重症急性胰腺炎治疗现状与发展.pptx
《重症急性胰腺炎治疗现状与发展.pptx》由会员分享,可在线阅读,更多相关《重症急性胰腺炎治疗现状与发展.pptx(43页珍藏版)》请在咨信网上搜索。
1、SHOCKDepartment of Surgery Ruijin Hospital,Medical College,Shanghai Jiaotong UniversitynWestern recordnviolent impact or blow,1743nphysiologic instability,1815nEastern recordn厥脱,内闭外脱I.Historical Aspect Initial records of shockInitial Explanation of shocknWesternnThomas Latta,1831nPatients with Chole
2、ranInfusion of fluids improvementHypovolemianEasternn邪毒内陷n气随血脱n阴亏气脱n气机郁闭n阴绝阳脱with the Rise of PhysiologynBurgeoning of Cardiovascular physiology in the end of 19CN,CrilenCVP dropped after hemorrhagenAnimal survival was increased after the infusion of salinenthe Use of Cardiac CatheterizationnBlood v
3、olume loss fall in Cardiac Outputwith the Combination of Physiology and BiochemistrynToxin theory of shock,Cannon&Baylissnimpairment of oxygen transportndevelopment of acidosisntoxin in severe muscle injury loss of vasomotor tone venous sequestration of blood hypotensionAntedate the Era of Critical
4、Care MedicinenExtensive physiologic research of Wigger,in early 1940snintegrating the Concepts of nimpaired oxygen deliverynoxygen debtntissue injury/death nthe concept of irreversible shocknprogressive systemic circulatory decompensationControversy on Lung&KidneynARDS nIntroduction of the flow dire
5、cted pulmonary artery catheter,in 1970n Noncardiogenic nature Not due to volume overloadnARF nMore prompt and aggressive resuscitationnIncidence ATN happens:hypoperfusionARDS happens:Defects in Cell Membrane Function and Vascular Permeability Hypovolemia/Toxin/CytokineHypoxiaARDSnA syndrome that res
6、ults from inadequate perfusion of tissues ninsufficient to meet metabolic demandnlead to cellular dysfunction,elaboration of inflammatory mediators,and celluar injuryn which may be limited,or widespreadn A continuum,ranging from subclinical deficits in perfusion to MODS or frank organ failure.nTissu
7、e hypoxia due to hypoperfusionnDefectsnInjuryII.Definition of shock A.组织低灌注所致细胞缺氧B.低血压C.酸中毒D.心功能不全E.以上都不对休克的根本问题是:nImpaired tissue perfusion nWider spectrum of shock presentations nRanging from occult tissue hypoxia to full-blown cardiovascular collapse or Multiple organ dysfunctionnImplication nala
8、rm earlierntreat earlierExplanationExplanationnTissue hypoperfusionntissue hypoxiananaerobic metabolism,acidosisninflammatory mediatersncirculatory redistributionnearly involvement of splanchnic circulationncellular injurynseptic complicationsnMODS ExplanationExplanationnO2 DebtnWhether DO2crit is i
9、ncreased in ARDS,or sepsis?nDelivery-dependent oxygen uptake=Hypoxiancause MODSnsupranormal levels supply of O2nprevent the progression of MODS?nProviding opportunity for interventionnProviding time for the disease to subsider Oxygen consumption(vO )2Oxygen delivery(DO2)O2 DebtExplanationExplanation
10、Circulatory redistributionnConceptnHomeostatic response to hypoperfusion to preserve oxygen delivery to heart and brain by selective diverting bloodnMechanismncatechols,angiotension II,Vasopressin,endothelin,TXA2 nConsequencenCellular and organ derangement MODS nBreakdown of the intestinal epithelia
11、l barriernbacterial and toxin translocation SIRSMODSExplanationExplanationnintrinsic obstruction of cap.Bednlow-flow states,hypothermia,and increased viscosityncap.Sludging:intravascular coagulation,platelet aggregation,other intraluminal debrisnpreventing RBC from reaching the tissues nextrinsic ob
12、struction of cap.Bednlocal tissue inflammation,edema,or hemorrhage,ACSnvessel wall permeability deficitThe changes in Microcirculatary LevelExplanationExplanationnHypovolemic ShocknHemorrhage-nPlasma losses-nCardiogenic ShocknIntrinsic-nExtrinsicnCompressive-nObstructive-III.Classificaion of Shock T
13、raumaGI BleedingRuptured aneurysmsBurnBowel obstructionMyocardial infarctionCardiomyopathyValvular Heart DiseaseCardiac Rhythm disturbanceMyocardial depression Tension pneumothoraxPericardial tamponadeHigh level of positive-pressure ventilationPulmonary embolismSurgical Shock 1Surgical Shock 1nNeuro
14、genic Shockne.g.nVasogenic ShocknSIRS,toxin nSeptic despite adequate fluid resucitationnTraumatic nAnaphylactic and AnaphylactoidnHypoadrenalSpinal cord injurySevere head injurySpinal cord anesthesiaSurgical Shock 2Surgical Shock 2nThe othersnThere may be a“”to be filled.n but“cellular shock”,such a
15、s poisoning,hypoxia,hypoglycemia,is not the syndrome,continuum,or tissue hypoxia due to hypoperfusion,may be excluded from the category of shock.各型休克的共同特点是:A.血压下降B.中心静脉压下降C.脉压缩小D.尿量减少E.有效循环血量锐减Secondary visceral impairement Microcirculatory changes Metabolic changesIV.Pathophysiologic staging of sho
16、ck Microcirculatory Stagingn nMicrocirculatory constrictive phasen nMicrocirculatory dilatation phasen nMicrocirculatory failure phase后微后微A微微V前括约肌前括约肌AV吻合支吻合支微微动动脉脉微微静静脉脉加重过程 只出不进/只过不进只进不出/进多出少Microcirculatory Structure Metabolic Changesnenergy metabolic abnormalityn无氧糖酵解,产能减少nmetabolic acidosisn引起微
17、血管扩张,等nbarrier function defects of membrane n累及基底膜,细胞膜,溶酶体膜 Secondary Visceral Impairmentn nHeart n nKidney n nLungn nBrainn nGastrointestinal tractn nLiverClinical Stagingn nShock compensatory stagen nnervous,restless,agitation,nervous,restless,agitation,n ncool,pale,thirsty,cool,pale,thirsty,n nta
18、chycardia,short of breathtachycardia,short of breathn nBP normal or increased,pulse pressure decreased,BP normal or increased,pulse pressure decreased,urinary output normal or decreasedurinary output normal or decreasedn nBlood loss Blood loss 20%20%,80020%20%,800800mlml 关于休克代偿期微循环改变,下列那一项是错误的:A.动静脉
- 配套讲稿:
如PPT文件的首页显示word图标,表示该PPT已包含配套word讲稿。双击word图标可打开word文档。
- 特殊限制:
部分文档作品中含有的国旗、国徽等图片,仅作为作品整体效果示例展示,禁止商用。设计者仅对作品中独创性部分享有著作权。
- 关 键 词:
- 重症 急性 胰腺炎 治疗 现状 发展
1、咨信平台为文档C2C交易模式,即用户上传的文档直接被用户下载,收益归上传人(含作者)所有;本站仅是提供信息存储空间和展示预览,仅对用户上传内容的表现方式做保护处理,对上载内容不做任何修改或编辑。所展示的作品文档包括内容和图片全部来源于网络用户和作者上传投稿,我们不确定上传用户享有完全著作权,根据《信息网络传播权保护条例》,如果侵犯了您的版权、权益或隐私,请联系我们,核实后会尽快下架及时删除,并可随时和客服了解处理情况,尊重保护知识产权我们共同努力。
2、文档的总页数、文档格式和文档大小以系统显示为准(内容中显示的页数不一定正确),网站客服只以系统显示的页数、文件格式、文档大小作为仲裁依据,平台无法对文档的真实性、完整性、权威性、准确性、专业性及其观点立场做任何保证或承诺,下载前须认真查看,确认无误后再购买,务必慎重购买;若有违法违纪将进行移交司法处理,若涉侵权平台将进行基本处罚并下架。
3、本站所有内容均由用户上传,付费前请自行鉴别,如您付费,意味着您已接受本站规则且自行承担风险,本站不进行额外附加服务,虚拟产品一经售出概不退款(未进行购买下载可退充值款),文档一经付费(服务费)、不意味着购买了该文档的版权,仅供个人/单位学习、研究之用,不得用于商业用途,未经授权,严禁复制、发行、汇编、翻译或者网络传播等,侵权必究。
4、如你看到网页展示的文档有www.zixin.com.cn水印,是因预览和防盗链等技术需要对页面进行转换压缩成图而已,我们并不对上传的文档进行任何编辑或修改,文档下载后都不会有水印标识(原文档上传前个别存留的除外),下载后原文更清晰;试题试卷类文档,如果标题没有明确说明有答案则都视为没有答案,请知晓;PPT和DOC文档可被视为“模板”,允许上传人保留章节、目录结构的情况下删减部份的内容;PDF文档不管是原文档转换或图片扫描而得,本站不作要求视为允许,下载前自行私信或留言给上传者【精***】。
5、本文档所展示的图片、画像、字体、音乐的版权可能需版权方额外授权,请谨慎使用;网站提供的党政主题相关内容(国旗、国徽、党徽--等)目的在于配合国家政策宣传,仅限个人学习分享使用,禁止用于任何广告和商用目的。
6、文档遇到问题,请及时私信或留言给本站上传会员【精***】,需本站解决可联系【 微信客服】、【 QQ客服】,若有其他问题请点击或扫码反馈【 服务填表】;文档侵犯商业秘密、侵犯著作权、侵犯人身权等,请点击“【 版权申诉】”(推荐),意见反馈和侵权处理邮箱:1219186828@qq.com;也可以拔打客服电话:4008-655-100;投诉/维权电话:4009-655-100。