中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2009年
10期
732-735
,共4页
阻塞性睡眠呼吸暂停%呼吸驱动%食管压力
阻塞性睡眠呼吸暫停%呼吸驅動%食管壓力
조새성수면호흡잠정%호흡구동%식관압력
Obstructive sleep apnea%Neural respiratory drive%Esophageal pressure
目的 使用表面电极记录膈肌肌电,评价OSAHS患者的呼吸努力及呼吸中枢驱动.方法 选择2007年6月至10月因存在打鼾、嗜睡等症状,怀疑OSAHS前来广州呼吸病研究所睡眠中心行整夜(>7h)多导睡眠(PSG)监测的患者11例,PSG监测同时记录食管压力,并通过胸部表面电极记录膈肌肌电活动信号,其中5例同时记录食管膈肌肌电信号.结果 当发生阻塞性呼吸暂停(OSA)时,表面电极记录的膈肌肌电信号(8.1±7.1)μV、食管膈肌肌电信号(21.1±10.7)μV和食管压信号(18.1±6.8)cm H_2O(1cm H_2O=0.098kPa)均逐渐增加.食管压变化幅度在呼吸暂停末达到最大值(31.1±13.4)cm H_2O,气流恢复后骤然降低(21.0±8.8)cm H_2O;体表膈肌肌电和食管膈肌肌电活动在气流恢复初期[(14.9±13.9)μV、(41.6±22.1)μV]仍继续增加,表面电极记录的膈肌肌电的最大均方根与食管压变化幅度在发生OSA时呈线性相关(r=0.66),而膈肌肌电与食管膈肌肌电在发生OSA时呈线性相关(r=0.72).结论 表面电极所记录的膈肌肌电可作为判断睡眠呼吸事件时呼吸努力存在与否的辅助方法,有助于鉴别睡眠呼吸暂停的类型.
目的 使用錶麵電極記錄膈肌肌電,評價OSAHS患者的呼吸努力及呼吸中樞驅動.方法 選擇2007年6月至10月因存在打鼾、嗜睡等癥狀,懷疑OSAHS前來廣州呼吸病研究所睡眠中心行整夜(>7h)多導睡眠(PSG)鑑測的患者11例,PSG鑑測同時記錄食管壓力,併通過胸部錶麵電極記錄膈肌肌電活動信號,其中5例同時記錄食管膈肌肌電信號.結果 噹髮生阻塞性呼吸暫停(OSA)時,錶麵電極記錄的膈肌肌電信號(8.1±7.1)μV、食管膈肌肌電信號(21.1±10.7)μV和食管壓信號(18.1±6.8)cm H_2O(1cm H_2O=0.098kPa)均逐漸增加.食管壓變化幅度在呼吸暫停末達到最大值(31.1±13.4)cm H_2O,氣流恢複後驟然降低(21.0±8.8)cm H_2O;體錶膈肌肌電和食管膈肌肌電活動在氣流恢複初期[(14.9±13.9)μV、(41.6±22.1)μV]仍繼續增加,錶麵電極記錄的膈肌肌電的最大均方根與食管壓變化幅度在髮生OSA時呈線性相關(r=0.66),而膈肌肌電與食管膈肌肌電在髮生OSA時呈線性相關(r=0.72).結論 錶麵電極所記錄的膈肌肌電可作為判斷睡眠呼吸事件時呼吸努力存在與否的輔助方法,有助于鑒彆睡眠呼吸暫停的類型.
목적 사용표면전겁기록격기기전,평개OSAHS환자적호흡노력급호흡중추구동.방법 선택2007년6월지10월인존재타한、기수등증상,부의OSAHS전래엄주호흡병연구소수면중심행정야(>7h)다도수면(PSG)감측적환자11례,PSG감측동시기록식관압력,병통과흉부표면전겁기록격기기전활동신호,기중5례동시기록식관격기기전신호.결과 당발생조새성호흡잠정(OSA)시,표면전겁기록적격기기전신호(8.1±7.1)μV、식관격기기전신호(21.1±10.7)μV화식관압신호(18.1±6.8)cm H_2O(1cm H_2O=0.098kPa)균축점증가.식관압변화폭도재호흡잠정말체도최대치(31.1±13.4)cm H_2O,기류회복후취연강저(21.0±8.8)cm H_2O;체표격기기전화식관격기기전활동재기류회복초기[(14.9±13.9)μV、(41.6±22.1)μV]잉계속증가,표면전겁기록적격기기전적최대균방근여식관압변화폭도재발생OSA시정선성상관(r=0.66),이격기기전여식관격기기전재발생OSA시정선성상관(r=0.72).결론 표면전겁소기록적격기기전가작위판단수면호흡사건시호흡노력존재여부적보조방법,유조우감별수면호흡잠정적류형.
Objective Measurement of esophageal pressure is considered to be the gold standard for assessing respiratory effort and neural respiratory drive but this requires placement of an esophageal catheter. We hypothesized that neural drive could be reflected by the diaphragm EMG recorded from chest wall surface electrodes. Methods We simultaneously recorded esophageal pressure and the chest wall diaphragm EMG in 11 patients with suspected obstructive sleep apnea/hypopnea syndrome during full night polysomnography. We also recorded the diaphragm EMG from esophageal electrode in 5 of the 11 subjects. Results Diaphragm EMG could be satisfactorily recorded from 9 of the 11 subjects. The root mean square of the chest wall diaphragm EMG increased gradually during the obstructive sleep apnea events and reached a maximal value at arousal. Similarly, the esophageal pressure increased gradually over the obstructive sleep apnea events and reached a maximal value at the end of apnea. There was a relation between the RMS of the diaphragm EMG recorded from the chest wall surface electrodes and esophageal pressure(r =0.66) and the diaphragm EMG(r =0.72) recorded from esophageal electrode during obstructive event. Conclusion The diaphragm EMG could be recorded from the chest wall surface electrodes in most subjects and can be used to demonstrate the presence of respiratory effort during apnoea/hyponea events.
