休克游浩元

benzodiazepines)
Hypovolaemic Shock
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LV preload is too low to support adequate stroke volume compensatory mechanisms: tachycardia, increased venous tone, increased vascular resistance, increased contractility, decreased urine output and Na+ reabsorption may help compensate for up to 1.5 L of blood loss shock develops when blood loss exceeds 2025% of normal circulating volume prolonged hypovolaemic shock leads to metabolic acidosis, then cardiogenic shock
休 克
Shock
Emergency Department the First Affiliated Hospital of NanChang University
南昌大学一附院 急诊科
游 You
休克的历史沿革（History of shock）
Circulation failure Description
PATHOGENESIS OF SHOCK 微循环机制
MICROCIRCULATION MECHANISMS
细胞分子机制
CELLULAR AND MOLECULAR MECHANISMS
MICROCIRCULATION MECHANISMS
代偿期（Compensatory stage）
失代偿期（Reversible decompensatory stage）
The HPA and neuroendocrine axes are triggered
Increased catecholamine release Increase glucocorticoid and mineralcorticoid release Activation of Renin-angiotensin system
Concept
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。
pericarditis
– acute pulmonary hypertension – aortic dissection – valvular (mitral stenosis, aortic stenosis)
Cardiogenic Shock
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cardiac index below 2 L/min/m2
The Shock Cycle
Consequences of Shock
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hypothermia coagulopathy acid-base disturbances electrolyte abnormalities cellular injury and Multi-System Organ Failure death
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 impediment and dysfunction of multiple organs.
Anaphylactic shock Cardiogenic shock Neurogenic shock
急性心力衰竭 强烈的神经刺激
【血液动力学分类】（Classification by hemodynamics）
Type 高排低阻性休克（Warm Shock Hyperdynamic shock ） Etiology G+感染性休克、 部分感染性休克 低排高阻性休克（Cold shock Hypodynamic shock ） 失血性、心源性休克、 大部分感染性休克
PCWP greater than 17-20 mmHg
Cardiogenic Shock
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causes:
–ischaemia –myocardial contusion –valvular disease –cardiomyopathy –myocarditis –dysrhythmias –septicaemia –pharmacologic
Distributive (hyperdynamic) Shock
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causes:
–SIRS (sepsis, burns, trauma, pancreatitis) –neurogenic (spinal trauma) –anaphylaxis / anaphylactoid –endocrine (thyroid, myxoedema, adrenal) –pharmacologic (vasodilators,
减压反射 窦弓反射
交感肾上 腺（+）儿 茶酚胺释 放
动静脉吻合支开放 前阻 力大 于后 阻力 灌少 流多
血管 收缩
缺血 缺氧
血管紧张素Ⅱ管加血压素 血栓素A2心肌抑制因子
Compensatory mechanisms (early shock)
A decrease in blood volume Stretch receptors in heart baroreceptors in aorta and carotid arteries
Simply...
oxygen requirement
>
oxygen delivery
ETIOLOGY AND CLASSIFICATION 1．病因（Etiology）
失血
Hemorrhagic shock Burn shock
大面积烧伤
严重创伤
感染 过敏
Traumatic shock
Infective shock
Distributive (hyperdynamic) Shock
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Hyperdynamic state with high cardiac output Normal to low filling pressures Decreased systemic vascular resistance Mixed venous oxygen may be normal or increased
Present
History
Microcircula the concept of shock
• A history of the 200 years to recognize shock:
“shake”, “attack” From superficial syndrome to microcirculatory level , cellular level, molecular level
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Hypovolaemic Shock
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causes:
–blood loss –polyuria –GI loss –burns –vasodilation –third space losses –vascular permeability
Obstructive Shock
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causes:
– tension pneumothorax – pulmonary emboli (thrombo-, air-, amniotic) – mediastinal tumours – pericardial tamponade, constrictive
• Circulatory level： blood pressure • Microcirculatory level： inadequate tissue perfusion • Cellular level and molecular level：
Frontier Exploratory stage，experimental therapies
The Shock Cycle
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various shock states may interrelate clinically to produce a mixed 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
（一）休克代偿期（Compensatory stage）
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。