充血性心力衰竭患者陈-施氏呼吸的发生机制-王菡侨教授-英文课件.ppt

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 apneas,Central 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, respectively,CSA 与OSA,when 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 importance,Diagnosis of CSA,In patients with 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),Cheyne-Stokes respiration (CSR) is a form of periodic breathing The ventilatory period is characterized by a prolonged waxingwaning pattern of tidal volume followed by central apnea or hypopnea. It is noteworthy that the patient in whom Cheyne first described this breathing disorder suffered from HF, atrial fibrillation, and a stroke, and undoubtedly had a low cardiac output and prolonged circulation time.,CSR can be observed both during sleep and wakefulness, although it appears to be far more common during sleep When 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 prolonged 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,AB（apnea length） =18s ，21s C =nadir of SaO2 BC （lung-tocarotid body circulation time）= 8 s ，26s BD (hyperpnea length) =7s，46s AD (cycle length ) =25 s, 65s Hall MJ, Am J Respir Crit Care Med 1996;154:376381,Pathophysiolory,hyperventilation,Respiratory control system instability Ventilation 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 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. 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 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.,arousals,in 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,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 overshoot Wake NREM PaCO2 is below the higher apnea threshold CSA CHF high sensitivity to PaCO2 CSR-CSA,Several 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.,Prevalence,Sin et al 450 patients: 33% with CSA vs 37% with OSA Because 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. Javaheri S 49% of male patients with systolic HF suffer from SA CSA 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 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 al 41.7% had periodic breathing with AHI15 Wang H, et al J Am Coll Cardiol 2007;49:16251631 胡克,等.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 CHF,Independent odds ratios for CSA in CHF Male Awake PCO238mmHg Age60 years Atrial fibrillation Higher 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-CSA,Once CSR-CSA initiated， it may participate in a pathophysiologic vicious cycle that contributes to deterioration in cardiovascular function,CSR-CSA contributes to sympathetic activation：,CSA cause cyclical surges in sympathetic nervous system activity (SNA) in synchrony with the ventilatory oscillations of CSR-CSA blood pressure and heart rate oscillate in concert with Cheyne-Stokes cycles, very much as they do during OSA The 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 afterload and, thus, work for the damaged myocardium Decrease myocardial contractility Ventricular arrhythmias Myocyte hypertrophy and adverse remodeling Lanfranchi PA, et al. Circulation 2003;107:727732.,The main clinical significance of CSR-CSA in HF is its potential to adversely influence survival. Several studies showed that CSR-CSA is a significant independent predictor of mortality in patients with HF AHI greater than 30 was an independent predictor of mortality Sin DD, et al. Circulation 2000;102:6166. Corra U, et al. Circulation 2006;113:4450. Javaheri S, et al. J Am Coll Cardiol 2007;49:20282034.,Dai Yumino et al Proc Am Thorac Soc Vol 5. pp 226236, 2008,1 Wang Hanqiao et al. JACC Epub 2007 Apr 2 2 Hanly PJ,et al Am J Respir Crit Care Med, 1996,153(1):272-6,SDB significantly reduce survival without cardiac 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 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 characteristic prolonged waxing-waning pattern of ventilation.,The 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-CSAinduced 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.,