<unk>  can be explained by mechanisms similar to those of orthopnea and typical<unk> . When a person is recumbent, or is lying down, blood is redistributed from the lower extremities and abdominal cavity (splanchnic circulation) to the lungs. Failure to accommodate this redistribution results in decreased vital capacity and pulmonary compliance, further causing the shortness of breath experienced in<unk> . In addition to the redistribution of blood in the body, most cases of<unk>  are accompanied by an increase in the overall work of breathing, often caused by abnormal pulmonary mechanisms. The perception of<unk>  is theorized to be a complicated connection between peripheral receptors, neural pathways, and the central nervous system. Receptors in the chest wall and central airways, as well receptors in the respiratory center of the central nervous system, produce an increased requirement for ventilation which is not matched by respiratory output, resulting in the conscious recognition of<unk> . Respiratory muscles and vagal afferent neural pathways relay information from the chest wall/airways to the central nervous system, facilitating the presentation of<unk> . In people with underlying congestive heart failure, this redistribution may overload the pulmonary circulation, causing increased pulmonary congestion. In congestive heart failure, left ventricular dysfunction will also increase pulmonary congestion, so further congestion caused by the redistribution of blood volume upon laying down will worsen any<unk> . Other theories exist for why<unk>  occurs, especially in those where<unk>  only occurs while sleeping. Theories include decreased responsiveness of the respiratory center in the brain and decreased adrenergic activity in the myocardium during sleep.
Paroxysmal nocturnal dyspnoea
Exercise intolerance
Expiratory apnea
Platypnea
Trepopnea
Sleep apnea
Periodic breathing
Generalized hypoxia