Effects of changes in central venous pressure on upper airway size in patients with obstructive sleep apnea.

Abstract

Intraluminal airway pressure and pharyngeal muscle activity are widely recognized as major determinants of the size and collapsibility of the upper airway. In addition, changes in the volume or pressure of tissue surrounding the pharyngeal airway may significantly influence its size. The present study used fast computed tomography (CT) to determine the effects of changes in central venous pressure (CVP) on upper airway size. Ten awake male patients with obstructive sleep apnea (OSA) were studied. Scans were performed at functional residual capacity (FRC) and at the end of a tidal inspiration (VTei) under three conditions of CVP: (1) at baseline (CVP nl) with patients lying supine; (2) at decreased CVP (CVP-) by inflating blood pressure cuffs to 40 mm Hg on both legs; and (3) at increased CVP (CVP+) by elevating both legs to 33 degrees. At FRC, changes in CVP had no significant effect on either mean or minimum cross-sectional area (CSA) of the upper airway. In contrast, an analysis of variance (ANOVA) indicated that alterations in CVP were associated with changes in mean CSA (p = 0.03) and to a lesser extent in minimum CSA (p = 0.07) at VTei. With the legs elevated (CVP+), neither mean nor minimum CSA showed any significant change with tidal breathing. However, after leg-cuff inflation (CVP-), highly significant increases in both mean (163 +/- 22 to 218 +/- 19 mm2, p = 0.001) and minimum (48 +/- 8 to 85 +/- 12 mm2, p = 0.02) CSA were detected. Changes in mean and minimum CSA with tidal breathing at baseline (CVP nl) were intermediate. These results indicate that changes in CVP significantly alter the response of the upper airway to tidal breathing. They further suggest that increases in upper airway size with tidal breathing may be related to reduction in venous blood volume in pharyngeal and neck tissues as the generation of negative intrathoracic pressure during inspiration increases venous return to the chest.

Sleep Apnea and Cardiovascular Disease

“…Consequent airway narrowing and increased airway resistance would require increased generation of negative intrathoracic pressures to maintain flow, thus theoretically predisposing to upper airway occlusion. 199 Indeed, in healthy volunteers, rapid displacement of Ϸ340 mL of fluid from the legs to the upper body, elicited by lower-body positive pressure, increased neck circumference and pharyngeal resistance to airflow, and reduced upper airway cross-sectional area. 200,201 Hence, decreased intravascular volume and attenuated venous congestion resulting from heart failure treatment could potentially reduce OSA severity.…”

Sleep Apnea and Heart Failure

“…This mechanism would explain a reduction in central but not obstructive events. If upper airway edema accumulated while the patient was in the recumbent position, 52,53 augmentation of cardiac output by overdrive pacing could have alleviated this edema and increased pharyngeal lumenal dimensions. Although the observations of Garrigue et al 51 have generated considerable interest, their implications for the treatment of sleep apnea in general and for sleep apnea in patients with HF in particular are not clear.…”

Investigation of the link between fluid shift and airway collapsibility as a mechanism for obstructive sleep apnea in congestive heart failure

“…(1996). They speculated that an increase in fluid surrounding the pharynx could result in increased extraluminal pressure.…”