SHOCK

1. 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.

2. Etiology and Classification • Hemorrhage and fluid loss • burn • trauma • infection • anaphylaxis • neural stimulation • acute heart failure Blood volume ↓ Effective circulatory volume ↓ Capacity of vascular bed↑ CO↓

3. Hemorrhagic shock Burn shock Traumatic shock Infectious shock Anaphylactic shock Neurogenic shock Cardiogenic shock Hypovolemic shock Vasogenic shock Cardiogenic shock

4. Process and pathogenesis Compensatory stage Ischemic anoxia stage Progressive stage Stagnant anoxia stage Refractory stage Microcirculatory failure stage

5. Compensatory stage Ischemic anoxia stage Alterations of MC vasoconstriction Increased pre-capillary resistance Arteriovenous shunt opening Tissue ischemia

6. Mechanism of MC disturbance Activation of sympathetic-adrenal medulla system Actions of angiotensin Ⅱ (AT-Ⅱ), Vasopressin, thromboxane (TXA2), endothelin (ET), etc.

7. 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 ↑

8. Clinical manifestations Pallor, cool limbs, decreased urine, thready pulse, narrowing pulse pressure, restless BP may be normal or decreased.

9. Progressive stage Stagnant anoxia stage Alterations of MC Vasodilation Blood sludge

10. 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

11. MC de-compensation clinical manifestation Decreased Bp, cyanosis, oliguria, coma

12. Refractory stage Microcirculatory failure stage • Hyper-coagulation state • acidosis • TF↑ • Endotoxin ↑ DIC No-reflow Organ failure lysosomal enzymes, active oxygen, cytokines

13. Mediators involved in shock Vasoactive amines catecholamine, histamine, 5-HT ET, angiotensin II, vasopressin, ANP,VIP, CGRP, kinin, β-endorphin Regulatory peptides TNF-α, IL-1, IL-6,IL-8, IFN, LT, PAF, TXA2, PGI2, PGE2 Inflammatory mediators

14. Alterations of metabolism and function Cell damage and apoptosis Multiple organ dysfunction syndrome (MODS)

15. MODS MODS is defined as a syndrome with progressive impairment of two or more organs due to severe trauma , infection or shock.

16. Etiology Infection Non-infectious factors severe trauma, surgery, burn, ischemia-reperfusion injury, antigen-antibody compound, severe hypoxia, tumor, etc.

17. 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

18. Brain dysfunction Gastrointestinal ischemia ulcer Liver dysfunction

19. 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