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The Predisposition to Inspiratory Upper Airway Collapse during Partial Neuromuscular Blockade

Klinik für Anästhesiologie und Intensivmedizin, and Klinik für Diagnostische Radiologie, Universitätsklinikum Essen; and Universität Duisburg-Essen, Essen, Germany

Correspondence and requests for reprints should be addressed to Priv. Doz. Dr. Matthias Eikermann, Oberarzt der Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Hufelandstrasse 55, D-45122 Essen, Germany. E-mail: meikermann{at}rics.bwh.harvard.edu

Rationale: Partial neuromuscular transmission failure by acetylcholine receptor blockade (neuromuscular blockade) or antibody-mediated functional loss (myasthenia gravis), even with a magnitude of muscle weakness that does not evoke respiratory symptoms, can evoke dysphagia and decreased inspiratory airflow, and increases the risk of susceptible patients to develop severe pulmonary complications.

Objectives: To assess whether impaired neuromuscular transmission predisposes individuals to inspiratory upper airway collapse, we assessed supraglottic airway diameter and volume by respiratory-gated magnetic resonance imaging, upper airway dilator muscle function (genioglossus force and EMG), and changes in lung volume, respiratory timing, and peripheral muscle function before, during, and after partial neuromuscular blockade in healthy, awake volunteers.

Measurements and Main Results: Partial neuromuscular blockade (train-of-four [TOF] ratio: 0.5 and 0.8) was associated with the following: (1) a decrease of inspiratory retropalatal and retroglossal upper airway volume to 66 ± 22 and 82 ± 12% of baseline, which was significantly more intense in the retropalatal area; (2) an attenuation of the normal increase in anteroposterior upper airway diameter during forced inspiration to 74 ± 18% of baseline; (3) a decrease in genioglossus activity during maximum voluntary tongue protrusion to 39 ± 19% (TOF, 0.5) and 73 ± 29% (TOF, 0.8) of baseline; and (4) no effects on upper airway size during expiration, lung volume, and respiratory timing.

Conclusions: Thus, impaired neuromuscular transmission, even to a degree insufficient to evoke respiratory symptoms, markedly impairs upper airway dimensions and function. This may be explained by an impairment of the balance between upper airway dilating forces and negative intraluminal pressure generated during inspiration by respiratory "pump" muscles.

Key Words: partial neuromuscular transmission failure • forced inspiration • upper airway size • upper airway dilator muscles • lung volume

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject It is unclear how important neuromuscular factors (in the absence of anatomic insufficiency) are in the pathogenesis of obstructive sleep apnea (OSA). What This Study Adds to the Field Our data show that impaired neuromuscular transmission, even to a degree insufficient to evoke respiratory symptoms, markedly impairs upper airway dimensions and function of the upper airway dilator muscles.

 

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