Role of nocturnal rostral fluid shift in the pathogenesis of obstructive and central sleep apnoea

Abstract

Obstructive sleep apnoea (OSA) is common in the general population and increases the risk of motor vehicle accidents due to hypersomnolence from sleep disruption, and risk of cardiovascular diseases owing to repetitive hypoxia, sympathetic nervous system activation, and systemic inflammation. In contrast, central sleep apnoea (CSA) is rare in the general population. Although their pathogenesis is multifactorial, the prevalence of both OSA and CSA is increased in patients with fluid retaining states, especially heart failure, where they are associated with increased mortality risk. This observation suggests that fluid retention may contribute to the pathogenesis of both OSA and CSA. According to this hypothesis, during the day fluid accumulates in the intravascular and interstitial spaces of the legs due to gravity, and upon lying down at night redistributes rostrally, again owing to gravity. Some of this fluid may accumulate in the neck, increasing tissue pressure and causing the upper airway to narrow, thereby increasing its collapsibility and predisposing to OSA. In heart failure patients, with increased rostral fluid shift, fluid may additionally accumulate in the lungs, provoking hyperventilation and hypocapnia, driving below the apnoea threshold, leading to CSA. This review article will explore mechanisms by which overnight rostral fluid shift, and its prevention, can contribute to the pathogenesis and therapy of sleep apnoea.

Figures

Figure 1. The role of overnight rostral fluid shift in the pathogenesis of obstructive and central sleep apnoea (OSA and CSA)

Overnight fluid shift from the legs to the neck can affect upper airway mechanics and lead to OSA, whereas fluid shift to the lungs can provoke hyperventilation, hypocapnia and CSA. CO, cardiac output; , partial pressure of carbon dioxide; PCWP, pulmonary capillary wedge pressure; UA, upper airway; UA-XSA, upper airway cross-sectional area.

Figure 2. Mechanisms influencing upper airway (UA) collapsibility in the pathogenesis of obstructive sleep apnoea (OSA)

A number of dynamic factors, including fluid shift into the neck, determine the active (pharyngeal dilator muscle activity) and passive (intra- and extraluminal pressure and pharyngeal wall compliance) properties of the UA which can increase UA collapsibility and lead to UA obstruction and OSA. REM, rapid eye movement sleep.

Figure 3. Magnetic resonance images of the upper airways from end-stage renal failure patients with (A) and without (B) obstructive sleep apnoea (OSA)

Significantly more pharyngeal wall oedema (arrows) is observed in the OSA patient, as indicated by lighter shade and as quantified by arbitrary units. Reproduced with permission from Elias et al. 2013.

Figure 4. Relationship between overnight ΔLFV and AHI in men and women with heart failure

A, correlation between overnight decrease in leg fluid volume (LFV) and apnoea–hypopnea index (AHI) in men with heart failure and either obstructive or central sleep apnoea. Central sleep apnoea was associated with greater overnight fluid shift. Reproduced with permission from Yumino et al. 2010. B, in women with heart failure, there is no correlation between overnight decrease in LFV and AHI. ΔLFV, overnight change in leg fluid volume. Reproduced with permission from Kasai et al. 2012.