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
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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 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, respec
2、tively,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
3、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 period
4、ic 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 undoubtedl
5、y 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 sl
6、eep, 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
7、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 ins
8、tability 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 centra
9、l 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 hyperventilati
10、on 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. Jav
11、aheri 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 v
12、entilatory 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
13、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
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- 充血 心力衰竭 患者 呼吸 发生 机制 王菡侨 教授 英文 课件
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