The respiratory system is responsible for gaseous exchange between the circulatory system and the outside world. Air is taken in via the upper airways (the nasal cavity, pharynx and larynx) through the lower airways (trachea, primary bronchi and bronchial tree) and into the small bronchioles and alveoli within the lung tissue.
Each branch of the bronchial tree eventually sub-divides to form very narrow terminal bronchioles, which terminate in the alveoli. There are many millions of alveoli in each lung, and these are the areas responsible for gaseous exchange, presenting a massive surface area over which gaseous exchange can occur.
Each alveolus is very closely associated with a network of capillaries containing deoxygenated blood from the pulmonary artery. The capillary and alveolar walls are one cell layer thick, allowing rapid exchange of gases by passive diffusion along concentration gradients.
CO2 moves into the alveolus because the concentration of CO2 is much lower in the alveolus than in the blood, and O2 moves out of the alveolus into the blood. The continuous flow of arterial blood through the capillaries prevents saturation of the blood with O2 and allows maximal transfer across the membrane.The respiratory system is responsible for gaseous exchange between the circulatory system and the outside world. Air is taken in via the upper airways (the nasal cavity, pharynx and larynx) through the lower airways (trachea, primary bronchi and bronchial tree) and into the small bronchioles and alveoli within the lung tissue.
The major excitatory drive to breathe originates in brain cells sensitive to CO2. Obstructive sleep apnea patients with narrow and collapsible upper airways experience increased collapsibility during REM sleep due to its accompanying atonia.
The frequency of breathing is lower and more regular in NREM sleep than in wakefulness. Upper airway resistance increases during sleep. Respiratory modulated inputs to brain cells are not lost in sleep but become function at a lower level.
Responses to carbon dioxide and oxygen levels remain intact during sleep. Regulation and changes in breathing are caused by chemical and mechanical inputs to parts of the brain that control ventilation. In patients with OSA there is a diminution of normal inputs. This facilitates upper airway obstruction because the muscles controlling the airway patency fail to properly compensate for the collapsing effects of the negative pressure generated by inhalation.
The end result of apnea is lower oxygen (hypoxia) and higher CO2 (hypercarboxia). The hypoxia can cause fatigue and ultimately brain damage. The hypercarboxia results in acidosis. The symptoms of acidosis are headache, confusion and possibly kidney damage.