The pharyngeo-tracheal lumen airway: an assessment of airway control in the setting of upper airway hemorrhage

Aspiration of blood from nasal and upper airway injuries is a common problem in trauma patients. The pharyngeo-tracheal lumen (PTL) airway uses a large balloon to occlude the oropharynx. We conducted a postmortem radiographic evaluation of the PTL airway's ability to control simulated upper airway hemorrhage using a barium solution. The PTL airway was inserted in ten patients and the barium solution was instilled in the nose until it was full. Radiographs were taken to determine the extent of containment of the radiopaque liquid. The PTL airway successfully controlled the simulated upper airway hemorrhage in nine of the ten cases studied including one patient with a cleft palate. There was leakage in the tenth case due to a balloon leak. The PTL airway may be the prehospital airway of choice in trauma patients due to its ability to control upper airway hemorrhage, but it requires further clinical testing.     

Factors affecting upper airway patency

We studied the following functional factors which affect upper airway patency. First, the effects of inspiratory resistive loading, increased pulmonary resistance, hypercapnic gas or hypoxic gas loading on the upper airway pressure-flow (P-F) relationship were studied. The upper airway P-F curves under these loading conditions shifted upward with load dependency. Secondly, effects of limb muscle contraction on upper airway resistance (Rua) were studied. Rua decreased reflexly during limb muscle contraction. Thirdly, effects of body position on the stability of the upper airway were studied. The upper airway was kept patent in the lateral position. Fourthly, effects of electrical stimulation of the genioglossus muscle on P-F relationship of upper airway were studied. P-F curves of upper airway shifted upward with increase in stimulation frequency. Fifthly, effects of nasal or oropharyngeal lubrication by artificial surfactant on the critical stimulation frequency (CSF) for upper airway opening were studied. Nasal or oropharyngeal lubrication decreased CSF. Based on these fundamental studies, we applied constrained lateral position, submental stimulation due to demand-type stimulator and nasal or oropharyngeal lubrication for treatment of patients with obstructive sleep apnea syndrome (OSAS). We found these three methods were effective in treatment of OSAS patients.     

Increased upper airway resistance in patients with airway narrowing.

The mean air flow resistance of the orolaryngeal (upper) airway was significantly increased in 7 of 11 patients with chronic airway obstruction, when compared with 6 controls. All the patients had noisy respiration with harsh breath sounds audible by auscultation over the larynx. The increase in resistance was greater during expiration than during inspiration. Since 4 patients had normal upper airway resistance, the signs were not invariably associated with upper airway narrowing and presumably could arise also in the chest. When increased, upper airway resistance was usually more than half the total airway resistance. It is suggested that this increase could only be due to narrowing of the glottis, probably by muscle activity. This narrowing may have had the same function as expiration through pursed lips. On the other hand, when present, the increased resistance through the upper airway during inspiration is unlikely to have had a useful function.     

Effect of nasal airway positive pressure on upper airway size and configuration

The effect of nasal airway positive pressure (NAPP) on upper airway size and configuration during wakefulness was studied by computerized tomography in 12 obese subjects with obstructive sleep apnea (OSA), seven weight- and age-matched subjects without OSA, and 12 normal subjects. NAPP of 10 to 12 cm H2O was associated with a significant increase in airway area throughout the upper airway in all three groups. The change in airway area per cm H2O NAPP increased from nasopharynx to hypopharynx. The change in airway area per cm H2O NAPP was significantly smaller in the OSA than in the normal subjects in the region of the soft palate. Electromyographic recordings of the genioglossus and alae nasi muscles with and without NAPP during wakefulness in five of the OSA and five of the normal subjects showed either a decrease or no change in phasic and tonic activity with NAPP. In a separate series of experiments in an additional five OSA and five normal subjects, NAPP of zero, 5, 10, and 15 cm H2O was associated with a linear increase in airway area at a given airway level. These results indicate that (1) the increase in pharyngeal cross-sectional area with application of NAPP during wakefulness is smaller in OSA than in normal subjects in the region of the soft palate and (2) changes in upper airway muscle activity may accompany changes in upper airway size and configuration.     

A heated humidifier reduces upper airway dryness during continuous positive airway pressure therapy.

Upper airway dryness is a frequent side-effect of nasal continuous positive airway pressure (nCPAP) therapy in obstructive sleep apnoea (OSA). In this situation, heated humidification is often used. Alternatively, oily nose drops are frequently applied to relieve dryness. The present study aimed to investigate the efficacy of a heated humidifier in comparison with oily nose drops. Twenty-four OSA patients complaining of serious nCPAP-related upper airway dryness were randomized to 6 weeks of treatment either with heated humidification (HC 100, Fischer & Paykel, Inc., Auckland, New Zealand) or oily nose drops (Colda-Stop, Desitin, Inc., Germany). The patients completed questionnaires on the degree and frequency of upper airway dryness, compliance with nCPAP, intention to terminate nCPAP and comfort during the nCPAP therapy. All 12 patients treated with heated humidification improved in terms of the degree and frequency of upper airway dryness, and reported greater comfort when using the nCPAP device. All patients in the heated humidification group intending to terminate nCPAP therapy because of upper airway dryness persisted with nCPAP on addition of humidification. In contrast, only five out of 12 patients (42%) in the oily nose drops group reported their degree of upper airway dryness to be improved (P = 0.003), only three patients (25%) reported an improvement in the frequency of upper airway dryness (P < 0.001), and only five patients (42%) reported greater comfort when using the nCPAP device with oily nose drops (P < 0.001). In the group using oily nose drops none of the three patients who intended to terminate nCPAP therapy persisted with nCPAP. Heated humidification is highly effective and superior to oily nose drops in reducing the symptoms of upper airway dryness during nCPAP.     

Magnetic resonance imaging of the upper airway in obstructive sleep apnea before and after chronic nasal continuous positive airway pressure therapy

Magnetic resonance imaging (MRI) provides high-resolution images of the upper airway and is useful for assessing conditions associated with increased tissue water content. To determine whether nasal continuous positive airway pressure (CPAP) changes awake upper airway morphology in obstructive sleep apnea (OSA), we performed awake upper airway MRI scans on five male patients with moderate to severe OSA before and after 4 to 6 wk of nasal CPAP therapy. MRI scans were performed using spin echo pulse sequences to examine detailed anatomy and inversion recovery sequences to assess mucosal water content. Patients did not have nasal CPAP applied during the MRI scans. Axial and sagittal images were obtained, and tracings were made of the upper airway, tongue, and soft palate. Utilizing computer graphics, cross-sectional areas and volumes were calculated for each anatomic structure. A subjective grading system was used to assess upper airway mucosal water content. Pharyngeal volume and minimum pharyngeal cross-sectional area increased (p less than 0.05) and tongue volume decreased (p less than 0.01) following chronic nasal CPAP therapy. The increase in pharyngeal volume occurred mainly in the oropharynx (p less than 0.01). Upper airway mucosal water content decreased in the oropharynx (p less than 0.05). We conclude that chronic nasal CPAP therapy during sleep in patients with OSA produces changes in awake upper airway morphology. These changes may be due to resolution of upper airway edema. The upper airway of patients with OSA can be accurately and repeatedly assessed using MRI.     

Mechanical properties of the upper airway

Abnormalities of upper airway mechanical properties are a well-recognized and important feature of the pathophysiology of the obstructive sleep apnea hypopnea syndrome (OSAHS). Recently, investigations enhanced our understanding of the factors that promote upper airway obstruction. In patients with OSAHS, anatomic narrowing of the pharyngeal airway, particularly in the lateral dimension with thickening of the lateral pharyngeal walls, is present. In addition, the passive upper airway (absent muscle activity) demonstrates increased collapsibility, which is modulated by caudal tracheal traction, mucosal surface forces, route of breathing, and the balance of intraluminal airway and extraluminal tissue pressures. In patients with OSAHS, pharyngeal dilator muscles (including the genioglossus and soft palate muscles) demonstrate a coordinated pattern of increased muscle activity while awake compared with normals. This is thought to represent a neuromuscular compensatory mechanism for the anatomically narrow, more collapsible upper airway. With the onset of sleep, the reflexes that drive this muscular compensation are diminished, leading to reduced muscle activity and predisposing the OSAHS patient to pharyngeal collapse. Better understanding of the mechanical properties of the upper airway in normals and patients with OSAHS should help in the development of new therapeutic strategies.     

Airway secretions influence upper airway patency in the rabbit

The hypothesis tested in these experiments was that the properties of the upper airway mucosal surface may be important in reopening of the closed airway, and that mucosal surface properties may depend on airway secretions. The intraluminal pressures required to close and reopen the upper airways were measured in the isolated upper airways of anesthetized rabbits. Atropine (0.1 mg/kg i.v.), given to reduce the volume of upper airway secretions, had no effect on closing or on reopening pressures. Stimulation of upper airway secretions in 6 animals with methacholine (0.2 mg/kg subcutaneously) changed closing pressures from -10.63 +/- 0.57 to -16.91 +/- 0.60 cm H2O (p less than 0.05) but made the airway less likely to reopen, changing reopening pressures from -3.45 +/- 0.48 to -2.12 +/- 0.39 cm H2O (p less than 0.04), and caused frequent failure of the airway to reopen spontaneously. Filling the upper airways with saline to mimic the hydrostatic forces present in the mucus-filled airway caused both closing and reopening pressures to become more negative. We conclude that reopening pressure is influenced by the secretions lining the airway surface, and, therefore, that airway closure and airway reopening may be substantially independent.     

Effect of ventilatory drive on upper airway patency in humans during NREM sleep

The pharynx is the site of upper airway obstruction during sleep. As a collapsible tube, pharyngeal patency is determined by transmural pressure and the compliance of the pharyngeal wall. Thus, several factors may influence upper airway patency including the activity of upper airway dilating muscles, the magnitude of caudal traction generated by thoracic inspiratory activity, vascular tone and mucosal surface forces. Changing ventilatory motor output influences upper airway patency primarily by altering dilating muscle activity or caudal traction. Increased ventilatory motor output enhances upper airway patency. Isolated reduction of ventilatory motor output has no significant effect on upper airway patency. However, upper airway narrowing or occlusion occur at the nadir of ventilatory drive during induced periodic breathing and during central apnea. The latter indicates that negative intraluminal pressure is not required for upper airway obstruction during sleep. Therefore, upper airway occlusion during sleep may be due to: (1) passive collapse of a compliant upper airway by gravitational factors or (2) active closure generated by the contraction of the pharyngeal constrictors.     

Effects of upper airway carbon dioxide on upper airway resistance and muscle activity in young guinea-pigs.

The upper airway (UA) of adult animals is known to contain carbon dioxide-sensitive receptors and UA CO2 reflexly affects breathing, UA dilator muscle activity and UA resistance. These effects may function in the control of UA patency. There is evidence that some UA reflexes are stronger in young than in adult animals, but it is not known whether CO2-sensitive receptors are present in the UA of young animals, and the effects of UA CO2 on UA resistance and on UA dilator muscle activity have not been investigated in young animals. The responses of ventilation, UA resistance and geniohyoid muscle electromyographic activity to warm air containing 10% CO2 applied to the isolated UA were measured in anaesthetized, vagotomized young guinea-pigs breathing spontaneously through a low-cervical tracheostomy. Upper airway carbon dioxide caused an increase in ventilation (46.7+/-16.3 to 49.9+/-16.8 mL x min(-1) x 100 g body weight(-1)) and upper airway resistance (56.8+/-14.8 to 63.7+/-17.7 cmH2O x L(-1) x s(-1) x kg body weight(-1)). Similar effects were obtained following vagotomy. Geniohyoid activity became apparent following vagotomy and this activity was reduced by upper airway carbon dioxide. These responses were abolished by topical anaesthesia of the upper airway. This suggests that the reflexes seen are due to carbon dioxide-sensitive receptors in the upper airway.     

Relationship of airway wall thickness to airway sensitivity and airway reactivity in asthma

Airway wall thickening has been assumed to cause airway hyperresponsiveness, but a protective effect against airway narrowing has also been suggested. We investigated the relationship between airway wall thickness as assessed by helical computed tomography and two components of airway responsiveness, airway sensitivity and reactivity, in patients with stable asthma with (n = 23) and without (n = 22) inhaled steroid treatment. A cross-section of the apical bronchus of the right upper lobe was obtained. Airway wall area corrected by body surface area was measured as an index of wall thickness. Airway sensitivity and reactivity were measured by continuous inhalation of methacholine, on the basis of the methacholine respiratory resistance dose-response curve. The eosinophil count in sputum was determined in 16 patients [steroid (+) group] and 14 patients [steroid (-) group]. In both groups of patients, airway sensitivity was not related to airway reactivity. Airway sensitivity was related to eosinophil count [r = 0.57 in the steroid (+) group and r = 0.49 in the steroid (-) group], but not to airway wall thickness. In contrast, airway reactivity negatively correlated with airway wall thickness [r = -0.56 in the steroid (+) group and r = -0.55 in the steroid (-) group] but not with eosinophil count. Our results suggest that airway wall thickening attenuates airway reactivity in patients with asthma. These findings may have important implications in pathophysiology and in the treatment of airway remodeling.     

Relationships among bacteria, upper airway, lower airway, and systemic inflammation in COPD

STUDY OBJECTIVE: The upper and lower airways are continuous. While upper airway symptoms are common in COPD patients, with accumulating evidence to suggest increased nasal inflammation, the relationships among upper airway, lower airway, and systemic inflammatory indexes have not been studied. We aimed to confirm that there is heightened nasal inflammation in COPD patients, to test the hypothesis that the degree of upper airway inflammation relates to the degree of lower airway inflammation, and to investigate the underlying associations with bacterial carriage and the systemic inflammatory response. DESIGN: Prospective cohort study. SETTING: Outpatient Department, London Chest Hospital, London, UK. PARTICIPANTS: Forty-seven patients with COPD and 12 control subjects of similar age, sex, and smoking status. MEASUREMENTS: Serum, nasal wash fluid, and sputum samples were obtained from 47 stable patients with COPD for the analysis of inflammatory indexes and bacterial colonization. Nasal wash fluid specimens were obtained from 12 control subjects. RESULTS: COPD patients had an increased nasal interleukin (IL)-8 concentration compared to control subjects (difference, 97.2 pg/mL; p = 0.009). The nasal IL-8 concentration in COPD patients correlated with that in sputum (r = 0.30; p = 0.039). In both the upper and lower airways of patients with COPD, the IL-8 concentration was associated with indexes of bacterial colonization. Patients colonized with a sputum potentially pathogenic microorganism had a higher total nasal bacterial load (difference, 1.5 log cfu/mL; p = 0.016). We did not find significant relationships between the degree of upper or lower airway inflammation, or bacterial carriage, and the systemic inflammatory response. CONCLUSIONS: COPD is associated with an increased nasal concentration of the neutrophil chemoattractant protein IL-8, the degree of which reflects that present in the lower airway. A relationship between lower airway bacterial colonization, postnasal drip, and higher nasal bacterial load may suggest a mechanism underlying this finding. This study is the first to report a correlation between the degree of upper and lower airway inflammation in COPD.     

The effects of breath-holds and Muller manoeuvres on upper airway carbon dioxide concentration in humans

BACKGROUND: Obstructive sleep apnoea is caused by collapse of the upper airway. The presence of CO(2) in the upper airway lumen evokes a number of reflexes which favour upper airway re-opening, and we have proposed previously that CO(2) would build up in the upper airway following airway collapse and that this would contribute to reflex airway re-opening. However, it is not known if CO(2) can transfer from the alveoli to the anatomical dead space of the upper airway during apnoea. OBJECTIVES: To determine if alveolar CO(2) can enter the upper airway during breath-holds and Muller manoeuvres. MATERIAL AND METHODS: With local ethics committee approval, 6 male volunteers (aged 22-48 years), following a quiet inspiration, carried out breath-holds and Muller manoeuvres until breaking point. CO(2) was measured continuously in samples obtained from the hypopharynx using an infrared analyser with a sample rate of 50 ml/min. Muller manoeuvres (forced inspirations against a closed upper airway) mimic the respiratory efforts which occur during obstructive apnoeas. RESULTS: In all cases, CO(2) increased progressively during apnoeas. There was a much larger increase in Muller manoeuvres (3.78 +/- 0.51%, mean +/- SEM at breaking point) compared to breath-holds. DISCUSSION: These results show that upper airway CO(2) concentration rises substantially during apnoeas and suggest that transfer of CO(2) from the lungs to the upper airway may evoke a number of reflex effects which could affect breathing and upper airway re-opening during obstructive apnoeas.     

Effects of sodium cyanide and nicotine on upper airway resistance in anesthetized dogs

The purpose of this study was to determine whether pharmacologic interventions which increase respiratory drive could also reduce flow resistance in the upper airway. Studies were performed in twelve anesthetized supine dogs. In six animals breathing spontaneously through the intact upper airway, intravenous administration of respiratory stimulants (sodium cyanide and nicotine) produced a dose-related decrease in upper airway. In nine animals, upper airway resistance was measured across the isolated upper airway. The stimulants produced a dose-related decrease in upper airway resistance. In both preparations inspiratory resistance fell at lower doses than expiratory resistance. Eventually a dose could be given which resulted in comparable, minimal values of resistance during both inspiration and expiration. Mechanisms for changes in resistance were clarified using lateral radiographs of the neck and transbronchoscopic views of the upper airway. Pharmacologic challenge resulted in a change in the route of airflow (from nose only to nose-and-mouth breathing) as well as a change in caliber of the airway at the level of the naso-pharynx and hyoid apparatus. In anesthetized dogs, respiratory stimulants will decrease upper airway resistance by increasing activation of upper airway muscles which may enlarge the airway, change the route of flow, and thus overcoming collapsing forces produced by increased chest wall muscle activation.     

Upper airway resistance during progressive hypercapnia and progressive hypoxia in normal awake subjects

Ventilatory motor output is known to influence the upper airway. Although inspiratory upper airway resistance decreases during progressive hypoxia or hypercapnia, the effects of hypoxia and hypercapnia on expiratory upper airway resistance remain unknown. In the present study, we attempted to examine whether the expiratory and the inspiratory upper airway resistances were modified in the same way by progressive hyperoxic hypercapnia or by progressive normocapnic hypoxia. Nine healthy subjects (five males, four females, 33+/-9 years) participated in the study. Inspiratory upper airway (iUAR) and expiratory upper airway resistances (eUAR) were calculated at flow 300 ml x s(-1). Both resistances were obtained during a baseline period and during progressive hyperoxic hypercapnia or progressive normocapnic hypoxia. In all subjects, iUAR and eUAR decreased significantly during hypercapnic or hypoxic challenge (P<0.05). eUAR was always lower than iUAR during hypercapnic challenge (P<0.0001) and during hypoxic challenge (P<0.0001). The authors conclude that expiratory upper airway resistance, as with inspiratory resistance, decreases during progressive hypercapnia or during progressive hypoxia. Pharyngeal dilator or constrictor muscle activities may be implicated.     

Humidified nasal continuous positive airway pressure in obstructive sleep apnoea.

Heated humidification of nasal continuous positive airway pressure (nCPAP) reduces upper airway symptoms and improves initial use in obstructive sleep apnoea syndrome (OSAS). The present study aimed to assess the effect of heated humidification of nCPAP on upper airway symptoms and initial use in obstructive sleep apnoea. This study was of a randomised, crossover design. Subjects with polysomnographically confirmed OSAS were randomised to 3 weeks nCPAP treatment with heated humidification (nCPAP-humid) or placebo humidification (nCPAP pl-humid). Objective and subjective nCPAP use, upper airway symptoms, and treatment satisfaction were compared. Thirty seven of 42 patients completed the protocol. nCPAP-humid reduced the frequency of adverse upper airway symptoms. nCPAP use over 3 weeks was greater with nCPAP-humid compared with nCPAP pl-humid. No difference was found between the treatment arms in terms of subjective treatment satisfaction or alertness. Heated humidification of nasal continuous positive airway pressure reduces upper airway symptoms and is associated with a small increase in initial use but not subjective sleepiness or treatment satisfaction. The results support the use of heated humidification as a strategy to reduce side-effects related to continuous positive airway pressure but not routine initial use.     

Chronic intermittent asphyxia impairs rat upper airway muscle responses to acute hypoxia and asphyxia

BACKGROUND: Obstructive sleep apnea (OSA) is a major clinical disorder that is characterized by multiple episodes of upper airway obstruction due to the failure of the upper airway dilator muscles to maintain upper airway patency. This results in chronic intermittent asphyxia (CIA) due to repetitive apneas, but very little is known about the effects of CIA on upper airway muscle function. OBJECTIVE: To test the hypothesis that CIA affects upper airway muscle activity and electromyogram (EMG) responses to acute hypoxia and asphyxia. DESIGN: Record upper airway EMG responses to acute hypoxia and asphyxia in control and CIA-treated rats. SETTING: Department of Physiology, Royal College of Surgeons in Ireland, Dublin, Ireland. MEASUREMENTS: Sternohyoid (SH) muscle and diaphragm (DIA) muscle EMG activities were recorded in both groups during normoxia, hypoxia (7.5% O(2) in N(2)), and asphyxia (7.5% O(2) and 3% CO(2)) under pentobarbitone anesthesia. RESULTS: Baseline SH EMG activity was significantly elevated in the CIA-treated rats compared to the controls, whereas DIA EMG activity was similar in the two groups. In addition, CIA significantly reduced SH EMG but not DIA EMG responses to acute hypoxia and asphyxia. CONCLUSIONS: The elevated upper airway muscle activity associated with OSA in humans during wakefulness is due at least in part to CIA. We propose that a reduction in the response of upper airway dilator muscles to acute asphyxia following upper airway obstruction is likely to cause further asphyxic insult, leading to a vicious feed-forward cycle exacerbating the condition. Our results suggest that CIA contributes to the pathophysiology of sleep-disordered breathing.     

Functional contribution of mandibular advancement to awake upper airway patency in obstructive sleep apnea

In the narrowed upper airway of patients with obstructive sleep apnea (OSA), a neuromuscular compensatory mechanism augments the activity of the upper airway dilator muscles in defense of upper airway patency, particularly during inspiration. We hypothesized that mechanical enlargement of the upper airway by a mandibular advancement oral appliance would permit a reduction in this neuromuscular compensation during wakefulness. To test this hypothesis, we focused on changes in the cross-sectional (CS) area of the upper airway before and after emplacement of a ventrally titrated oral appliance in 12 awake OSA patients. The CS areas at the end of tidal expiration (CS area-EET) and at the nadir of intraluminal pressure during inspiration (CS area-IN) were obtained using videoendoscopy. The median apnea–hypopnea index decreased with mandibular advancement. Before mandibular advancement, there was no difference between CS area-EET and CS area-IN in the velopharynx, oropharynx, and hypopharynx. This indicates that upper airway dilator muscle activity increased during inspiration to counteract the intraluminal negative pressure of the upper airway. After mandibular advancement, CS area-EET increased in the velopharynx, oropharynx, and hypopharynx, but CS area-IN was unchanged at any level and was less than CS area-EET in the velopharynx and oropharynx. These findings suggest that mandibular advancement enlarges the upper airway and may reduce upper airway dilator muscle activity during inspiration. We conclude that oral appliances act to return the upper airway towards a normal configuration and pattern of muscle function in OSA patients.     

Upper airway reflexes

It is usually assumed that upper airway pressure receptors mediate the reflexes involved in sleep apneas, but many other receptors may be involved, including those responding to chemical stimuli. The reflexes to upper airway negative pressure have been further studied, and the timing of their inputs shown to be important. Their effects on the cardiovascular system, including cerebral blood flow, have been emphasized. The central nervous pathways for the upper airway reflexes and their relationship to the neuronal circuits of the respiratory rhythm generator are being analyzed, but no clear pattern has emerged. Many neurotransmitters have been identified, usually on the motor pathways, which points to possible therapeutic approaches. The central nervous pharmacology and the neuronal pattern for the cough reflex have been described, and a similar approach to other upper airway reflexes, especially those involved in sleep apneas, would be valuable.     

Translaryngeal jet ventilation and end-tidal PCO2 monitoring during varying degrees of upper airway obstruction

STUDY OBJECTIVES: To explore the ventilatory adequacy of translaryngeal jet ventilation (TLJV) during partial upper airway obstruction and the usefulness of monitoring end-tidal CO2 (PETCO2) during this condition. DESIGN: Prospective, nonrandomized, sequential crossover design. SETTING AND PARTICIPANTS: Apneic dog model (five dogs; mean weight, 23 kg). INTERVENTIONS: Animals were intubated with a 9.0-mm endotracheal tube with the tip positioned above the cricothyroid membrane. Upper airway obstructions of 40%, 69%, and 80% were created. TLJV was performed through the cricothyroid membrane using a 13-gauge catheter with 100% oxygen, 45 psi, 15 breaths per minute, and 30% inspiratory time for 15 minutes at each upper airway obstruction. Data collected at baseline (no upper airway obstruction) and one-minute intervals included arterial blood pressures, continuous PaCO2 measurements, and PETCO2 at the TLJV catheter tip and above the level of obstruction. Arterial blood gases were obtained at 0 and 15 minutes. Data were analyzed using Pearson's correlation, analysis of variance, and Turkey's multiple comparisons (significance, P less than .05). MEASUREMENTS AND RESULTS: Baseline values for all variables did not significantly differ at the onset of each testing phase. Mean pH increased significantly from baseline during 69% upper airway obstruction (7.36 to 7.54, P less than .05) and 80% upper airway obstruction (7.39 to 7.61, P less than .01). Mean PaCO2 decreased significantly from baseline during all upper airway obstructions: 40% upper airway obstruction (39.9 to 33.6 mm Hg, P less than .01), 69% upper airway obstruction (38.3 to 25.6 mm Hg, P less than .001), and 80% upper airway obstruction (36.2 to 18.2 mm Hg, P less than .001). PaCO2, PETCO2, and pH differed significantly between each level of upper airway obstruction (P less than .01). PETCO2 was significantly correlated with PaCO2 (r = .84, P less than .001) and did not significantly differ from PaCO2. No signs of barotrauma were observed in any animal at any degree of upper airway obstruction. CONCLUSION: TLJV during partial upper airway obstruction in our model provided safe and adequate-to-supranormal minute ventilation. In fact, marked hypocapnia and alkalemia occurred at levels of 69% and 80% upper airway obstruction, thus dispelling concepts that TLJV may cause hypercapnia during partial upper airway obstruction. PETCO2 correlates well with PaCO2 and may be valuable for monitoring ventilation when using TLJV in the nonobstructed or partially obstructed upper airway.