What We Already Know about This Topic
❖ Although sitting posture improves symptoms in many patients with obstructive sleep apnea (OSA), whether it alters collapsibility of the pharyngeal airway during anesthesia is unknown
What This Article Tells Us That Is New
❖ In nine patients with OSA during general anesthesia with neuromuscular blockade, change from supine to sitting position significantly improved collapsibility of the pharyngeal airway
PHARYNGEAL airway obstruction impairs both spontaneous breathing and mechanical ventilation leading to severe hypoxemia during sleep or anesthesia.1
Presence of obstructive sleep apnea (OSA) is an independent risk factor for difficult and/or impossible mask ventilation during anesthesia induction.2,3
Establishment of airway management strategies for prevention or reversal of pharyngeal airway obstruction in anesthetized and paralyzed patients with OSA, therefore, is a significant task assigned to anesthesiologists responsible for patients' safety during perioperative periods.
Compared with supine posture, sitting posture is reported to decrease OSA frequency particularly in more obese patients with OSA,4
suggesting significant improvement of pharyngeal airway patency during sitting posture. However, no study has assessed postural changes of pharyngeal airway dimensions during sleep and anesthesia. In awake patients with OSA, previous studies demonstrated variable influences of sitting posture on the pharyngeal airway dimensions,5–10
possibly because of compensatory increase of the genioglossal muscle activity in response to the postural change from sitting to supine.7
Whereas significant decrease of upper airway closing pressure during sitting posture was reported in sleeping patients with OSA,11
pharyngeal muscle activity was not controlled during the closing pressure measurements in this study, and both structural and neural factors contributed to the influences of sitting posture on pharyngeal airway collapsibility.
We have developed a method for exclusively evaluating structural properties of each pharyngeal segment independently of the neural factors12
and successfully applied the methodology for assessing influences of various mechanical interventions on pharyngeal airway patency under general anesthesia.13–15
Accordingly, our primary purpose in this study was to test the hypothesis that sitting posture improves pharyngeal airway patency even under absence of neural mechanisms. We compared static pharyngeal mechanics of the passive pharynx during supine posture with those during sitting posture in anesthetized and paralyzed patients with OSA.
Materials and Methods
Subjects and Sleep Studies
Informed consent was obtained from all subjects after the aim and potential risks of the study were fully explained to each. The investigation was approved by the Hospital Ethics Committee (Graduate School of Medicine, Chiba University, Chiba, Japan).
We studied nine consecutive male patients with OSA who were interested in undergoing uvulopalatopharyngoplasty as a treatment for their OSA and were scheduled to have endoscopic assessment of their pharyngeal mechanics to determine whether they were favorable candidates for this procedure.16
Exclusion criteria in this study included (1) difficulty in performing mandible advancement and head extension, (2) presence of clinical symptoms suggesting chronic heart failure, (3) presence of pulmonary aspiration risk, and (4) presence of a beard, which potentially may cause a mask leak. All had histories of excessive daytime sleepiness, habitual snoring, and witnessed repetitive apnea. Sleep disordered breathing was evaluated by a pulse oximeter (Pulsox-5; Minolta, Tokyo, Japan) at home. All subjects were instructed to attach an oximetry finger probe before sleep and to remove the probe on awakening. After checking quality of the recordings of arterial oxygen saturation (Spo2
), oximetry variables were calculated by computer software.12–16
Although the oximetry evaluation alone does not clarify the nature of sleep-disordered breathing, we believe that all nine patients can be safely diagnosed as having OSA based on the oximetry results and the clinical symptoms.17
OSA diagnosis was confirmed by standard full polysomonography in seven patients with OSA. Recordings include bilateral electroencephalograms, bilateral electrooculograms, submental electromyogram, leg electromyograms, electrocardiogram, airflow measurement with a thermistor at the mouth and nose, thoracoabdominal wall motions, Spo2
, snoring over a microphone, and body position. Apnea was defined as absence of airflow for more than 10 s. Hypopnea was determined upon an apparent reduction of airflow for more than 10 s with reduction of Spo2
by more than 4% from the baseline. Apneic events were classified as obstructive, mixed, and central, and the apnea-hypopnea index was calculated as the total number of the obstructive or mixed apnea and hypopnea events per hour of sleep.
Preparation of the Subjects
Each subject was initially premedicated with 0.5 mg atropine. Studies were performed with the subjects in either supine position or sitting at a 62° angle on an adjustable medical stretcher trolley, with the neck in a comfortable neutral position. The sitting angle was chosen because it was the most upright position safe for an anesthetized and paralyzed patient without restraint equipment. A modified tight-fitting nasal mask was used. Care was taken to prevent air leaks from the mask, particularly when the airway was pressurized above 20 cm H2
O. Use of a chin strap maintained contact of the upper and lower incisors and eliminated air leaks through the mouth. Air leaks through the mask and mouth were detected by inadequate increase in the airway pressure (PAW
) and manual palpation. General anesthesia was induced by intravenous infusion of propofol (2 mg/kg) and intravenous injection of a muscle relaxant (vecuronium 0.2 mg/kg). General anesthesia with total paralysis was maintained by continuous infusion of propofol (6-10 mg · kg−1
) while the subject was ventilated through the nasal mask with positive pressure through an anesthetic machine. Complete paralysis was confirmed by no responses to train-of-four stimulations at the ulnar nerve. Spo2
and an electrocardiogram were continuously monitored, and blood pressure was noninvasively measured every 5 min. A slim endoscope (3 mm OD; FB10×; Pentax, Tokyo, Japan) was inserted through a 10-mm diameter hole in a modified nasal mask and into a naris (fig. 1
). A modified silicone rubber plug with continuous bubbles (15 mm OD; SILICOSEN type L; Shin-Etsu Polymer Co., Ltd., Tokyo, Japan) tightly plugged the hole and held the endoscope to prevent leakage around them. The tip of the scope was placed at the upper airway to visualize the retropalatal airway space (airway space behind the soft palate) and the retroglossal airway space (airway space behind the base of the tongue). A closed-circuit camera (ETV8; Nisco, Saitama, Japan) was connected to the endoscope, and the pharyngeal images were recorded on a videotape. Reading of PAW
, measured by a water manometer, was simultaneously recorded on the videotape.
To determine the pressure-area relation of the pharynx, the anesthetic machine was disconnected from the nasal mask. The latter was in turn connected to a pressure-control system capable of accurately manipulating PAW from +20 to −20 cm H2O in a stepwise fashion. Cessation of mechanical ventilation resulted in apnea caused by complete muscle paralysis. PAW was immediately increased up to 20 cm H2O, dilating the airway. While the subject remained apneic for 2 to 3 min, PAW was gradually reduced from 20 cm H2O to a closing pressure (P′close) of the retropalatal airway in a stepwise fashion. The latter represented the pressure at which complete closure of the retropalatal airway occurred, as evident on the video screen. In this experimental setting, the retroglossal PAW was not reduced below the retropalatal PAW. Spo2 was maintained above 95% during the apneic tests. This procedure of experimentally induced apnea allowed construction of the pressure-area relation of the visualized pharyngeal segment. The subject was manually ventilated for at least 1 min before and after the apneic test. Distance between the tip of the endoscope and the narrowing site was measured with a wire passed through the aspiration channel of the endoscope. Measurements were made for the retropalatal and retroglossal airways with patients lying supine and sitting at a 62° angle. Care was taken to maintain the neutral neck position throughout the procedure, particularly when the patient was in the sitting position, although we did not measure the head angle. After measurements of the static pharyngeal mechanics, lung volume changes from the supine to the sitting position were measured with a spirometer connected to a tightly fitted full facemask at atmospheric pressure. Patent airway was maintained during the lung volume measurement by triple airway maneuver (mandible advancement, neck extension, and mouth opening) with the use of two hands. Airway opening and absence of mask leak were confirmed by progressive increase of spirometer tracing in response to the postural change.
The technique and accuracy of conversion of the monitor pharyngeal image to an absolute value of cross-sectional area have been reported previously.15,18
In short, magnification of the imaging system was estimated at 1.0-mm interval distances between the endoscopic tip and the object (1-cm2
grid) in range of 5-30 mm, producing a relation between distance and pixels corresponding to 1 cm2
. At a defined value of PAW
, the image of the pharyngeal lumen was traced and counted pixels included in the area (SigmaScan version 2.0; Systat Software, Inc., San Jose, CA). The pixel number was converted to the pharyngeal cross-sectional area according to the distance-magnification relation. Using tubes of known diameter, we tested the accuracy of our cross-sectional area measurements.15
For a constant distance, the measured areas were systematically deviated from actual areas. The largest known area tested (0.95 cm2
) was underestimated by 11% because of image deformation at outer image area, and the smallest known area tested (0.03 cm2
) was overestimated by 13% because of reduction in image resolution. The measured luminal cross-sectional area (A) was plotted as a function of PAW
. We defined P′close
as the pressure corresponding to the zero area. At high values of PAW
, relatively constant cross-sectional areas were revealed; therefore, maximum area (Amax
) was determined as the mean value of the highest three PAW
(18, 19, and 20 cm H2
O). As reported previously,12–16
the pressure-area relation of each pharyngeal segment was fitted by the following exponential function: A = Amax
− B × exp(K × PAW
), where B and K are constants. A nonlinear least-squares technique was used for the curve fitting, and the quality of the fitting was provided by coefficient r2
(SigmaPlot version 2.0; Systat Software, Inc.). A regressional estimate of P′close
, which corresponds to an intercept of the curve on the PAW
axis, was calculated from the following equation for each pharyngeal segment: P′close
) × K−1
. The shape of the pressure-area relation was described by the value of K. When the pressure-area relation is curvilinear, compliance of the pharynx, defined as a slope of the curve, varies with changes in PAW
. Therefore, a single value of compliance calculated for a given PAW
does not represent collapsibility of the pharynx for entire ranges of PAW
. By contrast, the K value represents a rate of changes in the slope of the curve. When the K value is high, small reduction of PAW
results in significant increase in compliance, leading to remarkable reduction in cross-sectional area. Accordingly, collapsibility of the pharynx increases with increasing K value. We suggest that both P′close
and K values represent collapsibility of the pharynx, whereby the former determines the position of the exponential curve and the latter characterizes the shape of the curve.
Our study indicates that a maximum SD of our primary variable, the P′close
of patients with OSA, is 2.8 cm H2
Neill et al.11
found a difference of 4.3 cm H2
O of upper airway closing pressure between supine and sitting (30° upper body elevation). Because the effect of 62° upper body elevation was assessed in this study, we expected that the P′close
difference between the positions would be greater than 5 cm H2
O. Appropriate sample size was determined to be seven or more for detecting the difference assuming α = 0.05 (two tailed) and 80% power (SigmaStat 3.1; Systat Software, Inc.). All values are expressed by median (10th-90th percentiles). Wilcoxon signed rank test was used for comparison of static mechanics variables between the supine and sitting positions (SigmaStat 3.1). Mann-Whitney rank sum test was used for comparison of the static mechanics variables between the pharyngeal segments. Spearman rank-order test was performed for correlation analyses between P′close
differences between the positions and anthropometric and sleep study data (SigmaStat 3.1). P
less than 0.05 (two-tailed) was considered significant.
Endoscopic measurements of static pressure-area relations of the retropalatal and retroglossal airways were successfully performed in both the supine and sitting positions in all patients. As listed in table 1
, anthropometric characteristics and sleep study data varied among the patients with OSA. Median values of these variables indicate that they were middle-aged, overweight patients with moderate to severe OSA.
shows representative endoscopic pharyngeal images during step PAW
changes in one patient, clearly demonstrating that the sitting position significantly increased the cross-sectional area for a given PAW
at both retropalatal and retroglossal airways compared with the supine position. Table 2
summarizes changes in the static mechanic variables of the retropalatal and retroglossal airways of the patients in the supine and sitting positions. As indicated by relatively high r2
values, the exponential function fitted reasonably well the measured pressure-area relations. Change from the supine to the sitting position significantly increased median Amax
from 1.25 to 1.91 cm2
at the retropalatal airway and from 1.75 to 2.42 cm2
at the retroglossal airway. The K values representing stiffness of the pharyngeal airway were not statistically different in the positions. The position change significantly decreased median P′close
from 2.20 to −3.47 cm H2
O at the retropalatal airway and from 2.67 to −5.31 cm H2
O at the retroglossal airway. The P′close
values in the sitting position were below atmospheric pressure in all patients, whereas those in the supine position were above the atmospheric pressure (fig. 3
). Median differences of the P′close
between the positions are 5.89 (3.73-11.6) cm H2
O and 6.74 (4.16-9.87) cm H2
O at retropalatal and retroglossal airways, respectively, and were not different in the pharyngeal segments. Median lung volume increase in response to the position change from the supine to the sitting position was 330 (140-564) ml.
presents results of Spearman correlation analyses between P′close
position differences and lung volume change during the position change, anthropometric, and sleep study variables. We found no significant association or tendency of indirect association between the lung volume and the P′close
changes. Interestingly, influences of sitting position on retropalatal airway collapsibility were smaller in patients with more severe obstructive sleep apnea. No correlation was found at the retroglossal airway.
We found that the postural change from supine to sitting enlarged both retropalatal and retroglossal airways and decreased P′close at both pharyngeal segments by approximately 6 cm H2O in completely paralyzed and anesthetized patients with OSA. The results clearly demonstrate that structural properties of the passive pharynx improve while patients are in the sitting posture.
Mechanisms of Pharyngeal Airway Patency Improvement during Sitting Position
Our results agree with the previous studies examining influences of sitting posture on pharyngeal collapsibility.11,19
Using nasal occlusion technique, Neill et al.11
found improvement of upper airway closing pressure from 0.3 ± 2.4 cm H2
O (supine) to −4.0 ± 3.2 cm H2
O (30° head elevation) in sleeping patients with OSA. By measuring pressure-flow relationship in non-OSA subjects under midazolam sedation, Ikeda et al.19
found significant reduction of the critical closing pressure from −8.2 ± 5.2 cm H2
O (supine) to −13.3 ± 4.9 cm H2
O (30° head elevation). These studies did not assess pharyngeal segments responding to the postural changes, and the neuromuscular factors were not controlled in their experimental conditions. Although our study does not completely address the mechanisms by which sitting posture improves pharyngeal airway patency, we have confirmed the results of the previous studies and evidenced significant contribution of structural factors to the mechanisms by eliminating the neuromuscular factors. We consider two possible structural mechanisms that operate near pharyngeal airway (local structural mechanism) and from a distance (structural mechanism from a distance) for development of pharyngeal obstruction.1
Patients with OSA have significantly larger soft tissue volume surrounding the pharyngeal airway for a given maxillomandibular enclosure size, resulting in upper airway anatomical imbalance.20,21
The soft tissues are not uniformly distributed within the maxillomandibular enclosure. The larger mass of the soft tissues, such as the tongue, anteriorly overrides on the pharyngeal airway wall while the patient is in the supine posture. In addition, the excessive anterior soft tissues are able to be displaced through the submandible region.22,23
Accordingly, postural changes of direction of gravity acting on the soft tissues may significantly influence the anatomical balance.24
In fact, we previously demonstrated that lateral posture significantly improved pharyngeal airway patency.14
As illustrated in figure 4
, a relatively larger vector of gravity perpendicular to the airway in the supine posture is divided into perpendicular and vertical components in the sitting posture. The perpendicular component of the gravity decreases during sitting posture and effective mass acting on the airway possibly decreases, possibly improving upper airway anatomical balance. In addition, gravity vertical to the airway created during sitting posture may displace the anterior soft tissue out of the maxillomandibular enclosure through the submandible region, improving anatomical imbalance. This longitudinal gravity may also increase longitudinal tension of the pharyngeal airway wall, stiffening the airway. In fact, Tsuiki et al.
found significant elongation of the pharyngeal airway during the postural change from supine to sitting.9
Furthermore, the postural change significantly alters venous blood distribution, decreasing total soft tissue volume inside the maxillomandibular enclosure. Redolfi et al.25
recently demonstrated importance of fluid distribution on the pharyngeal airway maintenance. Pae et al.7
reported significant reduction of the tongue volume during the sitting posture supporting this possibility. These are speculative with little evidence and need to be tested in the future studies.
Recent studies suggest significant involvement of lung volume changes in development of OSA. Heinzer et al.26
demonstrated that a 0.77-l lung volume increase during sleep in obese patients with OSA decreased the apnea hypopnea index by approximately half. Our group found significant reduction of retropalatal P′close
in response to 0.7-l lung volume increase in anesthetized and paralyzed patients with OSA.13
Direct association between P′close
improvement and body mass index suggested greater lung volume dependence in obese patients with OSA. Therefore, in this study, we measured lung volume change from supine to sitting posture to examine potential contribution of the lung volume to the observed P′close
change as an alternative structural mechanism operating at a distance from the pharyngeal airway. However, we failed to find significant association between the P′close
improvement and lung volume changes in response to the postural change. This may not necessarily mean that the lung volume mechanism is unimportant in the postural improvement of the pharyngeal airway patency. Only one OSA patient with body mass index greater than 30 kg/m2
was included in this study, and his lung volume increased by only 100 ml during sitting posture. The absolute lung volume changes in this study were unexpectedly small compared with those in previous studies, possibly because of a different degree of head elevation and positioning of the lower legs.27
In particular, the total number of subjects tested in this study (n = 9) is small; therefore, the absence of a relation between the P′close
improvement and lung volume changes should be cautiously interpreted. Future studies need to examine contribution of the lung volume to postural changes of pharyngeal collapsibility in morbidly obese patients with OSA.
Induction of general anesthesia places patients at risk for both respiratory and circulatory derangements. The supine posture with the head in the sniffing position is a current standard for anesthesia induction. Compared with the supine posture, head-up posture significantly prolonged the apnea tolerance period in obese patients.28
Valenza et al.27
clearly demonstrated that the beach chair position and application of positive end expiratory pressure improved lung mechanics and oxygenation in obese patients. This study further demonstrated significant increase of the pharyngeal airway size and improvement of pharyngeal collapsibility in patients with OSA. It is noteworthy that the sitting posture successfully reduced the pharyngeal closing pressure below the atmospheric pressure in all patients with OSA, indicating that the sitting posture is the most effective mechanical intervention among the other postural interventions.29
Taken together, respiratory function during anesthesia induction is best maintained by placing the patient in sitting posture with the head in the sniffing position while applying positive end expiratory pressure and the triple airway maneuver with two hands.30
Despite these respiratory advantages, the sitting posture potentially decreases cerebral blood flow as a result of induced hypotension.31,32
Accordingly, the beneficial effects of the sitting posture during anesthesia induction must be weighed against hemodynamic derangements particularly in patients with OSA with cardiovascular comorbidities, and the patient should be returned to the supine posture immediately after successful placement of a endotracheal tube.
In conclusion, postural change from supine to sitting significantly enlarged pharyngeal cross-sectional area and decreased closing pressures at both retropalatal and retroglossal airways in anesthetized and paralyzed patients with obstructive sleep apnea. Sitting may be an advantageous posture compared with supine posture during induction of anesthesia in these patients for airway maintenance. The possible value of the sitting position during general anesthesia induction should be investigated further in obese patients with OSA.
The authors appreciate the assistance of Sara Shimizu, M.D. (Head of the Department of Plastic Surgery, JFE Kawatetsu Chiba Hospital, Chiba, Japan), who greatly helped to improve the manuscript.
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