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1、休 克,Shock,南昌大学一附院急诊科 游,You,Emergency Department the First Affiliated Hospital of NanChang University,休克的历史沿革（History of shock）,Development of the concept of shock,A history of the 200 years to recognize shock: “shake”, “attack” From superficial syndrome to microcirculatory level , cellular level, mo
2、lecular level Circulatory level： blood pressure Microcirculatory level： inadequate tissue perfusion Cellular level and molecular level： Frontier Exploratory stage，experimental therapies,机体在严重失血失液、感染、创伤等强烈致病因素作用下，有效循环血量急剧减少，组织血液灌流量严重不足，导致各重要生命器官和细胞的功能代谢障碍及结构损害的全身性病理过程。休克是一急性的综合征。在这种状态下，全身有效血流量减少，微循环出
3、现障碍，导致重要的生命器官缺血缺氧。即是身体器官需氧量与得氧量失调。,Concept,Shock is a dangerous systemic pathologic process under the effect of various drastic etiological factors, characterized by acute circulatory failure including decreased effective circulatory blood volume, inadequate tissue perfusion, cellular metabolism imp
4、ediment and dysfunction of multiple organs.,Simply.,oxygen requirement,oxygen delivery,1病因（Etiology）,ETIOLOGY AND CLASSIFICATION,【血液动力学分类】（Classification by hemodynamics）,2.分类（Classification by initial changes ）,Hypovolemic shock (Decreased blood volume)低血容量性休克 各种病因引起的机体血容量减少所致的休克。 Vasogenic shock (
5、low-resistance shock or distributive shock)血液分布性休克 外周血管扩张，血管床容量增加，大量血液淤滞在扩张的小血管内，使有效循环血量减少而引起的休克。 Cardiogenic shock (Inadequate cardiac output)心源性休克 由于心泵功能障碍，心输出量急剧减少，有效循环血量和微循环灌流量显著下降所引起的休克。 Obstructive shock (obstruction of blood flow outside of the heart ) 阻塞性休克,Distributive (hyperdynamic) Shock,
6、Hyperdynamic state with high cardiac output Normal to low filling pressures Decreased systemic vascular resistance Mixed venous oxygen may be normal or increased,Distributive (hyperdynamic) Shock,causes: SIRS (sepsis, burns, trauma, pancreatitis) neurogenic (spinal trauma) anaphylaxis / anaphylactoi
7、d endocrine (thyroid, myxoedema, adrenal) pharmacologic (vasodilators, benzodiazepines),Hypovolaemic Shock,LV preload is too low to support adequate stroke volume compensatory mechanisms: tachycardia, increased venous tone, increased vascular resistance, increased contractility, decreased urine outp
8、ut and Na+ reabsorption may help compensate for up to 1.5 L of blood loss shock develops when blood loss exceeds 20-25% of normal circulating volume prolonged hypovolaemic shock leads to metabolic acidosis, then cardiogenic shock,Hypovolaemic Shock,causes: blood loss polyuria GI loss burns vasodilat
9、ion third space losses vascular permeability,Obstructive Shock,causes: tension pneumothorax pulmonary emboli (thrombo-, air-, amniotic) mediastinal tumours pericardial tamponade, constrictive pericarditis acute pulmonary hypertension aortic dissection valvular (mitral stenosis, aortic stenosis) vena
10、-caval compression,Cardiogenic Shock,cardiac index below 2 L/min/m2 PCWP greater than 17-20 mmHg,Cardiogenic Shock,causes: ischaemia myocardial contusion valvular disease cardiomyopathy myocarditis dysrhythmias septicaemia pharmacologic,various shock states may interrelate clinically to produce a mi
11、xed picture hypovolaemic shock may lead to acidosis and result in cardiogenic shock septic shock may lead to hypovolaemia as a result of microbial toxins, cytokines, and capillary permeability,The Shock Cycle,The Shock Cycle,Consequences of Shock,hypothermia coagulopathy acid-base disturbances elect
12、rolyte abnormalities cellular injury and Multi-System Organ Failure death,PATHOGENESIS OF SHOCK,微 循 环 机 制 MICROCIRCULATION MECHANISMS,细 胞 分 子 机 制 CELLULAR AND MOLECULAR MECHANISMS,微循环的组成 微动脉、后微动脉 毛细血管前括约肌 真毛细血管 通血毛细血管（直捷通路） 动-静脉吻合支 微静脉。,直捷通路：微动脉 后微动脉和通血毛细血管 微静脉 迂回通路：微动脉 后微动脉 毛细血管前括约肌 真毛细血管网 微静脉 动静脉短
13、路：微动脉 动静脉吻合支 微静脉,前、后阻力血管的特点两点同： 1.对儿茶酚胺的敏感性不同 2.对缺氧酸中毒的耐受性不同,1. Alterations of microcirculation perfusion （微循环变化的特点） 少灌少流或少灌多流；微循环缺血、缺氧。 fluid and no perfusion,图2 微循环休克早期,（一）休克代偿期（Compensatory stage）,微循环变化的机制,减压反射 窦弓反射,血管收缩,前阻力大于后阻力灌少流多,动静脉吻合支开放,大出血 血容量减少 心输出量下降 血压下降,缺血缺氧,交感肾上腺（+）儿茶酚胺释放,血管紧张素管加血压素 血
14、栓素A2心肌抑制因子,Compensatory mechanisms (early shock),休克早期微循环的代偿,1）血容量增加 组织液回流加速 2）心输出量增加 回心血量增加 心肌收缩增强 心率加速 3）维持动脉血压 心输出量增加 外周阻力增加 4）血流重新分布,Compensatory mechanisms,precapillary resistance vessel to contract， to decrease capilary hydrostatic pressure.,fluid and no perfusion,CNS ,烦燥不安 神志清楚,休克病因,交感肾上腺髓质,休克
15、早期的临床表现,交感-肾上腺髓质系统兴奋和儿茶酚胺大量释放是 不同类型休克的共同通路。,血管收缩无选择性,（3）代偿意义（Compensatory signification ） 动脉血压的维持（Maintain arterial blood pressure）,缺血缺氧期的临床表现 （Clinical manifestation in Ischemic hypoxia stage） 脸色苍白、 四肢冰凉、尿量减少（多为功能性急性肾衰） 脉搏细速、脉压减少 烦燥不安、出冷汗 血压可急降(失血)、也可微降，甚至正常(代偿),mild tachycardia; bounding pulse Lev
16、el of Consciousness: lethargy, confusion, combativeness Skin: delayed capillary refill; cool and clammy Blood Pressure: normal or slightly elevated Respirations: rapid and shallow,Early Stage (compensated shock): Compensatory mechanisms are able to maintain perfusion of vital organs,The ischemic hyoxia stage is a reversible com- pansatory stage. Eliminating pathogenic factors and restoring blood volume
