Collapsibility of the Upper Airway at Different Concentrations of Propofol Anesthesia

2005 ◽  
Vol 103 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Peter R. Eastwood ◽  
Peter R. Platt ◽  
Kelly Shepherd ◽  
Kathy Maddison ◽  
David R. Hillman
Keyword(s):  
Upper Airway ◽  
Inspiratory Flow ◽  
Electromyographic Activity ◽  
Flow Limitation ◽  
Genioglossus Muscle ◽  
Airway Collapsibility ◽  
Effect Site Concentration ◽  
Intramuscular Electrodes ◽  
Upper Airway Collapsibility ◽  
Spontaneously Breathing

Background This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it. Methods Upper airway collapsibility was determined from pressure-flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 mug/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 +/- 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects. Results With increasing depth of anesthesia, (1) critical closing pressure progressively increased (-0.3 +/- 3.5, 0.5 +/- 3.7, and 1.4 +/- 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 microg/ml respectively; P < 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 +/- 9.9% of maximum at 2.5 microg/ml to 0.8 +/- 0.5% of maximum at 6.0 microg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 microg/ml but not at propofol concentrations of 4.0 and 6.0 microg/ml, whereas phasic EMGgg was unchanged. Conclusions Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

Neostigmine/Glycopyrrolate Administered after Recovery from Neuromuscular Block Increases Upper Airway Collapsibility by Decreasing Genioglossus Muscle Activity in Response to Negative Pharyngeal Pressure

2010 ◽  
Vol 113 (6) ◽  
pp. 1280-1288 ◽  
Author(s):  
Frank Herbstreit ◽  
Daniela Zigrahn ◽  
Christof Ochterbeck ◽  
Jürgen Peters ◽  
Matthias Eikermann
Keyword(s):  
Neuromuscular Blockade ◽  
Lung Volume ◽  
Muscle Activation ◽  
Neuromuscular Block ◽  
Upper Airway ◽  
Acetylcholinesterase Inhibitors ◽  
Genioglossus Muscle ◽  
Pharyngeal Pressure ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Background Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function. Methods We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges. Results Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection. Conclusion Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.

Collapsibility of the Upper Airway during Anesthesia with Isoflurane

2002 ◽  
Vol 97 (4) ◽  
pp. 786-793 ◽  
Author(s):  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
David R. Hillman
Keyword(s):  
Lung Volume ◽  
Critical Pressure ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Flow Limitation ◽  
Anesthetic Depth ◽  
Volume Collapse ◽  
End Tidal ◽  
Spontaneously Breathing

Background The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. Methods To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. Results The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. Conclusions Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

scholarly journals Evolution of Changes in Upper Airway Collapsibility during Slow Induction of Anesthesia with Propofol

2009 ◽  
Vol 111 (1) ◽  
pp. 63-71 ◽  
Author(s):  
David R. Hillman ◽  
Jennifer H. Walsh ◽  
Kathleen J. Maddison ◽  
Peter R. Platt ◽  
Jason P. Kirkness ◽  
...  
Keyword(s):  
Bispectral Index ◽  
Critical Pressure ◽  
Upper Airway ◽  
Index Score ◽  
Loss Of Consciousness ◽  
Electromyographic Activity ◽  
Verbal Command ◽  
Effect Site ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Background Upper airway collapsibility is known to increase under anesthesia. This study assessed how this increase in collapsibility evolves during slow Propofol induction and how it relates to anesthesia-induced changes in upper airway muscle activity and conscious state. Methods Nine healthy volunteers were studied. Anesthesia was induced with Propofol in a step-wise manner (effect-site concentration steps of 0.5 microg x ml(-1) from 0 to 3 microg x ml(-1) and thereafter to 4 microg x ml(-1) and 6 microg x ml(-1) [target-controlled infusion]). Airway patency was maintained with continuous positive airway pressure. Pharyngeal collapsibility was assessed at each concentration by measuring critical pressure. Intramuscular genioglossus electromyogram and anesthetic depth (bispectral index score) were monitored throughout. Loss of consciousness was defined as failure to respond to loud verbal command. Results Loss of consciousness occurred at varying Propofol effect-site concentrations between 1.5 and 4.0 microg x ml(-1). Initially genioglossus electromyographic activity was sustained with increases in Propofol concentration, increasing in some individuals. At or approaching loss of consciousness, it decreased, often abruptly, to minimal values with an accompanying increase in critical pressure. In most subjects, bispectral index score decreased alinearly with increasing Propofol concentration with greatest rate of change coinciding with loss of consciousness. Conclusions Slow stepwise induction of Propofol anesthesia is associated with an alinear increase in upper airway collapsibility. Disproportionate decreases in genioglossus electromyogram activity and increases in pharyngeal critical closing pressure were observed proximate to loss of consciousness, suggesting that particular vulnerability exists after transition from conscious to unconscious sedation. Such changes may have parallels with upper airway behavior at sleep onset.

scholarly journals Effects of leptin and obesity on the upper airway function

2012 ◽  
Vol 112 (10) ◽  
pp. 1637-1643 ◽  
Author(s):  
Mikhael Polotsky ◽  
Ahmed S. Elsayed-Ahmed ◽  
Luis Pichard ◽  
Christopher C. Harris ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Upper Airway ◽  
Leptin Deficiency ◽  
Airway Function ◽  
Airway Collapsibility ◽  
Neuromuscular Responses ◽  
Neuromechanical Control ◽  
Nasal Pressure ◽  
Upper Airway Collapsibility ◽  
Spontaneously Breathing ◽  
Deficient Mice

Obesity is associated with alterations in upper airway collapsibility during sleep. Obese, leptin-deficient mice demonstrate blunted ventilatory control, leading us to hypothesize that ( 1) obesity and leptin deficiency would predispose to worsening neuromechanical upper airway function and that ( 2) leptin replacement would acutely reverse neuromuscular defects in the absence of weight loss. In age-matched, anesthetized, spontaneously breathing C57BL/6J (BL6) and ob− /ob− mice, we characterized upper airway pressure-flow dynamics during ramp decreases in nasal pressure (PN) to determine the passive expiratory critical pressure (PCRIT) and active responses to reductions in PN, including the percentage of ramps showing inspiratory flow limitation (IFL; frequency), the PN threshold at which IFL developed, maximum inspiratory airflow (Vimax), and genioglossus electromyographic (EMGGG) activity. Elevations in body weight were associated with progressive elevations in PCRIT (0.1 ± 0.02 cmH2O/g), independent of mouse strain. PCRIT was also elevated in ob− /ob− compared with BL6 mice (1.6 ± 0.1 cmH2O), independent of weight. Both obesity and leptin deficiency were associated with significantly higher IFL frequency and PN threshold and lower Vimax. Very obese ob− /ob− mice treated with leptin compared with nontreated mice showed a decrease in IFL frequency (from 63.5 ± 2.9 to 30.0 ± 8.6%) and PN threshold (from −0.8 ± 1.1 to −5.6 ± 0.8 cmH2O) and increase in Vimax (from 354.1 ± 25.3 to 659.0 ± 71.8 μl/s). Nevertheless, passive PCRIT in leptin-treated mice did not differ significantly from that seen in nontreated ob− /ob− mice. The findings suggest that weight and leptin deficiency produced defects in upper airway neuromechanical control and that leptin reversed defects in active neuromuscular responses acutely without reducing mechanical loads.

Effects of continuous negative airway pressure-related lung deflation on upper airway collapsibility

1993 ◽  
Vol 75 (3) ◽  
pp. 1222-1225 ◽  
Author(s):  
F. Series ◽  
I. Marc
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Linear Regression Analysis ◽  
Upper Airway ◽  
Flow Limitation ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Lung Deflation ◽  
The Relationship ◽  
Negative Airway Pressure

Continuous negative airway pressure (CNAP) causes a decrease in lung volume, which is known to increase upper airway resistance by itself. We studied how this lung volume change could modify upper airway collapsibility with five normal awake subjects. In a first trial, pressure in a nasal mask (Pm) was progressively decreased in 3- to 5-cmH2O steps (CNAP). In a second trial, changes in lung volumes resulting from CNAP were prevented by applying simultaneously an equivalent level of negative extrathoracic pressure into a poncho-type respirator [isovolumetric CNAP (CNAPisovol)]. For each trial, we examined the relationship between the maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding Pm by least-squares linear regression analysis and determined the critical pressure. We also determined the Pm threshold corresponding to the first Pm value below which flow limitation occurred. Flow limitation was observed in each subject with CNAP but in only two subjects with CNAPisovol. In these two subjects, the Pm threshold values were -20 and -9 cmH2O with CNAP and -39 and -16 cmH2O with CNAPisovol, respectively. Critical pressures for the same two subjects were -161 and -96 cmH2O with CNAP and -202 and -197 cmH2O with CNAPisovol, respectively. We conclude that CNAP-induced decreases in lung volume increase upper airway collapsibility.

scholarly journals Upper airway collapsibility and patterns of flow limitation at constant end-expiratory lung volume

2012 ◽  
Vol 113 (5) ◽  
pp. 691-699 ◽  
Author(s):  
Robert L. Owens ◽  
Bradley A. Edwards ◽  
Scott A. Sands ◽  
James P. Butler ◽  
Danny J. Eckert ◽  
...  
Keyword(s):  
Pressure Drop ◽  
Lung Volume ◽  
Upper Airway ◽  
Inspiratory Pressure ◽  
Flow Limitation ◽  
Pressure Drops ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Measure Change ◽  
Upper Airway Collapsibility

The passive pharyngeal critical closing pressure (Pcrit) is measured using a series of pressure drops. However, pressure drops also lower end-expiratory lung volume (EELV), which independently affects Pcrit. We describe a technique to measure Pcrit at a constant EELV. Continuous positive airway pressure (CPAP)-treated obstructive sleep apnea (OSA) patients and controls were instrumented with an epiglottic catheter, magnetometers (to measure change in EELV), and nasal mask/pneumotachograph and slept supine on nasal CPAP. Pcrit was measured in standard fashion and using our novel “biphasic technique” in which expiratory pressure only was lowered for 1 min before the inspiratory pressure was dropped; this allowed EELV to decrease to the drop level before performing the pressure drop. Seven OSA and three controls were studied. The biphasic technique successfully lowered EELV before the inspiratory pressure drop. Pcrit was similar between the standard and biphasic techniques (−0.4 ± 2.6 vs. −0.6 ± 2.3 cmH2O, respectively, P = 0.84). Interestingly, we noted three different patterns of flow limitation: 1) classic Starling resistor type: flow fixed and independent of downstream pressure; 2) negative effort dependence within breaths: substantial decrease in flow, sometimes with complete collapse, as downstream pressure decreased; and 3) and negative effort dependence across breaths: progressive reductions in peak flow as respiratory effort on successive breaths increased. Overall, EELV changes do not influence standard passive Pcrit measurements if breaths 3–5 of pressure drops are used. These results also highlight the importance of inspiratory collapse in OSA pathogenesis. The cause of negative effort dependence within and across breaths is not known and requires further study.

Supplemental Carbon Dioxide Stabilizes the Upper Airway in Volunteers Anesthetized with Propofol

2018 ◽  
Vol 129 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Katarina Jennifer Ruscic ◽  
Janne Bøgh Stokholm ◽  
Johann Patlak ◽  
Hao Deng ◽  
Jeroen Cedric Peter Simons ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Deep Level ◽  
Muscle Tone ◽  
Secondary Analysis ◽  
Upper Airway ◽  
Dependent Manner ◽  
Genioglossus Muscle ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Closing Pressure

Abstract Background Propofol impairs upper airway dilator muscle tone and increases upper airway collapsibility. Preclinical studies show that carbon dioxide decreases propofol-mediated respiratory depression. We studied whether elevation of end-tidal carbon dioxide (Petco2) via carbon dioxide insufflation reverses the airway collapsibility (primary hypothesis) and impaired genioglossus muscle electromyogram that accompany propofol anesthesia. Methods We present a prespecified, secondary analysis of previously published experiments in 12 volunteers breathing via a high-flow respiratory circuit used to control upper airway pressure under propofol anesthesia at two levels, with the deep level titrated to suppression of motor response. Ventilation, mask pressure, negative pharyngeal pressure, upper airway closing pressure, genioglossus electromyogram, bispectral index, and change in end-expiratory lung volume were measured as a function of elevation of Petco2 above baseline and depth of propofol anesthesia. Results Petco2 augmentation dose-dependently lowered upper airway closing pressure with a decrease of 3.1 cm H2O (95% CI, 2.2 to 3.9; P < 0.001) under deep anesthesia, indicating improved upper airway stability. In parallel, the phasic genioglossus electromyogram increased by 28% (23 to 34; P < 0.001). We found that genioglossus electromyogram activity was a significant modifier of the effect of Petco2 elevation on closing pressure (P = 0.005 for interaction term). Conclusions Upper airway collapsibility induced by propofol anesthesia can be reversed in a dose-dependent manner by insufflation of supplemental carbon dioxide. This effect is at least partly mediated by increased genioglossus muscle activity.

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