Presentation on theme: "SHOCK Background concept Shock is a severe pathological process under the effect of various types of etiological factors, characterized by acute circulatory."— Presentation transcript:
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 neural stimulation acute heart failure Blood volume ↓ Capacity of vascular bed ↑ CO↓ Effective circulatory volume ↓
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 Vasodilation Blood sludge Alterations of MC
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 DIC Hyper-coagulation state acidosis TF↑ Endotoxin ↑ Organ failure lysosomal enzymes, active oxygen, cytokines No-reflow