《儿童重症哮喘》课件.ppt

动态过度充气的恶性循环 * CPAP/PEEP 对抗auto-PEEP 消除吸气肌所增加的呼吸做功 缩短吸气时间，减少Ti/Ttot 扩张萎陷的气道和肺泡 一般PEEP小于15cmH2O 呼气末正压通气 * 应用镇静剂，甚至肌松剂，消除患者自主呼吸，保持镇静 注意气道湿化和分泌物清除 镇静肌松剂 * 肌松剂 阿片类药物 镇静剂 琥珀胆碱、罗库溴铵 芬太尼 异丙芬、氯胺酮 机械通气的镇静和肌肉松弛 1 2 3 4 吸痰、扩张支气管等降低气道阻力 设置PEEPp小于PEEPi 镇静、肌松、镇痛和控制体温 允许性高碳酸血症通气策略 减轻过度通气的方法 * * Asthma is a chronic inflammatory disorder of the airways This bronchoscopic view of an airway shows the normal appearance of a healthy airway, contrasted with inflammation (reddening and swelling) and narrowing of the asthmatic airway Microscopic examination of biopsy and lavage samples taken through the bronchoscope has established that inflammatory changes are present in asthma of all grades of severity, including recently diagnosed asthma * * 哮喘症状是“冰山的一角” 平时我们所看到患者哮喘症状，只是哮喘疾病的这座冰山露出水面的那一小部分。水面下的部分才是哮喘真正的病因，更大更危险。所以，哮喘治疗不能仅对症，更要对因。 * * 哮喘是一慢性炎症性疾病，有间断性发作，包括慢性持续性炎症基础上的急性炎症。 哮喘的急性炎症伴随着支气管收缩，血浆渗漏/水肿，血管扩张和粘液高分泌。 哮喘的慢性炎症伴随着上皮下纤维化、平滑肌增生/肥大，粘液腺增生和新血管的形成。 如果哮喘未经控制或未得到很好的控制，气道的持续性炎症导致结构改变（重构），从而降低了短程激素改善FEV1的程度。 * * * * 我们知道，药物经气雾剂的定量阀门喷入口腔， 有10－20％的微小颗粒悬浮药物随吸入气流进到肺部小气道及细小支气管，真正发挥直接而强效的抗炎作用。 80－90％咽下，经胃肠道吸收入血，被肝脏代谢，即‘首过效应’失活,代谢产物进入全身循环，称其量为A。经肺循环入血的药物量非常少，几可忽略称为B。A+B为药物代谢产物进入全身循环的总量。 丙酸氟替卡松(氟替卡松)口服生物利用度不到1％，是现有糖皮质激素中最小的，对全身引起的副作用微乎其微。 一种理想的药物除副作用越小越好外，疗效极其重要。 * * Both in vivo studies and computer models using monodisperse aerosols have demonstrated that inhaled particles deposit in the airways by one of three (3) principle mechanisms: inertial impaction, gravitational sedimentation, and Brownian diffusion (a fourth is electrostatic precipitation). Larger particles (i.e. 5 microns) deposit in the upper and conducting airways primarily via the mechanism of inertial impaction. The fraction absorbed through the gut will be drug dependent. Particles in the 2-5 micron range deposit primarily by sedimentation under the force of gravity. However, when particles are sufficiently small (i.e. 2 microns), diffusion becomes the principle mechanism of deposition. Some of these smaller particles wi