Upper Airway Resistance Rationale

Changes in upper airway muscle activity can influence upper airway caliber (16, 30). Therefore, measurements of upper airway resistance can be used to indirectly assess changes in upper airway muscle activity. However, upper airway resistance is also influenced by changes in mucosal vasculature, body position (e.g., supine versus prone), head position (e.g., extended versus flexed), lung volume, and application of continuous positive airway pressure (31, 32). Upper airway resistance also has a direct but nonlinear relationship with flow.

Methodology

Resistance is calculated by measuring the pressure drop across the airway at a given flow. The upper airway includes the larynx, pharynx, and nasal and oral cavities. Upper airway resistance can be measured during oral or nasal breathing. Determination of total upper airway resistance requires measurement of the pressure drop between the subglottic airway and the nares or mouth. Resistance across the nasal, pharyngeal, or laryngeal segments of the upper airway can be determined by measuring the pressure drop across the particular segment of interest (33). Measurement of subglottic pressure requires the percutaneous or transnasal placement of a catheter attached to a pressure transducer into the extrathoracic trachea (34). Because of the technical difficulty of both methods, most studies of upper airway resistance exclude the laryngeal airway from their measurements.

Figure 3. Electromyogram (EMG) of the genio-glossus (GG) muscle during two obstructive apneas (OSAs) in nonrapid eye movement sleep. Airway closure (horizontal lines) is associated with a decrease in GG activation. GG activation progressively increases during the obstructive, apneas but airway reopening, as evidenced by the resumption of tracheal breathing sounds, does not occur until there is a large burst of GG activity. The time constant of the oxygen saturation signal delays the appearance of the oxygen saturation nadir until after airway reopening. EEG = electroencephalogram; SaO2 = arterial oxygen saturation.

Figure 3. Electromyogram (EMG) of the genio-glossus (GG) muscle during two obstructive apneas (OSAs) in nonrapid eye movement sleep. Airway closure (horizontal lines) is associated with a decrease in GG activation. GG activation progressively increases during the obstructive, apneas but airway reopening, as evidenced by the resumption of tracheal breathing sounds, does not occur until there is a large burst of GG activity. The time constant of the oxygen saturation signal delays the appearance of the oxygen saturation nadir until after airway reopening. EEG = electroencephalogram; SaO2 = arterial oxygen saturation.

Supraglottic airway resistance is the pressure drop from the level of the epiglottis to the airway opening (mouth or nose) at a given flow (Figure 4). A face mask connected to a pneumo-tachograph is attached via an airtight seal to the individual to measure flow. Mask pressure, that is, pressure at the nares or mouth, is measured from a port in the mask. The intralumenal airway pressure measurement requires an invasive procedure. After topical anesthesia of one nasal passage, a catheter attached to a pressure transducer is advanced to the level of the epiglottis and secured at the nose. To eliminate the influence of kinetic energy, the pressure is measured from a side port near the sealed tip of the catheter. Because changes in the position of the catheter can influence the measurements, studies should be designed so that the control and experimental recordings are obtained without repositioning or removing the catheter. The catheter can be filled with air or water. An air-filled catheter has the potential to become occluded with fluid. Once in position, pressure from the water-filled catheter at zero flow must be obtained to determine the contribution of hydrostatic pressure to the measurements. Pressure transducer-tipped catheters have also been used to measure pharyngeal pressure. However, these catheters work best in a completely dry or fluid environment such as the intravascular space and esophagus. The repetitive wetting and drying of the transducer surface in the pharynx frequently results in an unacceptable drift of the signal.

Upper airway resistance is calculated by dividing the pressure drop across the airway at a particular flow by that flow. The units of measurement are cm H2O ■ L-1 ■ second-1. It is important to state whether the measurements are obtained during inspiration or expiration as, even at the same flow, upper airway resistance during inspiration is not the same as upper airway resistance during expiration. Measurements on different breaths should also be obtained from the same portion of inspiration or expiration as the pressure-flow relationships during each of the two respiratory phases may show hysteresis.

An alternative method used to quantify upper airway resistance is to describe the entire pressure-flow curve on inspiration or expiration by fitting the pressure and flow data to a second-order equation. Numerous equations have been used, including the Rohrer equation: P = K1V + K2V2 (Equation 1), where P is pressure, V is flow, and K1 and K2 are constants. The presence of two constants in this equation makes statistical comparisons difficult and, therefore, another frequently used equation is: P = KV2 (Equation 2). Changes in upper airway resistance can be assessed indirectly by measuring total pulmonary resistance with the passage of an esophageal balloon. This method is valid if resistance across the lower airways remains constant. Therefore, these measurements must be obtained at a given lung volume.

The measurement of upper airway resistance requires two pressure transducers to measure the pressure drop across the airway and a pneumotachograph connected to a differential pressure transducer for the measurement of flow. Pressure is calibrated in cm H2O and flow in L ■ second-1. As the measurements are obtained under dynamic conditions, the three signals should remain in phase up to a frequency of 10 Hz.

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