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Estimation of upper airway dynamics using neck inductive plethysmography

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Estimation of upper airway dynamics using neck inductive plethysmography

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Content ESTIMATION OF U PPER AIRWAY DYNAMICS USING NECK INDUCTIVE PLETHYSMOGRAPHY by Chih-Ming C hen A T hesis P re s e n te d to the FACULTY OF THE GRADUATE SCHOOL UNIVERSITY OF SOUTHERN CALIFORNIA In Partial Fulfillment of the R equirem ents for the D egree MASTER OF SCIENCE (BIOMEDICAL ENGINEERING) May 1995 C opyright 1995 Chih-Ming C hen This thesis, written by C hih-M ing Chen under the guidance o f h is F a c u lty Committee and approved by all its members, has been presented to and accepted by the School of Engineering in partial fulfillment of the re quirements for the degree of Faculty Committee Chairman DEDICATION: To my Father and Mother and to Grace for their love and support. ACKNOWLEDGMENTS: I wish to express my most enthusiastic gratitude and deep appreciation to Dr. Michael C. K. Khoo for his continued supervision, guidance, and understanding throughout this research. I also would like to thank him for the encouragement, enormous time and patience he expanded in discussing my problems. I also wish to thank Mr. Jeffrey W. Birnbaum for his invaluable assistance. My gratitude goes also to all my friends for their friendship and encouragement. I would like to take this opportunity to express my appreciation to my parents and Grace C. C. Cheng for all their support, love, and patience throughout my life. TABLE OF CONTENTS DEDICATION A CKNOWLEDGMENTS LIST OF FIGURES ABSTRACT 1. INTRODUCTION 2. LITERATURE REVIEW 2.1. Basic Anatomy of Upper Airway 2.1.1. Mouth 2.1.2. Nasal Cavity 2.1.3. Pharynx 2.1.4. Larynx 2.2. Distribution of Airway R esistance 2.3. Breathing and the Upper Airway R esistance 2.3.1. N asal Breathing 2.3.1.1. Nasal Valve 2.3.1.2. Nasal Erectile M ucosa 2.3.2. Oral Breathing 2.3.3. Parapalatal Airways 2.3.4. Pharyngeal Airway 2.4. T ypes of Airway Obstruction 2.4.1. Transm ural P ressu re and UAO 2.4.2. Flow-Volume Loop and Airway Obstruction 2.5. S leep A pnea 2.5.1. T ypes of S leep A pnea 2.5.2. M echanism of UAO during Sleep 2.5.2.1. Upper Airway Patency 2.5.2.2. C hem oreceptor R e sp o n se s 2.5.2.3. Local Reflexes 2.6. Respiratory Inductive Plethysm ography 29 2.6.1. Principle of RIP 29 2.6.2. Calibration of RIP 30 2.6.3. Neck inductive Plethysm ography 31 3. METHODS 33 3.1. Experimental A pparatus 33 3.2. Experimental Protocol 35 3.3. D ata Analysis 36 3.3.1. Data Calibration 36 3.3.2. Data Analysis 38 3.3.2.1. D ata Classification 39 3.3.2.2. Analysis Method 43 4. RESU LTS 46 4.1. NUAO and PUAO 46 4.2. CUAO 54 5. DISCUSSION AND CONCLUSIONS 57 R EFER E N C E S 62 APPENDIX 65 V LIST OF FIGURES Figure__________________________________________________ Page 1. Upper airway: mouth or nasal cavity, pharynx, and larynx. 5 2. Formula illustrating upper airway dynamics in respiration. 9 3. The distribution of airway resistance in the respiratory tract. 9 4. Diagrammatic divisions of a nasal cavity. 11 5. Measured nasal resistances at sites within a nasal cavity. 12 6. The parapalatal (palatoglossal and palatopharyngeal) airways. 16 7. Pressures affecting the intrathoracic and extrathoracic upper airway. 18 8. Behavior of an extrathoracic upper airway obstruction throughout the respiratory cycle. 20 9. Behavior of an intrathoracic upper airway obstruction during the respiratory cycle. 20 10. Characteristic flow-volume loop in airway obstruction. 22 11. Types of sleep apnea. 24 12. Balance of forces that sustain upper airway patency. 26 13. Transducer bands of the respiratory inductive plethysmography placed around the rib cage and abdomen. 30 14. Experimental apparatus. 34 15. Management of CPAP during experimentation. 35 16. Typical waveforms of V and Pes. 38 17. The representative waveforms of CUAO. 39 18. The representative waveforms of PUAO. 40 19. The representative waveforms of NUAO. 43 20. Definition of AResp and APes. 21. Definition of AResp and Gaw. 22. Gaw versus AResp in the ACPAP case of the NUAO state. 45 45 48 23. Data sets distribution between Gaw and AResp in the ACPAP case of the NUAO state. 48 24. Data sets distribution between Gaw and AResp in the DCPAP case of the NUAO state. 49 25. Experimental relationships between Gaw and AResp in the ACPAP case of the NUAO state. 50 26. Experimental relationships between Gaw and AResp in the DCPAP case of the NUAO state. 51 27. Experimental relationships between Gaw and AResp in the DCPAP case of the NUAO state including CPAP=0 cmH2 condition. 51 28. Experimental relationship between Gaw and AResp in the ACPAP case of the PUAO state. 53 29. Experimental relationship between Gaw and ARe sp in the DCPAP case of the PUAO state. 53 30. Experimental relationship between APes and AResp in CUAO state. 55 31. Experimental relationship between APes and AResp in the ACPAP case of the CUAO state. 56 32. Experimental relationship between APes and AResp in the DCPAP case of the CUAO state. 56 33. Comparison of NUAO and PUAO in ACPAP case. 59 34. Comparison of CUAO between CPAP= 0 and CPAP=3 cmH20. 60 vii ABSTRACT The goal of this experiment was to use the neck inductive plethysmography (NIP) technique to estimate the upper airway dynamics of a representative subject with obstructive sleep apnea (OSA) during inspiration in the various levels of continuous positive airway pressure (CPAP). The NIP was mainly employed to detect the cross-sectional area (CSA) changes of the upper airway. Measurements of nasal airflow (Vt), esophageal pressure (Pes)- neck respitrace (Resp). and nasal mask pressure (Pmask) were recorded simultaneously and used to determine three variables, the upper airway conductance (Gaw). the neck CSA changes (AResp), and the changes of esophageal pressure (APes), for illustrating the upper airway dynamics in the no obstruction (NUAO), partial obstruction (PUAO), and complete upper airway obstruction (CUAO) categories. AResp and Gaw showed a highly significant relationship during inspiration at various CPAP conditions in both the NUAO and the PUAO categories. In the CUAO studies, APes was linearly proportional to the AResp- These experimental results demonstrate that the NIP may be useful for characterizing the upper airway dynamics of patients with OSA without the need for invasive procedures such as the placement of a catheter into the upper airway. Chapter 1 INTRODUCTION Sleep apnea syndrome is characterized by multiple obstructive or mixed apneas during sleep associated with repetitive episodes of loud snoring and microarousals. There are three types of sleep apnea: (1) central apnea, characterized by cessation of air flow resulting from termination of respiratory effort; (2) obstructive apnea, characterized by cessation of air flow despite persistent respiratory effort; (3) mixed apnea, characterized by the occurrence of an early central phase and a late obstructive phase. A modest degree of obesity is often associated with sleep apnea syndrome, but many patients with the disorder are not significantly overweight. They may exhibit anatomical abnormalities of the upper airway or demonstrate a short, thick neck. The treatment of sleep apnea syndrome includes both medical and surgical approaches. The ultimate surgical approach to obstructive sleep apnea is tracheostomy, a procedure most often recommended in severe cases associated with life-threatening cardiac disease. The most successful nonsurgical approach to sleep apnea syndrome has been the use of the continuous positive airway pressure (CPAP). Now CPAP has been increasingly recognized as an important therapeutic modality for sleep apnea. The key events in sleep apnea are now well known, but underlying causes are still ambiguous. What are the actual procedures that induce people to develop upper airway obstruction (UAO) during sleep? There is evidence that each of the various theoretical causes does contribute to sleep apnea, and perhaps more l importantly, each may dominate in different patients. In other words, although sleep apnea study recordings may look identical in any sample of patients, some may be the result of structural defects, whereas others may be entirely the result of neuromuscular abnormalities. Actually, many of the patients having obstructive sleep apnea have a pre-existing UAO. In other words, while patients have an extrathoracic obstruction, the negative pressure inside the extrathoracic airway tends to suck the airway closed and then increase the obstruction during inspiration. Thus, most patients with obstructive sleep apnea have a pre-existing abnormality that causes an UAO (29). The estimation of the upper airway dynamics, therefore, may be useful to explain the upper airway collapse mechanism associated with obstructive sleep apnea. During the inspiratory cycle of respiration, airflow is directly related to the pressure difference between atmospheric and intrathoracic (inspiratory) pressures and inversely related to respiratory resistance (see 2.2 distribution of airway resistance). Lower atmospheric pressure, or any lesion increasing resistance to airflow would increase the respiratory effort needed to maintain airflow. When inspiratory airflow accelerated, intraluminal pressure suddenly drops in the area of narrowing due to the Venturi effect, and the airway is further compromised. Precisely speaking, while the intraluminal negative pressure of the airway reaches a critical point, the combination of redundant tissues and the loss of pharyngeal muscle tone causes airway collapse during inspiration. This process continues with repetitive inspiratory effort for the duration of the apnea until it ends with a brief awakening (arousal). 2 In order to investigate the upper airway dynamics of the patients with OSA, a modification of respiratory inductive plethysmography (RIP) named neck inductive plethysmography (NIP) was employed in this experiment. The ability of RIP to distinguish central and obstructive apnea had been suggested to use in the sleep laboratory. However, if respiratory efforts are weak, the RIP can fail to differentiate between central and obstructive apnea. Staats and coworkers (27) indicated a method of using esophageal manometry in this instance. In the method, NIP appears to be capable of detecting these minute respiratory efforts, even when rib cage and abdomen signals are flat. Recently, Lustro and colleagues (28) present a method of using NIP to assess cross-sectional area (CSA) changes of the extrathoracic airways via an inductive plethysmograph band placed around the upper part of the neck. Results present evidence on the reliability of measuring CSA of extrathoracic airways by NIP in healthy subjects during resistive breathing. The objective of this study was to use the NIP technique to investigate the upper airway dynamics of a representative subject with OSA during the application of various levels of CPAP. For the management of CPAP, a procedure of proportionately ascending CPAP (ACPAP) in increments of 2 cmH20 from 3 to 15 cmH20 was applied after the starting of CPAP=0 cmH20 situation. Subsequently, a corresponding procedure of CPAP from 13 to 3 cmH20 , descending CPAP (DCPAP), was also utilized to the patient (see 3.2 experimental protocol). During the experiment, nasal airflow (Vt), esophageal pressure (Pes), neck respitrace (Resp), and nasal mask pressure (Pmask) were simultaneously recorded during the first and second stages of nonrapid-eye-movement (NREM) sleep in each CPAP condition of the ACPAP and DCPAP case. According to the recorded data, it was 3 classified into three groups: no upper airway obstruction (NUAO), partial upper airway obstruction (PUAO), and complete upper airway obstruction (CUAO). In order to illustrate the respiratory properties among them, upper airway conductance (Gaw). the neck CSA changes (AResp). and the changes of esophageal pressure (APes) were defined (see 3.3.2.2 analysis method). The results of this experiment showed a highly significant relationship between AResp. measured by NIP, and Gaw during inspiration at various CPAP levels regardless of whether there was no obstruction or partial obstruction (Fig. 25, 26, 28, and 29). During obstructive apnea, our results demonstrated a significant linear relationship between APes and AResp (Fig. 30, 31, and 32). These empirical conclusions verify that the NIP is a useful noninvasive method for the estimation of upper airway dynamics of patients with OSA. 4 Chapter 2 LITERATURE REVIEW 2.1 Basic Anatomy of Upper Airway The respiratory system can be divided into three parts: upper airway, lower airway and lungs. The upper airway can be defined as that portion of the respiratory tree from the nasal cavity to the carina trachea, encompassing the nasal cavity or mouth, pharynx, and larynx (Fig. 1). These components of the upper airway will be described briefly later. Nasal cavity — Palate - Pharynx Epiglottis Larynx Trachea jjj'L —X - Bronchi Lung Esophagus Diaphragm Figure 1. Upper airway: mouth or nasal cavity, pharynx, and larynx. 5 The upper airway has three major functions: ventilation, swallowing, and speech. For ventilation, the upper airway must remain patent, but for the other functions, it must narrow or close. Ventilation continues during sleep whereas swallowing and speech cease. However, it decreases during normal sleep. In addition, ventilation must be maintained when the nose is occluded or, alternatively, when the mouth is closed. These conflicting functions in one anatomical region is complicated, and it is not surprising that intermittent failure of ventilation occurs. Under pathological conditions, ventilation may also cease when the upper airway collapses. These normal and abnormal events will be discussed later. 2.1.1 Mouth The mouth includes the vestibule (between the lips and cheeks and the teeth and gums) and the oral cavity (encompassing the teeth, gums, alveolar arches, hard and soft palates, and tongue). Except the functions of mastication and swallowing, the mouth provides a parallel airway with the nose and, as a respiratory passage, it can bypass the nasal airway partially or completely. 2.1.2 Nasal Cavity As the anatomically superior part of the airway, the nose serves the following functions: (1) it acts as a respiratory conduit for airflow; and (2) the nasal mucosa warms and humidifies inspired air. The paired nasal cavities each consists of an anterior alar region in continuity with a caval portion. In the nasal alar area, the anterior skeleton is cartilaginous and consists of the septum medially and paired alar cartilages laterally. Each lower lateral cartilage extends from the alar wing to 6 the columella and overlaps the upper lateral cartilage to which it is attached by a fibrous joint. For the nasal cavum, its walls consist of rigid bone. Bony projections from the lateral wall, of which the middle and inferior turbinates are the most important, increase mucosa to a large region. The erectile mucosa alters the lumen of this cavity. 2.1.3 Pharynx The pharynx, shaped like a cone, is a muscular tube covered by a mucosa and submucosa. Anteriorly, the nasal cavities and mouth open into the nasopharynx and oropharynx, respectively. The pharynx extends from the base of the skull to the esophagus and epiglottis and includes the nasopharynx and the oropharynx, which join to form the hypopharynx. It is necessarily a compliant and muscular passage with few skeletal restrictions, and enables brief performance of swallowing to convey material from the mouth and from the mucociliary transport system of the air passages to the esophagus. Apart from these momentary swallowing interruptions, the pharynx has to provide an adequate respiratory airway. 2.1.4 Larynx The larynx, between the pharynx and trachea, is a cartilaginous framework, lying at the base of the neck (between the third /fourth and sixth cervical vertebrae), interiorly attached to the trachea and superiorly opening into the pharynx. It includes two generating sound vocal folds (formerly known as cords) composed of ligament and muscle with a covering of mucosa. Except the function of phonation, 7 the larynx is the uppermost component of the respiratory tract. The primary function of the larynx is as a valve to seal off the ain/vay, preventing foreign substances from entering the respiratory tract. Other functions are to ensure free passage of air into and out of the lung and to prevent air escape during effortful activities. However neuromuscular coordination between pharyngeal and laryngeal dilators and constrictors is essential for control of breathing and swallowing. 2.2 Distribution of Airway Resistance In the simplest terms, resistance to the flow of gas through an airway is described by an equation that relates the flow per unit time (airflow) to the pressure difference or gradient between the ends of the tube (Fig. 2). According to this formula, the distribution of the airflow resistance will be easily presented. The cross-sectional area of the upper airway is quite narrow immediately above the vocal cords and in the larynx and trachea. Since the velocity of flow is high and secondary eddies are formed in this area, turbulent flow exists in the upper airway. The resistance to airflow is high with turbulent flow; that is, the pressure required to maintain such a flow is high. The pressure required for turbulent flow is summarized by the equation P o c V2; the pressure is directly proportional to the density of the gas and the square of the flow. For the lower airway, however, the cross-sectional area increases progressively and it leads to a progressive diminution of the linear velocity of the gas flow. This produces laminar flow. The pressure required is proportional to this flow. The resistance in such situation is very low compared with turbulent flow. airflow A pressure R esistance = T J L A P ressu re Airflow Figure 2. Formula illustrating upper airway dynamics in respiration. The distribution of airway resistance in the respiratory tract is shown as Figure 3. Total airway resistance in normal subjects may be divided into two parts, the first part is in the central airways with turbulent flow (80 to 90% of total resistance) and the second part is due to the laminar flow in the peripheral airways, which are defined as those with internal diameter of less than 2 mm (10 to 20% of the total resistance) (29). CROSS SECTIONAL AREA DISTRIBUTION OF AIRWAY RESISTANCE 2 cm2 PROGRESSIVE DIVISIONS OF AIRWAYS LARYNX & TRACHEA 5 0% 13-19 cm2 LARGE AIRWAYS > 2 mm 2 0 -8 0 cm2 / Cross Sectional Area Figure 3. The distribution of airway resistance in the respiratory tract. 9 2.3 Breathing and The Upper Airway Resistance The performance of breathing and the function of respiration are not synonymous. The meaning of breathing is the transport of air in through the upper and lower airways to the alveolar cells with sufficient pressure, moisture, warmth, and cleanliness to secure optimal conditions for oxygen uptake and for elimination of carbon dioxide brought to the alveoli by the blood stream (33). Nose, pharynx, larynx, and upper trachea account for the upper airway resistance during nose breathing and mouth, pharynx, larynx, and upper trachea account for the upper airway resistance during mouth breathing. For normal either mouth or nose breathing, inspiration is the result of contraction of the respiratory muscles enlarging the thoracic cage. The distending pressure generated by the muscles is dissipated in overcoming the elasticity and resistance. As the previous description, the upper airway contributes greatly to total airway resistance in mammals, constituting about one-half of the total airway resistance. However several factors alter the upper airway resistance. It decreases with increasing lung volume and breathing frequency. Exercise and breathing increased concentrations of CO2 decrease the resistance. In contrast, vascular congestion and low ambient air temperature increase the upper airway resistance (1). There exists a wide variability in the sam e individual at the different times. 2.3.1 Nasal Breathing The healthy nose provides a advantageous breathing route. McCaffrey and Kern (3) showed that the hypercapnia decreases nasal airway resistance in proportion to the partial pressure of the inspired CO2 and to the increase in minute 10 ventilation. This decreased nasal airway resistance counteracts the increase in pulmonary airway resistance in response to the hypercapnia. Moreover in comparison with other segments of the breathing passages, its resistance to respiratory airflow is high. The principal nasal components that regulate respiratory airflow to cause high resistance are the structural of the nasal valve and the lumen- regulation erectile mucosa. In fact by the measurements of pressure and flow of respiratory air at different sites within healthy nasal cavities, Haight and Cole (2) found that resistance is concentrated in the regions of high-velocity flow in a specific anterior nasal segment a few millimeters in length (Fig. 4 and Fig. 5). < / > o N III (J z < cc - I < co < z 2 4 6 8 10 DEPTH IN NOSE (cm) Figure 4. Diagrammatic divisions of a nasal cavity: A, vestibular entrance; B, resistive valve region; C, minimally resistive cavum. (From Eccles 1987, p 41) 11 0 N X E _o 01 o Z s (/> C O UJ cc < C O < z 10 CONGESTED UNTREATED 5 DECONGESTED 0 8 10 6 2 4 DEPTH IN NOSE (cm) Figure 5. Measured nasal resistances at sites within a nasal cavity. Resistance is localized at 2 to 3 cm in the congested, untreated, and decongested mucosal state. There is little resistance change in cavum between 3 and 10 cm. (From Haight, Cole, 1983) 2.3.1.1 Nasal Valve The nasal valve constitutes the major airflow resistive segment of the respiratory airways (2). It is a dynamic segment of the airway with a length of several millimeters, and its lumen follows a much longer and narrower course dorsally than ventrally. This segment is confined to a short, narrow region bridging the piriform aperture and extends from the caudal edge of the upper lateral cartilage in the vestibule to the anterior end of the bony inferior turbinate in the cavum (34). The anterior bony cavum contains inferior turbinate erectile mucosa, lateral-wall erectile mucosa anterior to the turbinate, and septal erectile mucosa, supported respectively by compliant alar tissues and the rigid cartilaginous septum. These elements combine to form dynamic valve that adjusts nasal airflow. It is 12 stabilized by cartilage and bone, modulated by voluntary muscles, and regulated by erectile tissues (32). 2.3.1.2 Nasal Erectile Mucosa Studies show that some erectile tissues, superimposed on structural elements of the stabilized anterior nose and the rigid bony cavum, narrows the skeletal nasal lumen. Moreover at critical sites, notably the nasal valve, airflow resistances are altered substantially by physiologic and pathologic changes in the degree of the erectile tissues swelling. This variable contribution to nasal airflow resistance is dependent mainly on the blood content of capacitance vessels that constitute the erectile components of the septal and lateral nasal walls (32). This erectile tissues is the nasal mucosa. The nasal mucosa, composed of an epithelium, subepithelial connective tissue, glands, nerves, and blood vessels (31), provides a protective barrier. When it is contacted by bacteria or by chemical or gaseous stimuli, the autonomic nervous system and anatomic control of the nasal mucosa provide reflex cholinergic responses which influence the beat and secretions of the mucosa through ciliary activity (33). For healthy nasal cavities, the magnitude of the nasal resistance is altered substantially by physiologic responses of erectile mucosa to irritants. Yet, in the absence of mucosal abnormality, the anterior location of resistance remains unchanged, and swelling of mucosa within the nasal cavum has little effect on airflow resistance of the nasal cavity by contrast with its effect in the valve region (Fig. 4 and Fig. 5). Computed tomographic (CT) studies (4,5) validate the clinical observation that nasal erectile mucosa accommodate to structural irregularities. It maintains a remarkably constant airway 13 width of 2 to 3 mm in the more patent nasal cavum despite septal irregularities. However the ability to adapt so as to maintain an appropriate airway is not unlimited. The reason is that structural irregularities, depending on site and size, can result in intermittent obstruction by cyclic or postural mucosal swelling at a narrowed site (32). 2.3.2 Oral Breathing Nasal breathing is involuntary, but mouth breathing occurs when there is difficulty breathing through the nose, such as in exertion, under stress, and when cardiac, pulmonary, or other illness hampers the supply of oxygen to the tissue. Thus, nasal versus mouth breathing is a "trade-off." Oral resistance is localized to the spontaneously positioned oral vestibule in awake subjects. It is of similar magnitude to resistance in the valve region of the nasal vestibule. In other words, the fact that the principal resistor of the breathing passages is located at the nasal respiratory portal (nasal valve) and a resistor of similar magnitude is located at the oral portal during spontaneous mouth breathing suggests that a similar function could be attributed to each. However the oral resistance is increased in sleep and even when the labial aperture is patent and the mouth provides an airway. In some cases, such as the burden of nasal breathing becoming intolerable, nasal breathing is shared with the parallel oral airway. Neither the open mouth nor mouth breathing is a reliable indicator of nasal resistance, but oral and nasal resistances each play a part in the regulation of respiratory airflow distribution between these parallel airways during oronasal breathing. Studies appear that in oronasal breathing the degree of nasal patency plays a part in distribution of respiratory air between mouth 14 and nose. However the mouth provides a far greater range of airflow resistances than the nose, and the variable cross section of the labial aperture is the major determinant of oral airflow resistance and resulting oronasal distribution of respiratory airflow (32). 2.3.3 Parapalatal Airways The parapalatal airways is the joining of the palatoglossal and palatopharyngeal airways (Fig. 6). There exists a soft palate. The palate can occlude either the nasal or the oral airway, and its position between tongue and posterior pharyngeal wall enables oronasal breathing to take place (6). The m easurement of respiratory airflow resistances above and below the soft palate have been made via healthy subjects breathing exclusively through the nose while awake. Results show resistance of the palatopharyngeal airway segm ent to be small compared with resistance of either the oral or nasal vestibules (7). For palatoglossal segment , studies also present similarly small resistance to airflow during oral breathing. Thus, the principal resistors affecting oronasal breathing and its distribution are situated at the oral and nasal portals rather than the parapalatal airways (32). 2.3.4 Pharyngeal Airway As above description, the palatoglossal and palatopharyngeal segm ents of awake healthy subjects present relatively small resistances to respiratory airflow. However during sleep, upper-airway dilator muscle tone is diminished, and under this circumstance, gravitational forces and flaccidity of the muscles force to narrow 15 the parapalatal and glossopharyngeal airways (Fig. 6). Further narrowing is promoted by compliance with the suction (subatmospheric) pressures generated within the pharyngeal lumen by inspiration against upstream resistances. Narrowing increases resistance to airflow, and, indeed, it has been noted that pharyngeal respiratory airflow resistance is elevated in apneic patients (8). Properly speaking, the pharyngeal walls collapse completely and occlude the airway if a critical inspiratory transmural pressure (described later) is achieved. As the closing pressure occludes the pharyngeal lumen, inspiratory efforts increase transmurai pressures further and seal the closure more tightly. This phenomenon result in an obstructive apnea and the obstructive apnea is maintained until arousal reactivates dilator muscle tone then restores airway patency (32). Palatopharyngeal Palatoglossal G lossopharyngeal S eg m en ts Figure 6. The parapalatal (palatoglossal and palatopharyngeal) airways. 16 2.4 Types of Airway Obstruction As already described, the upper airway encom passes the nasal cavity or mouth, pharynx, and larynx. Obstruction in the upper airway has important physiological differences from obstruction in the lower respiratory tract. The differences are mainly related to two factors. The first factor is whether the diameter of the airway at the site of the obstruction changes with the respiratory cycle. If the obstruction changes with the phase of respiration, it is called the variable obstruction; if it doesn't change, it is called the fixed obstruction. The second factor is the location of the lesion. An obstruction in the upper airway behaves quite differently from an intrathoracic obstruction. The diameter of the airway at the site of an obstruction is related to the pressure inside and outside the airway. With a fixed obstruction, the airway at the site of the obstruction is too stiff to change its dimensions as these pressures change. If the obstruction is dynamic, the diameter of the airway will increase when the pressure in the airway exceeds the pressure around the airway. However, when the pressure in the airway is less than the pressure around the airway, the diameter of the airway will decrease, thus creating the obstruction. In order to distinguish the differences between extrathoracic and intrathoracic obstruction, understanding the transmural pressures across the large central airways is very important. 2.4.1 Transmural Pressure and UAO Understanding the nature of transmural pressures across the large central airways, during both expiratory and inspiratory phases of the respiratory cycle, is essential to interpreting the effects of obstructing lesions of the central airways. 17 Figure 7 illustrates the different pressures affecting the intrathoracic and extrathoracic upper airway. The extrathoracic upper airway is surrounded by atmospheric pressure, whereas the intrathoracic upper airway is surrounded by pleural pressure. However the exact anatomic site of this transition between the extra- and intrathoracic airway is not well defined because it may vary with longitudinal movement of the extension of the neck (31). Thus, there is a zone in the region of the thoracic inlet where varying effects may been seen. Extrathoracic Airway Atm ospheric Pressure Intratracheal Pressure Intrathoracic Airway Pleural Pressure Figure 7. Pressures affecting the intrathoracic and extrathoracic upper airway. Transmural pressure is calculated by subtracting the pressure outside the object from that inside it. Therefore transmura! pressure = Pjnside - Poutside Using this formula, luminal transmural pressure equals intraluminal minus extraluminal pressure, or 18 Ptransm ~ Pil "Pel where Ptransm is transmural pressure Pj| is intraluminal pressure, and Pel is extraluminal pressure. Clearly, if the intraluminal pressure exceeds the external pressure, the airway remains open. Conversely, if the extraluminal pressure exceeds the intraluminal pressure, the lumen of the airway tends to collapse. Therefore, a positive transmural pressure tends to open the airway, whereas a negative transmural pressure tends to collapse the airway. For a normal inspiration, the expanding chest cage and the descending diaphragm increase intrathoracic volume and creates a negative intrathoracic pressure due to decompression of gases within the thorax. Compared to atmospheric pressure outside the chest, the action of the normal inspiration creates a pressure gradient, so that air rushes in and expands the lungs through the opening mouth or nose. The rushing air causes a negative pressure inside the extrathoracic airway, and at the same time, however, there is a relative positive pressure (normal atmospheric pressure) outside the airway. Thus, there is a normal tendency of the extrathoracic airway to collapse during inspiration. Nevertheless this tendency is countered by the relative rigidity of the airway in the neck, as well as the neural innervation of the pharynx, which keeps the pharynx taut in order to prevent upper airway collapse (31). For pathophysiology, the degree of extrathoracic variable obstruction is increased during inspiration. The falling pressure within the trachea results in a decrease in the transmural pressure, causing the trachea to collapse and worsening the obstruction. With expiration, the intraluminal pressure of the trachea rises, causing a relative increase in the 19 transmural p ressu re and lessen in g th e d eg re e of obstruction with concom itant im provem ent of airflow (Fig. 8). EXPIRATION INSPIRATION > P atm Figure 8. Behavior of an extrathoracic upper airway obstruction throughout the respiratory cycle. Ptr: intratracheal pressure. Patm: atmospheric pressure. EXPIRATION INSPIRATION Ptr < Ppl Figure 9. Behavior of an intrathoracic upper airway obstruction during the respiratory cycle. Ptr: intratracheal pressure. Ppl: pleural pressure. 20 In intrathoracic obstruction, the forced expiration generates a positive pleural pressure exceeding the intraluminal pressure. This causes a decrease in the transmural pressure and collapses the airway, thus worsening the obstruction. In inspiration, the pleural pressure becomes more negative than the intraluminal pressure. This causes an increase in the transmural pressure, thereby lessening the obstruction and improving flow (Fig. 9). 2.4.2 Flow-Volume Loop and Airway Obstruction Using flow-volume curves, the kind of airway obstruction can be diagnosed. In the case of an extrathoracic variable obstruction, the inspiratory portion of the flow-volume loop would show a plateau (due to the decrease in transmural pressure during inspiration), whereas the expiratory portion of the curve would appear closer to normal (Fig. 10A). Conversely, an intrathoracic variable obstruction shows a plateau in the expiratory portion of the flow-volume loop (due to a negative transmural pressure during that portion of the respiratory cycle), w hereas the inspiratory curve would appear normal (Fig. 10B). If the plateau is present in the portion of both the inspiratory and expiratory flow-volume loops, it is a fixed upper airway obstruction regardless of whether the obstruction is intra- or extrathoracic (Fig. 10C) (31). 21 Expiratory flo w RV TLC Inspiratory flo w A Expiratory flo w Inspiratory flo w B RV TLC Expiratory flo w Inspiratory flo w TLC RV Figure 10. Characteristic flow-volume loop in (A), variable extrathoracic airway obstruction. (B), variable intrathoracic airway obstruction. (C), fixed intra- or extrathoracic airway obstruction. 22 2.5 Sleep Apnea In 1965 Gastaut, Tassinari, and Duron discovered that certain obese patients have the experience of abrupt and repetitive obstruction of the airway hundreds of times during a sleep night. Since then research on respiration during sleep speeded and revealed that respiratory physiology during sleep differs dramatically from that of wakefulness (9). The most exciting phenomenon is still the transient cessation of breathing during sleep. This behavior is called sleep apnea. Sleep apnea is most common in men and postmenopausal women, and its prevalence increases with age. Sleep apnea is also positively associated with obesity and a history of chronic alcohol intake. Certain features of jaw and facial structure may predispose an individual to sleep apnea. The key events in sleep apnea are now well known, but underlying causes are still uncertain. What are the real procedures that let people develop upper airway obstruction during sleep? There is evidence that each of the various theoretical causes does contribute to sleep apnea, and perhaps more importantly, each may dominate in different patients. In other words, although sleep apnea study recordings may look identical in any sample of patients, some may be the result of structural defects, whereas others may be entirely the result of neuromuscular abnormalities. 2.5.1 Types of Sleep Apnea Sleep apnea is defined as a greater-than-ten second pause in respiration during sleep, even though the lungs are entirely normal (30). Such patients have recurrent episodes of apnea resulting in a periodic breathing pattern. Three type of 23 apnea are observed. They are central, obstructive and mixed apnea (Fig. 11). In central sleep apnea, a patient is observed without the airflow and respiratory musculature activity. Obstructive apnea is characterized by contraction of the respiratory muscles but absent airflow. Mixed apnea is a central apnea followed immediately by an obstructive apnea (29). In general, the medical complications of central sleep apnea are not so clear as those in obstructive sleep apnea, and patients with central sleep apnea tend to be somewhat older than those with obstructive sleep apnea. CENTRAL A A A ____________ / \ / \ / \ ~ Airflow / \ / \ / ^ \ w Respiratory Muscle Activity OBSTRUCTIVE a / w w _ _ _ /Ja m A/\AyLyw\y\y\Ai v AAA. MIXED /V w v - - - - - - - - - - - - -A/W /i I VAA/ I _____ I 10 sec TIME Figure 11. Types of sleep apnea. Central: absence of muscle activity and airflow. Obstructive: absence of airflow in the presence of muscle activity. Mixed: central followed by obstructive apnea. Actually, many of the patients having obstructive sleep apnea have a pre existing UAO. As already described, while patients have an extrathoracic obstruction, the negative pressure inside the extrathoracic airway tends to suck the airway closed and then increase the obstruction during inspiration (see 2.4.1 24 transmural pressure and UAO). Thus, most patients with obstructive sleep apnea have a pre-existing abnormality that causes an UAO (29). 2.5.2 Mechanism of UAO during Sleep For sleep apnea, a structural abnormality in the upper airway is one important factor, but it is the only "cause" in some cases. Lower jaw disproportion, retrognathia, and obesity are well-known effects in sleep apnea. Many studies, however, indicate that neurophysiological and control abnormalities are also dominant factors in many patients. A major clinical problem is how to separate anatomical from neurophysiological components of sleep apnea. Actually, there is no easy way to partition the contribution of each of these components. Using the idea of balance of forces, which control upper airway patency, is a convenient way to explain UAO (10). 2.5.2.1 Upper Airway Patency The forces controlling upper airway patency are summarized in Figure 12. It offers a convenient visual framework to explain some of the interactions of respiratory muscle pump function and upper airway function. Upper airway patency is dependent on the balance between the tendency to collapse, induced by upper airway suction pressure, and upper airway dilator muscle activity. The suction pressure is a negative pressure, intraluminal pressure, during inspiration (see 2.4.1 transmural pressure and UAO). Hence, it is the key force provoking occlusion during sleep. Normally, the upper airway remains patent because the force exerted 25 by the upper airway dilator muscles exceeds the intraluminal pressure during inspiration. Respiration involves close coordination between respiratory pump muscles, particularly the diaphragm, and upper airway dilator muscles. The key force sustaining the airway open is muscle tone generated by the upper airway dilator muscles. Dilator muscle activity, by tensing the pharyngeal walls, makes the airway more rigid. They are driven by reflexes sensitive to changes in arterial oxygen and carbon dioxide, the same chemoreceptors that drive the respiratory pump muscle (35). Open Closed AIRWAY Reflex Local Airway Suction Inspiratory Drive Upper Airway Drive Dilator Muscle Tone Central Breathing Control Central Chem oreceptors Peripheral Chem oreceptors Figure 12. Balance of forces that sustain upper airway patency. The two major forces are airway suction pressure and upper airway dilator tone, and these are in turn influenced by other factors. (From Saunders and Sullivan 1994, p408) 26 2.5.2.2 Chemoreceptor Responses A number of studies in animals demonstrate that the upper airway dilator muscles receive drive from the respiratory control centers in the brain stem, which are sensitive to hypoxic and hypercapnic stimulation. The human upper airway musculature also responds to hypoxic and hypercapnic stimuli with activation of at least the genioglossus muscles (dilator muscles). Obstructive apnea can be induced in some healthy human subjects following a brief period of externally imposed hyperventilation during sleep. For the peripheral or central chemoreceptors, the difference in timing between the drive to the upper airway dilator muscles and to the inspiratory pump muscles may be an important mechanism in producing UAO (11). In other words, if inspiration is possibly initiated before there is any activation of dilator muscles, the upper airway is at risk of closure by the suction. There are some evidences supporting for this mechanism as a trigger of obstructive apnea. For example, sleeping animals and humans display an apneic threshold to arterial carbon dioxide levels (12). If normal human subjects are hyperventilated by external means to a minimal degree, apnea occurs at a highly reproducible level of arterial carbon dioxide. This phenomenon had been demonstrated in anesthetized subjects. Any circumstance that might cause instability of breathing, for example sleep onset, is a potential cause of apnea by this mechanism. 2.5.2.3 Local Reflexes An important set of reflexes originates in neural receptors that are located in the upper airway itself. A wide range of stimuli are detected by these neural 27 receptors. When there are unusual or abnormal event in upper airway, the responses of neural receptors are considered to be defensive rather than regulatory. However, evidence demonstrates that upper airway pressure-sensitive reflexes play an essential moment-to-moment role in upper airway patency in animals (13,14,15). These reflexes are markedly depressed by anesthesia and reduced in sleep. Upper airway negative suction pressure lengthens the duration of inspiration, augments the genioglossus activity, and reduces the peak effort of the inspiratory pump muscles. Importantly, this load-compensating reflex protects the upper airway in two ways. By stimulating dilator muscle activity (first way) and lengthening inspiratory time (second way), the reflex reduces the need for high suction pressure in the upper airway (14). Similar reflexes have been observed in normal adult humans during wakefulness. Evidence shows that there is an increase in genioglossus activity following the application of suction pressure to the upper airway (16,17). However, these reflexes are abolished after upper airway anesthesia (18). Inducing upper airway collapse with suction pressure in awake patients with UAO is possible (19). This possibility indicates that loss of these reflexes is likely to play a role in the pathogenesis of UAO. These reflexes also exist during sleep, but are less clear. Evidence showed that upper airway anesthesia in normal subjects can induce sleep-disordered breathing (20). This suggests the presence of a neurally mediated reflex that is operative during sleep. Observation demonstrated that the first occluded breath in both neonates and animals is associated with an increase in genioglossus activity (21,22). Moreover, a simple method had been used to examine these reflexes during sleep. The details of these experiments are 28 described extensively elsewhere (23,24). The results show that the loss of these reflexes may be an important part of the transition from snoring to sleep apnea. The most important concept from all discussions is that upper airway reflexes protect us from upper airway closure, at least during wakefulness. There is growing evidence that these reflexes are also operative during sleep. 2.6 Respiratory Inductive Plethysmography Respiratory inductive plethysmography (RIP) can produce waveforms which can be separated into measurements of tidal volume, airflow, expiratory and inspiratory time, and thoracoabdominal motion. The basic idea of RIP relies on the assumption that the respiratory system moves with two degrees of freedom, the abdomen and the rib cage. During normal inspiration, the diaphragm descends and displaces the abdomen while the rib cage expands outward. It was first described by Konno and Mead (25) in 1967. 2.6.1 Principle of RIP RIP now is the most widely accepted methods of measuring ventilation in a noninvasive and quantitative manner. Generally, this technique utilizes transducers to monitor not only tidal volumes, but also ventilatory frequency and breathing pattern. The transducers consist of two coils of insulated wire sewn sinusoidally onto each band placed around the chest wall and abdomen (Fig. 13). The coils are connected to a small oscillator. This oscillator generates frequency-modulated signals that are proportional to alterations in the self-inductance of the coil. The changes of cross-sectional area in the bands cause the orientation of the insulated 29 wire to be altered, resulting in a change in oscillatory frequencies due to changes in self-inductance. These signals are sent to a demodulator-calibrator unit that converts the signal into a proportional voltage that can be amplified and recorded. Figure 13. Transducer bands of the respiratory inductive plethysmography placed around the rib cage and abdomen. 2.6.2 Calibration of RIP Many different calibration procedures have been described and assessed for the RIP. These various procedures affect the accuracy and validity of RIP measurements. Calibration of the RIP is based on the assumption that the respiratory system behaves as a simple physical system with two moving parts: the abdomen and rib cage. Consequently, tidal volume measured at the mouth is equivalent to the sum of volume changes of the rib cage and abdomen. This concept of two degrees of freedom forms the basis of the various techniques that 30 can be used to calibrate the RIP during wakefulness or sleep. The classic calibration technique is the isovolume maneuver calibration procedure (IMC). It calibrates any noninvasive respiratory monitor that measures both the rib cage and abdomen contributing to tidal volume. Another calibration method, two-posture simultaneous equation method (SEM), is based on the principles of the IMC procedure (36). It suits the case of body position changes causing the contribution of the rib cage and abdomen to tidal volume between each compartment. However, obstructive apnea cannot be detected by RIP when the SEM calibration has been performed (36). Recently, Sackner and coworkers (26) developed a modification of the single posture technique that permits calibration of the RIP without the use of a spirometer or pneumotachograph and, thus, is particularly suited to clinical monitoring in critically ill patients. 2.6.3 Neck Inductive Plethysmography The ability of RIP to distinguish central and obstructive apnea had been suggested for use in the sleep laboratory. However, if respiratory efforts are weak, the RIP can fail to differentiate between central and obstructive apnea. Staats and coworkers (27) indicate a method of using esophageal manometry in this instance. A modification of RIP that includes neck inductive plethysmography (NIP) appears to be capable of detecting these minute respiratory efforts, even when rib cage and abdomen signals are flat. Recently, NIP had been used to measure changes in cervical cross section. Lustro and colleagues (28) present evidence on the reliability of measuring cross-sectional area of extrathoracic airways by NIP in healthy 31 subjects during resistive breathing. Further studies are required to asse ss its validity in the diagnosis of sleep related breathing disorders. 32 Chapter 3 METHODS 3.1 Experimental Apparatus By applying neck inductive plethysmography (NIP), this experiment was designed to investigate the respiratory properties in upper airway of a subject with obstructive apnea at different continuous positive airway pressure (CPAP) conditions. In order to investigate the subject's methodological situation, four measurements were recorded - nasal airflow (V) measured by pneumotachograph, negative esophageal pressure (P es) detected by a pressure transducer at level of supraglottis, nasal mask pressure (Pmask). and neck Respitrace (Resp) via a NIP to measure changes in C SA of the underlying neck. In this experiment, a pneumotachograph was included in the circuit to provide a simultaneous measurement of airflow. A tight-fitting nasal mask was used to isolate the subject's nose and its tubing was connected to one side of the pneumotachograph (model 3700, Hans Rudolph). An airway m anagem ent system providing different CPAP was also connected by tubing to the other side of the pneumotachograph. In addition, the transducer band of the NIP surrounded subject's neck to measure Resp- For measuring these physiological parameters, the subject's mouth was always sealed with tape to prevent air leak during the experiment. V was measured using a differential pressure transducer across the pneumotachograph, Pmask was measured using a pressure transducer connected to a pressure tap on the nasal 33 mask, and P es was measured using a pressure transducer tipped catheter inserted via the nose into the upper airway. However, a preamplifier was employed in circuit to amplify Resp because the signal generated from the transducer of NIP was at the mV level. The final measurements of these four physiological parameters sent to the computer for further processing and analysis. The experimental apparatus is shown in Figure 14. CPAP pneumotachograph differential pressure - transducer pressure transducer preamplifier Bmask. Resp NIP Figure 14. Experimental apparatus. 34 3.2 Experimental Protocol The objective of this experiment was to investigate the respiratory properties in the upper airway of a representative subject with OSA during the application of various levels of CPAP. For the management of CPAP, a procedure of proportionately ascending CPAP (ACPAP) in increments of 2 cmH20 from 3 to 15 cmH20 was applied after the starting of CPAP=0 cmH20 situation. Subsequently, a corresponding procedure, descending CPAP (DCPAP), was utilized from 13 to 3 cmH20 (Fig. 15). The patient with OSA was placed in the supine posture during sleep, then four physiological parameters — V, Pes, Pmask. and Resp— were simultaneously measured during NREM sleep in stages 1 and 2. These four analog signals with electrical waveform were led into a 486 based personal computer equipped with a analog-to-digital converter (ADC) circuit. For each CPAP condition of the ACPAP and DCPAP case, data was recorded for about 7 minutes at sampling rate 100 pts/s via ADC. 15 1 3 1 1 /F" i ,/iv 0 cmH20 A scending CPAP 13 11 D escending CPAP Figure 15. Management of CPAP during experimentation: ascending CPAP immediately ensued by descending CPAP. 35 3.3 Data Analysis The recored data were stored by the waveform playback software, WINDAQ, which provided an easy way to review and analyze acquired waveforms. After reviewing the data, MATLAB was chosen for data analysis and graphics in this experiment. The interface between WINDAQ and MATLAB had been developed (see Appendix). 3.3.1 Data Calibration Except Resp. calibrations of V, Pes, and Pmask were required prior to analyzing for this experiment. V was calibrated with 500 ml syringe, so the following equation was employed to find the calibration coefficient p: pxE[(Af(i)-Bl)xAt] = 0 .5 x B n where Af represents measured inspiratory airflow, Bl is the baseline during recording, B n is the breath number, and At is the time interval (A t= 0 .0 5 ). After calculating, p is equal to 2.19. For calculating Pes and Pmask. the simplest method, linear equation, was used. Therefore, the following equations were applied to the calibration: Pes = - 40.36xMsi - 63.65 (cmH20) Pmask = - 5.51 xMS2 - 0.41 (CIT1 H 2 O ) V = 2.19xMS3 + 0.075 (liter/sec) where Ms1, Ms2 and Ms3 are the original data of Pes. Pmask and V .respectively. 36 Via inspection, calibrated data was classified into three types for further studies: complete upper airway obstruction (CUAO), partial upper airway obstruction (PUAO), and no upper airway obstruction (NUAO). The typical waveforms were demonstrated in Figure 16. According to these types, subsequent methodology was developed. 20 w" 10 “ -10 -20 -30 0 20 40 60 80 100 120 140 160 180 200 Tima (0.05 s e c ) 20 — 10 9, I 0 -10 - 20, 0 20 40 60 80 100 120 140 160 180 200 (A) Tima (0.05 sec) Pes C U A O PU A O v > < 5 5 -20 -30 140 160 180 200 ( 0.05 se c ) 60 100 120 Time Pes -10 -20 100 120 140 160 180 200 60 20 (B) Time (0.05 s e c ) 37 N U A O — -10 -20 -30 60 100 120 TImo 140 160 160 200 (0.05 se c ) Pos -20 0 20 60 60 100 120 140 160 100 200 Tima (0.05 sa c) Figure 16. Typical waveforms of V and Pes: (A) CUAO, (B) PUAO, and (C),NUAO. 3.3.2 Data Analysis Before illustrating the analysis methods, the relationship between CPAP (both ACPAP and DCPAP) and the three classified types (CUAO, PUAO and NUAO) should be demonstrated (Tab. 1). NUAO exists in all conditions of CPAP, and PUAO in the conditions of CPAP= 5, 7, and 9 cmH20; nevertheless, CUAO exists only in the CPAP conditions equal to 0 and 3 CIT1 H 2 O . CPAP (cmH20) 0 3 5 7 9 11 13 15 CUAO X X PUAO X X X NUAO X x X X X x x x Table 1. Relationship between CPAP and different types of upper airway obstruction. Mark "x" represents existence. 38 3.3.2.1 Data Classification The representative waveforms of CUAO, PUAO, and NUAO in the ACPAP case were shown in Figure 17, 18, and 19, respectively. According to these three different types of obstruction, some variables will be defined later to investigate the properties between them and CPAP. (see 3.3.2.2 analysis method) CPAP*0 cmH20 10 0 60 100 160 200 250 300 Tim* 360 400 460 600 (0.05 SOC) 0 60 100 160 200 250 300 Time 350 400 450 600 (0.05 s e c ) 0 60 100 150 200 250 300 Time 350 400 450 500 (0.05 sec) (A) CPAPO cmH20 10 •10 350 400 460 600 (0.05 sec) 0 60 100 160 200 250 300 Time 60 0 60 100 160 200 250 Tlmo 300 350 400 450 500 (0.05 sec) 0 60 100 150 200 260 Tim* 300 360 400 450 500 (0.05 SOC) Figure 17. The representative waveforms of CUAO in cases of (A) CPAP=0, and (B) CPAP=3. 39 CPAP«5 cmH20 6 0 - N 0 0: 60 100 160 200 250 300 360 400 Time (0.05 sac) •so> 60 100 150 200 Tima 300 350 400 (0.05 sec) (A ) 60 100 150 200 Tim# 250 350 400 (0.05 s e c ) CPAP»7cmH20 •* 5 0 ■ - ■ - -■ ■ 50 100 150 200 250 300 350 400 Tima (0.05 sec) 50 100 160 200 250 300 350 400 Tima (0.05 sec) ■ ■ ■ ■ (B) 60 100 160 200 250 300 350 <00 Tlmo (0.05 ioc) CPAP*9 cmH20 •50 -- 50 100 150 200 250 300 350 400 Tima (0.05 sec) •60 60 100 150 200 250 300 350 400 Tima (0.05 sec) (C ) 50 100 150 200 250 300 350 400 Tims (0.05 «ec) Figure 18. The representative waveforms of PUAO in cases of (A) CPAP=5, (B) CPAP=7, and (C) CPAP=9. 40 CPAP*0cmH20 100 w 1° -100 60 1 0 2 0 - 2 ( A ) 60 100 160 Tim* 60 100 160 Tima 200 60 1C 0 160 Tim# 250 300 (0.05 so c) - I ... I.. 250 300 (0.05 so c) 250 300 (0.05 see) * 0 5 60 ^ ° -60 Reip < B ) CPAP*3 cmH20 60 100 160 Tlmo 60 100 160 Tlmo 200 ■ » 60 100 160 Tlmo 250 300 (0.05 soc) 250 300 (0.05 so c) 250 300 (0.05 sec) CPAP«5cmH20 s # 60 100 150 200 Tlmo Pes 60 100 160 Tlmo 200 (C) 60 100 160 Tlmo 250 300 (0.05 sec) 250 300 (0.05 sec) 250 300 (0.05 sec) 41 CPAP-7 cmH20 50 1 0 •50 ( 2 0 ■ 2 A / X / ' V / V / ^ SO 100 160 200 PM 60 100 160 200 (0) 60 100 160 Tima 250 300 (0.05 sac) 250 300 (0.05 sac) 250 300 (0.05 sac) 60 M I ” •50 ( l ° ~ 2 Q ( 0.5 0 50 (E ) CPAP-9 cmH20 100 150 200 Tima 100 160 200 Tima 50 100 150 Tima 250 300 (0.05 sac) 250 300 (0.05 sec) 250 300 (0.05 sec) 50 w 1 ° •50 ( _ 2 0 f ° ~ 2 0 t 0.5 0 50 (F) CPAP-11 cmH20 100 150 200 Tima 100 150 Tima 200 100 160 200 Tima 250 300 (0.05 sac) 250 300 (0.05 sec) 250 300 (0.05 se c ) 42 F ig u re 19. T he represen tative w aveform s of NUAO in all c a s e s o f C PAP. 3.3.2.2 Analysis Method As described earlier, the calibrated data in both ACPAP and DCPAP ca se s w ere classified by three different types of obstruction - CUAO, PUAO, and NUAO (see 3.3.2.1 data classification). After inspecting the physiological features am ong them, som e variables relying on only the inspiration part of each respiration cycle w ere defined. For the CUAO case, variables AResp and APes w ere defined (Fig. 20) and em ployed to investigate physiological properties of OSA; furthermore, another variable Gaw w as defined in PUAO and NUAO ca se s in addition to AResp (Fig- 21). Originally, Gaw w as defined a s the following: G aw = Afp / [ (Pi-Pm l) - (P2*Pm2) ] ° r Gaw = A fp /[(P i-P 2) - ( P mi-Pm 2)] w here P mi is the m ask pressure corresponding to the airflow at the beginning of inspiration, and P m2 is the m ask pressure corresponding to the airflow at the peak of inspiration. Since the difference in m ask pressure (Pm 1-Pm2) is always less than 10% of the esophageal pressure difference (P 1-P 2 ) in this study (i.e. (P-|- P 2)>:>(Pm 1-Pm2)). therefore the definition of Gaw in Figure 21 w as used to calculate the airway conductance. Gaw is the upper airway conductance which is inverse proportional to airway resistance as outlined in section 2.2. For PUAO, note that there w as a significant ph ase lag betw een AResp and Pes, such that th ese two signals were almost completely out of phase. For this reason, the values of AResp corresponding to inspiratory V w ere considered negative. 44 Pes APes P2 R1 Resp AResp R2 A P es = P2 - P1 AResp = R2 - R1 Figure 20. Definition of A R esp and APes f° r CUAO case. P ea k Pes P2 Resp AResp R2 R2 Resp AResp R1 G aw = Afp / (P1-P2) AResp = R2 - R1 Figure 21. Definition of A R esp and Gaw for (A) PUAO and (B) NUAP. 45 Chapter 4 RESULTS 4.1 NUAO and PUAO NUAO existed in all conditions of ascending a s well a s descending C PAP procedure in this experim ent (see table 1). Originally, variable APe s w as also included to investigate the respiratory properties of NUAO in addition to AResp and Gaw, but studies show ed that only G aw and AResp dem onstrated a significant correlation. For the ACPAP case, Figure 22 illustrates the changing relationship betw een Gaw and ARasp during the procedure of proportionately ascending CPAP in increm ents of 2 cm H20 from 3 to 15 cm H20 (Fig. 22. (B) ~ (H)) after CPAP equals 2 cm H20 (Fig. 22. (A)). This procedure led to one phenom enon - AResp d escended gradually and Gaw increased simultaneously w hen CPAP conditions w ere less than 9 cmH20; however, when CPAP conditions w ere equal to or more than 9 cm H2O , AResp never descended but Gaw still increased. The joining of Figure 22 from (A) to (H) formed Figure 23 provided an advantageous m ethod for observation in NUAO studies. (A ) CPAP=0 cmH20 3 3.5 A (Uter-sec’-cmHzO-’) 46 G ) m AResp N ) o o cn cn o ro c o ro to cn A Resp o ro o bi “ 0 ++ C O O C O - O i AResp t O — I------------- i— 0 0 1 o Q > ro € ro cn C C D 3 X ro O & * % i i c o cn 4^ CPAP=9 cmH20 o CD AResp AResp ro o o cn ro ro oi c o O D ) € c C D o 3 X o ro o o bi "0 ro co co cn AResp ro cn O o > ro 3 co . ro E S T C / 3 C D C O X ro o “ i------------- 1 ------------- r CPAP=15 cmH20 c l2 - w Q ) 5 ’ (H) 0.5 1.5 2 Gaw 2.5 3 3.5 4 (LHer-S8C'1 'anH20 '1 ) Figure 22.G aw versus ARe sp in the ACPAP case of the NUAO state: (A) CPAP=0, (B) CPAP=3, (C) CPAP=5, (D) CPAP=7, (E) CPAP=9, (F) CPAP=11, (G) CPAP=13, (H) CPAP=15 (cmH20 ). 2.5 a h *+ +++ H ++ +++ 0.5 H r # ' v +++ + + + +++f+++^.+ ++++ 0.5 1.5 2.5 3.5 A (Ut9r.sec'''CmH20 _l) Gaw Figure 23. Data sets distribution between Gaw and AResp in the ACPAP case of the NUAO state (CPAP from 0 to 15 C I T 1H2 O). As described already, after ACPAP manipulation, a corresponding and su b seq u en t procedure, DCPAP, from 15 to 3 C IT 1 H2O w as applied (see 3.2 experim ental protocol). In order to com pare DCPAP with ACPAP, the CPAP=0 C IT 1 H2O condition in the ACPAP case w as also presented in the results of the 48 DCPAP case. Figure 24 dem onstrated the results. In Figure 24, the data sets with mark '+' in a circle represented the CPAP=0 cm H 20 condition. Obviously, the results of Figure 23 and 24 show ed that the distribution sh ap es of the data sets in the DCPAP c a se and the ACPAP case of the NUAO state w ere quite similar, but there w as a slight degree of discontinuity betw een CPAP=3 and CPAP=0 in the DCPAP c a se (Fig. 24). 2.5 + + CL V ) « a : < + + + + , .+ • * * - . 0.5 2.5 0.5 Gaw Figure 24. Data sets distribution between Gaw and AResp in the DCPAP case of the NUAO state (CPAP from 15 to 3 cmH20). Mark '+' with circle represented the CPAP=0 cm H 20 condition in the ACPAP case. M ethods for finding empirical relationships betw een variables w as required b eca u se the mathematical relationships betw een variables w as the goal of this study. All the data obtained from this experiment showed curvilinear relationships betw een variables; therefore, a polynomial curve fitting technique (Horner's method) 49 w as em ployed. Curves A and B (second degree polynomials) in Figure 25 and 26 (ACPAP and DCPAP respectively) were the m athem atical relationships betw een Gaw andAResp. The dashed lines represent the 95 percent confidence interval for predictions. The reason for dividing the data sets into two parts is that their physiological properties are different. The interface w as located in the CPAP condition betw een 7 and 9 cm H20. As shown in Figure 26, the data (double circle) obtained from the CPAP=0 cm H 20 condition w ere not included to predict the curve A. However, the predicting results including th ese data set w as revealed in Figure 27. 2.5 curve A a curve B 0.5 1.5 0.5 2.5 Gaw Figure 25. Experimental relationships between Gaw and AResp in the ACPAP case of the NUAO state. The interface between curve A and B was located in the CPAP condition between 7 and 9 cmH20. 2.5 ^ curve A ® Q curve B 0.5 1.5 2.5 0.5 Gaw Figure 26. Experimental relationships between Gaw and AResp in the DCPAP case of the NUAO state. The interface between curve A and B was located in the CPAP condition between 7 and 9 cmH20. 2.5 curve A a > 1.5 0.5 0.5 3.5 2.5 Gaw Figure 27. Experimental relationships between Gaw and AResp in the DCPAP case of the NUAO state including CPAP=0 cmH2 condition. The interface between curve A and B was located in the CPAP condition between 7 and 9 C IT 1 H2O. 51 According to the results of Figures 25 and 26, physiological properties of the NUAO can be elucidated. Curve A dem onstrates that the neck CSA changes (AResp) diminished rapidly and upper airway conductance (Gaw) increased simultaneously while CPAP increased. Curve B show s that the CSA chan g es of the neck w as very little while upper airway conductance still increased w hen CPAP increased from 9 to 15 cmH20. PUAO only existed for CPAP equal to 5, 7, and 9 cm H 20 (see 3.2 experimental protocol). The sam e m ethods used in the NUAO c a se w ere also applied in the PUAO case to find the mathematical relationship betw een the G aw and AResp variables. The second degree curves in Figure 28 (ACPAP case) and 29 (DCPAP case) dem onstrate the results. According to the definition of AResp (s e e 3.3.2.2 analysis method), the positive AResp m eans the airway tends to extend and negative AResp m eans the airway tends toward obstruction during inspiration. Moreover, the absolute value of AResp indicated the m agnitude of neck CSA changes. Therefore, the results of PUAO showed similar respiratory properties with NUAO ca se except that NUAO caused upper airway extension but PUAO induced upper airway obstruction. 52 • 0.1 • 0.2 +/ + + A + S -0.3 -0.4 ■0.5 3.5 4 (Uler-sec'-cmHsO"') 3 2.5 0.5 1 1.5 2 Gaw 0 Figure 28. Experimental relationship between Gaw and AResp in the ACPAP case of the PUAO state. (CPAP conditions: 5, 7, and 9 C IT 1 H2O) •0.1 •0.2 ++ + + + A •0.4 + v + / -0.5 0 0.5 3.5 1 1.5 2.5 3 4 2 Gaw (Uter-sBC-'-cmHjO"') Figure 29. Experimental relationship between Gaw and AResp in the DCPAP case of the PUAO state. (CPAP conditions: 5, 7, and 9 cmH20) 53 4.2 CUAO In this experiment, CUAO only appeared in the conditions of CPAP=0 and CPAP=3 cm H20. For CUAO, the relationships betw een APes and AResp w ere investigated to reveal the respiratory properties in the upper airway of a subject with OSA. According to the definition of APes and AResp and using the polynomial curve fitting technique (second degree), the data sets and the experim ental relationships betw een APes and AResp w ere obtained and shown in Figures 30, 31, and 32. Figure 30 shows the results in CPAP=0 cm H20 condition, and Figures 31 and 32 represent the results in the CPAP=3 cm H20 condition of the ACPAP and DCPAP cases, respectively. Obviously, in Figures 30, 31, and 32 all the experim ental relationships betw een APes and AResp are alm ost like straight lines with positive slope, but actually they w ere second order polynomials. It illustrates our belief that APes is approximately linearly proportional to AResp- As outlined already, the transm ural pressure is defined a s the intraluminal pressure of the upper airway less the extraluminal (atm ospheric) pressure. For pathophysiology, if the extraluminal pressure exceeds the intraluminal pressure, the upper airway tends to collapse. Conversely, if the intraluminal pressure ex ceed s the extraluminal pressure, the upper airway remains open. Therefore, a negative transm ural pressure tends to collapse the upper airway, w hereas a positive transm ural pressure tends to splint the upper airway (Fig. 8). For this experiment, variable APes w as defined a s the definition of transm ural pressure. During inspiration, the falling esophageal pressure Pes within the upper airway resulted in the negative APes (transmural pressure). As Figures 30, 31, and 32 show, the negative APes caused the upper airway to collapse and w orsened the obstruction b ecau se the AResp w as also negative simultaneously. Moreover, the experim ental 54 results illustrated that the changes of esophageal pressure (APes) w ere linearly proportional to the neck CSA changes (AResp). •0.2 -0.4 •0.6 o o - 0.8 O o - 1.2 -1.4 - 1.6 -10 -20 •40 -30 -70 -60 -50 APes -100 -90 -80 Figure 30. Experimental relationship between APes and AResp in CUAO state. (CPAP=0 cmH20) 55 •100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 A Pes (cmH2 0) Figure 31. Experimental relationship between APes and AResp in the ACPAP case of the CUAO state. (CPAP=3 cmH20) - 0.2 -0.4 J* ' Oo/oO -0.6 - 0.8 Q. « < U cr < - 1.8 •100 -90 -80 -70 -60 -40 -30 -20 -10 0 ■50 A Pes (cmHjO) Figure 32. Experimental relationship between APes and AResp in the DCPAP case of the CUAO state. (CPAP=3 cmH20) Chapter 5 DISCUSSION AND CONCLUSIONS A method to a ss e s s CSA changes of the upper airway by using an inductive plethysm ograph band placed around the upper part of the neck has been presented. The experimental results strongly suggest the reliability of measuring CSA changes of the upper airway by NIP in healthy subjects during resistive breathing (28). In the NUAO studies, the significant relationships betw een airway conductance and neck CSA changes over a wide range of CPAP levels w ere found, as shown in Figures 25, 26, and 27. Comparing the ACPAP case with the DCPAP case, the slope of curve A in Figure 26 w as steeper than that of curve A in Figure 25. This evidence suggests the existence of hysteresis in the m echanics of the upper airway, which may not be entirely surprising. This conclusion is yet to be validated b ecau se it should be supported by a much larger sam ple of patients with OSA. Except for this feature, the results suggest similar upper airway dynamics betw een the ACPAP and the DCPAP case. Increasing the level of CPAP from 0 to 7 cm H20 increased the inspiratory upper airway conductance and this correlated strongly with larger amplitudes of NIP output. However, when CPAP w as increased to 9 cm H 20 or higher, the NIP indicated no further changes in amplitude although airway conductance still increased. From visual inspection of the waveforms of airflow, it is clear that PUAO only existed in the CPAP = 5, 7, and 9 cm H20 conditions. The characteristics of the 57 upper airways during PUAO have been illustrated (Fig. 28, 29). As described already, the absolute value of AResp represented the m agnitude of neck CSA changes, and the sign of AResp indicated the direction of the neck m ovem ent. In other words, the airway extension indicated the AResp value w as positive like NUAO, and the negative AResp value in PUAO studies reflected that the upper airway w as obstructed. Actually, the experimental relationships betw een airway conductance and neck CSA changes showed that the physiological properties of the PUAO studies w ere similar with that of the NUAO studies except NUAO caused airway extension different from PUAO induced airway obstruction. Furthermore, a quantitative difference betw een PUAO and NUAO in the ACPAP case w as illustrated in Figure 33. For convenience, the sam e CPAP conditions betw een 5 and 9 cm H 20 w ere considered b ecau se PUAO only existed in CPAP= 5, 7, and 9 C 1 7 1 H2O conditions. In Figure 33, the dotted curve A and solid curve B represented the NUAO and PUAO cases, respectively. It show ed that the absolute values of AResp in the NUAO state w ere always bigger than those in PUAO state. Furthermore, there w as a significant difference in the slopes betw een NUAO and PUAO while airway conductance w as less than 2.2 Liter-sec-1 -cm l^O -1. In other words, at the sam e CPAP condition, the m agnitude of the airway extension in the NUAO state w as much larger than that of airway obstruction in the PUAO state. 58 cu rve A: NUAO cu rve B : PUAO + + + - * H - Q. < 0.8 0.6 c u r v e A .++ 0.4 c u r v e B 0.2 3.5 2.5 0.5 Gaw (UtePsec-,’C m H 20"’) Figure 33. Comparison of NUAO and PUAO in ACPAP (CPAP= 5, 7, and 9 cmF^O). In the CUAO studies, the relationship betw een APes and AResp w as investigated to reveal the mechanical properties in the upper airway of the subject with OSA. Clearly, APes w as defined as transmural pressure in this experiment. The negative and positive transmural pressure tends to collapse and splint the upper airway, respectively (Fig. 8). During inspiration, the falling eso phageal pressure resulted in the negative APes reflecting the collapse of the airway if AResp w as also negative simultaneously. The experimental results dem onstrated the truth described above and show ed that a significant linear relationship w as found betw een the changes of esophageal pressure (APes) and the neck CSA changes (AResp) during inspiration in the CPAP conditions equal to 0 and 3 C IT 1 H2O in both ACPAP and DCPAP c a se s (Fig. 30, 31, and 32). 59 Moreover, in order to com pare the CUAO betw een CPAP=0 and CPAP=3 cm H20, the three linear fits of the experimental results of Figure 30, 31, and 32 are dem onstrated in Figure 34. It clearly shows that at the sam e APes, the absolute AResp value of linel is always bigger than that of Iine2 and Iine3. In other words, at the sam e APes, the magnitude of the airway collapse in the CPAP=0 C IT 1 H2O condition w as always larger than that in CPAP=3 cm H20 condition in both ACPAP and DCPAP cases. However, there is a small difference in slopes betw een the ACPAP and the DCPAP case. The slope of the DCPAP c a se (line 3) is steep er than that of the ACPAP case (line 2). This phenom enon w as similar with the NUAO studies - the slope of curve A in Figure 26 w as steep er than of curve A in Figure 25. line 2 -0.5 line 3 -0.6 line 7 -0.7 - 0.8 line I. CPAP=0 cmH20 line 2. CPAP=3 cmH20 In ACPAP case line 3: CPAP=3 cmH2Q In DCPAP case -20 -30 -40 -60 -50 APes -70 -80 -100 -90 Figure 34. Comparison of CUAO between CPAP= 0 and CPAP=3 cmH20 . 60 In summary, the results of this experim ent show ed a highly significant relationship betw een the upper airway conductance and the neck CSA changes m easured by NIP during inspiration at various CPAP levels, no m atter w hat the NUAO or the PUAO studies (Fig. 25, 26, 28, and 29). The critical point of the neck CSA ch an g es w as located in the CPAP condition betw een 7 and 9 C IT 1 H2O. Therefore, while the CPAP conditions w ere smaller than 9 C IT 1 H2O, the m agnitude of the airway extension of the NUAO or the magnitude of the airway collapse of the PUAO w as proportional to the upper airway conductance. Furthermore, in CUAO studies, sim ultaneous m easurem ents of CSA mutation of the neck by noninvasive NIP and esophageal pressure by invasive transducer show ed a significant linear relationship betw een the changes of esophageal pressure (APes) and the neck CSA chan g es (AResp) (Fig- 30, 31, and 32). Thus, it seem s reasonable to presum e that neck CSA changes are a good reflection of the changes of esophageal pressure. In conclusion, this experim ent had shown that NIP is a useful and noninvasive m ethod for the estimation of upper airway dynam ics of a patient with OSA. Further studies are required to a sse ss its validity in the diagnosis of a much larger sam ple of patients with OSA. 61 REFERENCES 1. Spann, R. W., and R. E. Hyatt. Factors affecting upper airway resistance in conscious man. J. Appl. Physiol. 31: 708-712, 1971. 2. Haight, J. S. J.,and P. Cole. The site and function of the nasal valve. Laryngoscope. 93(1): 49-55, 1983. 3. McCaffrey, T. V., and Kern, E. B. Response of nasal airway resistance to hypercapina and hypoxia in man. Ann. Otol. Rhinol. Laryngol. 88: 247-252, 1979. 4. Cole, P., J. S. J. Haight, K. Naito, et al. Magnetic resonance image of the nasal airway. Am. J. Rhinol. 3(2): 63-67, 1989. 5. Zinreich, S. J., D. W. Kennedy, A. J. Kumar, et al. MR imaging of normal nasal cycle: Comparison with sinus pathology. J. Comput. Assist. Tomogr. 2(6): 1014-1019, 1988. 6. Rodenstein, D. O., and D. C. Stanescu. The soft palate and breathing. Am. Rev. Respir. Dis. 134: 311-325, 1986. 7. Cole, P., A. Ayiomamitis, M. Ohki. Anterior and posterior rhinomanometry. Rhinology 27: 257-262, 1989. 8. Anch A. M., J. E. Remmers, Bunce, H. I. 1.1. Supraglottic airway resistance in normal subjects and patients with occlusive sleep apnea. J. Appl. Physiol. 53(5): 1158-1163, 1982. 9. Orem, J., and Barnes, C. D. (Eds), Physiology in sleep. New York: Academic Press, 1980. 10. Trach, B. J., R. T. Brouilette. The respiratory function of the pharyngeal musculature: relevance to clinical obstructive apnea. In: "Wenner-Gren Symposium on Central Nervous Control Mechanisms in Regular Periodic and Irregular Breadline: Physiological and Clinical Aspects in the Adult and Perinatal States", Edt 1' Euler, H. Lagercrantz, New York: pergamon Press, 1980. 11. Hwang, J. C., W. M. St John, Bartlett, D. Jr. Afferent apthways for hypoglossal and phrenic responses to changes in upper airway pressure. Resp. Physiol. 55: 341-354, 1984. 12. Skatrud, J. B., and Dempsey, J. A. Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation. J. Appl. Physiol. 55: 813-822,1983. 62 13. Mathew, O. P., Y. K. Abu-Osba, B. T. Thach. Influence of upper airway pressure changes on genioglossus muscle respiratory activity. J. Appl. Physiol. 52: 438-444, 1982. 14. Mathew, O. P., J. P. Farber. Effect of upper airway negative pressure on respiratory timing. Resp. Physiol. 54: 252-268, 1983. 15. McNamara, S. G., F. G. Issa, E. Szeto, and C. E. Sullivan. Influnce of negative pressure applied to the upper airway on the breathing pattern in unanaesthetized dogs. Resp. Physiol. 65: 315-329, 1986. 16. Leiter, J. C., Daubenspeck, J. A. Selective reflex activation of the genioglossus in humans. J. Appl. Physiol. 68: 2581-2587, 1990. 17. Horner, R. L., Innes J. A., Murphy, K., and Guz, A. Evidence for reflex upper airway dilator muscle activation by sudden negative aireay pressure in man. J. Physiol. (Lond.) 436: 15-29, 1991. 18. Horner, R. L., Innes, J. A., Holden, H. B., and Guz, A. Afferent pathway(s) for pharyngeal dilator reflex to negative airway pressure in man: a study using upper airway anaesthesia. J. Physiol. (Lond.) 436: 31-44, 1991. 19. Suratt, P. M., Wilhoit, S. C., and Cooper, K. Induction of airway collapse with subatomospheric pressure in awake patients with sleep apnea. J. Appl. Physiol. 57: 140-146, 1984. 20. McNicholas, W. T., Coffey, M., McDonnel, T., O'Regan, R., and Fitzgerald, M . X. Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anaesthesia. Am. Rev. Respir. Dis. 135: 1316-1319, 1987. 21. Carlo, W. A., Miller, M. J., and Martin, R. J. Differential response of respiratory m uscles to airway occlusion in infants. J. Appl. Physiol. 59: 847-852, 1985. 22. Cohen, G., and Henderson-Smart, D. J. Upper airway muscle activity during nasal occlusion in newborn babies. J. Appl. Physilo. 62: 2026-2030, 1987. 23. Issa F. G., Sullivan C. E. Upper airway closing pressures in snorers. J. Appl. Physiol. 57:528-535, 1984. 24. Issa F. G., Sullivan C. E. Upper airway closing pressures in obstructive sleep apnea. J. Appl. Physiol. 57: 520-527, 1984. 25. Konno, K., Mead, J. Measurement of the separate changes of rib cage and abdomen during breathing. J. Appl. Physiol. 22: 407, 1967. 26. Sackner, M. A., Watson, H. Belsito, A. S., Feinerman, D., Suarez, M., Gonzales, G., Bizousky, F., and Krieger, B. Calibration of respiratory inductive plethysmography during natural breathing. J. Appl. Physiol. 66: 410-420, 1989. 63 27. Staats, B.A., Bonekat, H. W., Harris, C. D. et al: Chest wall motion in sleep apnea. Am. Rev. Respir. Dis. 130: 59-63, 1984. 28. Lustro, G, Stanescu, D., Dooms, G., et al: Hypopharyngeal and neck cross-sectional changes monitored by inductive plethysmograph. J. Appl. Physiol. 68(6): 2649-2655, 1990. 29. Kryger, M. H. Abnormal control of breathing and sleep disorders. In: "Introduction to Respiratory Medicine." Edited by M . H. Kryger, 2nd edition, New York: Churchill Livingstone, 1990. 30. Fletcher, E. C. History, techniques, and definitions in sleep related respiratory disorders. In: "Abnormalities of Respiration during Sleep", Edited by E. C. Fletcher, Orlando: Grune & Stratton, 1986. 31. Roberts, J. T. Clinical management of the airway. In: "Pulmonary Function Tests to Evaluate the Airway", Eds. C. G. W. Dahlberg, and C. A. Hales, Philadelphia: W. B. Saunders, 1994. 32. Cole, P. The nose. In: "The Respiratory Role of the Upper Airways", Edited by P. Cole, Mosby, 1993. 33. Barelli, P. A. Nasopulmonary physiology. In: "Behavioral and Psychological Approaches to Breathing Disorders", Eds. Timmons, B. H., and Ley R., New York: Plenum Press, 1994. 34. Cole, P. Nasal Airflow Resistance. In: "Respiratory function of the Upper Airway", Eds. Mathew, O. P., and Sant'Ambrogio, G., New York: Marcel Dekker, 1988. 35. Cistulli, P. A., and Sullivan, C. E. Pathophysiology of Sleep Apnea. In: "Sleep and Breathing", Eds. Saunders, N. A., and Sullivan C. E., 2nd edition, New York: Marcel Dekker, 1994. 36. Branson, R. D., and Campbell, R. S. Impedance pneumography, apnea monitoring, and respiratory inductive plethysmography. In: "Monitoring in Respiratory Care", Eds. R. M. Kacmarek, D. Hess, and J. K. Stoller, Mosby, 1992. 64 APPENDIX Purpose of this C Program: Transfer the ASCII data of the WINDAQ to the MATLAB type data. User enters the following command under the M.S. DOD environment for data transfer: <fname> <ipdata> <opdata> <nofchn> fname: the filename of the executive program ipdata: the input ASCII data of WINDAQ opdata: the output data suited for MATLAB nofchn: the number of the channel for displaying the measurements in WINDAQ #include <fcntl.h> #include <stdio.h> #include <io.h> #include <stdlib.h> #include <math.h> #include <sys\types.h> #include <sys\stat.h> #define BUFFSIZE 12 char buff[BUFFSIZE]; main(argc.argv) int argc; char *argv[]; { FILE "outfile; int inhandle,bytes,i,j,k,chn,cnt; char string[5][15],buffer[50]; double f,E,temp; float val; cnt=1; if(argc != 4) { printf("Format: <filename> <indata> <outdata> <num of chn>"); exit(O);} if((inhandle = open(argv[1],0_RDONLY | 0_BINARY)) < 0 ) { printffCan't open file %s.",argv[1]); exit(O);} if((outfile = fopen(argv[2],"w")) == NULL) { printffCan't open file %s.",argv[2]); exit(O);} chn=atoi(argv[3]); while((bytes=read(inhandle,buff,BUFFSIZE)) > 0 ) { for(i=0;i<bytes/12;i++) { for(k=0;k<7;k++) string[0][k]=buff[k]; string[0][k+1]='\0'; for(k=0;k<3;k++) 65 string[1][k]=buff[k+8]; string[1][k+1]='\0'; f=atof(string[0]); E=atof(string[1]); temp=pow(10.0,E); val=(float)(f*temp); fprintf(outfile,"%10.4f ",val); if(chn==cnt) { fprintf(outfile,"\n"); cnt=0; } > /* for */ cnt++; } /* while*/ close(inhandle); fclose(outfile); return (0); } 66 INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer. The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps. Each original is also photographed in one exposure and is included in reduced form at the back of the book. 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Asset Metadata

Creator Chen, Chih-Ming (author)

Core Title Estimation of upper airway dynamics using neck inductive plethysmography

School Graduate School

Degree Master of Science

Degree Program Biomedical Engineering

Degree Conferral Date 1995-05

Publisher University of Southern California (original), University of Southern California. Libraries (digital)

Tag engineering, biomedical,OAI-PMH Harvest

Language English

Contributor Digitized by ProQuest (provenance)

Advisor Khoo, Michael Chee-Kuan. (committee chair), Maarek, Jean-Michel (committee member), Marmarelis, Vasilis A. (committee member)

Permanent Link (DOI) https://doi.org/10.25549/usctheses-c18-7395

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