Development of alpha-tocopherol acetate nanoparticles: influence of preparative processes.

We studied different methods of preparing alpha-tocopherol acetate (ATA) nanoparticles, which are to be used in targeting the lungs as aerosols in order to prevent cigarette smoke toxicity. Poly-(lactide) nanoparticles were prepared using nanoprecipitation and solvent evaporation techniques, which produced, respectively, too small and too large nanoparticles to be aerosolized. The emulsification-diffusion method produced 2 months stable nanoparticles with a size between (500-700 nm). Increasing ATA concentration (1-7 mg/mL) induced a decrease in the association rate (97-93%) and in the adsorbed ATA rate (7-4.5%), which was associated with variations of Zeta potentials (-27.5 to -24.3 mV) and decrease in polymeric wall thickness and density.

Abdominal muscle activity in sleep apnea during continuous positive airway pressure titration.

STUDY OBJECTIVES: The aim of this study was to investigate whether presence of expiratory abdominal muscle activity (EAMA) in obstructive sleep apnea syndrome (OSAS) patients during nasal continuous positive airway pressure (nCPAP) is due to either nCPAP overprescription or nCPAP underprescription. DESIGN: Airflow, esophageal pressure (Pes), and gastric pressure (Pga) were routinely measured during polysomnography aimed at determining the optimal nCPAP level, and the magnitude of EAMA was evaluated in relation to the nCPAP level and to the conventional indexes of upper-airway obstruction used during nCPAP titration. PATIENTS: The study was performed 12 patients with OSAS. RESULTS: Six patients displayed sustained EAMA, ie, EAMA lasting > 3 min, and characterized by a decrease in abdominal diameter and a paradoxical rise in Pga during expiration. In all six patients, EAMA decreased gradually as nCPAP neared optimal levels, and then disappeared when the optimal nCPAP level was achieved. The decrease in EAMA as nCPAP increased was associated with an increase in minute ventilation, decreases in both inspiratory and expiratory resistance, a decrease in Pes swing, and the normalization of the inspiratory flow contour. CONCLUSIONS: We conclude that the EAMA observed in some OSAS patients might be an indirect marker of upper-airway obstruction, and that the presence of EAMA during nCPAP titration might indicate a suboptimal nCPAP level rather than a deleterious effect of nCPAP.

Combined effects of a nasal dilator and nasal prongs on nasal airflow resistance.

STUDY OBJECTIVES: Nasal prongs (NPs), when used to assess nasal flow, can result in dramatic increases in nasal airflow resistance (NR). The aim of this study was to investigate whether the NP-induced increases in NR could be corrected by the simultaneous use of an internal nasal dilator (ND). DESIGN: NR was estimated by posterior rhinomanometry, in the basal state (NRb), and while breathing with NP (NRp), with ND (NRd), and with both ND and NP (NRd + p). PARTICIPANTS: The study was performed in 15 healthy subjects. MEASUREMENTS AND RESULTS: NR (mean NRb [+/- SEM], 2.5 +/- 0.4 cm H(2)O/L/s) significantly decreased with ND (NRd = 1.4 +/- 0.2 cm H(2)O/L/s; p < 0.001) and significantly increased with NP (NRp = 3.8 +/- 0.8 cm H(2)O/L/s; p < 0.001). A significant logarithmic relationship was found between NRd and NRb (r(2) = 0.95; p < 0.0001), and a significant exponential relationship was found between NRp and NRb (r(2) = 0.99; p < 0.0001). While breathing with both ND and NP, NRd + p was significantly lower than NRb (1.9 +/- 1.4 cm H(2)O/L/s; p < 0.02). CONCLUSIONS: Our results demonstrate that the ND tends to slightly overcorrect the NP-induced increase in NR and suggest that, in view of the possible effects of NPs on upper airway resistance, the combination of both devices might be used for nasal airflow monitoring during nocturnal polysomnography in patients presenting with highly resistive nares.

Respiratory impedance response to continuous negative airway pressure in awake controls and OSAS.

The aim of the study was to determine whether the response of respiratory impedance (Zrs) to decreasing levels of continuous negative airway pressure (CNAP) during wakefulness, differs in controls and subjects with obstructive sleep apnoea syndrome (OSAS). Zrs was measured by the forced oscillation technique (4-32 Hz) in 15 controls and 21 patients with OSAS (apnoea/hypopnoea index >20 per sleep hour) with normal lung function, in the basal state and with application of decreasing CNAP of -5, -10, and -15 hPa. Respiratory resistance was extrapolated to 0 Hz (R0) and estimated at 16 Hz (R16) by linear regression analysis of respiratory resistive impedance versus frequency. Respiratory elastance (Ers) and inertance (Irs) were estimated by multilinear regression analysis of respiratory reactance versus frequency, and resonance frequency (RF) was determined as RF=(1/2pi)(Ers/Irs)0.5. In both groups, R0, R16, Ers and RF significantly increased as the CNAP level decreased (p <0.0001 for all). R0, Ers, and RF increased significantly more in OSAS than in controls (p < 0.01, 0.001, and 0.0001, respectively), independently of the severity of obesity. Receiver operator characteristic curves showed that the parameter which best detected OSAS was RF, with a sensitivity of 81% and 93% specificity for the 13.6 Hz cut-off point. The results of the present study suggest that the response of respiratory impedance to decreasing continuous negative airway pressure levels, might allow detection of obstructive sleep apnoea syndrome in subjects with normal lung function.

Effects of nasal prongs on nasal airflow resistance.

STUDY OBJECTIVES: The aim of this study was to investigate whether nasal prongs, which have been proposed to assess nasal flow during sleep, affect nasal airflow resistance (NR). DESIGN: NR was estimated by posterior rhinomanometry at a 0.5 L/s flow, under eight conditions: in the basal state, and with seven different nasal prongs. PARTICIPANTS: The study was performed in 17 healthy supine subjects, 8 of whom had basal NR values within the normal range (< or = 2 cm H(2)O.L(-1).s, group 1), and 9 had increased basal NR values (> 2.5 cm H(2)O.L(-1).s, group 2), because of nare narrowness and/or deviated nasal septum. MEASUREMENTS AND RESULTS: NR increased significantly while breathing with nasal prongs (p < 0.0001 in both groups). The changes in NR (DeltaNR) induced by the different nasal prongs were characterized by large intersubject and intrasubject variability, with a maximum DeltaNR of 24.2 cm H(2)O.L(-1).s. Significant differences were found between the DeltaNR induced by the different nasal prongs (p < 0.001 in group 1, and p < 0.0003 in group 2), and for six of them, DeltaNR was significantly higher in group 1 than in group 2 (p < 0.02). CONCLUSIONS: This study demonstrates that nasal prongs can markedly increase NR in subjects presenting with nare narrowness and/or deviated nasal septum. Further investigations that would include nocturnal polysomnography are still required to evaluate the possible influence of nasal prongs on the diagnosis of obstructive sleep apnea syndrome and its severity.

Effects of mandibular advancement on respiratory resistance.

Mandibular advancing devices are proposed as nonsurgical treatment for certain patients with an obstructive sleep apnoea syndrome. Since they act by increasing the upper airway calibre, the aim of the present study was to investigate the changes in respiratory resistance (Rrs) resulting from mandibular advancement. Rrs was measured at the nose by the forced oscillation technique (4-32 Hz). Ten normal subjects were studied under three conditions: resting mandibular position, passive mandibular advancement steadied by a wax bite, and voluntary advancement, in random order. Respiratory resistance was extrapolated to 0 Hz (R0) and estimated at 16 Hz (R16) by linear regression analysis of respiratory resistive impedance versus frequency. R0 (mean+/-SEM=3.5+/-0.2 cmH2O x L(-1) x s in the resting position) decreased significantly with passive advancement (2.9+/-0.2 cmH2O x L(-1) x s, p<0.001), but remained unchanged with voluntary mandibular advancement (3.6+/-0.2 cmH2O x L(-1) s). Similar results were obtained for R16. The results of this study demonstrate that the effects of mandibular advancement on upper airway resistance differ, depending on whether advancement is passive or active, and suggest that in order to simulate the actual effects of therapeutic devices, mandibular advancement should be passive.

Effects of continuous negative airway pressure on lung volume and respiratory resistance.

This study was designed to determine the responses of lung volume and respiratory resistance (Rrs) to decreasing levels of continuous negative airway pressure (CNAP). Twenty normal subjects were studied in the basal state and under CNAP levels of -5, -10, and -15 hPa. Rrs was measured by the forced oscillation technique (4-32 Hz). End-expiratory lung volume (EELV) and tidal volume (VT) were measured by whole body plethysmography. Rrs was extrapolated to 0 Hz (R(0)) and estimated at 16 Hz (R(16)) by linear regression analysis of Rrs vs. frequency. Specific Rrs, SR(0) and SR(16), were then calculated as R(0) (EELV + VT/2) and R(16) (EELV + VT/2), respectively. EELV significantly decreased, whereas R(0), R(16), SR(0), and SR(16) significantly increased, as the CNAP level decreased (P < 0.0001 for all). At the lowest CNAP level, R(0) and R(16) reached 198 +/- 13 and 175 +/- 9% of their respective basal values. The CNAP-induced increase in R(0) was significantly higher than that in R(16) (P < 0.004). Our results demonstrate that the CNAP-induced increase in Rrs does not result from a direct lung volume effect only and strongly suggest the involvement of other factors affecting both intrathoracic and extrathoracic airway caliber.

Combined effects of a mechanical nasal dilator and a topical decongestant on nasal airflow resistance.

The goal of this study was to compare the isolated and combined effects of two treatments being used to reduce nasal airflow resistance (NR): an internal nasal mechanical dilator (Nozovent; Prevancure; Sté Pouret, Paris, France) and a topical decongestant, fenoxazoline hydrochloride (Aturgyl; Synthelabo; Le Plessis-Robinson, France). The study was performed in 17 healthy subjects. NR was estimated by active posterior rhinometry at a 0.5 L/s flow under four conditions: in the basal state, with the internal nasal mechanical dilator, after treatment with fenoxazoline hydrochloride, and with both fenoxazoline hydrochloride and the mechanical dilator. The mean NR (+/- SD) decreased from 1.65+/-0.54 cm H2O/L/s in the basal state to 1.02+/-0.27 cm H2O/L/s with the mechanical dilator (p < 0.001), 1.03+/-0.47 cm H2O/L/s with fenoxazoline hydrochloride (p < 0.001), and 0.48+/-0.15 cm H2O/L/s with both the mechanical dilator and fenoxazoline hydrochloride (p < 0.001). The decreases in NR observed after using either the mechanical dilator (deltaNR(N)) or fenoxazoline hydrochloride (deltaNR(A)) were not significantly different. The decrease in NR observed with both (deltaNR(N + A)) was not significantly different from the sum deltaNR(N) + deltaNR(A): 1.16+/-0.53 cm H2O/L/s vs 1.25+/-0.63 cm H2O/L/s, respectively (p > 0.05). deltaNR(N + A) strongly correlated with deltaNR(N) + deltaNR(A): deltaNR(N + A) = 0.80 (deltaNR(N) + deltaNR(A)) + 0.15 (r = 0.96; p < 0.0001). However, the slope of the regression line of deltaNR(N + A) vs deltaNR(N) + deltaNR(A) was significantly lower than unity (p < 0.003). These results demonstrate that, although not totally additive, the effects of using the mechanical dilator and fenoxazoline hydrochloride are cumulative. Further studies that include patients with nasal obstruction would allow us to better evaluate the benefit of a therapy combining both treatments.

Respiratory resistive impedance as an index of airway obstruction during nasal continuous positive airway pressure titration.

Esophageal pressure amplitude (DeltaPes), inspiratory pulmonary resistance (RLI) and inspiratory flow limitation score (FS) are used as indices of upper airway obstruction for the titration of nasal continuous positive airway pressure (nCPAP) in patients with obstructive sleep apnea syndrome (OSAS). This study was designed to determine whether oscillatory respiratory resistive impedance at 16 Hz (RFO) might be proposed as an alternative index. Eleven OSAS patients were studied during a night of polysomnography-controlled nCPAP titration. Nasal flow (V) and airway opening and esophageal pressures (Pao and Pes, respectively) were continuously measured during nasal breathing, and forced-flow oscillations (FO) were applied for 5 min at each nCPAP level. RLI was calculated by linear regression analysis of resistive pressure versus V over inspiration. R FO was obtained by linear regression analysis of respiratory resistive impedance versus frequency. Application of FO affected neither sleep nor pulmonary mechanics. RFO correlated with RLI in all patients. RFO did not correlate with DeltaPes in two patients, and was not significantly related to FS in five patients. This study demonstrates the applicability of the FO technique in sleeping patients receiving nCPAP, and the reliability of RFO for assessing pulmonary resistance. RFO might therefore be proposed as a quantitative index of airway obstruction for nCPAP titration.

Heavy snoring with upper airway resistance syndrome may induce intrinsic positive end-expiratory pressure.

We studied eight heavy snorers with upper airway resistance syndrome to investigate potential effects of sleep on expiratory airway and lung resistance, intrinsic positive end-expiratory pressure, hyperinflation, and elastic inspiratory work of breathing (WOB). Wakefulness and non-rapid-eye-movement sleep with high- and with low-resistance inspiratory effort (H-RIE and L-RIE, respectively) were compared. No differences in breathing pattern were seen across the three conditions. In contrast, we found increases in expiratory airway and lung resistance during H-RIE compared with L-RIE and wakefulness (56 +/- 24, 16 +/- 4, and 11 +/- 4 cmH2O . 1(-1) . s, respectively), with attendant increases in intrinsic positive end-expiratory pressure (5.4 +/- 1.8, 1.4 +/- 0.5, and 1.3 +/- 1.3 cmH2O, respectively) and elastic WOB (6.1 +/- 2.2, 3.7 +/- 1.2, and 3.4 +/- 0.7 J/min, respectively). The increase in WOB during H-RIE is partly caused by the effects of dynamic pulmonary hyperinflation produced by the increased expiratory resistance. Contrary to the Starling model, a multiple-element compliance model that takes into account the heterogeneity of the pharynx may explain flow limitation during expiration.

Effects of different mechanical treatments on nasal resistance assessed by rhinometry.

The goal of this study was to compare the effectiveness of three treatments aiming to reduce nasal airflow resistance (NR): an external nasal strip device (Respir+), an internal nasal mechanical dilator (Nozovent), and a topical decongestant (Pernazène). NR was estimated by active posterior rhinometry at both a 0.5 L/s flow (NRF) and a 1 cm H2O pressure (NRP), under four conditions: in the basal state, with Respir+, with Nozovent, and after treatment with Pernazène. The efficacy of each treatment was assessed by the percentage changes in NRF and NRP (%NRF and %NRP, respectively). The study was performed in 15 healthy subjects. The efficacy of the treatments was significantly different, depending on whether it was evaluated by NRF or by NRP (p<0.02), with %NRF and %NRP values, respectively, equal to the following: 88+/-20% and 91+/-14% with Respir+, 58+/-17% and 70+/-13% with Nozovent, and 55+/-29% and 69+/-22% with Pernazène. NRF remained unchanged with Respir+, whereas it significantly decreased with Nozovent and Pernazène (p<0.0001). No significant difference was observed between the effects of the two latter treatments. These results demonstrate that Nozovent, which involves no risk of side effects or drug interactions, is an effective treatment to improve nasal breathing. Nozovent might therefore be recommended as an alternative to topical decongestants, for certain subjects presenting with nasal obstruction.

Nasal airflow resistance measurement: forced oscillation technique versus posterior rhinomanometry.

This study was designed to determine whether nasal airflow resistance (Rn) which is nonlinear during tidal breathing, can be assessed by the forced oscillation (FO) technique. Rn values obtained by the FO technique and extrapolated to 0 Hz (Rn,FO) were compared to those assessed by posterior rhinomanometry at maximal tidal inspiratory flow (Rn,m), at a 0.5 L x s(-1) flow (Rn,F), and at a 1 hPa transnasal pressure (Rn,P). All Rn estimates were derived from the same inspiratory and expiratory nasal flow and transnasal pressure signals obtained during tidal nasal breathing whilst a forced flow was applied at the nose via a rigid nasal mask in 23 healthy volunteers, of whom 14 had additional measurements after vasoconstrictor treatment. In the basal state, no significant difference, and significant correlations (p<0.0001) were found between Rn,FO and the other Rn estimates. Only the regression line of Rn,FO versus Rn,m was not significantly different from the identity line. After nasal decongestion, Rn,P became significantly higher than the other Rn estimates (p<0.005). The regression line of Rn,FO versus Rn,m remained nonsignificantly different from the identity line. Similar results were observed regarding the percentage values of the different Rn estimates after decongestant treatment. This study shows that, despite its nonlinearity, Rn can be assessed by the FO technique, and that Rn,FO and Rn,m could be indifferently used as physiological indices of nasal patency. As the FO technique is more difficult to implement than the conventional rhinomanometry, its interest in rhinology appears not to be obvious.

Respiratory resistive impedance in obstructive patients: linear regression analysis vs viscoelastic modelling.

The aim of this study was to test the ability of a simple two segment model to describe the frequency dependence of resistive impedance in obstructive patients, and to investigate the significance of parameters derived from this model. The study was performed in 38 patients, in the basal state and after inhalation of 200 micrograms salbutamol. Impedance data measured over 4-32 Hz were fitted by a general four parameter viscoelastic model describing gas redistribution, and completed by an inertial component. This model yielded Newtonian resistance (Rmin) and maximal resistance (Rmax = Rmin plus delayed resistance due to gas redistribution). Resistive impedance data were also submitted to linear regression analysis over the 4-16 and 17-32 Hz frequency ranges, which respectively, yielded resistive impedance extrapolated at 0 Hz (R0) and resistive impedance estimated at 32 Hz (R32). R0 and R32 were compared to Rmax and Rmin, respectively. The airway response to salbutamol inhalation was assessed by the percentage changes in these parameters (R0%, R32%, Rmax%, and Rmin%, respectively). Significant linear correlations (p < 0.0001) were found between R0 and Rmax, R32 and Rmin, and R0% and Rmax%. Furthermore, the linear regression lines of R0 vs Rmax, and R0% vs Rmax%, were not significantly different from the identity line. These results demonstrate that resistive impedance extrapolated at zero frequency is equivalent to maximal resistive impedance, and can be proposed as an index, not only of the level of airway obstruction, but also of its reversibility.

Evaluation of an auto-nCPAP device based on snoring detection.

We evaluated an auto-nasal continuous positive airway pressure (nCPAP) prototype (MC+; SEFAM, Nancy, France) in which apnoea/hypopnoea detection was disabled and nasal mask pressure vibration detection was the only mode of pressure setting. The device was tested in 15 previously untreated obstructive sleep apnoea patients during a night with polysomnography. We observed that a single night of auto-nCPAP improved the apnoea/hypnoea index (AHI) (12 +/- 21 vs 51 +/- 31 disordered breathing events.h-1 of sleep (mean +/- SD)), the awakening-arousal index (13 +/- 20 vs 40 +/- 26 arousals.h-1 of sleep), and duration of slow wave sleep (102 +/- 49 vs 71 +/- 56 min) but not of rapid eye movement (REM) sleep (55 +/- 31 vs 64 +/- 38 min). Auto-nCPAP was effective (apnoea/hypopnoea and arousal indices < 10 events.h-1) in all but three patients. Auto-nCPAP was ineffective in one patient, whose obstructive respiratory events were not preceded by nasal mask pressure vibration detection, and in two patients who were quasi-permanent mouth breathers. Snoring detection may be effective in sleep apnoea syndrome with heavy snoring and without permanent mouth breathing, during the first night of nasal continuous positive airway pressure treatment.

Pulmonary clearance and lung function: influence of acute tobacco intoxication and of vitamin E.

Cigarette smoking increases the alveolar epithelial permeability to small solutes, as assessed by the pulmonary clearance of aerosolized 99mTc-labeled diethylenetriaminepentaacetate. The involvement of lipid peroxidation in this increased clearance was tested in eight asymptomatic young smokers by investigating the effects of a 3-wk supplementation with oral vitamin E (1,000 IU/day) on pulmonary clearance according to a protocol designed as a single-blind crossover study. Indexes of acute tobacco intoxication (exhaled CO, carboxyhemoglobin, and urinary cotinine) and lung function parameters [including Krogh factor (KCO)] were also studied. Under control conditions, pulmonary clearance was abnormally increased (2.93 +/- 0.78%/min), whereas KCO was in the normal range. Pulmonary clearance correlated strongly with expired CO (P < 0.04), HbCO (P < 0.005), urinary cotinine (P < 0.003), and KCO (P < 0.004). Supplementation with vitamin E, a highly efficient antioxidant, neither decreased the pulmonary clearance nor altered the above correlations. However, the strong correlations observed between pulmonary clearance and indexes of acute tobacco intoxication, which reflect the amount of inhaled smoke and the resultant oxidant stress, do not allow exclusion of the involvement of lipid peroxidation in the pulmonary clearance increase observed in smokers.

Inspiratory work of breathing in ventilated preterm infants.

In ventilated newborns, part of the inspiratory work of breathing (WOB) may be due to the inspiratory efforts preceding inspiratory ventilator flow. This study was designed to quantify the contribution of these efforts to WOB. WOB was evaluated in six intubated preterm infants ventilated by the Dräger Babylog 8000. The ventilatory modes studied were intermittent mandatory ventilation (IMV), continuous positive airway pressure (CPAP), and assist-control ventilation at 10 (ACV10) and 15 (ACV15) cmH2O peak pressure. Mouth flow (V) and esophageal pressure (Pe) were recorded, and WOB was estimate from the area delineated by the esophageal pressure-volume curve, where volume is the time integral of V. Calculation of WOB started either at the onset of the infant's inspiratory flow (WOBi), or at the beginning of the infant's inspiratory muscle efforts, detected on Pe and confirmed on the V tracing (WOBm). WOBm was found to be significantly higher than WOBi under all ventilatory conditions studied. The difference in work of breathing (delta W) between WOBm and WOBi did not depend on the type of ventilatory mode. When delta W was related to WOBm, it amounted to about 30% of WOBm in IMV and CPAP, and 60% in ACV (P < 0.05, ACV15 vs. IMV). These results suggest that, in preterm infants connected to a ventilator, inspiratory efforts preceding flow inspiration might account for a large fraction of the inspiratory work of breathing.

A new correction technique for measuring respiratory impedance through an endotracheal tube.

Measurement of respiratory impedance (Zrs) in intubated patients requires corrections for flow-dependent resistance and air compression inside the endotracheal tube (ET). The purpose of this study was to test a new correction technique for these effects. We therefore studied 110 patients in two conditions: breathing normally (C1), or breathing through an ET placed at the mouth (C2). In C1, we measured pressure and flow signals at the mouth, and in C2, at the ET inlet, during application of a pseudorandom forced excitation (4-32 Hz). In C1, respiratory impedance was calculated directly as Z1. In C2, pressure data were first corrected for the flow-dependent resistance of the ET, and respiratory impedance was then corrected both for gas compression inside the set-up and ET inertance (impedance Z2). Strong linear relationships were found between the reference and corrected estimates of the resistance at 6 Hz, the frequency dependence of resistance and the resonant frequency. The mean normalized distance between Z1 and Z2 observed in the patients over the 4-32 Hz frequency range was about 14% for resistance and 12% for reactance (-9% and -4%, respectively, when considering the algebraic value of the distance). This slight underestimation of both components of impedance might be due to an overcorrection of pressure for the flow-dependent resistance of the ET. We conclude that, in intubated patients, newly tested corrections for the mechanical contribution of the endotracheal tube may yield a fair estimate of respiratory impedance when pressure is measured at the inlet of the endotracheal tube.

Respiratory resistance by end-inspiratory occlusion and forced oscillations in intubated patients.

Measurement of respiratory impedance by the forced oscillation technique (FOT) in intubated patients requires corrections for the flow-dependent resistance, inertance, and air compression inside the endotracheal tube (ETT). Recently, we published a method to correct respiratory impedance for the mechanical contribution of the ETT. To validate this correction, we compared the respiratory resistance obtained with this method (Rfo) to the intrinsic (Rmin) and total resistances (RT) measured by the airway-occlusion technique (OCT) in 16 intubated sedated paralyzed ventilated patients. The FOT was applied at functional residual capacity in the 4- to 32-Hz frequency range, whereas the OCT was performed at the end of a normal constant-flow inspiration. Rmin corrected with Rfo measured at 16 and 32 Hz [Rfo(16) = 1.10 x Rmin + 0.10 cmH2O.s.l-1, r = 0.96, P < 0.001; Rfo(32) = 0.93 x Rmin + 0.72 cmH2O.s.l-1, r = 0.97, P < 0.001]. RT corrected with Rfo at 4 Hz [Rfo(4) = 1.11 x RT - 1.48 cmH2O.s.l-1; = 0.92; P < 0.001]. We conclude that the FOT improved by correction for the behavior of the ETT is in good agreement with the OCT in intubated patients.

Topical upper airway anaesthesia with lidocaine increases airway resistance by impairing glottic function.

OBJECTIVE: To assess if two different forms of upper airway topical anaesthesia induce similar changes in airway flow resistance (Rrs). DESIGN: Serial measurements of Rrs before and after topical anaesthesia with acqueous or paste lidocaine. SETTING: Lung function test laboratory. PARTICIPANTS: 9 normal men with documented normal lung function tests. INTERVENTIONS: 2 different session of topical upper airway anaesthesia with 100 mg of liquid 5% lidocaine and 100 mg of 2% lidocaine paste, respectively. MEASUREMENTS AND RESULTS: Rrs was measured by the random noise forced oscillation technique. Fiberoptic upper airway examination was performed in two subjects. Rrs increased on average by 81% after lidocaine spray and by 68% after lidocaine paste (p < 0.005, respectively) with no difference in the magnitude of Rrs increase between the two modes of anaesthesia studied. This increase lasted 13 +/- 3 min (spray) and 12 +/- 3 min (paste), respectively (p = ns). Fiberoptic examination of the two most responders showed inspiratory laryngeal collapse. CONCLUSIONS: Topical upper airway anaesthesia transiently increases Rrs with no specific effects regarding the drug presentation. Laryngeal dysfunction may be one mechanisms involved in Rrs increase following upper airway topical anaesthesia. Such findings may explain some poor respiratory tolerance reported during endoscopy.