SHOCKn nShen Hongn nZhejiang University School of Medicine. n n2003.2.17Historical Aspectsn nThe concept of shock has evolved over the centuries from the earliest The concept of shock has evolved over the centuries from the earliest description in antiquity of traumatic wounds and hemorrhage.description in antiquity of traumatic wounds and hemorrhage.n nHippocratic facies (460380 B.C.): tourniguet. BloodlettingHippocratic facies (460380 B.C.): tourniguet. Bloodlettingn nGalen (A.D. 130200): erroneous knowledge of anatomy. Ligation of Galen (A.D. 130200): erroneous knowledge of anatomy. Ligation of bleeding vesselsbleeding vesselsn nVesalius. William Harvey (16 centuries): anatomy and circulation of Vesalius. William Harvey (16 centuries): anatomy and circulation of the cardiovascular systemthe cardiovascular systemn nA French military surgeon: the use of simple bandagesA French military surgeon: the use of simple bandagesn nThomas Latta: in 1831. infusion of intravenous fluids into hypo-Thomas Latta: in 1831. infusion of intravenous fluids into hypo-volemic patients inflicted with cholera caused clinical improvent.volemic patients inflicted with cholera caused clinical improvent. Pathogenesis:n n a. vasomotor exhaustion: neurogenic theorya. vasomotor exhaustion: neurogenic theoryn n b. traumatic toxemia: cannon. Bay(World War I) b. traumatic toxemia: cannon. Bay(World War I)n n c. hypovolemia: Keith, Blalock(experiments on dogs) c. hypovolemia: Keith, Blalock(experiments on dogs)n n d. fat embolism; d. fat embolism;n n e. acidosis e. acidosisn n f. adrenal dysfunction f. adrenal dysfunction Pathogenesis:n nresuscitation, individual argan dysfunction, cellular derangements(Korean, Vietnam conflict). n nShock lung. ARDS n nmolecular biology, inflammatory mediator, n nmetabolic support, oxygen delivery, organ ischemia, sepsis.II. Definition of shockn nA syndrome results from inadequate perfusion of tissues alterations in cellular metabolism, cellular dysfunction and cellular injury, MODS due to tissue hyperfusion, hypoxia.n nOxygen delivery; oxygen debt; oxygen demand exceeds the oxygen supply.III. Cause, classification of shock1. hypovolemic shockn n1) hemorrhagic losses: trauma, gastrointestinal bleeding ruptured aneurysm.n n2) plasma volume losses: extravascular fluid sequestration, pancreatitis, burns, bowel obstruction.2. cardiogenic shockn ndinminished cardiac outputn nintrinsic causeintrinsic causen nextrinsic causeextrinsic causen nmyocardial infarctionn ncardiac rhythm disturbances.n nTension pneumothoraxn npericardial tamponade3. neurogenic shockn nfailure of the sympathetic nervous system to maintain normal vascular tone.n nSpinal cord injury, severe head injury. Spinal anesthesia4. vasogenicn nendogenous or exogenous vaso-active mediatorsn nsystemic inflammatory response syndrome(SIRS)n nsepsis (infectious)sepsis (infectious)n nnoninfectiousnoninfectiousn nAnaphylacticn nHypoadrenaln ntraumaticIV. Pathophysiology of shockImpaired tissue perfusionTissue hypoxiaAnaerobicmetabolismAcidosisCellular dysfunctionSIRS / SepsisMultiple organ dysfunction syndromeInflammatoryMediatorsCirculatoryredistributionIschemia/ReperfusionPathophysiology:n nRole of hypoxian nAnaerobic metabolism and acidosisn nHyperlactatemian nCirculatory redistributionn nImpairment of gut perfusionAnaerobic metabolism and acidosisGlucoseGlycogenlactatePyruvateAcetyl CoACitricAcidcyclemitochondriacytosolAerobicglycolysisAnaerobicglycolysisCirculatory redistributionn nVaso-constrictive factors:n nCatechol, angiotensin II, vasopressin, endothelin, thromboxan A2n nVaso-dilatory:n nNitric oxide, prostaglandin E2, prostacyclin, interleukin-2, bradykinin.Impairment of gut perfusion:n nSubsequent bacterial or toxin translocationn nSystemic inflammatory response, MODSI. baroreceptors n nVasomotor center(medulla)n nSympathetic neural outputn nIncreased systemic vascular resistancen nIncreased venous return to the heartn nArteriolar vasoconstriction(cutaneous tissue. Skeletal muscle. Renal and splanchnic vascular beds)II. adrenal medullary output tachycardia, enhanced cardiac contractilityIII. Antidiuretic hormone(posterior pituitary)nVasoconstrictionnWater reabsorption in the distal tubule of the kidneyIV. rennin(kidney)n nAngiotensin I (liver)n nAngiotensin II (lungs)n nvasoconstrictorn naldosterone(adrenal cortex) reabsorption of sodiumV. microcirculatory autoregulationMediator of shock and sepsisn nEndotoxinn nComplement fragmentsn nEicosanoidsn nLeukotrienes, Prostaglandins, ThrobomxanesLeukotrienes, Prostaglandins, Throbomxanesn nCytokines:n nInterleukins(IL1, IL2, IL6); TNF-a; CSF, Interleukins(IL1, IL2, IL6); TNF-a; CSF, GCSF,GM-CSF; IFN-rGCSF,GM-CSF; IFN-rn nNeuroendocrine mediators: n ncatechols, cortisol, glucagonscatechols, cortisol, glucagonsV. diagosis and management of shock: General approachKeep SaO2 90% Optimize cardiac index Optimize HbKeep SaO2 90% Optimize cardiac index Optimize Hbsupply supplemental supply supplemental O2 mechanical O2 mechanical ventilation, if ventilation, if necessarynecessaryMay need early May need early hemodynamic monitoringhemodynamic monitoring11-1311-13g/dlg/dlAssess volume status(preload)Assess volume status(preload)PCWP15 volume expansionPCWP15 consider volume if PCWP15 consider volume if PCWP18PCWP18Reassess to keep:Reassess to keep:PCWP 15-18 mmHgPCWP 15-18 mmHgMAP 60-80 mmHgMAP 60-80 mmHgSvO2 65-70%SvO2 65-70% Delivery independent O2 Delivery independent O2 consumptionconsumptionGoals metGoals metGoals not metGoals not metTreat inciting cause of shock Treat inciting cause of shock control inflammatory response control inflammatory response nutritional supportnutritional supportInotropic support (b agonism)Inotropic support (b agonism)Dobutamine Dobutamine DopamineDopamineEpinephrineEpinephrine注：此图表注：此图表太大，一个太大，一个幻灯页面不幻灯页面不能全部显示能全部显示Consider vasodilatorsNitroglyceninNitroglyceninNitroprussideNitroprussideConsider a agonistNorepinephrineNorepinephrineEpinephrineEpinephrineNeosynephrineNeosynephrinePlusDopamineGoals metGoals not metReassessTreat inciting cause of shock control inflammatory response nutritional support注：此图表注：此图表太大，一个太大，一个幻灯页面不幻灯页面不能全部显示能全部显示SPECIFIC SHOCK SYNDROMESClinical signs and symptoms of hemorrhagic shock based on severity of blood loss Clinical signs and symptoms of 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 decreasednormaldecreaseddecreasedmarkeddecreasednormaldelayeddelayedabsentNormalMild tachypneaMarked tachypneaMarked tachypneanormalanxiousconfusedlathargicnormal20-30ml/hr20ml/hrnegligible注：此图表注：此图表太大，一个太大，一个幻灯页面不幻灯页面不能全部显示能全部显示Traumatic shockn nHypovolemic shock withn n1. larger volume lossesn n2. greater fluid sequestration in the extravascular compartmentsn n3. more intense activation of inflammatory mediators development of SIRSn n4. microcirculatory derangementsn n5. MODS frequently occurTraumatic shock ntreatmentn n1. excessive fluid requirementsn n2. mechanical ventilationn n3. pulmonary artery catheter monitoringn n4. cardiovascular supportShock Associated with SIRS, Sepsis, and MODSn nSIRS: two or more of followingn n1. temperature greater than 38 or less than 36n n2. heart rate greater than 90 beats per minuten n3. respiratory rate greater than 20 breaths per minute or PaCO2 less than 32mmHgn n4. white blood cell count greater than 12,000 per cu mm, less than 4000 per cu mm or greater than 10% band formsVII. Diagnosis of hypovolemic shockn n1. clinical history; n n2. physical findings; n n3. blood tests. n n4. characteristic hemodynamicsn n1. low right and left sided filling pressures(low 1. low right and left sided filling pressures(low central venous pressure, low PCWP)central venous pressure, low PCWP)n n2. decreased cardiac output, decreased SvO22. decreased cardiac output, decreased SvO2n n3. increased systemic vascular resistance3. increased systemic vascular resistanceVIII. Treatmentn nPatients airway; adequate ventilation, oxygenationn nFluid replacement isotonic electrolyte solutionsn nCrystalloid - Ringers lactate solutionCrystalloid - Ringers lactate solutionn nBlood transfusion - type-specific type O packed red Blood transfusion - type-specific type O packed red blood cellsblood cellsn nGuide treatmentn nIf absent If absent n nmonitor the central venous pressuremonitor the central venous pressuren nPlace a pulmonary artery catheterPlace a pulmonary artery cathetern nThen: urinary output rate of 0.5 to 1.0 ml/kg/hourn nThe pneumatic anti-shock garmentn nColloid solution; hyper-tonic saline(controversy)SEPSISn nSepsis: the presence of SIRS in association with culture-proven infectionn nSeptic shock: sepsis with hypotension 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.n nMutiple organ dysfunction syndrome (MODS): the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.Mortality raten 26% SIRSSepsisMortality rate: 7%16%n4%SepsisSeptic shock Mortality rate: 7%46%nMODS mortality range from 20% to 100% depending on the number of failed organs severity of illness scoring systemsMODSn nPrimary MODSn nIschemicn nReperfussionn ndirect insultn nSecondary MODS(two-hit model)n nexaggerated uncontrolled systemicn ninflammatory responseclinical features:n nfever, tachycardia, hypotension, oliguria (obtundation, coma)altered mental status. Leukocytosis or leukopenia increased or decreased systemic vascular resistance. n nPositive microbial culturesn ngram-negative bacteria gram-negative bacteria n nescherichia coli, klebsiellaescherichia coli, klebsiellan npseudomonaspseudomonasn nstaphylococcus streptococcus spices,fungal, viral , staphylococcus streptococcus spices,fungal, viral , protozoalprotozoaln npneumonia, gastrointestinal perforation biliary tract infection, urinary tract infection burn woundsThe Two-hit Theory of MODSFirstHit11MODSMODSDeathDeathRecoveryRecoverySystemicInflammatoryresponseSecondHitAmplifiedAmplifiedSystemicSystemicInflammationInflammationresponseresponse2 2 MODSMODSRecoveryDeathDeath1. Pulmonary failure ARDSnMortality exceeds 50%n nventilation perfusion abnormalitiesn npulmonary edeman nhypoxemian ndecreased functional residual capacityn ndecreased infiltrates on chest X-rays2. Gastrointestinal dysfunctionnGastritis. Ulcerations. Pancreatitis; cholesystitis, mal-absorption, mucosal atrophy, translocation of bacteria or toxins.3. Renal dysfunctionn nTissue hypoperfusion n nTissue damage by activated infalammatory cells and their mediatorsn nUremia electrolyte disturbances dialysis4. Cardiac dysfunctionn n1 depreesed coronary blood flown n2 direct endotoxin toxicityn n3 myocardia depressant factor(TNF)5. CNS manifestation of MODSnGCS scoring; mental status the patients best eye opening, verbal and motor responsesTreatmentn nTo prevent the progression to MODS. To improve oxygen delivery and oxygen comsumptionn nOxygen delivery: Volume expansion;Provision of red blood cell mass;Use of pharmacologic agents:Beta agonists & Vasodilatorsn nFor monitoring: e.g. pulmonary artery cathetern nFor hemodynamic and other physiologic evaluationn nAntibiotics: to detect possible sources of Antibiotics: to detect possible sources of infection(culture)infection(culture)n nSurgical debridementSurgical debridementn nDrainageDrainagen nNutritional supportNutritional supportThe End