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1、 CSR-CSA 王 菡 侨 河北医科大学第三附属医院 呼吸睡眠科Definition of CSA Central sleep apneasCentral 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 least 10 seconds, respect

2、ivelyCSA 与OSAwhen 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 CSACSR can be observed both during sleep and wakeful

3、ness, although it appears to be far more common during sleepWhen it occurs during sleep, it is simply a form of CSA with a prolonged hyperpnea. When specifying the occurrence of CSR during sleep, we have used the term Cheyne-Stokes respiration with central sleep apnea (CSR-CSA).The presence of a pro

4、longed hyperpnea with a waxing-waning pattern of tidal volume, and prolonged cycle duration, that distinguishes CSR from other forms of periodic breathing as idiopathic CSA or high-altitude periodic breathing without HF In patients with HF with CSR-CSA, PaCO2 tends not to increase much more from wak

5、efulness to sleep compared to the apneic threshold does. Loop gain Xie A et al, Am J Respir Crit Care Med 2002;165:12451250. Ferrier K et al, Chest 2005;128:21162122.This chronic hyperventilation occurs because of pulmonary vagal irritant receptor stimulation by pulmonary congestion and increases in

6、 central and peripheral chemosensitivity. Lowering wedge pressure with drugs or CPAP is associated with a rise in PaCO2 and alleviation of CSRCSA. Solin Pet al Circulation 1999;99:15741579.Javaheri S. N Engl J Med 1999;341:949954.Solin P et al, Am J Respir Crit Care Med 2000;162:21942200.arousalsin

7、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 与OSA Several additional factors, such as metabolic alkalosis, low functional residual

8、capacity, upper airway instability, prolongation of circulation time and hypoxia, may further contribute to respiratory instability and CSRCSA.PrevalenceSin et al 450 patients: 33% with CSA vs 37% with OSABecause this was a sleep clinic population, the prevalence of CSR-CSA may not have been represe

9、ntative of its prevalence in the general population with HF.Javaheri S49% of male patients with systolic HF suffer from SACSA occurs in about 37%, and OSA in 12%Wang and colleagues performed sleep studies on 218 consecutive patients with HF (168 men and 50 women with LVEF 45%) enrolled from a single

10、 HF clinic between 1997 and 2004 without regard to suspicion of sleep apnea. The prevalence of CSR-CSA, defined as an AHI greater than or equal to 15 of which more than 50% were central, was 21%. Hu Ke et al41.7% had periodic breathing with AHI15 Wang H, et al J Am Coll Cardiol 2007;49:16251631胡克,等.

11、中华老年医学杂志,2002,21(1):15-18.patients 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. Wang H, et al. J Sleep Res 2006;15:321328.Risk factors for CSA in CHFIndependent odds ratios for CSA

12、in CHFMaleAwake PCO238mmHgAge60 yearsAtrial fibrillationHigher pulmonary capillary wedge pressure , and LV end-diastolic volume Sin DD, et al Am J Respir Crit Care Med 1999;160:11011106. Tkacova R, et al Am J Respir Crit Care Med 1997;156:15491555.Cardiovascular Effects of CSR-CSAOnce CSR-CSA initia

13、ted, it may participate in a pathophysiologic vicious cycle that contributes to deterioration in cardiovascular functionCSR-CSA contributes to sympathetic activation: CSA cause cyclical surges in sympathetic nervous system activity (SNA) in synchrony with the ventilatory oscillations of CSR-CSA bloo

14、d pressure and heart rate oscillate in concert with Cheyne-Stokes cycles, very much as they do during OSAThe sympathetic stimulatory effects of CSR-CSA are not isolated to sleep, but also carry over into wakefulness.Naughton MT, et al. Am J Respir Crit Care Med, 1995;152:473479.Increase preload and

15、afterload and, thus, work for the damaged myocardiumDecrease myocardial contractilityVentricular arrhythmiasMyocyte hypertrophy and adverse remodelingLanfranchi PA, et al. Circulation 2003;107:727732.The main clinical significance of CSR-CSA in HF is its potential to adversely influence survival.Sev

16、eral studies showed that CSR-CSA is a significant independent predictor of mortality in patients with HFAHI greater than 30 was an independent predictor of mortalitySin DD, et al. Circulation 2000;102:6166. Corra U, et al. Circulation 2006;113:4450.Javaheri S, et al. J Am Coll Cardiol 2007;49:202820

17、34.Dai 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):272-6SDB significantly reduce survival without cardiac transplantation (transplant-free survival) Summary In patients with HF, CSR-CSA is com

18、mon and is due to respiratory control system instability secondary to the effects of elevated LV filling pressures, pulmonary congestion, increased central and peripheral 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 precipitating central apneas, they do sculpt the hyperpneic period into the characteristi

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