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1、休克病理生理 Shock Pathophysiology,Shock is a pathological process of decreased effective circulating blood volume,tissue perfusion,cell metabolism disorder and impaired function. It is a syndrome caused by a variety of etiologies,normal circumstances（1） The arteriovenous anastomosis is closed .（2） Only 2
2、0% of capillaries open alternately, with hemoperfusion. （3） Capillary opening and closing are regulated by the relaxation and contraction of the anterior sphincter of the capillary,phase of microcirculation ischemia ： （1） Sympathetic excitement and adrenalin, norepinephrine secretion increased ， Art
3、erioles, arterioles, posterior arterioles, anterior sphincter constriction of capillaries （2） Arteriovenous anastomosis is open and blood flows directly from the arteriole to the venules. （3） Insufficient capillary hemoperfusion ,hypoxia,1） Arterioles and arterioles contract, arteriovenous anastomos
4、es remain open, and little blood enters capillaries. （2） As a result of hypoxia, histamine, bradykinin, hydrogen ion and other vasomotor substances increase, after the arteriole and capillary anterior sphincter relaxation, capillary opening, vascular volume expansion, blood flow into the capillary i
5、s very slow,Ecchymosis period of microcirculation,3）As a result of sympathetic excitement, adrenaline and norepinephrine secretion increased (and perhaps histamine role), so venules and venules contraction, capillary resistance increased, resulting in telangiectasia congestion,Ecchymosis period of m
6、icrocirculation,1） Due to severe hypoxia and acidosis of tissues, capillary wall is damaged and permeability increases, blood concentration in capillaries, blood flow stagnation; In addition, blood coagulation increased, resulting in disseminated intravascular coagulation in the microcirculation,Mic
7、rocirculation clotting period,2） Due to the formation of microthrombus, anoxia and metabolic disorders are more serious in tissues, intracellular lysosomes rupture, tissue cell necrosis, resulting in serious dysfunction of organs,Microcirculation clotting period,3） As a result of coagulation, coagul
8、ation factors (such as thrombin, fibrinogen, etc.) and platelets are consumed in large quantities, fibrin degradation products increase, and blood coagulation is reduced; The walls of the blood vessels are damaged and extensive bleeding occurs,Microcirculation clotting period,Release of inflammatory
9、 mediators and generation of O2- after ischemia reperfusion injury,After the rupture of lysosome membrane, in addition to releasing many hydrolases that cause cell autolysis and tissue damage, it can also produce myocardial inhibitory factor (MDF), bradykinin and other toxic factors. After the injur
10、y of mitochondrial membrane, the degradation of membrane lipid produces toxic products such as thrombin and leukotriene, presenting mitochondrial swelling, disappearance of mitochondrial cristae, and impaired oxidative phosphorylation of cells, which affects energy production,Release of inflammatory
11、 mediators and ischemia-reperfusion injury, severe trauma, infection and shock can stimulate the body to release excessive inflammatory mediators to form a waterfall chain amplification reaction,Second strike of multiple organ dysfunction syndrome,Hypoxia damages pulmonary capillary endothelial cell
12、s and alveolar epithelium and reduces surface active substances,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肺) Secondary damage to internal organs during shock (lungs,During resuscitation, if a large amount of stored blood is used, more microaggregates may cause pulmonary microcirculation embolization, resulting in partial alveo
13、lar collapse, atelectasis and edema, partial pulmonary vascular occlusion or hypoperfusion, resulting in increased pulmonary shunt and dead ventilation, and in severe cases, acute respiratory distress syndrome (ARDS,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肺) Secondary damage to internal organs during shock (lungs,Because the
14、 blood pressure drops, catecholamines secrete increases, causes the kidney enters the ball vasospasm and the effective circulation volume to reduce, the kidney filter rate obviously drops and produces the oliguria,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腎) Secondary damage to internal organs during shock (kidney,During shock
15、, renal blood flow redistributes and redirects to the medulla, leading not only to decreased urine filtration, but also to renal tubular necrosis in cortical areas and acute renal failure,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腎) Secondary damage to internal organs during shock (kidney,Cerebral hypoxia may result from decre
16、ased cerebral perfusion pressure and blood flow. Ischemia, CO2 retention and acidosis can cause brain cell swelling, increased vascular permeability, resulting in cerebral edema and increased intracranial pressure. The patient can appear consciousness obstacle, serious person can produce encephalopa
17、thy, coma,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(腦) Secondary damage to internal organs during shock (brain,Blood flow in the coronary arteries decreases, leading to ischemia and acidosis, which can damage the heart muscle and cause focal necrosis when blood clots form in the microcirculation. Myocardium is vulnerable to is
18、chemia and reperfusion injury, and electrolyte abnormalities will affect the systolic function of myocardium,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(心) Secondary damage to internal organs during shock (heart,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肝) Secondary damage to internal organs during shock (liver,Shock can cause liver ischemia and hypoxic in
19、jury, and can destroy liver synthesis and metabolism. Central lobular hemorrhage and necrosis of liver cells are seen,休克時(shí)內(nèi)臟器官的繼發(fā)性損害(肝) Secondary damage to internal organs during shock (liver,Biochemical examination showed abnormal metabolism of ALT and serum ammonia. The detoxification of damage liver and metabolization ability all drop, can cause endotoxemia, aggravate already metabolic disorder and acidosis
休克病理生理(英文版)ppt課件
