit) of the segment. Therefore, for the collapsible segment of this tube Pcrit=Pout.Now consider the effect of Pout on flow through the collapsible segment. In Figure 1B, we have set the pressure within the box at +10 cm H2O (Pout=+10) and applied a pressure of +5 cm H2O upstream to the collapsible segment (Pus=+5). Under these conditions (Pin<Pout, +5< + 10), the segment remains occluded and there is no flow through the tube. There can be no flow as long as the Pus is below Pcrit (+10 cm H2O). We will refer to the circumstance of Pus<Pcrit as condition 1. This condition is analogous to zone 1 of the pulmonary vasculature of West et al.35West JB Dollery CT Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures.J Appl Physiol. 1964; 19: 713-724Crossref PubMed Google ScholarLet us now examine the effect of an increase in Pus to a level above Pcrit (+15 cm H2O, Fig 1C). Because the Pus exceeds Pcrit, the collapsible segment opens and flow begins. In this example, let us assume that the pressure immediately downstream to the collapsible segment (Pds) remains below Pcrit (+9 cm H2O). Under these circumstances, the downstream end of the collapsible segment collapses or flutters to maintain its intraluminal pressure at +10 cm H2O. The reason for this phenomenon can be understood intuitively. If the intraluminal pressure at the site of collapse were to exceed +10 cm H2O (Pcrit) and the site opened widely, the intraluminal pressure at the site would fall to below Pcrit because of the lower pressure in the rigid segment immediately downstream. The decrease in intraluminal pressure at the site to below Pcrit would cause it to collapse and the flow to cease. Cessation of the flow would cause the pressure at the site to become +15 cm H2O (Pus), the site would reopen, and the sequence would begin again. Thus, when Pds is less than Pcrit, the downstream end of the collapsible segment collapses or flutters.How does collapse of the collapsible segment affect flow through the tube? Collapse of the segment fixes the pressure at its downstream end at Pcrit. Therefore, the pressure gradient driving flow through the tube becomes fixed at Pus-Pcrit and remains independent of changes in Pds (Pcrit is the effective downstream pressure for flow as long as Pds<Pcrit). Because the pressure gradient driving flow is fixed, flow also becomes fixed and does not exceed a maximal level (Vmax) even if Pds falls further. The Vmax of the collapsible segment is given by the following equation: V˙max=(Pus−Pcrit)/Rusequation (a) where Rus is the resistance of the portion of the tube upstream to the site of collapse. Because collapse of the collapsible segment limits flow through the tube at Vmax, it is termed the flow-limiting site (FLS). Therefore, when Pus exceeds Pcrit and Pds is less than Pcrit, collapse of the FLS fixes flow through the tube at Vmax. This circumstance will be referred to as condition 2. This condition is analogous to zone 2 of the pulmonary vasculature of West et al.35West JB Dollery CT Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures.J Appl Physiol. 1964; 19: 713-724Crossref PubMed Google ScholarNow consider the influence of alterations in Pus on the level of Vmax under model conditions 1 and 2. The relationship between Pus and Vmax for our model is illustrated in Figure 2. As long as Pus is less than +10 cm H2O, there is no flow (condition 1, Figure 1B). When the Pus exceeds +10 cm H2O (the Pcrit of the collapsible segment), Vmax increases linearly with Pus (condition 2, Figure 1C). From equation (a), the Pus at 0 flow is Pcrit and the slope of the relationship between Vmax and Pus is 1/Rus.Figure 2This figure demonstrates the effect of progressively increasing the pressure upstream to the collapsible segment (Pus, Figs 1B+C) on maximal flow through the tube ( V˙max). Until the Pus exceeds +10 cm H2O (Pcrit), the tube remains collapsed and occluded (condition 1). Above +10 cm H2O, V˙max and Pus are linearly related with a slope of 1/Rus as long as the pressure downstream from the collapsible segment is less than Pcrit (condition 2).View Large Image Figure ViewerDownload (PPT)Finally, let us examine the effect of increasing Pds above Pcrit on flow through the tube. In Figure 1D, the pressure downstream from the collapsible segment is increased to +11 cm H2O. Because the pressure throughout the collapsible segment is now greater than the Pcrit, the collapsible segment will open widely. There will be no flow limitation (as in condition 2) and the flow through the tube will be determined from the following equation: V˙=(Pus−Pds)/Requation (b) where R is the resistance of the entire tube between the upstream and downstream reference points. We will refer to this circumstance as condition 3. This condition is analogous to zone 3 of the pulmonary vasculature of West et al.35West JB Dollery CT Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures.J Appl Physiol. 1964; 19: 713-724Crossref PubMed Google ScholarThe Pharyngeal Airway as a Collapsible TubeThe advantage of modeling the pharyngeal airway as a collapsible tube is that the model can be used to examine the factors causing airflow obstruction even though the precise mechanisms are not fully understood. At present, much remains to be learned about the interactions of the pharyngeal muscles that maintain the pharyngeal airway patency during sleep. Nevertheless, if the pressure-flow relationships of the pharyngeal airway are described empirically by a simple model, then that model can be used to organize our thinking and to predict pharyngeal airway function, regardless of the physiologic mechanisms responsible. Although at first glance, the upper airway does not resemble a tube running through a box, its pressure-flow relationships are remarkably similar to those of the model that we have presented. In the following discussion, we encourage the reader to focus on the similarity between empirically observed flow through the pharyngeal airway during sleep and that predicted by the model of flow through collapsible tubes.Similarities Between Pharyngeal Airway Obstruction and the ModelThe pharyngeal airway of man during sleep demonstrates three distinct levels of patency that parallel the three conditions of the model of flow-through collapsible tubes discussed above. Individuals with obstructive sleep apnea have a pharyngeal airway that is completely occluded during sleep. The appearance of the human airway during an obstructive apnea is illustrated in Figure 3 by three midsagittal views of the pharyngeal airway of a patient with obstructive sleep apnea. Figure 3A illustrates his patent pharyngeal airway during wakefulness. Figures 3B and 3C demonstrate the progressive collapse of his pharyngeal airway during sleep. The appearance of the completely occluded pharyngeal airway in Figure 3C resembles the appearance of the collapsible segment of the model in condition 1 (Fig 1B). Unlike subjects with obstructive apnea, individuals who snore have a pharyngeal airway that collapses and flutters with inspiration during sleep. The fluttering of the airway, snoring, or obstructive hypopnea, is associated with the limitation of inspiratory flow38Cistulli PA Sullivan CE. Pathophsiology of sleep apnea.in: Saunders NA Sullivan CE 2nd ed. Sleep and breathing. Marcel Dekker, New York1994: 407Google Scholar and closely resembles model condition 2 (Fig 1C). In contrast to the preceding two groups who demonstrate complete and partial pharyngeal airway obstruction during sleep, individuals who breathe normally during sleep have a pharyngeal airway that is widely patent like a collapsible tube under condition 3 (Fig 1D). Thus, obstructive sleep apnea, snoring, and obstructive hypopnea, and normal breathing resemble the three levels of patency in collapsible tubes.Figure 3This figure illustrates the progressive obstruction of the pharyngeal airway of a patient with sleep apnea during sleep. In A, the airway is open during wakefulness. Collapse begins at the level of the nasopharynx and oropharynx (B) and progresses to include the hypopharynx (C). The collapsed pharyngeal airway resembles the collapsible segment of the model in condition 1 (Fig 1B).View Large Image Figure ViewerDownload (PPT)To understand the behavior of the pharyngeal airway during obstructive apnea, let us compare the airflow patterns of the pharynx to those of the model. If the pharyngeal airway during obstructive apnea resembles condition 1 of the model (Fig 1B), then it behaves like a collapsible tube when Pus is less than Pcrit. For the pharyngeal airway during inspiration, Pus is atmospheric pressure. Therefore, the Pcrit of the pharyngeal airway during obstructive apnea must be greater than atmospheric pressure. What are the determinants of the Pcrit of the pharyngeal airway? Referring back to the model, we observe that the Pcrit is equal to the Pout, the pressure surrounding the collapsible segment of the tube. To apply this model to the pharyngeal airway, we can think of the pharyngeal airway wall as a thin, very collapsible mucosal membrane (ignoring its muscle mass). The Pout of the pharyngeal airway consists of the pressures exerted on the airway by the pharyngeal muscle (resulting from its mass and the pressure resulting from its contraction) and the tissues surrounding the pharyngeal airway. Therefore, the pharyngeal airway Pcrit is a pressure that is equal to the pressure exerted on the pharyngeal airway by these same structures. Because the Pcrit is equal to the pressures tending to collapse the airway, it is an index of pharyngeal airway collapsibility (the greater the Pcrit, the more collapsible the airway). Thus, during obstructive apnea, the airway is occluded because the Pcrit of the pharyngeal airway is greater than atmospheric pressure. The pharyngeal airway is too collapsible to remain open at atmospheric pressure.Modeling the Response to Nasal CPAP in Obstructive Sleep ApneaNow let us examine the effect of an increase in nasal pressure (PN, analogous to Pus) above the pharyngeal Pcrit in a patient with an obstructive apnea. When we raise the PN from atmospheric pressure to a pressure above the pharyngeal Pcrit, the pharyngeal airway is no longer occluded and airflow resumes when the patient inspires. If PN is slightly above Pcrit, the pressure downstream from the collapsible segment of the pharynx (laryngeal pressure) will fall below Pcrit during inspiration. Under these conditions, as the patient inspires, collapse of the pharynx will lead to flow limitation manifested as snoring or hypopnea (condition 2). If PN is high enough, the downstream laryngeal pressure will not fall below Pcrit during inspiration. Consequently, airflow will occur as the patient inspires without pharyngeal collapse or flow limitation (condition 3). Therefore, when the PN is raised above Pcrit in a patient with obstructive apnea, the degree of airflow obstruction (condition 2 or condition 3) depends on the difference between PN and Pcrit.When obstructive sleep apnea patients sleep with nasal CPAP, inspiratory airflow patterns are qualitatively similar to those predicted from the model above. Figure 4 demonstrates the recordings of the airflow, esophageal pressure (Pesoph), and PN for one supine obstructive sleep apnea patient as the PN is progressively increased during stage 2 sleep. Notice the absence of inspiratory airflow (Fig 4A) when the PN is below a threshold level (Pcrit, condition 1). When the PN is raised above the Pcrit, inspiratory airflow is present, but becomes limited to a maximal level ( V˙Imax), independent of the continued decrease of downstream laryngeal pressure (reflected in Pesoph, Figs 4B through D). The dissociation of inspiratory airflow from Pesoph suggests that laryngeal pressure has fallen below the pharyngeal Pcrit (condition 2). Finally, at higher levels of PN, inspiratory flow and downstream pressure parallel each other (Fig 4E). This suggests that at higher levels of PN, the laryngeal pressure does not fall below Pcrit during inspiration, and inspiratory flow limitation does not occur (condition 3). Therefore, as PN is increased during sleep in a patient with obstructive sleep apnea, the upper airway passes through the three levels of patency observed in a collapsible tube.Figure 4This figure demonstrates the nasal airflow, esophageal pressure (Pesoph), and nasal mask pressure (PN) of an obstructive sleep apnea patient during sleep as PN is progressively increased. With increasing PN, the patient's pharyngeal airway progresses from complete apnea without inspiratory flow (condition 1, A), to hypopnea/snoring with progressively higher levels of maximal inspiratory flow (condition 2, B through D), to complete airway patency (condition 3, E). The arrows in B through D identify maximal inspiratory flow at each level of PN for the coordinates plotted in Figure 5. See text for further discussion.View Large Image Figure ViewerDownload (PPT)The response of inspiratory airflow to nasal CPAP administration can be examined in more detail to define a relationship of V˙Imax to PN for the obstructive sleep apnea patient (similar to the relationship of Vmax to Pus in the model, Fig 2). Smith and associates39Smith PL Wise RA Gold AR et al.Upper airway pressure-flow relationships in obstructive sleep apnea.J Appl Physiol. 1988; 64: 789-795Crossref PubMed Scopus (342) Google Scholar examined the relationship of V˙Imax to PN in six patients with obstructive sleep apnea. They consistently observed a linear relationship between V˙Imax and PN that intercepted the x-axis at Pcrit (defined as the value of PN at VImax=0, Fig 5). Thus, in obstructive sleep apnea patients, the pressure-flow relationships of the pharyngeal airway are similar to those of a simple collapsible tube and can be used to define a Pcrit in obstructive apnea that is greater than atmospheric pressure.Pcrit and the Spectrum of Pharyngeal CollapsibilityUsing the model of a simple collapsible tube, we can also predict the pressure-flow relationships of the normal pharyngeal airway during sleep. In contrast to obstructive sleep apnea patients, normal individuals have patent pharyngeal airways without inspiratory flow limitation during sleep. In other words, at atmospheric pressure, their pharyngeal airways are in condition 3. If the pharyngeal airway of normal individuals also behaves like a collapsible tube, then the Pcrit of their airway must be substantially below atmospheric pressure. To test this hypothesis, Schwartz and associates40Schwartz AR Smith PL Wise RA et al.Induction of upper airway occlusion in sleeping individuals with subatmospheric nasal pressure.J Appl Physiol. 1988; 64: 535-542Crossref PubMed Scopus (282) Google Scholar decreased the nasal pressure of normal individuals during sleep. Normal subjects slept in supine position while wearing a nasal mask attached to a vacuum source. The PN was progressively lowered during nonrapid eye movement (NREM) sleep while inspiratory flow, PN, and Pesoph were measured. With progressive lowering of PN, each subject demonstrated snoring (inspiratory flow limitation, condition 2). Figure 6 demonstrates a plot of V˙Imax against PN for one of the normal subjects. As PN was decreased, V˙Imax decreased in a linear fashion until it fell to zero as the PN approached the Pcrit of the pharyngeal airway (-9 cm H2O). Below Pcrit, there was no inspiratory airflow (condition 1) and the normal individual resembled a patient with obstructive sleep apnea (Fig 7). For the group of normal subjects, the Pcrit was −13.5±3.4 cm H2O. Therefore, similar to the pharyngeal airway in obstructive sleep apnea, the pressure-flow relationships of the normal pharyngeal airway can be predicted by a model of flow through a collapsible tube. The two airways differ only in the values of their Pcrit: Pcrit in patients with
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