重症急性胰腺炎治疗现状与发展.ppt

SHOCK,Department of Surgery Ruijin Hospital, Medical College, Shanghai Jiaotong University,Western record violent impact or blow, 1743 physiologic instability, 1815 Eastern record 厥脱，内闭外脱,I. Historical Aspect,Initial records of shock,Initial Explanation of shock,Western Thomas Latta, 1831 Patients with Cholera Infusion of fluids improvement,Hypovolemia,Eastern 邪毒内陷 气随血脱 阴亏气脱 气机郁闭 阴绝阳脱,with the Rise of Physiology,Burgeoning of Cardiovascular physiology in the end of 19CN, Crile CVP dropped after hemorrhage Animal survival was increased after the infusion of saline the Use of Cardiac Catheterization Blood volume loss fall in Cardiac Output,with the Combination of Physiology and Biochemistry,Toxin theory of shock, Cannon & Bayliss impairment of oxygen transport development of acidosis toxin in severe muscle injury loss of vasomotor tone venous sequestration of blood hypotension,Antedate the Era of Critical Care Medicine,Extensive physiologic research of Wigger, in early 1940s integrating the Concepts of impaired oxygen delivery oxygen debt tissue injury / death the concept of irreversible shock progressive systemic circulatory decompensation,Controversy on Lung & Kidney,ARDS Introduction of the flow directed pulmonary artery catheter, in 1970 Noncardiogenic nature Not due to volume overload ARF More prompt and aggressive resuscitation Incidence ,ATN happens: hypoperfusion,ARDS happens:,Defects in Cell Membrane Function and Vascular Permeability,Hypovolemia / Toxin /Cytokine,Hypoxia,ARDS,A syndrome that results from inadequate perfusion of tissues insufficient to meet metabolic demand lead to cellular dysfunction, elaboration of inflammatory mediators, and celluar injury which may be limited, or widespread A continuum, ranging from subclinical deficits in perfusion to MODS or frank organ failure. Tissue hypoxia due to hypoperfusion Defects Injury,II. 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:,Impaired tissue perfusion Wider spectrum of shock presentations Ranging from occult tissue hypoxia to full-blown cardiovascular collapse or Multiple organ dysfunction Implication alarm earlier treat earlier,Explanation,Tissue hypoperfusion tissue hypoxia anaerobic metabolism, acidosis inflammatory mediaters circulatory redistribution early involvement of splanchnic circulation cellular injury septic complications MODS,Explanation,O2 Debt Whether DO2crit is increased in ARDS, or sepsis ? Delivery -dependent oxygen uptake = Hypoxia cause MODS supranormal levels supply of O2 prevent the progression of MODS ? Providing opportunity for intervention Providing time for the disease to subsider,Oxygen consumption(vO ),2,Oxygen delivery(DO2),O2 Debt,Explanation,Circulatory redistribution,Concept Homeostatic response to hypoperfusion to preserve oxygen delivery to heart and brain by selective diverting blood Mechanism catechols, angiotension II, Vasopressin, endothelin,TXA2 Consequence Cellular and organ derangement MODS Breakdown of the intestinal epithelial barrier bacterial and toxin translocation SIRSMODS,Explanation,intrinsic obstruction of cap. Bed low-flow states, hypothermia, and increased viscosity cap. Sludging: intravascular coagulation, platelet aggregation, other intraluminal debris preventing RBC from reaching the tissues extrinsic obstruction of cap. Bed local tissue inflammation, edema, or hemorrhage, ACS vessel wall permeability deficit,The changes in Microcirculatary Level,Explanation,Hypovolemic Shock Hemorrhage - Plasma losses - Cardiogenic Shock Intrinsic - Extrinsic Compressive - Obstructive -,III. Classificaion of Shock,Trauma,GI Bleeding,Ruptured aneurysms,Burn,Bowel obstruction,Myocardial infarction,Cardiomyopathy,Valvular Heart Disease,Cardiac Rhythm disturbance,Myocardial depression,Tension pneumothorax,Pericardial tamponade,High level of positive-pressure ventilation,Pulmonary embolism,Surgical Shock 1,Neurogenic Shock e.g. Vasogenic Shock SIRS, toxin Septic despite adequate fluid resucitation Traumatic Anaphylactic and Anaphylactoid Hypoadrenal,Spinal cord injury,Severe head injury,Spinal cord anesthesia,Surgical Shock 2,The others There may be a “ ” to be filled. but “cellular shock”, such as 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 changes,IV. Pathophysiologic staging of shock,Microcirculatory Staging,Microcirculatory constrictive phase Microcirculatory dilatation phase Microcirculatory failure phase,后微A,微V,前括约肌,AV吻合支,微动脉,微静脉,加重过程 只出不进/只过不进只进不出/进多出少,Microcirculatory Structure,Metabolic Changes,energy metabolic abnormality 无氧糖酵解，产能减少 metabolic acidosis 引起微血管扩张，等 barrier function defects of membrane 累及基底膜，细胞膜，溶酶体膜,Secondary Visceral Impairment,Heart Kidney Lung Brain Gastrointestinal tract Liver,Clinical Staging,Shock compensatory stage nervous, restless, agitation, cool, pale, thirsty, tachycardia, short of breath BP normal or increased, pulse pressure decreased, urinary output normal or decreased Blood loss 20% ，800ml,Shock inhibiting stage faint, dullness, confusion, coma cyanosis, dyspnea extremities cold and wet, pulse fast and weak oliguria, anuria BP decreased Blood loss20% ，800ml,关于休克代偿期微循环改变， 下列那一项是错误的：,A. 动静脉短路开放 B. 直捷通道开放 C. 微动脉收缩 D. 微静脉收缩 E. 毛细血管内血液淤积,V. Diagnosis and patient monitoring,Causes and Prediction Conventional monitoring Mental status Skin temperature Blood pressure, Pulse rate Urinary output (30ml/hr) Special monitoring CVP (15, 20) Blood routine test/Arterial blood gas analysis/Electrolytes PCWP(615mmHg) CO CI Serum lactate concentration Arterial blood gas analysis DIC: PLT/FDP,VI. Measurement of Shock,一般紧急处理 Urgent measurement 补充血容量 Resuscitation 积极处理原发病 Treat inciting cause of shock 纠正酸碱平衡失调 Control electrolytes, and acid base derangement 血管活性药物的应用 Inotropic agent 治疗DIC，改善微循环 Treat DIC, improve microcirculation 皮质类固醇和其它药物的应用 Corticosteroids 心理支持与呵护,Reestablishment of urinary output to a rate of 0.5-1.0ml per kg. Per hour A normal heart rate and blood pressure Adequate capillary refill Normal sensorium Normal CVP and PWCP,i. Volume Resuscitation & Initial end-points,Fluid resuscitation,End-point reaching,Optimize Oxygen Delivery,Keep SaO290% Optimize Cardiac Index Optimize Hb Supply supplemental O2 Early hemodynamic monitoring 11-13 g/dl Ventilator, if necessary,Assess volume status(preload),Reassess,Keep: PCWP15-18 mmHg, MAP 60-80mmHg, Delivery independent O2 consumption,Goal meet Goal not meet,Treat inciting cause of shock Control SIRS Nutritional support,Inotropic support beta agonism,Goal meet,Goal not meet,Consider Vasodilator, alpha agonist,Initial resuscitation of patients in Shock,PCWP,15, Volume expansion,18, Consider volume;,18 Diurese,A. 心功能不全 B. 血容量不足 C. 血容量过多 D. 血管张力升高 E. 以上都不是,休克病人经补液后，血压仍低。5 10 min内经静脉注入等渗盐水250ml，如血压上升，而中心静脉压不变，提示：,? Timing & Strategy,!,!,!,Effort & Effect,ii. Current Strategy for Shock Solution,Prevention, early Identification, early and specific treatment for Shock and MODS,感染 创伤 烧伤 SAP,SIRS,代谢 紊乱低氧 乏氧代谢,休克,复苏失败,痊愈,MODS,好转,MODS,第 二 次 打 击,心源性、神经源性因素,低血容量,血 管 源 性,Primary,Secondary,（感染）,(24h),死亡,1. Hypovolemic shock,Symptom a decrease in pulse pressure tachycarida and hypotension urine output falls normal skin turgor is lost mental status changes - in a progressive fashion apprehension, anxiety, complete obtundation CVP decrease Treatment Resuscitation & Control the inciting cause of shock,Specific,2. Traumatic shock,Type Vasogenic shock that begins as hypovolemic shock Character - refractory to fluid replacement therapy Larger volume losses, greater fluid sequestration More intense activation of inflammatory mediators Development of SIRS Devastating soft tissue injuries Machanism increasing microvascular permeability, Excessive fluid requirement Frequently Require mechanical ventilation, Pulmonary artery catheter monitoring Cardiovascular support Operation,Specific,3. Septic shock,Type Vasogenic shock, Refractory to fluid replacement therapy Definition Sepsis with hypotension despite adequate fluid resuscitation along with the presence of manifestations of hypoperfution such as lactic acidosis, obliguria, or acute alteration in mental status Mechanism Cytokines Vasodilatation, Increasing microvascular permeability, Excessive fluid requirement,Specific,Treatment of Septic shock,Resuscitation Control infection Normalization of electrolytes, acid base dearangement Inotropic agent Corticosteroids Nutritional support, deal with DIC, organ function support,Specific,4. Anaphylactic and Anaphylactoid shock,Mechanism Inflammatory mediators C3a, C5a, Histamine, Kinnins, Prostaglandins symptoms Vasodilatation, increased capillary permeability bronchospasm, airway edema, circulatory collapse Treatment Epinephrine 0.3-0.5ml s.c. / 0.5-5ug/min / bolus 0.1-0.2ml 缩血管 Aminophylline Corticosteroids Antihistamine,Immunologically Mediated: byIgE antibody,Not Immunologically Mediated: Radiographic contrast dyes, narcotics,Specific,5. Cardiogenic Shock,Symptom Weak or slow pulse rate tachycarida or bradycardia urine output falls Cough, pink foam