課件春5-shock克氏外科學(xué)

1、SHOCKShen HongZhejiang University School of Medicine. Historical AspectsThe concept of shock has evolved over the centuries from the earliest description in antiquity of traumatic wounds and hemorrhage.Hippocratic facies (460380 B.C.): tourniguet. BloodlettingGalen (A.D. 130200): erroneous knowledge

2、 of anatomy. Ligation of bleeding vesselsVesalius. William Harvey (16 centuries): anatomy and circulation of the cardiovascular systemA French military surgeon: the use of simple bandagesThomas Latta: in 1831. infusion of intravenous fluids into hypo-volemic patients inflicted with cholera caused cl

3、inical improvent. Pathogenesis: a. vasomotor exhaustion: neurogenic theory b. traumatic toxemia: cannon. Bay(World War I) c. hypovolemia: Keith, Blalock(experiments on dogs) d. fat embolism; e. acidosis f. adrenal dysfunction Pathogenesis:resuscitation, individual argan dysfunction, cellular derange

4、ments(Korean, Vietnam conflict). Shock lung. ARDS molecular biology, inflammatory mediator, metabolic support, oxygen delivery, organ ischemia, sepsis.II. Definition of shockA syndrome results from inadequate perfusion of tissues alterations in cellular metabolism, cellular dysfunction and cellular

5、injury, MODS due to tissue hyperfusion, hypoxia.Oxygen delivery; oxygen debt; oxygen demand exceeds the oxygen supply.III. Cause, classification of shock1. hypovolemic shock1) hemorrhagic losses: trauma, gastrointestinal bleeding ruptured aneurysm.2) plasma volume losses: extravascular fluid sequest

6、ration, pancreatitis, burns, bowel obstruction.2. cardiogenic shockdinminished cardiac outputintrinsic causeextrinsic causemyocardial infarctioncardiac rhythm disturbances.Tension pneumothoraxpericardial tamponade3. neurogenic shockfailure of the sympathetic nervous system to maintain normal vascula

7、r tone.Spinal cord injury, severe head injury. Spinal anesthesia4. vasogenicendogenous or exogenous vaso-active mediatorssystemic inflammatory response syndrome(SIRS)sepsis (infectious)noninfectiousAnaphylacticHypoadrenaltraumaticIV. Pathophysiology of shockImpaired tissue perfusionTissue hypoxiaAna

8、erobicmetabolismAcidosisCellular dysfunctionSIRS / SepsisMultiple organ dysfunction syndromeInflammatoryMediatorsCirculatoryredistributionIschemia/ReperfusionPathophysiology:Role of hypoxiaAnaerobic metabolism and acidosisHyperlactatemiaCirculatory redistributionImpairment of gut perfusionAnaerobic

9、metabolism and acidosisGlucoseGlycogenlactatePyruvateAcetyl CoACitricAcidcyclemitochondriacytosolAerobicglycolysisAnaerobicglycolysisCirculatory redistributionVaso-constrictive factors:Catechol, angiotensin II, vasopressin, endothelin, thromboxan A2Vaso-dilatory:Nitric oxide, prostaglandin E2, prost

10、acyclin, interleukin-2, bradykinin.Impairment of gut perfusion:Subsequent bacterial or toxin translocationSystemic inflammatory response, MODSI. baroreceptors Vasomotor center(medulla)Sympathetic neural outputIncreased systemic vascular resistanceIncreased venous return to the heartArteriolar vasoco

11、nstriction(cutaneous tissue. Skeletal muscle. Renal and splanchnic vascular beds)II. adrenal medullary output tachycardia, enhanced cardiac contractilityIII. Antidiuretic hormone(posterior pituitary)VasoconstrictionWater reabsorption in the distal tubule of the kidneyIV. rennin(kidney)Angiotensin I

12、(liver)Angiotensin II (lungs)vasoconstrictoraldosterone(adrenal cortex) reabsorption of sodiumV. microcirculatory autoregulationMediator of shock and sepsisEndotoxinComplement fragmentsEicosanoidsLeukotrienes, Prostaglandins, ThrobomxanesCytokines:Interleukins(IL1, IL2, IL6); TNF-a; CSF, GCSF,GM-CSF

13、; IFN-rNeuroendocrine mediators: catechols, cortisol, glucagonsV. diagosis and management of shock: General approachKeep SaO2 90% Optimize cardiac index Optimize Hbsupply supplemental O2 mechanical ventilation, if necessaryMay need early hemodynamic monitoring11-13g/dlAssess volume status(preload)PC

14、WP15 consider volume if PCWP18Reassess to keep:PCWP 15-18 mmHgMAP 60-80 mmHgSvO2 65-70% Delivery independent O2 consumptionGoals metGoals not metTreat inciting cause of shock control inflammatory response nutritional supportInotropic support (b agonism)Dobutamine DopamineEpinephrine注：此圖表太大，一個幻燈頁面不能全

15、部顯示Consider vasodilatorsNitroglyceninNitroprussideConsider a agonistNorepinephrineEpinephrineNeosynephrinePlusDopamineGoals metGoals not metReassessTreat inciting cause of shock control inflammatory response nutritional support注：此圖表太大，一個幻燈頁面不能全部顯示SPECIFIC SHOCK SYNDROMESClinical signs and symptoms o

16、f hemorrhagic shock based on severity of blood loss Percent loss of circulating bloodvolume(volume loss for 70kg male)Pulse rateSystolic pressurePulse pressureCapillary refillRespirationsCentral nervous systemUrine output15%(40%(2000ml)normal100120140nonpalpablenormalnormalweak decreasedmarked decre

17、asednormaldecreaseddecreasedmarkeddecreasednormaldelayeddelayedabsentNormalMild tachypneaMarked tachypneaMarked tachypneanormalanxiousconfusedlathargicnormal20-30ml/hr20ml/hrnegligible注：此圖表太大，一個幻燈頁面不能全部顯示Traumatic shockHypovolemic shock with1. larger volume losses2. greater fluid sequestration in th

18、e extravascular compartments3. more intense activation of inflammatory mediators development of SIRS4. microcirculatory derangements5. MODS frequently occurTraumatic shock treatment1. excessive fluid requirements2. mechanical ventilation3. pulmonary artery catheter monitoring4. cardiovascular suppor

19、tShock Associated with SIRS, Sepsis, and MODSSIRS: two or more of following1. temperature greater than 38 or less than 362. heart rate greater than 90 beats per minute3. respiratory rate greater than 20 breaths per minute or PaCO2 less than 32mmHg4. white blood cell count greater than 12,000 per cu

20、mm, less than 4000 per cu mm or greater than 10% band formsVII. Diagnosis of hypovolemic shock1. clinical history; 2. physical findings; 3. blood tests. 4. characteristic hemodynamics1. low right and left sided filling pressures(low central venous pressure, low PCWP)2. decreased cardiac output, decr

21、eased SvO23. increased systemic vascular resistanceVIII. TreatmentPatients airway; adequate ventilation, oxygenationFluid replacement isotonic electrolyte solutionsCrystalloid - Ringers lactate solutionBlood transfusion - type-specific type O packed red blood cellsGuide treatmentIf absent monitor th

22、e central venous pressurePlace a pulmonary artery catheterThen: urinary output rate of 0.5 to 1.0 ml/kg/hourThe pneumatic anti-shock garmentColloid solution; hyper-tonic saline(controversy)SEPSISSepsis: the presence of SIRS in association with culture-proven infectionSeptic shock: sepsis with hypote

23、nsion despite adequate fluid resuscitation, along with the presence of manifestations of hypoperfusion, including, but not limited to, lactic acidosis, oliguria, or an acute alteration in mental status.Mutiple organ dysfunction syndrome (MODS): the presence of altered organ function in an acutely il

24、l patient such that homeostasis cannot be maintained without intervention.Mortality rate 26% SIRSSepsisMortality rate: 7%16%4%SepsisSeptic shock Mortality rate: 7%46%MODS mortality range from 20% to 100% depending on the number of failed organs severity of illness scoring systemsMODSPrimary MODSIsch

25、emicReperfussiondirect insultSecondary MODS(two-hit model)exaggerated uncontrolled systemicinflammatory responseclinical features:fever, tachycardia, hypotension, oliguria (obtundation, coma)altered mental status. Leukocytosis or leukopenia increased or decreased systemic vascular resistance. Positi

26、ve microbial culturesgram-negative bacteria escherichia coli, klebsiellapseudomonasstaphylococcus streptococcus spices,fungal, viral , protozoalpneumonia, gastrointestinal perforation biliary tract infection, urinary tract infection burn woundsThe Two-hit Theory of MODSFirstHit1MODSDeathRecoverySyst

27、emicInflammatoryresponseSecondHitAmplifiedSystemicInflammationresponse2 MODSRecoveryDeath1. Pulmonary failure ARDSMortality exceeds 50%ventilation perfusion abnormalitiespulmonary edemahypoxemiadecreased functional residual capacitydecreased infiltrates on chest X-rays2. Gastrointestinal dysfunctionGastritis. Ulcerations. Panc