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| {{Infobox_Disease | | | {{Infobox_Disease | |
| Name = Cheyne-Stokes respiration | | | Name = Cheyne-Stokes respiration | |
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| ICD9 = {{ICD9|786.09}} | | | ICD9 = {{ICD9|786.09}} | |
| }} | | }} |
| {{SI}} | | {{Cheyne-Stokes respiration}} |
| {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | | {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} |
| | ==[[Cheyne-Stokes respiration overview|Overview]]== |
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| ==Overview== | | ==[[Cheyne-Stokes respiration historical perspective|Historical Perspective]]== |
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| '''Cheyne-Stokes respiration''' (also known as periodic breathing) is an abnormal pattern of breathing characterized by periods of breathing with gradually increasing and decreasing [[tidal volume]] interspersed with the brain to compensate quickly for changing serum [[partial pressure]] of [[oxygen]] and [[carbon dioxide]].
| | ==[[Cheyne-Stokes respiration classification|Classification]]== |
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| Sleep disordered breathing was first described by Cheyne in 1818 in a 60 year old obese man with heart failure. In 1854, Stokes described a similar pattern of breathing that eventually culminated in apnea. The term [[Cheyne-Stokes respiration]] (CSR) describes a pattern of breathing with a crescendo – decrescendo variation in tidal volume separated by periods of central apnea or hypopnea.
| | ==[[Cheyne-Stokes respiration pathophysiology|Pathophysiology]]== |
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| It is seen primarily in patients with [[congestive heart failure]], and in those who have suffered a stroke, but is also seen in patients with other CNS processes such as [[tumor]]s, [[meningitis]], [[encephalitis]] and [[trauma]], as well as patients exposed to [[high altitude sickness|high altitudes]]. Patients with CSR have fragmented sleep with frequent arousals and desaturations. These cause problems with quality of life, as well as cardiopulmonary physiology.
| | ==[[Cheyne-Stokes respiration causes|Causes]]== |
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| == Epidemiology and Demographics == | | ==[[Cheyne-Stokes respiration differential diagnosis|Differentiating Cheyne-Stokes respiration from other Diseases]]== |
| === Association with Congestive Heart Failure (CHF) ===
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| Although the incidence of CSR is unknown, it seems to be fairly common in patients with New York Heart Association (NYHA) class III and IV disease.
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| * One study found that 45% of patients with moderate, stable, optimally treated CHF had CSR with an apnea – hypopnea index (AHI) >20. These episodes were associated with a SaO2 < 90% for ¼ - ½ of total sleep time. The patients were also found to have a significant increase in the number of episodes of nocturnal [[ventricular arrhythmias]].
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| * Another study found that although the cardiac parameters did not differ between patients, those with [[CHF]] and CSR has reduced total sleep time, reduced sleep efficiency, increased proportion of stages I, II, and NREM sleep and reduced REM sleep. By definition, they had higher AHIs, however the degree of [[hypoxemia]] during desaturation did not differ between the groups.
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| * The recurrent desaturations and arousals experienced by patients with [[CHF]] and CSR have been associated with an increase in nocturnal angina and [[ventricular arrhythmias]]. It has also been shown that these patients have higher circulating plasma norepinephrine levels, which can obviously worsen afterload and [[heart failure]].
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| === Association with Stroke === | | ==[[Cheyne-Stokes respiration epidemiology and demographics|Epidemiology and Demographics]]== |
| CSR was once thought only to occur with bilateral or large deeper strokes, however is now recognized to be much more common, and can be seen in patients with ischemic [[stroke]] in any location.
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| * One study identified CSR in 59% of patients with supratentorial stroke, and in 40% with infratentorial stroke. The patients with CSR had a significant decrease in SaO2 as compared to those without CSR, and the authors raised the concern for potential worsening of [[ischemia]] in the peri-infarct zone, due to low sats in these patients.
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| == Pathophysiology & Etiology== | | ==[[Cheyne-Stokes respiration risk factors|Risk Factors]]== |
| === Pathophysiology in Patients with CHF ===
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| The exact mechanisms responsible for the development of CSR are unknown. Among the more important factors are hyperventilation, and a prolonged circulatory time.
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| * [[Hyperventilation]] and resultant [[hypocapnia]], is thought to occur in patients with [[CHF]] due to stimulation of pulmonary mechanoreceptors by interstitial edema.
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| *:* Patients with [[CHF]] and CSR have been found to have lower awake and sleep PaCO2 levels, and increased minute ventilation as compared to patients with [[CHF]] without CSR.
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| *:* In addition, the [[apnea]] threshold (the PaCO2 below which [[apnea]] occurs) also seems to be increased in patients with [[CHF]] and CSR.
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| *:* Furthermore, [[hypoxemia]] shifts the ventilatory response curve for CO2 up and to the left (higher ventilation at any given CO2). This reduces the stability of the ventilatory control system.
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| *:* Thus, [[hyperventilation]] reduces the PaCO2 below the [[apnea]] threshold, and as PaCO2 rises, an exaggerated ventilatory response causes the PaCO2 to fall below the [[apnea]] threshold, and a vicious cycle ensued.
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| * Prolonged circulatory time, as a marker of severity of [[CHF]], is directly correlated to the duration of sleep spent in CSR, as well as the cycle length of each episode.
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| *:* This is due to an increase in the oscillation around a set point PaO2 and PaCO2. As circulatory time increases, the PaO2 and PaOC2 become more out of phase with the respiratory pattern set by the ventilatory control centers (carotid body and medulla).
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| * It also seems that patients with [[CHF]] have less ability to buffer changes in PaCO2, i.e. the system is underdamped. This results from the fact that [[CHF]] causes a decrease in FRC, which reduces total body stores of CO2 and O2. It has been shown that, as total body stores of CO2 decrease, the body is not able to buffer the transient changes in PaCO2 as well.
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| === Pathophysiology in Patients with Stroke === | | ==[[Cheyne-Stokes respiration natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| There is a lot less data on the mechanisms of CSR in patients with CNS disease, than in patients with [[CHF]]. Some potential mechanisms include a delay in afferent, efferent neural transmission, delays in central processing of afferent signals, slowed brain blood flow, and altered chemoresponsiveness with a heightened ventilatory responsiveness.
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| == Differential Diagnosis == | | ==Diagnosis== |
| * [[Stroke]]
| | [[Cheyne-Stokes respiration history and symptoms| History and Symptoms]] | [[Cheyne-Stokes respiration physical examination | Physical Examination]] | [[Cheyne-Stokes respiration laboratory findings|Laboratory Findings]] | [[Cheyne-Stokes respiration electrocardiogram|Electrocardiogram]] | [[Cheyne-Stokes respiration chest x ray|Chest X Ray]] | [[Cheyne-Stokes respiration CT|CT]] | [[Cheyne-Stokes respiration MRI|MRI]] | [[Cheyne-Stokes respiration echocardiography|Echocardiography]] | [[Cheyne-Stokes respiration other imaging findings|Other Imaging Findings]] | [[Cheyne-Stokes respiration other diagnostic studies|Other Diagnostic Studies]] |
| * [[Drugs]]
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| * [[Heart Failure]]
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| * [[Hypoxia]]
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| * [[Subdural hematoma]]
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| * [[Uremic coma]]
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| === Chest X Ray === | | ==Treatment== |
| [[Congestive heart failure]] maybe present | | [[Cheyne-Stokes respiration medical therapy|Medical Therapy]] | [[Cheyne-Stokes respiration surgery|Surgery]] | [[Cheyne-Stokes respiration primary prevention|Primary Prevention]] | [[Cheyne-Stokes respiration secondary prevention|Secondary Prevention]] | [[Cheyne-Stokes respiration cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Cheyne-Stokes respiration future or investigational therapies|Future or Investigational Therapies]] |
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| == Treatment == | | ==Case Studies== |
| Obviously, [[CHF]] is associated with an increased mortality. The data concerning CSR and mortality is equivocal. It is unclear if CSR actually increases mortality from [[CHF]] (which would make physiologic sense), or is just a marker of more severe disease. <br><br>
| | [[Cheyne-Stokes respiration case study one|Case#1]] |
| It has been shown that CSR can resolve in a majority of patients with adequate treatment of the underlying [[CHF]].
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| * [[ACE inhibitor]]s have been associated with a 50% reduction in the frequency of apnea and desaturation in patients with class II – III [[CHF]]. The exact mechanism remains unknown, but improved circulatory time is a leading contender.
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| * Nocturnal oxygen (2-3 L/min) has been shown to reduce the duration of CSR, improve [[hypoxemia]], sleep, and daytime cognitive function patients with severe [[CHF]]. The long term effects of nocturnal oxygen in these patients, however, remain unproven.
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| *:* Low-flow oxygen was also found to reverse both CSR and desaturations in patients with acute strokes.
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| *:* It is felt that eliminating [[hypoxemia]] reduces the gain of the respiratory control system. It also reduces respiratory drive, thus resulting in an increase in PaCO2 as well.
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| * One study showed that 3.3 mg/kg of [[theophylline]] bid reduced the AHI (from 37 to 18), and duration of sleep with SaO2 < 90% (23% vs. 6%) in patients with [[CHF]] / obstructive sleep apnea (OSA).
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| *:* Theophylline has also been shown to reverse CSR and desaturation in patients with acute stroke.
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| * Another study found that administering 3% CO2 to 6 patients with [[CHF]] and CSR reduced the duration of CSR from 62% to 2.2% of sleep time.
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| * The mechanisms by which continuous positive airway pressure (CPAP) improves central sleep apnea (CSA) in patients with CHF are likely multifactorial.
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| *:* By increasing functional residual capacity (FRC), and therefore intrathoracic pressure, [[afterload]] and [[preload]] are reduced, and [[cardiac output]] increases. This results in a shorter circulation time. In patients with low filling pressures, however, the decrease in [[preload]] can reduce [[cardiac output]].
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| *:*:* Several studies have shown improvement in [NYHA classification]] in patients with [[CHF]]/CSR, and with [[CHF]] alone, who were treated with CPAP.
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| *:*:* Additionally, Naughton et.al. showed that nasal CPAP caused an increase in left ventricular ejection fraction (LVEF), a decrease in heart rate (HR), and an increase in quality of life, as measured by [[dyspnea]], [[fatigue]], emotional well being and disease mastery.
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| *:* CPAP, usually in pressures of 8 – 12 cm H20, can also eliminate [[apnea]]s (and therefore arousals), as well as desaturations. The reduction in sympathetic tone may be another mechanism for improved [[CHF]].
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| *:* By increasing PaO2, the gain of the system is reduced (as above).
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| *:* CPAP can also increase the PaCO2. The mechanism of this is likely multifactorial, and includes a reduction in ventilatory effort caused by improvement in [[pulmonary edema]], a reduction in arousal mediated [[hyperventilation]], and by reducing the gain of the ventilatory system by increasing PaO2.
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| *:*:* This may drive the PaCO2 over the [[apnea]] threshold. Additionally, increased body CO2 stores can help buffer transient changes in PaCO2.
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| *:* Unfortunately, there are no good studies that recommend using sleep studies in the routine evaluation of [[CHF]]. However, if a patients [[CHF]] is maximally treated, preliminary data would suggest performing sleep studies in patients with signs and symptoms of obstructive sleep apnea (OSA), CSR and possibly in patients with nocturnal angina or [[arrhythmia]].
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| ==References==
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| #The Diagnosis of Stupor and Coma by Plum and Posner, ISBN 0195138988
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| #Agus Agus, Z.S., Cheyne-Stokes respiration in congestive heart failure, in UpToDate, September 27, 1996.
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| #Andreas, S., et.al., Cheyne-Stokes respiration and prognosis in congestive heart failure, Am J Cardiol 1996; 78: 1260-1264. PMID 8960586 | |
| #Hanly, P., Zuberi, N., Gray, R., Pathogenesis of Cheyne-Stokes respiration in patients with congestive heart failure, Chest 1993; 104: 1079-1084. PMID 8404170
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| #Hudgel, D.W. et.al. Mechanism of sleep-induced periodic breathing in convalescing stroke patients and healthy elderly subjects, Chest 1993; 104: 1503-1510. PMID 8222815
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| #Nachtmann, A., et.al., Cheyne-Stokes respiration in ischemic stroke, Neurology 1995; 45: 820-821. PMID 7723977
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| #Naughton, M. et.al., Role of hyperventilation in the pathogenesis of central sleep apnea in patients with congestive heart failure, Am Rev Respir Dis 1993; 148: 330-338. PMID 8342895
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| #Naughton, M.T., et.al., Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure, Am J Respir Crit Care Med 1994; 150: 1598-1604. PMID 7952621
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| #Naughton, M.T., et.al., Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure, Am J Respir Crit Care Med 1995; 151: 92-97. PMID 7633695
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| #Quaranta, A.J., et.al., Cheyne-Stokes respiration during sleep in congestive heart failure, Chest 1997; 111: 467-473. PMID 9041998
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| {{Circulatory system pathology}} | | {{Circulatory system pathology}} |
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| [[pl:Oddech Cheyne'a-Stokesa]] | | [[pl:Oddech Cheyne'a-Stokesa]] |
| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| | [[Category:Medical signs]] |
| [[Category:Signs and symptoms]] | | [[Category:Signs and symptoms]] |
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