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

Abstract

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. 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. 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 < 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 < 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. 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.