Modulating effects of hypoxia and hypercarbia on glottic closing force

Aspiration has been identified as one of the independent risk factors for development of respiratory tract infections, the incidence of which varies from 10% to 65% in patients in intensive care units. The primary defense mechanism for protection of the lower airway is the glottic closure reflex (GCR), elicited by stimulation of the internal branch of the superior laryngeal nerve. This reflex, once considered highly stable, is now considered vulnerable to a growing number of clinical factors. This study was designed to explore the biomechanical effects of hypoxia and hypercarbia, common occurrences among critically ill patients, on the GCR.

Five adult male Yorkshire pigs were used in the study. Both internal superior laryngeal nerves were simultaneously stimulated with bipolar platinum-iridium electrodes. The glottic closing force (GCF) was then measured by placing a pressure transducer between the adducting vocal folds under 3 different protocols: protocol 1 (control), protocol 2 (hypoxia: partial pressure of arterial oxygen [PaO2] levels of 90, 70, and 50 mm Hg), and protocol 3 (hypercarbia: partial pressure of arterial carbon dioxide [PaCO2] levels of 60 and 70 mm Hg). Six readings were recorded under each experimental paradigm, and Student's t-test was applied to calculate the statistical significance against the control.

Hypoxia reduced the GCF to 75%, 40%, and 29% of control for PaO2 levels of 90, 70, and 50 mm Hg, respectively, and hypercarbia reduced the GCF to 40% and 27% of control for PaCO2 levels of 60 and 70 mm Hg, respectively.

This is the first study that highlights the biomechanical impact of hypoxia and hypercarbia on the GCR, providing a unified explanation for the increased incidence of life-threatening aspiration in critically ill patients with such alterations.