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