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Pathophysiology and Treatment of Cheyne-Stokes Respiration Thorax: First Published As 10.1136/Thx.53.6.514 on 1 June 1998

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Pathophysiology and Treatment of Cheyne-Stokes Respiration Thorax: First Published As 10.1136/Thx.53.6.514 on 1 June 1998 514 Thorax 1998;53:514–518 Pathophysiology and treatment of Cheyne-Stokes respiration Thorax: first published as 10.1136/thx.53.6.514 on 1 June 1998. Downloaded from M T Naughton Cheyne-Stokes respiration is a disorder charac- results from hyperventilation, prolonged circu- terised by recurrent central apnoeas during lation time, and reduced blood gas buVering sleep alternating with a crescendo-decrescendo capacity.21 pattern of tidal volume.12 It is often observed in patients with congestive heart failure, usually HYPERVENTILATION during stages 1 and 2 non-REM sleep when Hyperventilation, the common pathophysi- ventilation is under chemical-metabolic ological feature of all forms of periodic breath- 2 control. Patients with Cheyne-Stokes respira- ing, causes PaCO2 levels to fall below the tion usually present with the symptoms of apnoeic threshold triggering a central apnoea. orthopnoea, paroxysmal nocturnal dyspnoea, Once the peripheral chemoreceptors sense an excessive daytime sleepiness and witnessed apnoea related rise in the PaCO2 level above the apnoeas in the setting of congestive heart apnoea threshold, hyperventilation recurs driv- 13 failure. Excessive weight and snoring may be ing the PaCO2 level below the apnoea threshold absent. Approximately 50% of patients with once again.2 symptomatic congestive heart failure have Increased central hypercapnic ventilatory sleep apnoea, mainly of the Cheyne-Stokes responsiveness has been reported to occur in respiration variety.4-6 As congestive heart failure Cheyne-Stokes respiration with congestive occurs in 1% of the adult population and dou- heart failure22 and in other forms of periodic bles in prevalence for each decade beyond 60 breathing in subjects without congestive heart years,7 Cheyne-Stokes respiration is common failure—namely, idiopathic non-hypercapnic but often left unrecognised. central sleep apnoea23 and high altitude peri- odic breathing.24 25 A significant positive corre- Adverse eVects lation between central hypercapnic ventilatory Based upon small case series, patients with responsiveness and percentage sleep time with congestive heart failure and Cheyne-Stokes Cheyne-Stokes respiration has also been 26 respiration have a significantly greater reported. Taken together, it would appear http://thorax.bmj.com/ mortality,89 particularly if present during that Cheyne-Stokes respiration is associated wakefulness,10 than those without Cheyne- with increased central chemosensitivity and Stokes respiration. Although Cheyne-Stokes explains the low mean PaCO2 observed during respiration is likely to arise as a result of sleep and wakefulness in patients with Cheyne- congestive heart failure, once present it is likely Stokes respiration.32728As the response time of to have adverse eVects upon cardiac function central chemoreceptors in normal subjects is of akin to a vicious cycle. Following an initial car- the magnitude of five minutes29 and the mean diac insult there is a compensatory increase in cycle length of Cheyne-Stokes respiration is 60 11 12 32830 sympathetic activity which in susceptible seconds, rapidly responsive peripheral on September 25, 2021 by guest. Protected copyright. patients causes hyperventilation,13 destabilises chemoreceptors are likely to play an integral respiratory control, and leads to Cheyne- part in the propagation of Cheyne-Stokes Stokes respiration. Once Cheyne-Stokes respi- respiration.29 Data in support of a significant ration is established, apnoea related hypoxae- positive relationship between increased periph- mia causes cardiac diastolic dysfunction.14 eral chemosensitivity and periodic breathing, Hypoxaemia and arousals lead to further however, are limited to idiopathic non- increases in sympathetic activity15 which con- hypercapnic central sleep apnoea23 and high tribute to potentially fatal arrhythmias16-18 and altitude periodic breathing.24 25 further cardiotoxicity.19 It is likely that one or more of the following Hyperventilation and resultant increased factors are likely to contribute to hyperventila- work of the respiratory muscles probably play a tion in congestive heart failure. part in the symptom of paroxysmal nocturnal dyspnoea1 and place an increased demand Hypoxaemia upon the already reduced cardiac output.20 Hypoxaemia may contribute to hyperventila- Finally, patients with congestive heart failure tion and Cheyne-Stokes respiration in conges- Alfred Sleep Disorders and Cheyne-Stokes respiration frequently tive heart failure through peripheral chemore- and Ventilatory Failure complain of fatigue and excessive daytime ceptor stimulation. However, in contrast to Service, Department of Respiratory sleepiness which relate to reduced amounts of high altitude periodic breathing where hypo- Medicine, Alfred total, slow wave, and REM sleep in association baric hypoxia stimulation of the peripheral Hospital, Commercial with marked sleep fragmentation due to arous- chemoreceptors is likely to be responsible for Road, Prahran 3181, als from sleep.5 the periodic breathing,24 hypoxia is thought not Victoria, Australia to be solely responsible for the development of M T Naughton Pathophysiology Cheyne-Stokes respiration in patients with Correspondence to: Instability of respiratory control underpins the congestive heart failure for the following Dr M T Naughton. development of Cheyne-Stokes respiration and reasons. Hyperventilation, in the absence of Pathophysiology and treatment of Cheyne-Stokes respiration 515 hypoxaemia, has been shown to trigger central is directly related to the length of the apnoeas during non-REM sleep induced by apnoea-hyperpnoea cycle and contributes to either mechanical hyperventilation in normal the crescendo-decrescendo respiratory Thorax: first published as 10.1136/thx.53.6.514 on 1 June 1998. Downloaded from subjects31 or by arousal induced hyperventila- pattern.28 30 tion in Cheyne-Stokes respiration3 and idi- opathic non-hypercapnic central sleep apnoea.32 Furthermore, supplemental oxygen REDUCED BLOOD GAS BUFFERING CAPACITY Reduced total body oxygen and carbon dioxide has been shown to attenuate rather than stores are considered factors that amplify the abolish Cheyne-Stokes respiration in patients blood gas oscillations in Cheyne-Stokes respi- with congestive heart failure.33-36 ration. Pulmonary function tests of patients with severe congestive heart failure reveal a Increased pulmonary vagal aVerent traYc restrictive ventilatory defect, and therefore Increased pulmonary vagal aVerent nerve traf- oxygen storage, which relate to cardiomegaly fic related to pulmonary venous congestion and and pleural e usions.44-46 Carbon monoxide pulmonary C fibre stimulation has been shown V transfer capacity is approximately 70% of pre- to induce rapid shallow breathing and hyper- dicted normal values in patients with severe ventilation in animal studies.37-40 In humans congestive heart failure and correlates inversely with congestive heart failure, those with with PCWP.46 Despite these findings, no Cheyne-Stokes respiration have a significantly significant di erences in pulmonary function greater pulmonary artery pressure (mean 34 V tests have been observed between those with mm Hg) than those without Cheyne-Stokes and without Cheyne-Stokes respiration.3927As respiration (mean 21 mm Hg).6 Moreover, patients with Cheyne-Stokes respiration hyper- there is a significant inverse correlation be- ventilate awake and asleep,327 total body tween awake pulmonary capillary wedge pres- 6 carbon dioxide stores are likely to be reduced, sure (PCWP) and awake PaCO . Finally, there 2 hence the carbon dioxide bu ering capacity is a tendency for the analogous condition high V will be diminished. 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 Treatment increased pulmonary artery pressures, but Generally, patients with Cheyne-Stokes respi- whether this is a cause and e ect relationship V ration suYcient to cause symptoms have more remains to be seen. than 20 apnoeas and hypopnoeas per hour sleep and should be considered for treatment.5 Increased sympathetic activity Treatment options can be broadly divided into Heistad et al reported a 20% increase in minute five groups: intensive heart failure treatment, http://thorax.bmj.com/ ventilation 10 minutes after a six minute respiratory stimulants, respiratory depressants, venous infusion of noradrenaline, an eVect that oxygen, and continuous positive airway pres- could be blocked by prior treatment with sure (CPAP). propranolol.13 As increased circulating nor- adrenaline levels and hyperventilation occur in congestive heart failure,11 12 particularly in INTENSIVE HEART FAILURE TREATMENT those with Cheyne-Stokes respiration, it is pos- Although it would seem prudent to ensure that sible that peripheral chemoreceptors bathed in patients with Cheyne-Stokes respiration are noradrenaline, or possibly central sympathetic on optimal medical treatment for congestive on September 25, 2021 by guest. Protected copyright. activation related to spontaneous arousals, pre- heart failure, and as a result the severity of cipitates Cheyne-Stokes respiration. Upper Cheyne-Stokes respiration would diminish, airway collapse towards the end of the central there are only limited supportive data. In apnoea, known to occur in Cheyne-Stokes patients with congestive heart failure a raised respiration,42 may also cause arousal from sleep PCWP is associated with greater mortality.47 and
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