机械通气的临床应用和进展课件.ppt

1、ICU ICU IN XIAMEN FIRST HOSPITAL IN XIAMEN FIRST HOSPITAL AFFILIATED TO FUJIAN MEDICAL AFFILIATED TO FUJIAN MEDICAL UNIVWERSITYUNIVWERSITY 张民伟张民伟ILV各种新模式？各种新模式？回归根本！回归根本！模式无自主呼吸或自主呼吸弱 IPPV SIMV较明显的自主呼吸 BIBAP ASB CPAP定容 BIBAP 定压定压参数：VT、f、Tins、PEEP、PAW、参数：Pins、f、Tins、PEEP、参数：PS、PEEP设置:FiO2、维维 持持 气气 体体

2、 交交 换换控控 制制 呼呼 吸吸 作作 功功 避免肺损伤避免肺损伤 Low lung pressure and High PEEPAmato,American Journal of Respiratory and Critical Care Medicine.1995;152:1835-1846 Amato,New England Journal of Medicine.1998;338:347-354 Patient-ventilator interaction自主呼吸中自主呼吸中“呼吸泵呼吸泵”的作用的作用呼吸系统呼吸系统和循环系和循环系统的和谐统的和谐工作工作自然自然进化的结进化的结果

3、果Diaphragm Position and Displacement during Tidal BreathingAwake spontaneousAnaesthetized spontaneousParalyzedSpontaneous breathingControlled ventilationWhat Is BIPAP?Intermittent CPAP (Dr.John Downs,1987)CPAP(cm H2O)Time(sec)02010Mechelle Williams RN ANP-CS,Susannah Kish RN CS CCRN CPANThe Universi

4、ty of Texas M D Anderson Cancer Center,Houston,TexasIntroduction:The use of analgesia on mechanically ventilated patients is acommon practice in the medical ICU.Analgesia management is generallyrelated to the patients dysynchrony and agitation on the ventilator.A newmode of ventilation(BiLevel)was i

5、ntroduced that should allow the patient tobe more comfortable.The current study compared the use of opioid in MICUpatients before and after the introduction of the new mode.Methods:A studydone in our ICU prior to the introduction of BiLevel quantitated the amount ofopioid use on mechanically ventila

6、ted patients.At that time the mode ofventilation was a combination of Assist Control or SIMV with PressureSupport.This study was used as the baseline for comparison.The datacollection methods of the previous study were duplicated on 10 consecutivepatients ventilated with BiLevel.Opioid usage was col

7、lected on day 1,2,3 andday 7 after institution of mechanical ventilation.All opioid dosages wereconverted to an equivalent parenteral dose of morphine sulfate for comparison.The data was analyzed using a two tailed unpaired t test.Results:Patients inthe two groups had similar demographics.Current gr

8、oup mean age was 57 andin the baseline group mean age was 53.Females comprised 56%of the patientsin the baseline and 40%in the current group.Patients in both groups hadsimilar etiologies for Respiratory Failure.Mean data is presented in the table.MorphineEquivalentDay 1Day 2Day 3Day 7OverallPre BiLe

9、vel77.10mg 142.5mg 204.17mg213 mg159.2mgPost BiLevel76.72mg 130.2mg 113.30mg41.34mg 90.4mgDifference(%decrease).38mg(0.49%)12.32mg(8.6%)90.87mg(44.5%)171.66(80.6%)68.8mg(43.2%)This represents a statistically significant decrease in opioid use of 43.2%in theBiLevel group on the days monitored.(p.01)C

10、onclusions:Analgesiamanagement of non-surgical patients ventilated with the BiLevel mode,asmeasured by opioid administration,decreased as compared to a previousbaseline study.Further studies examining the relationship of analgesia andsedation management related to ventilator mode are warranted.C.Hrm

11、ann et al.(1997)Acta Anaesthesiol Scand 41(supp.111):152-155)C.Hrmann et al.(1997)Acta Anaesthesiol Scand 41(supp.111):152-155)呼吸机所致肺损伤呼吸机所致肺损伤呼吸机所致肺损伤(Ventilator induced lung injury,VILI)是机械通气的重要并发症，其发生率占机械通气的0.5%-39%，死亡率高达13%-35%。主要有肺气压伤、肺容积伤、肺萎陷伤、肺生物伤所致。呼吸机所致肺损伤呼吸机所致肺损伤肺气压伤(barotrauma)由于气道压过高导致的张

12、力性气胸,肺间质,纵隔和皮下气肿,心包和腹膜后积气,气腹,系统性气体栓塞(统称为肺泡外气体)。气压伤发生的机制为:肺泡和周围血管间隙的压力梯度增大,导致肺泡破裂,形成肺间质气肿,气体再沿支气管血管鞘进入纵隔,并沿其周边间隙进入皮下组织,心包,腹膜后和腹腔。若脏层胸膜破裂,气体可进入胸腔。最终可形成肺间质、纵隔和皮下气肿,心包和腹膜后积气以及胸和气腹。气体进入肺循环则引起气体栓塞。8 cm H2O for 20 min30 cm H2O for 20 min呼吸机所致肺损伤呼吸机所致肺损伤肺容积伤(volutrauma)研究者比较了高压高容通气,低压高容通气和高压低容通气对健康兔的影响,发现高容

13、通气均能产生高通透性肺水肿,而高压低容通气则无肺损伤发生,因此认为气压伤实质上为容积性肺损伤(volume damage)。容积伤的形成主要与过大的吸气末肺容积对肺泡上皮和血管内皮的过度牵拉(overstretch)有关。呼吸机所致肺损伤呼吸机所致肺损伤肺萎陷伤(atelectrauma)ALI 呼气末容积过低时,肺泡和终末气道的周期性开闭可致 肺表面活性物质大量损失,加重肺不张和肺水肿。同时,由于ALI 病变的不均一性,在局部的扩张肺泡和萎陷肺泡之间产生很强的剪切力(shearing force)也可以引起严重的肺损伤。呼吸机所致肺损伤呼吸机所致肺损伤肺生物伤(biotrauma)机械性因素

14、使血管内皮细胞脱落,为炎性细胞活化,与基底膜粘附并进而进入肺内创造了机会,由此激发的炎症反应所致的肺损伤称为肺生物伤,它对VILI 的发展和最终结局也产生重要的影响。肺损伤-多脏器功能衰竭David Carney,MD;Crit Care Med 2005 Vol.33.No.3(suppl)Figure 1.In vivo photomicrographs of the same normal(A and B)and acutely injured lung(C and D).Alveoli at peak inspiration(A)and end expiration(B)in the

15、normal lung are very stable with littlechange in size during tidal ventilation(dots).High positive inspiratory pressure(PIP)and low PEEPinjurious ventilation causes a ventilator-induced lung injury resulting in alveolar instability.Injuredalveoli at peak inspiration(C)are inflated(dots)and totally c

16、ollapse(arrows)end expiration(D),demonstrating severe instability during tidal ventilation.Figure 2.Alveolar stability assessed by subtracting the area of the alveolus at inspiration(I)from thatat expiration(E)using computer image analysis.The higher the I-E,the more unstable the alveoli.Normal alve

17、oli(control)are very stable.Tween lavage deactivates surfactant and causes alveolarinstability(5 mins).Without additional positive end-expiratory pressure(PEEP),alveoli remainsignificantly unstable for 180 mins(TWEEN).Increasing PEEP(TWEEN PEEP)rapidly stabilizesalveoli.from Am J Respir Crit Care Me

18、d(30)Am J Respir Crit Care Med(38).)Figure.Confocal images of subpleural alveoli(top,control and injury).Red nuclei(propidium iodidePI)mark the injured cells(top,injury).Bar graph,mean number of PI-positive cells per alveolus;mL/kg,tidal volume;ZEEP,0 positive end-expiratory pressure;PEEP,positive e

19、nd-expiratory pressure.Figure 4.Left panel,rat lung ventilated with high tidal volumelow airway pressure for 20 mins.A typeII epithelial cell(PII)is intact,whereas a type I epithelial cell is injured(arrows).The basementmembrane is denuded(arrows)and lined with cell debris and fibrinous deposits(hya

20、line membranes).AS,alveolar space,i.e.,interstitial edema;ca,capillary lumen(original magnification 7,100).Rightpanel,high-pressure ventilation plus positive end-expiratory pressure.Type I cells are intact(arrows)with the only pathology being endothelial blebs.En,endothelial cell;PII,original magnif

21、ication,7,100).(Reproduced with permission from Am J Respir Crit Care Med(39).)David Carney,MD;Crit Care Med 2005 Vol.33.No.3(suppl)Am J Respir Crit Care Med(41).)Figure 5.Laser confocal images of normal(left)and edematous(right)subpleural alveoli in a rat.Normal air-filled alveoli on the left and e

22、dema(solid white)filled alveoli on the right.Figure 6.Theoretical stresses imparted on epithelial cells during airway reopening.A,a collapsedcompliant airway is forced open by a finger of air.Circles show how the stresses of reopening mightaffect epithelial cells.B,a fluid-filled narrow channel is c

23、leared by a finger of air.Circles show how thestresses of fluid clearance might affect epithelial cells.from Am J Respir Crit Care Med(42).)Figure 7.Alveolar number(#Alveoli/Field)and alveolar stability(I-E)before(before RM),during(during RM),and after a recruitment maneuver(RM)with either 5(positiv

24、e end-expiratory pressure PEEP 5 after RM)or 10(PEEP 10 after RM)cm H2O PEEP added.Note that with only 5 cm H2O PEEPafter RM(PEEP 5 after RM)that alveoli recollapse(fall in#alveoli/field)and the alveoli that remain open were unstable(increased I-E).Adding PEEP(PEEP 10 after RM)prevented both recolla

25、pse and instability.from Am J Respir Crit Care Med(29).)Figure 8.In vivo photomicrographs of subpleural alveoli in the rat after lung injury by saline lavageventilated with either conventional mechanical ventilation(CMV)or high-frequency oscillatory ventilation(HFOV)using a 2.5-internal diameter tra

26、cheal tube.With CMV,a group of alveoli are seeninflated during inspiration(dots)but collapse with expiration(arrows).Alveoli are very stable withHFOV during ventilation.The same alveolus is seen with HFOV at inflation and exhalation(dots).David Carney,MD;Crit Care Med 2005 Vol.33.No.3(suppl)MORTALIT

27、Y52%MORTALITY37%肺保护性通气策略肺保护性通气策略呼气末正压通气(PEEP):通过呼气末正压,防止肺泡塌陷,使已塌陷的肺泡复张,提高功能残气量,降低肺内右向左分流,改善通气与血流的比例和弥散功能,提高肺顺应性,降低呼吸功,提高SaO2。确定最佳PEEP 的方法有:(1)在相同吸气流速下改变PEEP 水平,观察气道峰压的同步变化,寻找峰压增加幅度开始大于PEEP 增加幅度的转折点对应的PEEP 水平。(2)可在机械通气过程中逐渐提高PEEP 水平,并同步测定气道平台压,计算肺顺应性,从中找出肺顺应性从升到降的转折点。(3)采用FiO2 与PEEP 两个参数交替式调节,以期使用最低F

28、iO2与PEEP,维持PaO2 在55 mmHg以上,肺保护性通气策略肺保护性通气策略Psafewindowzone of overdistensionVatelectraumavolutraumaLIPUIPzone of derecruitment and atelectasisAmato et al.,AJRCCM 152:1835-46(1995)改容量控制通气为压力限制型通气模式,维持整个通气期间吸气峰压不超过3540cmH2O 吸气平台压不超过3035cmH2O。z控制通气(PCV)、z压力支持通气(/ASB/PSV),z双相气道正压(BIPAP)、z压力调节容量控制(PRVC)。

29、肺保护性通气策略肺保护性通气策略 长吸气时间策略:,改变呼吸比,延长吸气时间甚至采用反比通气(21,31,41)。,应用此策略的目的是降低吸气峰压、提高气道平均压,形成适当水平的内源性PEEP,利于萎陷的肺泡复张,促进氧合。肺保护性通气策略肺保护性通气策略容许性高碳酸血症(PHC):L使用上述通气策略将导致部分ARDS 患者发生不同程度的高碳酸血症,然而动物实验和临床均证明一定水平的高碳酸血症带来的危害远比大VT 造成的肺容量损伤的危害小的多,因而提出了容许性高碳酸血症的概念。L 目前人们最关注的问题是实行PHC 过程中高碳酸血症究竟可以允许到什么水平?或者说PHC 的安全线到底为多少?现有资

30、料表明,只要血氧饱和度正常,PaCO2 75110 mmHg 缓慢上升,不会引起明显的临床症状,有报道PaCO2 超过125mmHg 但其神志仍清楚者。但目前多数学者认为PaCO2 不超过80 mmHg 是安全的,pH 值一般以不低于7.22 为宜。其上升速度不应超过10mmHg/h,缓慢增加的目的在于细胞内部酸性物质可以充分代偿。下降速度调整为1020mmHg/h,下降速度过快会导致碱中毒和中枢障碍,以致撤机困难。L由于高碳酸血症可使呼吸运动增强,使自主呼吸与呼吸机对抗,此时可适当应用镇静剂和神经肌肉阻滞剂,然而有报道停药后其神经肌肉阻滞作用延长6h 至7d以上者,也有发生肌病的可能。PHC

31、 的绝对禁忌证包括颅内压升高(颅内损伤、出血、占位性病变)、脑血管病、心功能严重损害等。L 相对禁忌证包括未纠正的低血容量、使用-受体阻滞剂及严重的代谢性酸中毒。由于酸中毒会抑制心肌及血管对儿茶酚胺的反应性,故对PHC 患者应给予肾上腺素能药物的支持,并避免应用-肾上腺素能阻滞剂。肺保护性通气策略肺保护性通气策略机械通气中常见并发症及原因%皮下气肿,%气道黏膜糜烂,%气管食管瘘,%气道狭窄,发生率1%2%,%气道感染,M无菌观念不强;M导管更换不勤,大量细菌附着;M导管外口不上机时无湿纱布复盖;M口咽鼻分泌物顺导管外壁流入气道;M湿化罐和连通管消毒不彻底,呼吸道的冷凝水返流进入终末细支气管;M

32、吸痰不及时或者气道湿化不够,黏膜干燥,纤毛运动减弱,排痰不畅,痰涎结痂,痰块堵塞,气道狭窄;M湿化罐加温不够,气道低温,小气道易痉挛,纤毛活动受限,影响排痰。机械通气中常见的并发症机械通气中常见失误及原因%上机时机不当,多为插管上机太晚,呼吸肌疲劳,加重了组织缺氧;拔管太早,多见全麻术后病人,未完全清醒,呼吸不畅,咳痰无力,吸痰不彻底,痰栓堵塞。%导管位置不妥:N 置管过浅。躁动剧咳、翻身过猛、转头幅度过大时易脱管;N 过深,若插入一侧支气管又行机械通气,就极易发生单肺通气的严重后果。N 误入食道,解剖不熟,操作生疏,声门上抬窥视不清所致。机械通气中常见失误及原因%选管和连接有误:6导管太粗,

33、造成鼻及气道黏膜损伤;6导管太细,气道阻力大,通气不良;6气囊破损漏气致通气量不足。6连通管道质量差,老化破损漏气;6连通管太长,死腔过大,CO2 排不出去;6连通管太短,影响头颈部活动,也易脱管;6气管导管弯曲成角,气道阻力增大压力上升。6呼吸机氧源脱落,未及时发现,造成低氧血症。%置管动作粗疏、镇静不充分,引起病人血压升高、心跳加快,易引发脑出血、心律失常、心衰等。%操作过程失误:气道压太大,吸痰时间太久，吸痰管负压太大,吸痰管选择不当，人机对抗，采用的模式不适应。机械通气中常见失误及原因机械通气中常见失误及原因CLINICAL 临床目标：临床目标：1.Reverse hypoxemia 改善低血氧症改善低血氧症2.Reverse respiratory acidosis 改善呼吸性酸毒症改善呼吸性酸毒症3.Relieve respiratory distress 减轻呼吸窘迫减轻呼吸窘迫4.Prevent or reverse atelectasis 预防和改善肺不张预防和改善肺不张5.Reverse respiratory muscle fatigue 改善呼吸肌肉疲劳改善呼吸肌肉疲劳 PRIMARY前前 提：提：Avoid Iatrogenic Lung Injury避免医源性避免医源性肺损伤肺损伤谢谢！