Obesity, Respiratory Mechanics and Its Impact on the Work of Breathing, Neural Respiratory Drive, Gas Exchange and the Development of Sleep-Disordered Breathing

Abstract

Obesity causes an increased load on the respiratory muscle pump that impacts on the work of breathing and requires high levels of neural respiratory drive. Elevated intra-abdominal pressures in obesity impose a preload on the diaphragm during inspiration, particularly in the supine posture. These forces contribute to a reduced transpulmonary pressure gradient in the thoracic compartment and affect operational lung volumes. Morbidly obese subjects breathe at low lung volumes, close to the residual volume (RV); their functional residual capacity shifts towards a less favourable part of the pressure-volume curve with a reduced compliance. At low lung volumes, the closing volume of the airway increases airway resistance further and contributes an intrinsic positive end-expiratory pressure. In the asleep subject, the reduced neuromuscular tone in the skeletal muscles results in increased upper airway collapsibility and, potentially, leads to obstructive sleep apnoea. Reduced respiratory muscle recruitment during sleep causes alveolar hypoventilation and obesity hypoventilation syndrome (OHS). The disadvantageous respiratory mechanics in obesity can be overcome by the use of continuous positive airway pressure to avoid upper airway collapse and noninvasive ventilation to support ventilation. Physiological changes observed with obesity are largely reversible following significant weight loss. It is important to consider the respiratory physiology in obesity when screening for sleep-disordered breathing in this population prior to iatrogenic interventions.