Susceptibility to Upper Airway Obstruction during Partial Neuromuscular Block 

1998 ◽  
Vol 88 (2) ◽  
pp. 371-378 ◽  
Author(s):  
Gilles D'Honneur ◽  
Frederic Lofaso ◽  
Gordon B. Drummond ◽  
Jean-Marc Rimaniol ◽  
Jean V. Aubineau ◽  
...  

Background Airway obstruction after anesthesia may be caused or exaggerated by residual neuromuscular block, with loss of muscle support for collapsible upper airway structures. Methods Six male volunteers were studied before treatment, during stable partial neuromuscular block with vecuronium at a mean train-of-four (TOF) ratio of 50% (95% CI, 36-61%), and after reversal by neostigmine. Catheter-mounted transducers were placed in the pharynx and esophagus to estimate, respectively, the upper airway resistance, and the work of breathing (calculated as the time integral of the inspiratory pressure developed by the respiratory muscles, esophageal pressure time product) during quiet breathing, during breathing 5% carbon dioxide, and while breathing with an inspiratory resistor. Breathing with pressure at the airway opening held at pressures from -5 to 40 cm H2O were also tested to assess airway collapsibility. Results Although breathing through a resistor increased upper airway resistance from 1.2 (0.67, 1.72) cm H2O x l(-1) x s to 2.5 (1.32, 3.38) cm H2O x l(-1) x s, and carbon dioxide stimulation reduced resistance to 0.8 (0.46, 1.33) cm H2O x l(-1) x s, no effect of partial neuromuscular block (mean TOF ratio, 52%) on upper airway properties could be shown. Conclusions Neuromuscular block with a TOF ratio of 50% can be present yet clinically difficult to detect in patients recovering from anesthesia. This degree of block has no effect on airway patency in volunteers, even during challenge. Airway obstruction during recovery from anesthesia thus is more likely to be caused by residual effects of general anesthetic agents or centrally acting analgesics, either alone or perhaps in concert with residual neuromuscular block.

1998 ◽  
Vol 85 (3) ◽  
pp. 860-866 ◽  
Author(s):  
Frédéric Lofaso ◽  
Anne Marie Lorino ◽  
Redouane Fodil ◽  
Marie Pia D’Ortho ◽  
Daniel Isabey ◽  
...  

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 ⋅ l−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.


1991 ◽  
Vol 71 (4) ◽  
pp. 1346-1354 ◽  
Author(s):  
D. A. Wiegand ◽  
B. Latz

Previous investigators (van Lunteren et al. J. Appl. Physiol. 62: 582–590, 1987) have suggested that the geniohyoid and sternohyoid muscles may act as upper airway dilators in the cat. To investigate the effect of geniohyoid and sternohyoid contraction on inspiratory upper airway resistance (UAR), we studied five adult male cats anesthetized with ketamine and xylazine during spontaneous room-air breathing. Inspiratory nasal airflow was measured by sealing the lips and constructing a nose mask. Supraglottic pressure was measured using a transpharyngeal catheter placed above the larynx. Mask pressure was measured using a separate catheter. Geniohyoid and sternohyoid lengths were determined by sonomicrometry. Geniohyoid and sternohyoid contraction was stimulated by direct muscle electrical stimulation with implanted wire electrodes. Mean inspiratory UAR was determined for spontaneous breaths under three conditions: 1) baseline (no muscle stimulation), 2) geniohyoid contraction alone, and 3) sternohyoid contraction alone. Geniohyoid contraction alone produced no significant reduction in inspiratory UAR [unstimulated, 17.75 +/- 0.86 (SE) cmH2O.l-1.s; geniohyoid contraction, 19.24 +/- 1.10]. Sternohyoid contraction alone also produced no significant reduction in inspiratory UAR (unstimulated, 15.74 +/- 0.92 cmH2O.l-1.s; sternohyoid contraction, 14.78 +/- 0.78). Simultaneous contraction of the geniohyoid and sternohyoid muscles over a wide range of muscle lengths produced no consistent change in inspiratory UAR. The geniohyoid and sternohyoid muscles do not appear to function consistently as upper airway dilator muscles when UAR is used as an index of upper airway patency in the cat.


2016 ◽  
Vol 64 (4) ◽  
pp. 970.1-970
Author(s):  
J Doumit ◽  
P Belvitch ◽  
I Rubinstein

RationaleUpper airway resistance is critical to the pathophysiology of obstructive sleep apnea (OSA). We have previously characterized a subset of patients with OSA who have evidence of reversible upper airways resistance as measured by spirometry. Specifically, these patients have an increased FEF50/FIF50 ratio which decreases with administration of a short acting bronchodilator. On average these patients had a lower BMI (average 27) compared to OSA patients as a whole suggesting the possibility of unique upper airway pathophysiology among this group. In the current study, we identify additional patients with OSA who have reversible upper airways obstruction on spirometry and characterize their compliance with CPAP therapy as compared to a traditional OSA population.MethodsWe retrospectively evaluated patients who had a sleep screen suggestive of OSA in the last 2 years. Patients who also had spirometry in the previous 5 years were identified for further analysis. Those patients with either normal spirometry or fixed obstructive defects who had a decrease in the FEF50/FIF50 ratio after administration of a short acting inhaled beta agonist (albuterol) were then characterized. We then measured objective CPAP adherence using data downloaded from the positive airway pressure device with adherence defined as CPAP use >4 hrs more than 70% of nights over a 30 day period.ResultsWe identified 70 patients with positive sleep screens who also had spirometry demonstrating normal of fixed lower expiratory obstruction with evidence of upper airways obstruction as demonstrated by a decreased FEF50/FIF50 ratio. Of these, 45 had a decrease in the FEF50/FIF50 ratio of more than 20% following administration of inhaled albuterol. Overall, CPAP adherence between those with reversible upper airways obstruction and those without was similar (23/45=51% vs 14/26=54%). However, subgroup analysis revealed a lower adherence rate among non-obese patients (BMI<30) with reversible airways obstruction (6/16=36%).ConclusionThe identification of a subset of patients with OSA who have evidence of decreased upper airway resistance in response to inhaled bronchodilator suggests unique pathology in this group. Decreased adherence to traditional OSA therapy with CPAP among these patients is additional evidence of differential pathophysiology requiring novel treatments. Specifically, treatment with a long acting beta agonist (LABA) prior to sleep may reduce upper airway obstruction and be better tolerated than CPAP.


1991 ◽  
Vol 70 (1) ◽  
pp. 430-438 ◽  
Author(s):  
R. M. Aronson ◽  
D. W. Carley ◽  
E. Onal ◽  
J. Wilborn ◽  
M. Lopata

Although a thoracic volume dependence of upper airway resistance and caliber is known to exist in seated subjects, the mechanisms mediating this phenomenon are unknown. To test the hypothesis that actively altered end-expiratory lung volume (EELV) affects upper airway resistance in the supine position and to explore the mechanisms of any EELV-induced resistance changes, we studied five normal males during wakefulness. Supraglottic upper airway resistance (Ruaw) was calculated at an inspiratory flow of 0.1 l/s. The genioglossal electromyogram was obtained with indwelling wire electrodes and processed as moving time average. End-tidal CO2 was monitored by infrared analyzer. Observations were made during four 20-breath voluntary maneuvers: two at high and two at low EELV in each subject. Each maneuver was preceded by a control period at functional residual capacity. At high lung volume the EELV was increased by 2.23 +/- 0.54 (SD) liters; Ruaw decreased to 67.8 +/- 35.1% of control, while tonic and phasic genioglossal activities declined to 79.0 +/- 23.1 and 72.4 +/- 29.8%, respectively. At low lung volume the EELV was decreased by 0.86 +/- 0.23 liters. Ruaw increased to 178.2 +/- 186.8%, while tonic and phasic genioglossal activities increased to 243.0 +/- 139.3 and 249.1 +/- 146.3%, respectively (P less than 0.0001 for all). The findings were not explained by CO2 perturbations or respiratory pattern. Multiple linear regression analysis indicated that the genioglossal responses blunted the EELV-induced changes in upper airway patency.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 68 (1) ◽  
pp. 154-160 ◽  
Author(s):  
A. D. Wolin ◽  
K. P. Strohl ◽  
B. N. Acree ◽  
J. M. Fouke

Continuous positive pressure applied at the nose has been shown to cause a decrease in upper airway resistance. The present study was designed to determine whether a similar positive transmural pressure gradient, generated by applying a negative pressure at the body surface around the neck, altered upper airway patency. Studies were performed in nine spontaneously breathing anesthetized supine dogs. Airflow was measured with a pneumotachograph mounted on an airtight muzzle placed over the nose and mouth of each animal. Upper airway pressure was measured as the differential pressure between the extrathoracic trachea and the inside of the muzzle. Upper airway resistance was monitored as an index of airway patency. Negative pressure (-2 to -20 cmH2O) was applied around the neck by using a cuirass extending from the jaw to the thorax. In each animal, increasingly negative pressures were transmitted to the airway wall in a progressive, although not linear, fashion. Decreasing the pressure produced a progressive fall in upper airway resistance, without causing a significant change in respiratory drive or respiratory timing. At -5 cmH2O pressure, there occurred a significant fall in upper airway resistance, comparable with the response of a single, intravenous injection of sodium cyanide (0.5-3.0 mg), a respiratory stimulant that produces substantial increases in respiratory drive. We conclude that upper airway resistance is influenced by the transmural pressure across the airway wall and that such a gradient can be accomplished by making the extraluminal pressure more negative.(ABSTRACT TRUNCATED AT 250 WORDS)


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