Effects of upper airway anesthesia on pharyngeal patency during sleep.

Pharyngeal patency depends, in part, on the tone and inspiratory activation of pharyngeal dilator muscles. To evaluate the influence of upper airway sensory feedback on pharyngeal muscle tone and thus pharyngeal patency, we measured pharyngeal airflow resistance and breathing pattern in 15 normal, supine subjects before and after topical lidocaine anesthesia of the pharynx and glottis. Studies were conducted during sleep and during quiet, relaxed wakefulness before sleep onset. Maximal flow-volume loops were also measured before and after anesthesia. During sleep, pharyngeal resistance at peak inspiratory flow increased by 63% after topical anesthesia (P less than 0.01). Resistance during expiration increased by 40% (P less than 0.01). Similar changes were observed during quiet wakefulness. However, upper airway anesthesia did not affect breathing pattern during sleep and did not alter awake flow-volume loops. These results indicate that pharyngeal patency during sleep is compromised when the upper airway is anesthetized and suggest that upper airway reflexes, which promote pharyngeal patency, exist in humans.

Lung mechanics and neuromuscular output during CO2 inhalation after airway anesthesia.

Airway anesthesia with aerosolized lidocaine has been associated with an increase in minute ventilation (VE) during CO2 inhalation. The increase in VE may be due to increased neuromuscular output or decreased mechanical load on breathing. To evaluate this we measured VE, breathing pattern, mouth occlusion pressure, and lung mechanics in 20 normal subjects during room-air breathing and then inhalation of 6% CO2-94% O2, before and after airway anesthesia. Measurements of lung mechanics included whole-lung resistance, dynamic and static compliance, and functional residual capacity. Airway anesthesia had no detectable effect on any measurements during room-air breathing. During CO2 inhalation, airway anesthesia produced increases in VE and mean inspiratory flow rate (VT/TI) and more negative inspiratory pleural pressure but had no detectable effect on lung mechanics or mouth occlusion pressure. Pleural pressure was more negative during the latter 25% of inspiration. We concluded that airway receptors accessible to airway anesthesia play a role in determining neuromuscular output during CO2 inhalation.

Ventilatory response during CO2 inhalation after airway anesthesia with lidocaine.

Airway anesthesia with inhaled aerosolized lidocaine has been associated with increases in minute ventilation (VE) and mean inspiratory flow rate (VT/TI) during CO2 inhalation. However, it is unclear whether these increases are local effects of the anesthesia or systemic effects of absorbed and circulating lidocaine. To evaluate this 20 normal subjects were treated on separate days with aerosolized lidocaine, intravenous lidocaine, aerosolized control solution, or intravenous control solution, and the effects of each treatment on VE and VT/TI were determined and compared during room-air breathing and inhalation of 5% CO2-95% O2. None of the treatments altered VE or VT/TI during room-air breathing. Aerosolized lidocaine produced small (5.9-6.0%) increases in VE and VT/TI during CO2 inhalation, but these effects were not present after intravenous lidocaine despite equivalent lidocaine blood levels. We concluded that the increases in VE and VT/TI after aerosolized lidocaine were local effects of airway anesthesia rather than systemic effects of absorbed and circulating lidocaine.

Lack of effect of airway anesthesia on hypoxic ventilation.

Airway anesthesia causes an increase in ventilation (VE) during hypercapnia. However, it is unclear if that is related to an effect of the anesthesia on all forms of stimulated V.E or just hypercapnic VE. After airway anesthesia, an increase in hypoxic VE would suggest the former, whereas absence of an increase would suggest the latter. Thus we compared VE before and after airway anesthesia during hypoxic VE. Normal subjects performed hypoxic rebreathing plus additional periods of sham hyperoxic rebreathing. There was no effect of airway anesthesia on the slope of the line relating VE and arterial O2 saturation. However, there was an upward shift in the line, attributable to an effect of anesthesia on hypercapnic VE present during rebreathing. Additional normal subjects performed eucapnic hypoxic breathing, and there was no effect of airway anesthesia on VE. We conclude that airway anesthesia has little or no effect on hypoxic VE. To date, only hypercapnic VE has been shown to be increased after airway anesthesia.

Ventilatory response to high-frequency airway oscillation in humans.

To investigate respiratory control during high-frequency oscillation (HFO), ventilation was monitored in conscious humans by respiratory inductive plethysmography during application at the mouth of high-frequency pressure oscillations. Studies were conducted before and after airway and pharyngeal anesthesia. During HFO, breathing became slow and deep with an increase in tidal volume (VT) of 37% (P less than 0.01) and inspiratory duration (TI) of 34% (P less than 0.01). Timing ratio (TI/TT) increased 14% (P less than 0.05) and respiratory frequency (f) decreased 12% (P less than 0.01). Mean inspiratory flow (VT/TI) did not change during HFO. Following airway anesthesia, VT increased only 26% during HFO (P less than 0.01), whereas significant changes in TI, TI/TT, and f were not observed. Pharyngeal anesthesia failed to diminish the effect of HFO on TI, TT, or f, although the increase in VT was reduced. These results indicate that 1) HFO presented in this manner alters inspiratory timing without affecting the level of inspiratory activity, and 2) receptors in the larynx and/or lower airways may in part mediate the response.

Neuromuscular response to resistive unloading: helium vs. bronchodilation.

To evaluate the neuromuscular response to resistive unloading, we compared the ventilatory and occlusion pressure (P100) response of normal subjects breathing 20.9% O2 in helium (He-O2) with their response to unloading produced by inhaled atropine sulfate. During He-O2 breathing airway resistance (Raw) fell by 49% of the base-line value on air, and P100 decreased by 20.8%. Minute ventilation, tidal volume, respiratory frequency, end-tidal Pco2, inspiratory and expiratory duration, and mean inspiratory flow were not significantly different when air was replaced by He-O2. In contrast, although atropine reduced Raw by an equivalent amount, there was no change in P100. Atropine had no significant effect on other respiratory variables, although a trend toward higher minute ventilation was noted. Fowler dead space increased after atropine but was not affected by He-O2. We conclude that, unlike He-O2 unloading, atropine unloading does not cause a reduction in occlusion pressure. This may be due to the effect of atropine on anatomical dead space which stimulates ventilation sufficiently to offset the fall in neuromuscular output due to resistive unloading.

Ventilatory and occlusion pressure responses to helium breathing.

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.