重症医学之ARDS课件讲义.pptxVIP

ARDS;ARDS的诊断，应用1994年AECC的标准: ①急性起病; ②氧合指数(PaO2/FiO 2 ) ≤200mm Hg〔无论呼气末正压(PEEP)水平〕; ③正位X 线胸片显示双肺均有斑片状阴影; ④肺动脉嵌顿压≤18 mm Hg, 或无左心房压力增高的临床证据。 如满足上述标准但PaO2/FiO2≤300 mm Hg ，则诊断为ALI。 ;病理及病理生理变化;;低氧发生机制： V/Q不匹配及分流增加;;PATHOPHYSIOLOGY;;ARDS: Exudative Phase;Proliferative/Sub acute phase Lasting for 6-10 days. Characterized by infiltration of the interstitium by fibroblasts and collagen. There is proliferation of the type 2 epithelial cells. PEEP may not be effective in this stage. Since pulmonary capillary inflammation causes narrowing of vessels, pulmonary hypertension sets in which may be aggravated by Hypoxic Pulmonary Vasoconstriction (HPV). This leads to increase in dead space.;Fibrotic/Chronic phase From 10-14 days onwards. There is large destruction resulting in emphysema and the dead space further increases. Functionally the oxygenation improves, but there is pulmonary vascular obliteration due to fibrosis. In survivors beyond 3-4 weeks, the lungs are completely remodeled by sparsely cellular collagenous tissue. PEEP is not at all effective here and an increase in PaO2 does not correlate to increase in FiO2. There is increased chance of barotraumas and volutrauma.;Proliferative stage and Fibrotic stage;ARDS: Fibroproliferative phase;;机械通气改善氧合;呼吸机相关肺损伤;;“gross” barotrauma;Increased microvascular permeability in dog lungs due to high airway pressures;The concept of“volumetrauma”;;跨肺压（transpulmonary pressure）;Ecw / Etot : 0.2 to 0.8;The concept of“Atelectrauma”;The concept of“biotrauma”;肺保护性通气策略;ARDS肺形态学与机械通气相关肺损伤;ARDS机械通气策略;;;;;;试验方案;;BALF与组织病理检查 SB组 轻度肺损伤 BALF中性粒细胞少，总蛋白水平低 ?病理肺损伤评分最低 重度肺损伤 BALF总蛋白水平高 病理肺损伤评分最高;CT分析肺通气及塌陷 轻度肺损伤 肌松组 非低垂ROI通气( 75%)，导致过度充盈显著增加 低垂ROI正常通气显著减少 SB组 低垂ROI塌陷肺泡减少，正常通气肺组织增加 更多气体进入低垂ROI 重度肺损伤 肌松组通气更均一 SB组通气主要位于低垂ROI，但低垂ROI呼气???塌陷肺泡增加，周期性塌陷最多;根据ALI动物模型，本研究证实 肺损伤较轻且可以维持较低的Pplat时，SB有助于肺复张 重度肺损伤时，过度SB加重肺损伤，肌松治疗通过防止过高的PL和驱动压，对肺起到保护作用;PEEP;PEEP;PEEP的选择 ;;;;ARDS在CT上两种经典变化;Recruitment Maneuvers;Recruitment Maneuvers;Prone