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SHOCK •Background •concept Shock is a severe pathological process under the effect of various types of etiological factors, characterized by acute circulatory failure, microcirculation(MC) disturbance, tissue hypoperfusion and cell and organ dysfunction. Etiology and Classification •Hemorrhage and fluid loss • burn • trauma • infection • anaphylaxis Blood volume ↓ Capacity of vascular bed↑ •neural stimulation • acute heart failure CO↓ Effective circulatory volume ↓ Hemorrhagic shock Burn shock Hypovolemic shock Traumatic shock Infectious shock Anaphylactic shock Vasogenic shock Neurogenic shock Cardiogenic shock Cardiogenic shock Process and pathogenesis Compensatory stage Ischemic anoxia stage Progressive stage Stagnant anoxia stage Refractory stage Microcirculatory failure stage Compensatory stage Ischemic anoxia stage Alterations of MC vasoconstriction Increased pre-capillary resistance Arteriovenous shunt opening Tissue ischemia Mechanism of MC disturbance Activation of sympathetic-adrenal medulla system Actions of angiotensin Ⅱ (AT-Ⅱ), Vasopressin, thromboxane (TXA2), endothelin (ET), etc. Compensatory significances Auto blood transfusion Venous constriction may mobilize the stored blood to return to the heart. Auto fluid infusion The reduced blood pressure in capillaries caused by the elevated pre-resistance may drive fluid shift from interstitial space to the vascular compartment Blood redistribution Peripheral resistance ↑,CO ↑,blood pressure ↑ Clinical manifestations Pallor, cool limbs, decreased urine, thready pulse, narrowing pulse pressure, restless BP may be normal or decreased. Progressive stage Stagnant anoxia stage Alterations of MC Vasodilation Blood sludge Mechanism of MC disturbance Metabolic lactic Acidosis decreasing the response of SMCs to CA and leading to vasodilation. Local accumulation of metabolic products histamine, kinins, adenosine, K+ Alterations of hemorrheology WBC rolling and adhesion, RBC and platelet aggregation Effect of endotoxin LPS (lipopolysaccharide), TNF, NO MC de-compensation clinical manifestation Decreased Bp, cyanosis, oliguria, coma Refractory stage Microcirculatory failure stage •Hyper-coagulation state •acidosis DIC •TF↑ •Endotoxin ↑ No-reflow Organ failure lysosomal enzymes, active oxygen, cytokines Mediators involved in shock Vasoactive amines Regulatory peptides catecholamine, histamine, 5-HT ET, angiotensin II, vasopressin, ANP,VIP, CGRP, kinin, βendorphin Inflammatory mediators TNF-α, IL-1, IL-6,IL-8, IFN, LT, PAF, TXA2, PGI2, PGE2 Alterations of metabolism and function Cell damage and apoptosis Multiple organ dysfunction syndrome (MODS) MODS MODS is defined as a syndrome with progressive impairment of two or more organs due to severe trauma , infection or shock. Etiology Infection Non-infectious factors severe trauma, surgery, burn, ischemia-reperfusion injury, antigenantibody compound, severe hypoxia, tumor, etc. Renal failure functional or parenchymal Acute respiratory distress syndrome (ARDS) micro-thrombosis pulmonary edema decreased active surfactant hyaline membrane Cardiac dysfunction ischemia and hypoxia electrolyte and acid-base disturbance MDF DIC endotoxin Brain dysfunction Gastrointestinal ischemia ulcer Liver dysfunction Pathophysiologic basis of prevention and treatment Etiologic treatment Improving microcirculation volume replacement acidosis correction vasoactive drugs application Blockage of humoral factors Cell and organ protection
