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1、 CSR-CSA 王王 菡菡 侨侨 河北医科大学第三附属医院河北医科大学第三附属医院 呼吸睡眠科呼吸睡眠科Definition of CSA Central sleep apneasnCentral sleep apneas and hypopneas arise from complete or partial reductions in central neural outflow to the respiratory muscles during sleep that lead to complete or partial cessation of airflow for at leas
2、t 10 seconds, respectivelyCSA CSA 与与与与OSAOSAnwhen studying patients with cardiovascular diseases, especially those with HF and stroke, where CSA is much commoner than in the general population, distinguishing central from obstructive events assumes greater importanceDiagnosis of CSAnIn patients with
3、 HF, a diagnosis of CSA can be established on overnight polysomnography, using either RIP or nasal pressure cannula for respiratory monitoring, when there is an AHI of at least 5 to 15, and when at least 50% of apneas and hypopneas are central.Cheyne-Stokes respiration (CSR)nCheyne-Stokes respiratio
4、n (CSR) is a form of periodic breathingnThe ventilatory period is characterized by a prolonged waxingwaning pattern of tidal volume followed by central apnea or hypopnea.nIt is noteworthy that the patient in whom Cheyne first described this breathing disorder suffered from HF, atrial fibrillation, a
5、nd a stroke, and undoubtedly had a low cardiac output and prolonged circulation time.nCSR can be observed both during sleep and wakefulness, although it appears to be far more common during sleepnWhen it occurs during sleep, it is simply a form of CSA with a prolonged hyperpnea. When specifying the
6、occurrence of CSR during sleep, we have used the term Cheyne-Stokes respiration with central sleep apnea (CSR-CSA).nThe presence of a prolonged hyperpnea with a waxing-waning pattern of tidal volume, and prolonged cycle duration, that distinguishes CSR from other forms of periodic breathing as idiop
7、athic CSA or high-altitude periodic breathing without HFAB（apnea length） =18s ，21sC =nadir of SaO2 BC （lung-tocarotidbody circulation time）= 8 s ，26sBD (hyperpnea length) =7s，46sAD (cycle length ) =25 s, 65s Hall MJ, Am J Respir Crit Care Med 1996;154:376381PathophysioloryhyperventilationnRespirator
8、y control system instabilitynVentilation is dependent mainly on the metabolic rather than the behavioral respiratory control system during sleep, and the primary stimulation for ventilation while asleep is PaCO2 Central apnea during sleep occurs when PaCO2 falls below the apnea threshold. CSR-CSA is
9、 present when central apnea occurs cyclically In patients with HF with CSR-CSA, PaCO2 tends not to increase much more from wakefulness to sleep compared to the apneic threshold does. Loop gain Xie A et al, Am J Respir Crit Care Med 2002;165:12451250. Xie A et al, Am J Respir Crit Care Med 2002;165:1
10、2451250. Ferrier K et al, Chest 2005;128:21162122. Ferrier K et al, Chest 2005;128:21162122.nThis chronic hyperventilation occurs because of pulmonary vagal irritant receptor stimulation by pulmonary congestion and increases in central and peripheral chemosensitivity. nLowering wedge pressure with d
11、rugs or CPAP is associated with a rise in PaCO2 and alleviation of CSRCSA. Solin Pet al Circulation 1999;99:15741579.Solin Pet al Circulation 1999;99:15741579.Javaheri S. Javaheri S. N Engl J Med 1999;341:949954.N Engl J Med 1999;341:949954.Solin P et al, Am J Respir Crit Care Med 2000;162:21942200.
12、Solin P et al, Am J Respir Crit Care Med 2000;162:21942200.arousalsnin OSA arousals act as a defense mechanism to terminate apneas, and activate pharyngeal muscles that allow resumption of airflow, in CSA they appear to instigate central， apneas by provoking ventilatory overshoot.CSA CSA 与与与与OSAOSAn
13、Increases in ventilation in response to arousals occur due to both nonchemical hand chemical factors. The abrupt change in state NREM Wake waking neurogenic drive to breathe lower PaCO2 setpoint ventilatory overshootnWake NREM PaCO2 is below the higher apnea threshold CSAnCHF high sensitivity to PaC
14、O2 CSR-CSA nSeveral additional factors, such as metabolic alkalosis, low functional residual capacity, upper airway instability, prolongation of circulation time and hypoxia, may further contribute to respiratory instability and CSRCSA.Prevalencen nSin et al Sin et al 450 patients: 33% with CSA vs 3
15、7% with OSA450 patients: 33% with CSA vs 37% with OSABecause this was a sleep clinic population, the prevalence of CSR-CSA may not have been representative of its prevalence in the general population with HF.n nJavaheri SJavaheri S 49% of male patients with systolic HF suffer from 49% of male patien
16、ts with systolic HF suffer from SASA CSA occurs in about 37%, and OSA in 12%CSA occurs in about 37%, and OSA in 12%n nWang and colleagues performed sleep studies on 218 Wang and colleagues performed sleep studies on 218 consecutive patients with HF (168 men and 50 consecutive patients with HF (168 m
17、en and 50 women with LVEF 45%) enrolled from a single HF women with LVEF 45%) enrolled from a single HF clinic between 1997 and 2004 without regard to clinic between 1997 and 2004 without regard to suspicion of sleep apnea. The prevalence of CSR-CSA, suspicion of sleep apnea. The prevalence of CSR-C
18、SA, defined as an AHI greater than or equal to 15 of which defined as an AHI greater than or equal to 15 of which more than 50% were central, was 21%.more than 50% were central, was 21%. n nHu Ke et alHu Ke et al 41.7% had periodic breathing with AHI41.7% had periodic breathing with AHI15 15 Wang H,
19、 et al J Am Coll Cardiol 2007;49:16251631 胡克胡克胡克胡克, ,等等等等. .中华老年医学杂志中华老年医学杂志中华老年医学杂志中华老年医学杂志,2002,21(1):15-18.,2002,21(1):15-18.npatients with HF, OSA and CSA can be part of a spectrum of periodic breathing whose predominant type can transform over time in response to alterations in cardiac function
20、. Wang H, et al. J Sleep Res 2006;15:321328.Risk factors for CSA in CHFn nIndependent odds ratios for CSA in CHFIndependent odds ratios for CSA in CHF MaleMale Awake PCOAwake PCO2 238mmHg38mmHg Age60 yearsAge60 years Atrial fibrillationAtrial fibrillationHigher pulmonary capillary wedge pressure , a
21、nd LV end-diastolic volume Sin DD, et al Sin DD, et al Am J Respir Crit Care Med Am J Respir Crit Care Med 1999;160:11011999;160:1101 1106.1106. Tkacova R, et al Tkacova R, et al Am J Respir Crit Care Med Am J Respir Crit Care Med 1997;156:15491555.1997;156:15491555.Cardiovascular Effects of CSR-CSA
22、nOnce CSR-CSA initiated， it may participate in a pathophysiologic vicious cycle that contributes to deterioration in cardiovascular functionCSR-CSA contributes to sympathetic activation： nCSA cause cyclical surges in sympathetic nervous system activity (SNA) in synchrony with the ventilatory oscilla
23、tions of CSR-CSA -blood pressure and heart rate oscillate in concert with Cheyne-Stokes cycles, very much as they do during OSAnThe sympathetic stimulatory effects of CSR-CSA are not isolated to sleep, but also carry over into wakefulness.n nNaughton MT, et al. Naughton MT, et al. Am J Respir Crit C
24、are MedAm J Respir Crit Care Med, 1995;152:473479., 1995;152:473479.nIncrease preload and afterload and, thus, work for the damaged myocardiumnDecrease myocardial contractilitynVentricular arrhythmiasnMyocyte hypertrophy and adverse remodelingn nLanfranchi PA, et al. Lanfranchi PA, et al. Circulatio
25、n Circulation 2003;107:727732.2003;107:727732.nThe main clinical significance of CSR-CSA in HF is its potential to adversely influence survival.nSeveral studies showed that CSR-CSA is a significant independent predictor of mortality in patients with HFnAHI greater than 30 was an independent predicto
26、r of mortalityn nSin DD, et al. Circulation 2000;102:6166.Sin DD, et al. Circulation 2000;102:6166.n n Corra U, Corra U, et al. Circulation 2006;113:4450.et al. Circulation 2006;113:4450.n nJavaheri S, et al. J Am Coll Cardiol 2007;49:20282034.Javaheri S, et al. J Am Coll Cardiol 2007;49:20282034.Da
27、i Yumino et al Proc Am Thorac Soc Vol 5. pp 226236, 20081 Wang Hanqiao et al. JACC Epub 2007 Apr 22 Hanly PJ,et al Am J Respir Crit Care Med, 1996,153(1):272-6Am J Respir Crit Care Med, 1996,153(1):272-6SDB significantly reduce survival without cardiac SDB significantly reduce survival without cardi
28、ac transplantation (transplant-free survival)transplantation (transplant-free survival) Summary In patients with HF, CSR-CSA is common and is due to respiratory control system instability secondary to the effects of elevated LV filling pressures, pulmonary congestion, increased central and periphera
29、l chemoreceptor sensitivity, reduced cerebrovascular blood flow, and possibly other factors. Central apnea occurs when PaCO2 falls below the threshold for apnea during sleep. Although low cardiac output and increased lung to chemoreceptor circulation time have not been shown to play a direct role in
30、 precipitating central apneas, they do sculpt the hyperpneic period into the characteristic prolonged waxing-waning pattern of ventilation.nThe majority of the evidence indicates that CSR-CSA increases the risk of premature death in HF. This adverse effect has been most closely linked with CSR-CSAin
31、duced sympathetic activation, although other as yet unidentified mechanisms may be involved Evidence from one multicenter randomized trial demonstrated that CPAP attenuated CSR-CSA in association with improved LV function, decreased SNA, and increased exercise performance. Further research should be done to make sure whether the therapy of CSA-CSR can improve the survival or reduced hospitalizations of CHF patients.
