Patients with primary abnormalities of the respiratory pump, eg, restrictive chest wall or neuromuscular affecting the respiratory muscles, provide similar lessons to the observant physician. Alveolar ventilation during the day is normal in early stages of such diseases. However, during non-REM sleep, alveolar ventilation declines and arterial blood gas values deteriorate. This manifests wakefulness-dependent influences descending probably onto the bulbar respiratory network acting to augment the motor output of inspiratory and/or expiratory bulbospinal neurons. This enhanced activity during wakefulness compensates for the chest wall restriction or respiratory muscle weakness. Sleep compromises such compensation. During non-REM sleep, the brain-stem network receives chemoreceptor feedback and generates a supra-normal output, but this does not provide a respiratory motor output adequate to maintain a normal level of alveolar ventilation. Interestingly, the effect of sleep in patients with obstructive or restructive lung diseases diverges from that in restrictive chest wall disease. In intrinsic lung diseases that do not compromise the mechanical action of the respiratory muscles, compensatory motor output is not lost during non-REM sleep (see REM atonia section, below), suggesting that different neural mechanisms are engaged during the respiratory motor compensation in the 2 situations. One possibility is that afferent traffic arising from the lung, chest wall, or pulmonary vasculature reflexedly enhance motor output in these lung diseases.
Sleeping and Breathing: Sleep Removes Wakeful Motor Compensations (Part 2)
October 17th, 2012