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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