Obesity effects on lung volume, transdiaphragmatic pressure, upper airway dilator and inspiratory pump muscle activity in obstructive sleep apnoea.

Abstract

Obstructive sleep apnoea (OSA) is a common respiratory disorder characterised by repetitive periods of upper airway (UA) collapse during sleep. OSA is more common in males and the obese but the reasons why remain poorly understood. Abdominal obesity, particularly common in males, is likely to indirectly modulate the amount of tension (tracheal traction) exerted on the UA by the trachea and other intrathoracic structures, potentially leading to increased UA collapsibility. Other factors such as lung volume changes with obesity, altered drive to UA muscles and exaggerated arousal responses are also likely to contribute to UA instability. An investigation of these potential contributing factors forms the basis of this thesis. In the first study, the effect of external abdominal compression on UA collapsibility during sleep was investigated in a group of obese male OSA patients. A large pneumatic cuff wrapped around the abdomen was inflated to increase intra-abdominal pressure, aiming to produce an upward force on the diaphragm, designed to reduce axial tension on the UA. Abdominal compression increased end-expiratory gastric (PGA) and end-expiratory transdiaphragmatic (PDI) pressure by ~50% and produced a significant rise in UA collapsibility compared to the cuff deflated condition. These data support that increased intra-abdominal pressure has a negative effect on UA function during sleep. This effect may help explain why obesity is the leading risk factor for OSA and why OSA affects men more than women, given that abdominal obesity is particularly common in obese males. In the second study, differences in minimum expiratory (tonic) diaphragm activity during wakefulness were compared between 8 obese OSA patients and 8 healthyweight controls. Changes in tonic diaphragm activity and lung volume following sleep onset were also compared between the two groups. There was no evidence of increased tonic diaphragmatic activity during wakefulness in obese OSA patients to support significant diaphragmatic compensation for abdominal compressive effects of obesity. There were small decrements in lung volume following sleep onset in both groups (<70 ml), with significantly greater lung volume and diaphragmatic EMG decrements when sleep onsets were immediately followed by respiratory events. While lung volume decrements at sleep onset were relatively small, this does not discount that UA function is not more sensitive to effects of reduced lung volume in obese OSA patients. To more closely investigate the potential interactive effects of obesity on physiological variables likely influencing UA function, the third study investigated the temporal relationships between a comprehensive range of relevant physiological variables leading into and following the termination of obstructive apnoeas during sleep in 6 obese OSA patients. Prior to UA obstruction, diaphragm and genioglossus muscle activity decreased, while UA resistance increased. Lung volume and end-expiratory PGA and end-expiratory PDI also fell during this period, consistent with diaphragm ascent. There was a substantial increase in ventilation, muscle activity and lung volume immediately following the termination of obstructive events. Respiratory events and arousals occurred in close temporal proximity prior to and following obstructive apnoeas, supporting that cyclical respiratory events and arousals may both help to perpetuate further events. The results from this study support that there is a ‘global’ loss in respiratory drive to UA dilator and pump muscles precipitating obstructive respiratory events. The associated decreases in UA dilator muscle activity and lung volume may therefore both contribute to the propensity for the UA to obstruct. In summary, increased intra-abdominal pressure was shown to negatively impact UA airway collapsibility during sleep. A decrease in lung volume at sleep onset and prior to UA obstruction further support that lung volume decrement, coincident with a decline in overall respiratory drive, potentially contributes to the propensity for airway obstruction. Further studies are needed to elucidate the relative contribution of relatively small changes in lung volume versus changes in respiratory and UA muscle activity per se on UA patency in OSA patients.