Capter 12Shock分析课件

1、1chapter 12. shock2the term was originated from greece, its initial meaning was:about 200 years ago, it was used first time by a france doctor to describe a pathologic process caused by trauma a violent collision or a heavy blow； the effect of such a collision or blow 2introduction3 acute circulator

2、y failureintroduction 3 microcirculation disturbance and the effects of pro-inflammatory mediators and anti-inflammatory mediatorsreduction of ecbvinadequate perfusion of vital organscellular metabolism disturbancedysfunction of organsthe pathogenic is complex, involving: shock is a general patholog

3、ic process, charactrized by: including:4shock syndrome classic clinical presentation of shock: 5introduction peripheral vasoconstriction severely diminished co inadequate blood flow to the brain and kidneysrespiratory compensation for metabolic acidosis pale and cold clammy skin hyperventilation oli

4、guriadulled sensorium ranging from agitation to stupor or comatachycardia with a thready pulsehypotension with a narrowed pulse pressure5section 1. etiology and classification of shock6hypovolemicshock 6section 1. 1. etiology and classification of shock (1) according to causes 1) loss of blood or fl

5、uid blood loss hemorrhagic shock fluid loss dehydration shock 2) burn burn shock 3) trauma traumic shock 4) infection infectious (endotoxic, septic) shock 5) anaphylaxis anaphylactic shock 6) acute heart failure cardiogenic shock 7) strong stimulation on nerve system neurogenic shock 7 (2) according

6、 to the initial changes of shock development sufficientblood volumeheart pumpnormal functionvascular bed volumenormalvasoconstriction and vasodilation3 major determinants of effective perfusion :perfectperfusion 2section 1.any of these determinants may influence the effect perfusion 8conditions nece

7、ssary for effective perfusionshocktypeinitialchanges 3 2 1 3section 1. 3 types of shock according to different initial changes sufficient blood decreased hypovolemic volume shock adequate capacity increased vasogenic of vascular bed shock normal function disturbed cardiogenic of heart pump shock 9se

8、ction 2.stages and pathogenesis of shock10microcirculation theory 3section 2.0 1 2 3 4 5 6 7 8 9 10bpprcabfpresented by lillehei in 1964. shock is a syndrome mainly of microcirculation impairment. the sympathetic-adrenal systemis consecutive excited all time during shock development, leading to decr

9、eased tissue perfusion by vasoconstriction. 11microcirculation impairment caused by intensive excitation of sympathetic-adrenal systemblood flow rather than blood pressureintensive excitation rather than failure or numbness of sympathetic-adrenal system 3 the common pathogenic link is the pathogenic

10、 key point is the mechanism is section 2.“microcirculation theory”of12vasoconstrictionvasoconstrictionvasodilationvasodilationeffect of neuro-humoral factors on smc of microvasculature catecholamines, at-ii vasopressin, txa2, et histamine, kinins, lactic acid adenosine, pgi, tnf, no neuropeptides (e

11、ndorphin) 5section 2. 5 1microcirculation: the circulation between microartery and microvein. the basic structural and functional unit of material metabolism and exchange between blood and tissue. it is regulated by neural-humoral factors.13section 2. local feedback regulation of capillary perfusion

12、： constriction of pre-capillary decreased blood local accumulation of sphincter and post-arteriole flow of products and histamine true capillary net increased response decreased response of smc to of smc to vasoconstrictive agents vasoconstrictive agents increased blood clearance of histamine and fl

13、ow of relaxation of pre-capillary metabolic products true capillary net sphincter and post-arteriole constriction relaxation 14 shock can be divided into 3 stages: 1. ischemic anoxia phase of shock (compensatory stage of shock ) 2. stagnant anoxia phase of shock (reversible decompensatory stage) 3.

14、refractory shock stageaccording to the changes in microcirculation and take hemorrhagic shock as an example stages of shock 1. ischemic anoxia phase of shock (compensatory stage of shock ) 2. stagnant anoxia phase of shock (reversible decompensatory stage) 3. refractory shock stage 1section 2.stage

15、i 115 (1) microcirculation and tissue perfusionpre-capillary sphincterpre-capillary sphincterarteriovenous shuntture-capillaryture-capillaryarteriolevenuleischemic anoxianormalarteriovenous shunt persistent peripheral vasoconstriction pre-capillary resistance, opening of arteriovenous shunt inflow o

16、utflow blood stasis or sludge stagnant anoxiature-capillaryarteriovenous shuntpre-capillary sphinctervenulearteriole 3 1 2 4 5section 2.stage ii22 1) prolonged tissue ischemia and hypoxia acidosis decreased response of smc to catecholamine 2) local accumulation of histamine, adenosine, k+, kinin atp

17、 k+ canal open k+ outflow ca + inflow 3) enteral endotoxin enter into blood activating macrophage tnf, no vasodilation(2) mechanism for stasis of microcirculation 1 2 3section 2.stage ii1)2)3)23 4) changes of hemorheology blood concentrated, blood viscosity, rbc and platelet aggregation blood flow s

18、low down wbc rolling, adhesion and activation releasing oxygen free radical and lysosome enzymes ec injury microcirculation impairment tissue injury 1 1section 2.stage ii24(3) formation of vicious cycle 1 2 3 4 5section 2.stage ii continuously ischemia and hypoxia capillary dilation, permeability, p

19、lasma leaking out changes of hemorheology sludging of blood, blood flow stasis blood pools in the capillary bed decreased peripheral resistance b.p sympathetic exciting 25 (4) clinical manifestations blood stasis in kidney renal blood flow blood stasis in oliguria (400ml/d) microcirculation cardiac

20、output or anuria (100ml/d) b.p. brain ischemia dull or coma blood stasis in skin cyanosis, clamminess, maculation41234section 2.stage ii26 1. ischemic anoxia phase of shock (compensatory stage of shock ) 2. stagnant anoxia phase of shock (reversible decompensatory stage) 3. refractory shock stagesta

21、ges of shock 1. ischemic anoxia phase of shock (compensatory stage of shock ) 2. stagnant anoxia phase of shock (reversible decompensatory stage) 3. refractory shock stagesection 2.stage iii27 this stage is also called microcirculatory failure stage as the responsibility of smc to any vasoactive dru

22、gs is lost. pre-capillary sphincterarteriovenous shuntture-capillaryvenulearteriolesection 2.stage iiidic formation28section 2.stage iii(1) disseminated intravascular coagulation formationthe mechanisms of dic in this stage: 1) blood concentrated, fibrinogen, rbc and platelet aggregation, blood visc

23、osity blood flow slow down 2) severe acidosis vascular ecs injury. 3) septic shock: bacteria and toxin mono/macrophage secreting cytokines monocyte and endothelium releasing tissue factor 4) traumatic shock: tissue factor release initiating the extrinsic clotting pathway 5) hetero-type blood transfu

24、sion hemolysis erythrocytin release 529 the consequences of dic:1) the microcirculation pathway completely blocked by microthrombi blood return to heart reduced sharply2) fibrinopeptide, fibrin degradation product (fdp) and complementvascular permeability aggravating microcirculation impairment3) bl

25、eeding ecbv further decreased.4) embolism and infarction of organs aggravating acute organ failure section 2.stage iii430(msod or msof)section 2.stage iii(2) multiple system organ dysfunction (msod) or failure (msof) prolonged and severe various humoral factors ischemia and hypoxia, ( lysosome enzym

26、es, acidosis active oxygen and cytokines) important vital organs “irreversible” injury it is suggested the development of refractory shock stage might be related to systemic inflammatory response syndrome (sirs) and compensatory anti-inflammatory response syndrome (cars).22131section 3.alteration of

27、 cell metabolismand multiple organ dysfunction32 in the microcirculation impairment theory, impairment of cell metabolism is thought to be secondly to the microcirculation impairment and is caused by hypoxia and acidosis. however, several facts was found recently, which suggest the primary cause of

28、shock may also damage cells directly. afterwards, the understanding for shock has been involved to the cellular and molecular levels.section 3.33 1. impairment of cell metabolism (1) oxygen deficiency and glycolysis enhancement atp, lactic acid (2) energy deficient, sodium pump dysfunction and na+,

29、h2o inflow cellular edema, hyperkalemia (3) lactic acid and co2 local acidosissection 3.334(1) cell injury 1) cell membrane damage2) mitochondria damage3) lysosome damage 2. cell injury and apoptosissection 3.4cell edema, tmp35(1) cell injury 1) cell membrane damage2) mitochondria damage3) lysosome

30、damage swelling, dysfunction of oxidation and phospholyration2. cell injury and apoptosissection 3.36 cell necrosis lysosome enzyme activate kinin system release generate toxic polypeptide (mdf) release histamine2. cell injury and apoptosis(1) cell injury 1) cell membrane damage2) mitochondria damag

31、e3) lysosome damage section 3.237section 3.secrete or release attack 3213(2) cell apoptosis the activated inflammatory cells cytokines, inflammatory mediators and oxygen free radicals vascular endotheliums,pmns, mono/ macrophages, lymphocytes and parenchymal cells of various organs. denaturing , apo

32、ptosis or necrosis383. multiple organ dysfunction syndromemods: more than 2 organs dysfunction occur successively in patients without pre-exit organ dysfunction(1) causes and category 1) causes infectious causes (severe infection in abdominal cavity, bile duct) non-infectious cause (severe trauma, o

33、peration, shock, i-r injury)2) clinical types rapid single-phase (directly caused by injurious factors) 13 weeks delayed two-phase (first hit second hit)section 3.mods39section 3.1mods1 (2) common mods 1) pulmonary dysfunction (83%100%) acute lung injury (ali) acute respiratory distress syndrome (ar

34、ds) clinical manifestation: acute respiratory failure characterized by progressive dyspnea, hypoxia, cyanosis, pulmonary edema, decreased pulmonary compliance.40section 3.4mods1234 pathogenesis: activated pmncytokinesmfinflammatory cascade, ofr pulmonary stasis, edema, bleeding diffusion ec injury t

35、ransparent disorder membrane formation pulmonary microcirculation embolism or thrombosis ventilation dysfunction in micro circulation /perfusion local atelectasis mismatching41section 3.4mods1234clinical manifestation: jaundice occurred in 5 days, bilirubin. 2) hepatic dysfunction (95%) bacteria and

36、 toxin from intestine kupffers cells activated hepatic il8 pmn attracted and adhesion cells tnf, il-1, ofr injury xanthine oxydase (rich in liver)ofr 42section 3.mods3) renal dysfunction acute renal failure (shock kidney) sympathetic, ang ii renal vasoconstriction, rbf functional renal failure ald,

37、adh (early stage) tubular reabsorption of h2o and na+ persistent ischemia, toxin, ofr, microthrombosis acute tubular necrosis parenchynal renal failure (atn) (persistent shock) 412343 4) gastrointestinal dysfunction mucosa edema, stress ulcer, intestinal ischemia necrosis, bleeding 5) cardial dysfun

38、ction heart dysfunction may occur at late stage. 6) others immune inhibition, coagulation dysfunction, cns dysfunction section 3.mods444. systemic inflammatory response syndrome sirs is defined as auto-magnified and destroyed inflammation, characterized by disseminated activation of inflammatory cel

39、ls and inflammatory mediator spillover. section 3.(sirs)2 (1) causes 1) severe infection (septicemia) 2) non- infectious hit (necrosis, ischemia, trauma, burn)45 (2) pathogenesis 1) activation and diffusion of inflammatory cells mf, pmn, ec and platelet 2) proinflammatory mediators spillover tnf, il

40、s(1,2,6,8), ifn, ltb4, paf, txa2, am, tf, 3) compensatory anti-inflammatory response syndrome (cars) stnfr, il-1ra, il-4, il-10, il-13, pge2, pgi2, section 3.(sirs)3shock & multiple organ dysfunctionimmune inhibition12346 pathophysiologic basis of shock prevention and treatmentsection 4.471. eti

41、ological prevention and treatment 2. pathogenetic treatment (1) correction of acidosis. (2) expansion of blood volume (3) application of vasoactive drugs reasonably (4) treatment of cell damage (5) application of proinflammatory mediator antagonists. (6) prevention of organ function failure section

42、4.48summarynshock is a dangerous general pathogenic process caused by various drastic etiological factors, characterized by acute circulatory failure including microcirculation impairment, inadequate perfusion of vital organs, cellular metabolism impediment and dysfunction of organs. n microcirculation impairment caused by intensive excitation of sympathetic-adrenal system is the common pathogenic link of shock. naccording to the different changes of microcirculation, shock can divided into 3 stages: ischemic