Heart failure 5-year-survival rate:25%=Multiple myeloma 5-year-survival rate:24%
Ovary 5-year-survival rate: 34%
Hypoxaemia
Hypoxaemia may contribute to hyperventilation and Cheyne-Stokes respiration in congestive heart failure through peripheral chemoreceptor stimulation. However, in contrast to high altitude periodic breathing where hypobaric hypoxia stimulation of the peripheral chemoreceptors is likely to be responsible for the periodic breathing,
24 hypoxia is thought not to be solely responsible for the development of Cheyne-Stokes respiration in patients with congestive heart failure for the following reasons. Hyperventilation, in the absence of hypoxaemia, has been shown to trigger central apnoeas during non-REM sleep induced by either mechanical hyperventilation in normal subjects
31 or by arousal induced hyperventilation in Cheyne-Stokes respiration
3 and idiopathic non-hypercapnic central sleep apnoea.
32 Furthermore, supplemental oxygen has been shown to attenuate rather than abolish Cheyne-Stokes respiration in patients with congestive heart failure.
33-36
Increased pulmonary vagal afferent traffic
Increased pulmonary vagal afferent nerve traffic related to pulmonary venous congestion and pulmonary C fibre stimulation has been shown to induce rapid shallow breathing and hyperventilation in animal studies.
37-40 In humans with congestive heart failure, those with Cheyne-Stokes respiration have a significantly greater pulmonary artery pressure (mean 34 mm Hg) than those without Cheyne-Stokes respiration (mean 21 mm Hg).
6 Moreover, there is a significant inverse correlation between awake pulmonary capillary wedge pressure (PCWP) and awake Pa
CO 2.
6 Finally, there is a tendency for the analogous condition high altitude periodic breathing to occur in patients with associated high altitude pulmonary oedema,
41 so Cheyne-Stokes respiration with congestive heart failure is associated with increased pulmonary artery pressures, but whether this is a cause and effect relationship remains to be seen.
Increased sympathetic activity
Heistad
et al reported a 20% increase in minute ventilation 10 minutes after a six minute venous infusion of noradrenaline, an effect that could be blocked by prior treatment with propranolol.
13 As increased circulating noradrenaline levels and hyperventilation occur in congestive heart failure,
11 12 particularly in those with Cheyne-Stokes respiration, it is possible that peripheral chemoreceptors bathed in noradrenaline, or possibly central sympathetic activation related to spontaneous arousals, precipitates Cheyne-Stokes respiration. Upper airway collapse towards the end of the central apnoea, known to occur in Cheyne-Stokes respiration,
42 may also cause arousal from sleep and thereby hyperventilation.
3 32