Download - SHOCK
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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.
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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 ↓
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Hemorrhagic shock
Burn shock
Traumatic shock
Infectious shock
Anaphylactic shock
Neurogenic shock
Cardiogenic shock
Hypovolemic shock
Vasogenic shock
Cardiogenic shock
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Process and pathogenesis
Compensatory stage
Ischemic anoxia stage
Progressive stage
Stagnant anoxia stage
Refractory stage
Microcirculatory failure stage
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Compensatory stage
Ischemic anoxia stage
Alterations of MC
vasoconstriction
Increased pre-capillary resistance
Arteriovenous shunt opening
Tissue ischemia
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Mechanism of MC disturbance
Activation of sympathetic-adrenal medulla system
Actions of angiotensin (AT- ), VasoprⅡ Ⅱessin, thromboxane (TXA2), endothelin (ET), etc.
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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 ↑
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Clinical manifestations
Pallor, cool limbs, decreased urine, thready pulse, narrowing pulse pressure, restless
BP may be normal or decreased.
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Progressive stage
Stagnant anoxia stage
Vasodilation
Blood sludge
Alterations of MC
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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 aggregat
ion
Effect of endotoxin
LPS (lipopolysaccharide), TNF, NO
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MC de-compensation
clinical manifestation
Decreased Bp, cyanosis, oliguria, coma
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Refractory stage
Microcirculatory failure stage
DIC
•Hyper-coagulation state
•acidosis
•TF↑
•Endotoxin ↑
Organ failure
lysosomal enzymes, active oxygen, cytokines
No-reflow
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Mediators involved in shock
Vasoactive amines catecholamine, histamine, 5-HT
Regulatory peptides ET, angiotensin II, vasopressin, ANP,VIP, CGRP, kinin, β-endorphin
Inflammatory mediatorsTNF-α, IL-1, IL-6,IL-8, IFN, LT, PAF, TXA2, PGI2, PGE2
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Alterations of metabolism and function
Cell damage and apoptosis
Multiple organ dysfunction syndrome
(MODS)
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MODS
MODS is defined as a syndrome with progressive impairment of two or more organs due to severe trauma , infection or shock.
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Etiology
Infection
Non-infectious factors
severe trauma, surgery, burn, ischemia-reperfusion injury, antigen-antibody compound, severe hypoxia, tumor, etc.
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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
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Brain dysfunction
Gastrointestinal ischemia ulcer
Liver dysfunction
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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