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.

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.

A threshold lung volume for optimal mechanical effects on upper airway airflow dynamics: studies in an anesthetized rabbit model

2012 ◽  
Vol 112 (7) ◽  
pp. 1197-1205 ◽  
Author(s):  
Kristina Kairaitis ◽  
Manisha Verma ◽  
Jason Amatoury ◽  
John R. Wheatley ◽  
David P. White ◽  
...  
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Rabbit Model ◽  
Upper Airway ◽  
Flow Limitation ◽  
Volume Increase ◽  
Mechanical Effects ◽  
Pharyngeal Pressure ◽  
Volume Resistance ◽  
Spontaneously Breathing

Increasing lung volume improves upper airway airflow dynamics via passive mechanisms such as reducing upper airway extraluminal tissue pressures (ETP) and increasing longitudinal tension via tracheal displacement. We hypothesized a threshold lung volume for optimal mechanical effects on upper airway airflow dynamics. Seven supine, anesthetized, spontaneously breathing New Zealand White rabbits were studied. Extrathoracic pressure was altered, and lung volume change, airflow, pharyngeal pressure, ETP laterally (ETPlat) and anteriorly (ETPant), tracheal displacement, and sternohyoid muscle activity (EMG%max) monitored. Airflow dynamics were quantified via peak inspiratory airflow, flow limitation upper airway resistance, and conductance. Every 10-ml lung volume increase resulted in caudal tracheal displacement of 2.1 ± 0.4 mm (mean ± SE), decreased ETPlat by 0.7 ± 0.3 cmH2O, increased peak inspiratory airflow of 22.8 ± 2.6% baseline (all P < 0.02), and no significant change in ETPant or EMG%max. Flow limitation was present in most rabbits at baseline, and abolished 15.7 ± 10.5 ml above baseline. Every 10-ml lung volume decrease resulted in cranial tracheal displacement of 2.6 ± 0.4 mm, increased ETPant by 0.9 ± 0.2 cmH2O, ETPlat was unchanged, increased EMG%max of 11.1 ± 0.3%, and a reduction in peak inspiratory airflow of 10.8 ± 1.0%baseline (all P < 0.01). Lung volume, resistance, and conductance relationships were described by exponential functions. In conclusion, increasing lung volume displaced the trachea caudally, reduced ETP, abolished flow limitation, but had little effect on resistance or conductance, whereas decreasing lung volume resulted in cranial tracheal displacement, increased ETP and increased resistance, and reduced conductance, and flow limitation persisted despite increased muscle activity. We conclude that there is a threshold for lung volume influences on upper airway airflow dynamics.

Effect of Blood Pressure Changes on Air Flow Dynamics in the Upper Airway of the Decerebrate Cat

1996 ◽  
Vol 84 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Alexander H. Mayor ◽  
Alan R. Schwartz ◽  
James A. Rowley ◽  
Shannon J. Willey ◽  
Boyd M. Gillespie ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Airway Obstruction ◽  
Critical Pressure ◽  
Air Flow ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Nasal Resistance ◽  
Flow Limitation ◽  
Decerebrate Cat ◽  
Arterial Blood

Background Previous studies suggest that upper airway neuromuscular activity can be affected by changes in blood pressure via a baroreceptor-mediated mechanism. It was hypothesized that increases in blood pressure would increase upper airway collapsibility predisposing to airway obstruction at a flow-limiting site in the hypopharynx. Methods To examine the effect of blood pressure on upper airway function, maximal inspiratory air flow was determined through the isolated feline upper airway before, during, and after intravenous infusion of phenylephrine (10-20 micrograms.kg-1.min) in six decerebrate, tracheotomized cats. Inspiratory flow, hypopharyngeal pressure, and pressure at the site of pharyngeal collapse were recorded as hypopharyngeal pressure was rapidly decreased to achieve inspiratory flow limitation in the isolated upper airway. Pressure-flow relationships were used to determine maximal inspiratory air flow and its mechanical determinants, the upper airway critical pressure (a measure of pharyngeal collapsibility), and the nasal resistance upstream to the site of flow limitation. Results An increased mean arterial blood pressure of 71 +/- 16 mmHg (mean +/- SD) was associated with significant decrease in maximal inspiratory air flow from 147 +/- 38 ml/s to 115 +/- 27 ml.sec-1 (P &lt; 0.01). The decrease in maximal inspiratory air flow was associated with an increase in upper airway critical pressure from -8.1 +/- 3.8 to -5.7 +/- 3.7 cm H2O (p &lt; 0.02), with no significant change in nasal resistance. When blood pressure was decreased to baseline by discontinuing the phenylephrine infusion, maximal inspiratory air flow and upper airway critical pressure returned to their baseline values. Conclusions Increased blood pressure increased the severity of upper airway air flow obstruction by increasing pharyngeal collapsibility. Previous studies relating baroreceptor activity to neuromuscular regulation of upper airway tone, are consistent with this effect being mediated by afferent activity from baroreceptors. These findings warrant further study because they suggest the possibility that upper airway obstruction in postoperative patients could either be caused or exacerbated by an increase in blood pressure.

Decrease in lung volume-related feedback enhances laryngeal reflexes to negative pressure

1992 ◽  
Vol 73 (3) ◽  
pp. 832-836 ◽  
Author(s):  
S. Zhang ◽  
O. P. Mathew
Keyword(s):  
Lung Volume ◽  
Negative Pressure ◽  
Upper Airway ◽  
Pressure Change ◽  
Inspiratory Flow ◽  
Lower Airway ◽  
Excitatory Effect ◽  
Peak Inspiratory Flow ◽  
Inspiratory Muscles ◽  
Pressure Pulses

Negative pressure applied to the upper airway has an excitatory effect on the activity of upper airway muscles and an inhibitory effect on thoracic inspiratory muscles. The role of lung volume feedback in this response was investigated in 10 anesthetized spontaneously breathing adult rabbits. To alter lung volume feedback, the lower airway was exposed to SO2 (250 ppm for 15 min), thereby blocking slowly adapting receptors (SARs). Negative pressure pulses (5, 10, and 20 cmH2O, 300-ms duration) were applied to the functionally isolated upper airway before and after SAR blockade. Tracheal airflow and electromyogram (EMG) of the genioglossus and alae nasi were recorded. Peak EMG, peak inspiratory flow, tidal volume, and respiratory timing of control breaths (3 breaths immediately preceding test) and test breaths were determined. Analysis of variance was used to determine the significance of the effects. Negative pressure pulses increased peak EMG of genioglossus and alae nasi and inspiratory duration and decreased peak inspiratory flow. These effects were larger after SAR blockade. We conclude that a decrease in volume feedback from the lung augments the response to upper airway pressure change.

Pressure transmission across the respiratory system at raised lung volumes in infants

1994 ◽  
Vol 77 (2) ◽  
pp. 1015-1020 ◽  
Author(s):  
D. J. Turner ◽  
C. J. Lanteri ◽  
P. N. LeSouef ◽  
P. D. Sly
Keyword(s):  
Lung Volume ◽  
Dynamic Pressure ◽  
Esophageal Pressure ◽  
Tidal Range ◽  
Lung Volumes ◽  
Pressure Transmission ◽  
Airway Opening ◽  
Forced Expiratory Flow ◽  
End Tidal ◽  
Volume Range

Forced expiratory flow-volume (FEFV) curves can be generated from end-tidal inspiration in infants with use of an inflatable jacket. We have developed a technique to raise lung volume in the infant before generation of FEFV curves. Measurements of pressure transmission to the airway opening by use of static maneuvers have shown no change with increasing lung volume above end-tidal inspiration. The aim of this study was to determine, under dynamic conditions (i.e., during rapid thoracic compression), whether the efficiency of pressure transmission across the chest wall is altered by raising lung volume above the tidal range. Dynamic pressure transmission (Ptx,dyn) was measured in five infants (age 6–17 mo). Jacket pressure (Pj), esophageal pressure, and volume were measured throughout passive and FEFV curves at lung volumes set by 10, 15, and 20 cmH2O preset pressure. The group mean Ptx,dyn was 37 +/- 6% (SE) of Pj at end-tidal inspiration, and no change was seen with further increases in lung volume. However, a mean decrease in Ptx,dyn of 42% was evident throughout the tidal volume range (i.e., from end-tidal inspiration to end expiration). Isovolume static pressure transmission (Ptx,st) was measured in three of the five infants by inflation of the jacket in a stepwise manner with the airway closed. Measurements were made at end-tidal inspiration and lung volumes at 10, 15, and 20 cmH2O preset pressure. Resulting changes in Pj, esophageal pressure, and airway opening pressure were compared using linear regressions to determine Ptx,st.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Differential effects of acute cerebellectomy on cough in spontaneously breathing cats

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253060
Author(s):  
M. Nicholas Musselwhite ◽  
Tabitha Y. Shen ◽  
Melanie J. Rose ◽  
Kimberly E. Iceman ◽  
Ivan Poliacek ◽  
...  
Keyword(s):  
Motor Behavior ◽  
Motor Pattern ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Adductor Muscle ◽  
Motor Drive ◽  
Mechanical Stimuli ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing

The role of the cerebellum in controlling the cough motor pattern is not well understood. We hypothesized that cerebellectomy would disinhibit motor drive to respiratory muscles during cough. Cough was induced by mechanical stimulation of the tracheobronchial airways in anesthetized, spontaneously breathing adult cats (8 male, 1 female), and electromyograms (EMGs) were recorded from upper airway, chest wall, and abdominal respiratory muscles. Cough trials were performed before and at two time points after total cerebellectomy (10 minutes and >1 hour). Unlike a prior report in paralyzed, decerebrated, and artificially ventilated animals, we observed that cerebellectomy had no effect on cough frequency. After cerebellectomy, thoracic inspiratory muscle EMG magnitudes increased during cough (diaphragm EMG increased by 14% at 10 minutes, p = 0.04; parasternal by 34% at 10 minutes and by 32% at >1 hour, p = 0.001 and 0.03 respectively). During cough at 10 minutes after cerebellectomy, inspiratory esophageal pressure was increased by 44% (p = 0.004), thyroarytenoid (laryngeal adductor) muscle EMG amplitude increased 13% (p = 0.04), and no change was observed in the posterior cricoarytenoid (laryngeal abductor) EMG. Cough phase durations did not change. Blood pressure and heart rate were reduced after cerebellectomy, and respiratory rate also decreased due to an increase in duration of the expiratory phase of breathing. Changes in cough-related EMG magnitudes of respiratory muscles suggest that the cerebellum exerts inhibitory control of cough motor drive, but not cough number or phase timing in response to mechanical stimuli in this model early after cerebellectomy. However, results varied widely at >1 hour after cerebellectomy, with some animals exhibiting enhancement or suppression of one or more components of the cough motor behavior. These results suggest that, while the cerebellum and behavior-related sensory feedback regulate cough, it may be difficult to predict the nature of the modulation based on total cerebellectomy.

Changes in end-expiratory lung volume during sleep in patients with occlusive apnea

1987 ◽  
Vol 63 (4) ◽  
pp. 1642-1647 ◽  
Author(s):  
R. M. Aronson ◽  
C. G. Alex ◽  
E. Onal ◽  
M. Lopata
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Esophageal Pressure ◽  
Inspiratory Pressure ◽  
Upper Airways ◽  
Airway Occlusion ◽  
Respiratory Inductive Plethysmography ◽  
Inductive Plethysmography

Eight patients with occlusive sleep apnea were monitored during non-rapid-eye-movement (NREM) sleep to study the factors that contribute to negative inspiratory pressure generation and thus upper airway occlusion. End-expiratory lung volume assessed by respiratory inductive plethysmography [sum of end-expiratory levels (SUM EEL)] increased early and decreased late during the ventilatory phases (P less than 0.0001, one-way analysis of variance). Inspiratory change in esophageal pressure (Pes) and peak inspiratory diaphragmatic and genioglossal electromyograms (EMGdi and EMGge) decreased while the inspiratory pressure generated for a given diaphragmatic activity (Pes/EMGdi) increased during the preapneic phase (P less than 0.0001, for all). Multiple regression analysis with Pes/EMGdi as the dependent variable (R2 = 0.90) indicated that both the changes in SUM EEL and EMGge significantly contributed to the model (P less than 0.008 and 0.004, respectively). These results indicate that end-expiratory lung volume fluctuates during NREM sleep in patients with occlusive apnea and suggest that these changes along with the changes in upper airway muscle activity contribute to the generation of negative inspiratory pressure, leading to the passive collapse of the upper airways.

Assessment of Changes in Upper Airway Obstruction by Automatic Identification of Inspiratory Flow Limitation During Sleep

2009 ◽  
Vol 56 (8) ◽  
pp. 2006-2015 ◽  
Author(s):  
Christian Morgenstern ◽  
Matthias Schwaibold ◽  
Winfried J. Randerath ◽  
Armin Bolz ◽  
Raimon Jane
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Upper Airway Obstruction ◽  
Automatic Identification ◽  
Flow Limitation

Effect of negative expiratory pressure on respiratory system flow resistance in awake snorers and nonsnorers

1999 ◽  
Vol 87 (3) ◽  
pp. 969-976 ◽  
Author(s):  
Claudio Tantucci ◽  
Alexandre Duguet ◽  
Anna Ferretti ◽  
Selma Mehiri ◽  
Isabelle Arnulf ◽  
...  
Keyword(s):  
Respiratory System ◽  
Supine Position ◽  
Flow Resistance ◽  
Upper Airway ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Upper Airways ◽  
Flow Interruption ◽  
Expiratory Flow ◽  
Spontaneously Breathing

In spontaneously breathing subjects, intrathoracic expiratory flow limitation can be detected by applying a negative expiratory pressure (NEP) at the mouth during tidal expiration. To assess whether NEP might increase upper airway resistance per se, the interrupter resistance of the respiratory system (Rint,rs) was computed with and without NEP by using the flow interruption technique in 12 awake healthy subjects, 6 nonsnorers (NS), and 6 nonapneic snorers (S). Expiratory flow (V˙) and Rint,rs were measured under control conditions with V˙ increased voluntarily and during random application of brief (0.2-s) NEP pulses from −1 to −7 cmH2O, in both the seated and supine position. In NS, Rint,rs with spontaneous increase inV˙ and with NEP was similar [3.10 ± 0.19 and 3.30 ± 0.18 cmH2O ⋅ l−1 ⋅ s at spontaneous V˙ of 1.0 ± 0.01 l/s and atV˙ of 1.1 ± 0.07 l/s with NEP (−5 cmH2O), respectively]. In S, a marked increase in Rint,rs was found at all levels of NEP ( P < 0.05). Rint,rs was 3.50 ± 0.44 and 8.97 ± 3.16 cmH2O ⋅ l−1 ⋅ s at spontaneous V˙ of 0.81 ± 0.02 l/s and atV˙ of 0.80 ± 0.17 l/s with NEP (−5 cmH2O), respectively ( P < 0.05). With NEP, Rint,rs was markedly higher in S than in NS both seated ( F = 8.77; P < 0.01) and supine ( F = 9.43; P < 0.01). In S,V˙ increased much less with NEP than in NS and was sometimes lower than without NEP, especially in the supine position. This study indicates that during wakefulness nonapneic S have more collapsible upper airways than do NS, as reflected by the marked increase in Rint,rs with NEP. The latter leads occasionally to an actual decrease in V˙ such as to invalidate the NEP method for detection of intrathoracic expiratory flow limitation.

Oxygen cost of breathing during fatiguing inspiratory resistive loads

1989 ◽  
Vol 66 (5) ◽  
pp. 2045-2055 ◽  
Author(s):  
F. D. McCool ◽  
G. E. Tzelepis ◽  
D. E. Leith ◽  
F. G. Hoppin
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Energy Utilization ◽  
Whole Body ◽  
Inspiratory Flow Rate ◽  
Inspiratory Muscles ◽  
Inspiratory Resistance ◽  
Resistive Loads

When a subject breathes against an inspiratory resistance, the inspiratory pressure, the inspiratory flow, and the lung volume at which the breathing task takes place all interact to determine the length of time the task can be sustained (Tlim). We hypothesized that the mechanism actually limiting tasks in which these parameters were varied involved the rate of energy utilization by the inspiratory muscles. To test this hypothesis, we studied four experienced normal subjects during fatiguing breathing tasks performed over a range of pressures and flows and at two different lung volumes. We assessed energy utilization by measuring the increment in the rate of whole body O2 consumption due to the breathing task (VO2 resp). Power and mean esophageal pressure correlated with Tlim but depended also on lung volume and inspiratory flow rate. In contrast, VO2 resp closely correlated with Tlim, and this relationship was not systematically altered by inspiratory flow or lung volume. The shape of the VO2 resp vs. Tlim curve was approximately hyperbolic, with high rates of VO2 resp associated with short endurance times and lower rates of VO2 resp approaching an asymptotic value at high Tlim. These findings are consistent with a mechanism whereby a critical rate of energy utilization determines the endurance of the inspiratory pump, and that rate varies with pressure, flow, and lung volume.

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