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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
•neural stimulation
• acute heart failure
Blood volume ↓
Capacity of vascular bed↑
CO↓
Effective circulatory volume ↓
Hemorrhagic shock
Burn shock
Traumatic shock
Infectious shock
Anaphylactic shock
Neurogenic shock
Cardiogenic shock
Hypovolemic shock
Vasogenic 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 (AT- ), VasoprⅡ Ⅱessin, 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 aggregat
ion
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
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
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, antigen-antibody 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
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