1、shock休克英文專題知識(shí)講座shock休克英文專題知識(shí)講座第1頁Whats shock？sick or unconsciousness？Introductionshock休克英文專題知識(shí)講座第2頁 hypotension？Introductionshock休克英文專題知識(shí)講座第3頁vasoconstrictive treatment vasodilative treatmentIntroductionshock休克英文專題知識(shí)講座第4頁 Lartin General Critical Reaction: strike and vibration 1731, Henri Francois Le

2、 Dran apply to medicine for the first timeI. Concept of Shockshock休克英文專題知識(shí)講座第5頁pale face cyanosis cold and clammy limbsoliguriafaint consciousnesshypotension1.Description of symptoms & signs“shock syndrome”I. Concept of Shockshock休克英文專題知識(shí)講座第6頁“sympathetic failure theory”sympathetic failure Bp shock2

3、.Acute circulatory disorderI. Concept of Shockshock休克英文專題知識(shí)講座第7頁blood volume ECBV（effective circulating blood volume） microcirculation disturbancessympathetic activation3.Microcirculation theoryI. Concept of Shockshock休克英文專題知識(shí)講座第8頁systemic inflammatory response syndrome, SIRS全身炎癥反應(yīng)綜合征pro-inflammator

4、y & anti-inflammatory factors4.Cellular and molecular levelI. Concept of Shockshock休克英文專題知識(shí)講座第9頁 Regardless of causes, shock is defined as a clinical condition and pathophysiologic process characterized by microcirculation dysfunction( inadequate blood flow vital organs, and inability of cell to met

5、abolize normally). causes acute circulatory failure microcirculation disturbance ECBV(effective circulatory blood volume) “l(fā)ow flow state” in vital organs abnormal cellular metabolism and function, tissue injury, dysfunction of vital organs shock I. Concept of Shockshock休克英文專題知識(shí)講座第10頁1.Loss of blood

6、 or fluid: Blood loss: peptic ulcer, varices due to portal hypertension Fluid loss: severe vomiting, diarrhea, intestinal obstruction (collapse)2.Burn: early stage: loss of body fluid, pain later stage: loss of body fluid, infection 3.Trauma: hemorrhage, severe pain4.Infection: G- infection release

7、of endotoxins sepsisII. Etiology of Shockshock休克英文專題知識(shí)講座第11頁5.Anaphylaxis: allergen combination of IgE and mast cellsrelease of histamine and bradykinin vasodilation and capillary permeabilityperipheral resistanceblood flow back to the heartcardiac outputBp, plasma exosmosisallergenII. Etiology of S

8、hockshock休克英文專題知識(shí)講座第12頁 6.Strong stimulation on nerve system: brain injury, the depressant action of drugs, general anesthesia, hypoxia, or lack of glucose, spinal anesthesia or spinal cord injury decreased sympathetic control 7.Heart & large blood vessels diseases: acute massive myocardial infarcti

9、on, acute myocarditis, perimyocarditis, cardiac tamponade, serious arrhythmias, myocardial diseases, cardiovalvular problems, etc. pumping function of the heart is impaired “cardiogenic shock”coronary artery disease, pulmonary embolism, etc. “extracardiac obstructive shock” II. Etiology of Shockshoc

10、k休克英文專題知識(shí)講座第13頁According to Etiology: 1、Hemorrhagic Shock 2、Dehydration Shock 3、Traumatic Shock 4、Burn Shock 5、Infectious Shock: endotoxic, septic 6、Cardiogenic Shock 7 、Extracardiac Obstructive Shock 8 、Anaphylactic Shock 9 、Neurogenic ShockIII. Classification of Shockshock休克英文專題知識(shí)講座第14頁 blood volu

11、me cardiac output blood vessels capacity According to the pathogenesis of shock :III. Classification of Shockmarked vasodilation “Hypovolemic Shock” “Cardiogenic Shock”“Vasogenic Shock”shock休克英文專題知識(shí)講座第15頁Conditions necessary for effective perfusionInitial event Shock type Clinical examplesSufficient

12、 blood volume Decreased Hypovolemic Hemorrhage shock Surgery Burns or trauma Vomiting or diarrheaAdequate capacity Increased Vasogenic Anaphylaxisof vascular bed shock Sepsis Normal function Impaired Cardiogenic Myocardial infarctionof heart pump shock Congestive heart Arrhythmiasshock休克英文專題知識(shí)講座第16頁

13、According to the Hemodynamicshyperdynamic shock(高排低阻型休克)cardiac outputperipheral resistance “warm shock”hypodynamic shock(低排高阻型休克)cardiac output peripheral resistance “cold shock”低排低阻型休克cardiac output peripheral resistance “decompensatory”III. Classification of Shockshock休克英文專題知識(shí)講座第17頁Microcirculati

14、on(MC): The capillaries, venules, and metarterioles of the circulatory system are collectively referred to as the microcirculation. 1.Function of microcirculation: It is here that exchange of gases, nutrients, and metabolites move between the tissues and the circulating blood. transport of nutrients

15、 to the tissues and removal of cellular excretaIV. Pathogenesis and Mechanisms of Shockshock休克英文專題知識(shí)講座第18頁微動(dòng)脈Arteriole 后微動(dòng)脈Metarteriole 毛細(xì)血管前括約肌Precapillary Sphincters 真毛細(xì)血管True capillary 通血毛細(xì)血管（直捷通路） Preferential channels 微靜脈Venule 動(dòng)靜脈短路Arteriovenous anastomosis后微動(dòng)脈2.Structure of microcirculation:I

16、V. Pathogenesis and Mechanisms of Shockshock休克英文專題知識(shí)講座第19頁 Arteriole Metarteriole Arteriovenous anastomosisPrecapillary Sphincters True capillaryPreferential channels VenuleIV. Pathogenesis and Mechanisms of Shock(1)precapillary & postcapillary vessels (resistance)(2)true capillary: extremely thin s

17、tructures with tubular walls of single-layer, highly permeable endothelial cells(3)three channels for blood flowshock休克英文專題知識(shí)講座第20頁 直捷通路（） thoroughfare channel 動(dòng)靜脈短路（） arteriovenous shunt 迂回通路 (營養(yǎng)通路) nutrient flow后微動(dòng)脈shock休克英文專題知識(shí)講座第21頁 “microcirculation disturbance” IV. Pathogenesis and Mechanisms

18、of Shockcompensatory stageprogressive stagerefractory stageshock休克英文專題知識(shí)講座第22頁Stage I: compensatory stageMicrocirculation changes2. Mechanism 3. Effects on body4. Main clinical manifestations .Treatment principleIV. Pathogenesis and Mechanisms of Shockshock休克英文專題知識(shí)講座第23頁Alterations of Microcirculati

19、on and Tissue Perfusion:Stage I: compensatory stageshock休克英文專題知識(shí)講座第24頁vasoconstriction arteriolar and pre-capillary sphincter constrictionpre- capillary resistance low perfusion postcapillary resistancelow flow arteriovenous shunt openingtissue perfusion tissue ischemia and hypoxia*degree of vasocon

20、striction is differentStage I: compensatory stage: “ischemic hypoxia stage”shock休克英文專題知識(shí)講座第25頁Mechanisms of Microcirculation Disturbance:vasoconstrictionarteriovenous shunt openingcauses(hemorrhage,etc)-receptor: skin, skeletal m., kidneys, abdominal organsrelease of catecholamine-receptor: arteriov

21、enous shuntSAMS(+) (sympathetic-adrenal-medulla system)“initial link”“result”Stage I: compensatory stageshock休克英文專題知識(shí)講座第26頁Stage I: compensatory stageMechanisms of Microcirculation Disturbance:ischemia & hypoxia in pancreas MDF (myocardial depressant factor,心肌抑制因子) vasoconstrictionPGI2 ischemia & hy

22、poxiaendothelial cells injuryRAAS(+)AngII renal blood volumecatecholamineTXA2plateletET endothelial cellsvaso-pressinshock休克英文專題知識(shí)講座第27頁 (2) several humoral factors: catecholamine, AngII (angiotensin II), vasopressin, TXA2, ET(endothelin) ,etc. Stage I: compensatory stageMechanisms of Microcirculati

23、on Disturbance: (3) production of PGI2 (1) activation of SAMS: vasoconstriction (4) production of MDF A summary for mechanism of stage I of shock:shock休克英文專題知識(shí)講座第28頁 (1) self-blood transfusion: 肝脾儲(chǔ)血庫、靜脈收縮、動(dòng)靜脈短路開放 “first defense line” venous constriction blood return to the heart cardiac output aldos

24、terone(ADS) & vasopressin(ADH) (2) self-fluid infusion: “second defense line” precapillary resistance postcapillary resistance capillary pressure fluid transfer from interstitial fluid to circulation (3) blood redistribution: -adrenoceptor:brain, coronary A. -adrenoceptor:skin, skeletal m., kidneys,

25、 abdominal organs (4) activation of SAMS: catecholamine myocardial contractilityStage I: compensatory stageEffects on Body:shock休克英文專題知識(shí)講座第29頁Stage I: compensatory stageMain Clinical Manifestations:pale facecool and clammy limbs96/minoliguriaconsciousness but restless105/85mmHgBp?shock休克英文專題知識(shí)講座第30頁

26、 “reversible compensatory stage” eliminating pathogenic factors & restoring blood volume and tissue perfusion 盡早消除休克動(dòng)因，補(bǔ)充血容量，預(yù)防向休克期發(fā)展。Stage I: compensatory stageTreatment Principle:shock休克英文專題知識(shí)講座第31頁Stage II: progressive stageMicrocirculation changes2. Mechanism 3. Effects on body4. Main clinical m

27、anifestations .Treatment principleIV. Pathogenesis and Mechanisms of Shockshock休克英文專題知識(shí)講座第32頁Alterations of Microcirculation and Tissue Perfusion:Stage II: progressive stageshock休克英文專題知識(shí)講座第33頁Stage II: progressive stage: “stagnant hypoxia stage”precapillary resistancehigh perfusionpostcapillary resi

28、stancelow flow tissue congestion and hypoxiashock休克英文專題知識(shí)講座第34頁1.Acidosis:anaerobic glycolysisproduction of lactic acidmetabolic acidosisresponse of arteriole and metarteriole to catecholamine vasodilationStage II: progressive stageMechanisms of Microcirculation Disturbance:2.Local accumulation of m

29、etabolic products: histamine, adenosine, Kinin3.Endotoxin: myocardial contractility activate mononuclear cells production of IL-1, TNF, and NO vasodilation, Bp5. Alteration of hemorheology: RBC aggregation and adhesion, WBC rolling and block, platelet aggregation and adhesion blood concentration & i

30、ncreased blood viscosity 4.Effects of humoral factors: endorphin(內(nèi)啡肽)vasomotor center(-)vasodilationshock休克英文專題知識(shí)講座第35頁WBC penetrate capillaryshock休克英文專題知識(shí)講座第36頁 Blockage of WBCshock休克英文專題知識(shí)講座第37頁白細(xì)胞附壁、滾動(dòng)、嵌塞shock休克英文專題知識(shí)講座第38頁組織間膠體venous stasisvasodilationcap permeability“self-blood transfusion” sto

31、pblood vessels capacityblood returnStage II: progressive stage (decompensated stage)Decompensated changes:self-blood transfusion and self-fluid infusion stopcap static pressureplasma exudation“self-fluid transfusion” stopshock休克英文專題知識(shí)講座第39頁 formation of vicious cyclecap static pressurecap permeabili

32、typlasma exudationblood concentration RBC aggregationmicrocirculation stasisvasodilationblood stasis,blood returnC.O.,Bp,sympathetic N.(+)tissue perfusionischemia,hypoxia,acidosisStage II: progressive stage (decompensated stage)Decompensated changes:shock休克英文專題知識(shí)講座第40頁Heart heart failureKidneysoligu

33、ra or anuriaSkincyanosisBpBrain dull or coma80/50mmHgStage II: progressive stageMain Clinical Manifestations:shock休克英文專題知識(shí)講座第41頁Stage III: refractory stageMicrocirculation changes and mechanism2. Effects on body3. Mechanism of refractory shockIV. Pathogenesis and Mechanisms of Shockshock休克英文專題知識(shí)講座第4

34、2頁Alterations of Microcirculation and Tissue Perfusion and its Mechanism:Stage III: refractory stageshock休克英文專題知識(shí)講座第43頁Stage III: refractory stage: “microcirculation failure stage”后微動(dòng)脈no any response to vasoactive drugs: blood flow stop no perfusion and no flowshock休克英文專題知識(shí)講座第44頁血細(xì)胞聚集成團(tuán)塊，似淤泥狀，在血管內(nèi)擺動(dòng)

35、shock休克英文專題知識(shí)講座第45頁Stage III: refractory stage DIC (disseminated intravascular coagulation) （1） alteration of hemorheology: blood stasis, concentration, viscosity, blood cells aggregation “hypercoagulable state”（2）acidosis（3）impairment of mono-macrophages system（4）imbalance of TXA2 and PGI2shock休克英文

36、專題知識(shí)講座第46頁 (3) MODS (multiple organs dysfunction syndrome, 多器官功效障礙) “circulatory failure” (1) DIC shock(2) capillary no-reflow phenomenon(無復(fù)流現(xiàn)象) (4) SIRS（systemic inflammatory response syndrome,全身炎癥反應(yīng)綜合征）Effects on Body:Stage III: refractory stageshock休克英文專題知識(shí)講座第47頁毛細(xì)血管無復(fù)流現(xiàn)象(capillary no-reflow phen

37、omenon)Concept: large amount of blood transfusion and fluid infusion Bp but capillary blood flow has no recovery 休克晚期即使大量輸血補(bǔ)液，血壓回升，有時(shí)仍不能恢復(fù)毛細(xì)血管血流，稱為無復(fù)流現(xiàn)象。Mechanism： （1） WBC adhesion and aggregation （2）capillary endothelial cells swelling （3）formation of extensive microthrombiblockage of capillariessh

38、ock休克英文專題知識(shí)講座第48頁SIRS (systmic inflammatory response syndrome，全身炎癥反應(yīng)綜合征) Concept：SIRS is a hard-controlling systemic inflammatory cascade caused by infectious or non-infectious factors. 因感染或非感染原因作用于機(jī)體而引發(fā)一個(gè)全身性炎癥反應(yīng)臨床綜合征。機(jī)體失控自我連續(xù)放大和自我破壞炎癥。 Mechanisms of SIRS in shock: severe ischemia, hypoxia of intest

39、inal tractimmunity and barrier function entergenic bacterial and endotoxins enter blood flowact on mono-macrophages systemSIRSStage III: refractory stageMechanism of refractory shock: DIC, SIRSshock休克英文專題知識(shí)講座第49頁后微動(dòng)脈后微動(dòng)脈后微動(dòng)脈后微動(dòng)脈ABCDshock休克英文專題知識(shí)講座第50頁Summary for the Mechanism of Shockneural-humeralc

40、ellularmicrocirculationtheorySAMS(+) microcirculation disturbances cell injuries, organ dysfunction “concept”Pro-inflammatory & anti-inflammatory factors imbalance “SIRS” causes cell injuries (structure, metabolism & function changes) “cellular level”shock休克英文專題知識(shí)講座第51頁 Neural-humeral mechanism:SAMS

41、Hypothalamus-pituitary-adrenocortical system(下丘腦-垂體-腎上腺皮質(zhì)系統(tǒng))RAASshock休克英文專題知識(shí)講座第52頁endothelin（ ET ，內(nèi)皮素 ） vasoconstrictors catecholamine (CA)include：epinephrine (EP) and norepinephrine (NE) angiotensin （Ang ，血管擔(dān)心素） vasopressin（ADH，血管升壓素） TXA2（thromboxane,血栓素A2） Neural-humeral mechanism:shock休克英文專題知識(shí)講

42、座第53頁CGRP （calcitonin gene-related peptide,降鈣素基 因相關(guān)肽）atrial natriuretic peptide （ANP ,心房鈉尿肽）endogenous opioid peptide （內(nèi)源性阿片肽）kinin NO vasodilators histamine-endorphin vasoactive intestinal peptide（VIP,血管活性腸肽）early: improve ischemia；myocardial contractility; C.O.later: hypotension; I-RI.7 Neural-hum

43、eral mechanism:shock休克英文專題知識(shí)講座第54頁Cell injury: Cellular and molecular mechanism:shock休克英文專題知識(shí)講座第55頁glycolysisATPlactic acid impaired Na+-K+ pump cell edemahyperkalemiametabolic acidosishypoxiaMit injuryATPlysosome injuryprotease releaseCell injury: Cellular and molecular mechanism:shock休克英文專題知識(shí)講座第56

44、頁Metabolism disturbances: Cellular and molecular mechanism:causeschangesresultATP，Na pump impairedNa and water inflowcell edemaATP，Na pump impairedextracellular K+hyperkalemiaanaerobic glycolysislactic acid metabolic acidosisearly: ventilation PaCO2 respiratory alkalosislater: shock lungventilation

45、respiratory acidosisshock休克英文專題知識(shí)講座第57頁V. Organ Dysfunctionshock休克英文專題知識(shí)講座第58頁1.Causes: renal perfusion endoxinsrenal damage2.Main clinical manifestations: oliguria, metabolic acidosis, hyperkalemia, azotemia(I) Effects on Kidneys: “shock kidney”休克時(shí)最易損害臟器之一renal perfusionGFRoliguriaAcute functional

46、renal failure early stage:shock休克英文專題知識(shí)講座第59頁 later stage:Acute parenchymal renal failurepersistent renal ischemia and thrombosisoliguriaanuriaacute renal tubular necrosisshock休克英文專題知識(shí)講座第60頁 renal tubular dilation upper: microthrombi lower: macrophagesshock休克英文專題知識(shí)講座第61頁(II) Effects on Lungs: “shock

47、 lung” 1. pulmonary edema: histamine, kinin, adenosine, etc capillary permeability vasodilation fluid transude from capillaries to tissue 2. pulmonary atelectasis: pulmonary perfusion production of surfactant(DPL) by type II alveolar cell alveolar collapse 3. pulmonary hemorrhage: DIC continuous ble

48、eding 4. alveolar hyaline membrane formation: capillary permeability plasma proteins deposit in alveolar cavityALI （acute lung injury） ARDS（acute respiratory distress syndrome）shock休克英文專題知識(shí)講座第62頁lung edemashock休克英文專題知識(shí)講座第63頁 vasodilation upper: normal lung tissue lower: lung edemashock休克英文專題知識(shí)講座第64頁

49、diffused lung edema shock休克英文專題知識(shí)講座第65頁alveolar hyaline membraneshock休克英文專題知識(shí)講座第66頁1. coronary blood volume:SAMS(+) HR, myocardial contractility oxygen consumption deterioration of myocardial hypoxia 2. water, electrolytes and acid-base disturbance: hyperkalemia, acidosis HR, myocardial contractilit

50、y 3. production of MDF: ischemic pancreas production of MDF myocardial contractility 4. myocardial DIC myocardial contractility 5. endotoxins damage myocardium 6. ATP myocardial contractility(III) Effects on Heart:shock休克英文專題知識(shí)講座第67頁hypoxia, acidosis ATP impaired Na+-K+ pump cytotoxic brain edema ly

51、sosome injury brain cell injury activation of complement (C3a,C5a) histamine, bradykinin capillary permeability vasogenic brain edema(IV) Effects on Brain:shock休克英文專題知識(shí)講座第68頁(V) Effects on Digestive System: enterogenous endotoxemia （腸源性內(nèi)毒素血癥)ischemiastasisbarrier functionendotoxin enter bloodstress

52、ulcerjaundice & hepatic encephalopathyshock休克英文專題知識(shí)講座第69頁 Definition: Dysfunctions of more than two organs occur successively in patients without pre-exist organ dysfunction defined as MODS.(VI) MODS(multiple organ dysfunction syndrome,多器官功效障礙綜合征): MSOF ( Multiple System Organ Failure,多系統(tǒng)器官衰竭 )high

53、incidence； great expense； high mortality shock休克英文專題知識(shí)講座第70頁 Causes:1.infectious causes: 70 septicemia 2.non-infectious causes: big operation severe traumashock休克英文專題知識(shí)講座第71頁causesincidencesevere traumaabout 10%after big operation8%22%massive burnabout 30%septicemia30%50%shock休克英文專題知識(shí)講座第72頁organs fa

54、iluremortality115%30%245% 55%380%4100%shock休克英文專題知識(shí)講座第73頁 Clinical classification: 1.速發(fā)單相型 (immediate monophase MODS, rapid single-phase type)2.遲發(fā)雙相型 (delayed dual phase MODS, delayed two-phases type)shock休克英文專題知識(shí)講座第74頁 速發(fā)單相型(rapid single-phase) “原發(fā)型（primary type）”“一次打擊型（one hit type）” caused by sho

55、ck,trauma,etc directly由損傷因子直接引發(fā) organs injury occur at the same time or simultaneously 器官損害同時(shí)或者相繼 develop rapidly, only one phase, only one peak病情發(fā)展快，只有一個(gè)時(shí)相，損傷只有一個(gè)高峰 This kind of MODS often takes place rapidly after the occurrence of shock and trauma. This kind of MODS is only one phase, i.e., there

56、 is only one peak of organ failure during the pathological processes.shock休克英文專題知識(shí)講座第75頁 遲發(fā)雙相型(delayed two-phase) “繼發(fā)型（secondary type）”“二次打擊型（double hit type）” remssion after the first hit 第一次打擊后出現(xiàn)一個(gè)緩解期 second hit 其后13周又受到第二次打擊發(fā)生MODS dual-phase, two peaks病情發(fā)展呈雙相，出現(xiàn)兩個(gè)損傷高峰 The first peak of organ fail

57、ure of patients with trauma, shock or hemorrhage usually appears in a short time. If the condition of those patients could not be effectively controlled, a second organ failure peak will appear in 3 to 5 days due to a rapidly happened septicemia. The course of the MODS described above shows a dual-phase progression with two peaks of organ failures. shock休克英文專題知識(shí)講座第76頁(I) Treatment of primary diseases (II) Symptomatic treatment: “improve microcirculation