pulmonary disorders
Central Sleep Apnea
Pathophysiology of Central Sleep Apnea
Unlike with Obstructive Sleep Apnea (OSA) , in which airway obstruction restricts airflow, central sleep apnea (CSA) is caused by alterations in respiratory drive, which during sleep is highly dependent on carbon dioxide levels. Two mechanisms are distinguished: Hypoventilation-related CSA:Decreasedventilatory drive causes transient decreases and/or pauses in respiration. Hyperventilation-related CSA:Increasedventilatory drive during sleep leads to hypocapnia which causes a compensatory fall in ventilation that, if abnormally prolonged, leads to recurrent central apnea with arousals. Hypoventilation-related CSA usually occurs in patients with a central nervous system or neuromuscular disorder that directly impairs ventilation, resulting in high CO2 levels (hypercapnia). Rarely, patients have an impaired chemoreceptor response to hypercapnia (primary alveolar hypoventilation). Paradoxically, most CSA involves periods ofhyperventilation. Transient increases in ventilation for any reason may overshoot the target carbon dioxide level, causing hypocapnia. In most people, compensatory mechanisms restore normal ventilation despite the hypocapnia. In patients with CSA, compensatory mechanisms do not respond quickly enough, and the hypocapnia causes periods of hypoventilation and/or apnea resulting in hypercapnia. Patients may cycle periodically between hyper- and hypoventilation, as in Cheyne-Stokes breathing, in which patients have brief periods of apnea followed by progressively faster and deeper breathing, which then becomes slower and shallower until they become apneic again and repeat the cycle. Disturbed ventilation occurs primarily during sleep because during wakefulness there are additional external stimuli for respiration. CSA can interfere with sleep enough to cause Insomnia and Excessive Daytime Sleepiness (EDS) . 