Sunday, February 10, 2013



Research history of the shock:

Some common signs:
Paleness or cyanosis
Cold and clammy skin 
Dulled sensorium

Traditional view : Hypotension

Traditional treatment principle: Raise BP

Today's point of view:

modern view : low perfusion

modern treatment principle :Improve perfusion

                                 blood pressure ×

                                 blood flow √

Content you should know:
III.Stages and their pathological changes and mechanisms 
IV.Organ dysfunction 
V.Treatment principles

First of all the Concept of a Shock: 

What actually shock is ?

 Shock is a dangerous clinical pathological process characterized by an acute circulatory failure, inadequate blood flow and oxygen delivery to the tissue of the body.

II. Classifications of shock: 

According to:


Perfusion factors

Cardiac output


Common character :Sharp drop of the ECBV

According to the causes:

1-Hypovolemic shock
2-Burn  shock
3-Traumatic  shock
4-Infectious  shock
5-Cardiogenic shock
6-Neurogenic shock
7-Anaphylactic shock

Perfusion Factors

Three determinants of effective perfusion

   Sufficient blood volume

   Normal function of heart pump
   Normal vasomoter function
 three types :

                     Hypovolemic shock

                     Cardiogenic shock

                     Vasogenic shock      
Cardiac output:

◆ Hypodynamic shock (Cold Shock):    inadequate or falling cardiac output
    seen in most of the shock

◆ Hyperdynamic shock (Warm shock): normal or high cardiac output 
      seen in anaphylactic shock , neurogenic shock and part of infectious  shock

III. Stages and their pathological 
     changes and mechanisms : 

 Phased basis: 

            The changes of microcirculation

The normal structure of microcirculation
Perfuse: Arteriole, Precapillary sphincter
Outflow: Venule

Take Hypovolemic shock as an example: 

Ischemic hypoxia Stage
Stagnant hypoxia Stage 
Organic failure Stage

1. Ischemic hypoxia Stage:

(1) Changes of microcirculation

          Decreased blood volume
     Sympathetic-adrenal system activation
 Capillary constriction     Arteriovenous shunt open
                         Tissue    hypoxia

(2) Significance of compensation

1-  Auto blood transfusion

       Auto blood transfusion 

Sympathetic-adrenal system activation
constriction of the capacitance vessel
Disgorging stored blood
“The first-line defensive response”

2- Auto fluid transfusion

 Mechanism of auto fluid transfusion 

Sympathetic-adrenal system activation
precapillary resistance > postcapillary resistance
            Hydrostatic pressure↓                                          
     promoting tissue fluid reflow to blood

   “The second-line defensive response”

3- Redistribution of blood volume 


Redistribution of blood volume

obvious constriction in Some organs’ vessel ,others are not
ensure adequate blood flow through the brain and heart

“The third-line defensive response”

 (3) Clinical  Manifestation


What are the determinants of Bp?

-Blood volume
-Heart pump
-Peripheral resistance

Mechanism of blood pressure does not drop:
  During the early stage of hypovolemic shock,
 the patient can maintain the normal BP.

   Acute or Severe blood loss and fluid loss Should be excepted

Question :  
      Is Bp the most important index in diagnosis and management of shock?


Other Manifestations :

    Sympathetic - adrenal   system   activation
            small blood vessel constriction      Activation of the sweat glands
            redistribution of blood
                       ↓                             ↓                
                    GFR↓                        ↓                
      HR↑      Urine output ↓          cool and moist skin

How about the consciousness of patient?

clear consciousness
agitate, restless

2. Stagnant hypoxia Stage

      Prolonged excitation of Sympathetic adrenal system
Widespread tissue hypoxia                                          
Acid metabolites produced:                                      Endothelial cell injury
Lactic acid,Histamine,Adenosine ,NO,etc
precapillary   postcapillary resistance is still high     permeability↑        
     ↓                        ↓    
blood fluid slowly,Congestion       < :::::::     RBC aggregation WBC rolling and block
                                                                      platelet aggregation and adhension
Venous return↓↓   :::: >   Bp↓↓

                Tissue hypoxia
     Acidosis and some cytokines
precapillary resistance < postcapillary resistance
               Slow blood flow
              Stagnant hypoxia    :::::: >    vicious circle

Clinical Manifestation 
   Stasis in microcirculation
  Returned blood volume↓              Congestion
                        ↓                                        ↓  
                      CO ↓                             Cyanosis
                ↓                ↓            ↓     
Renal blood flow ↓           Cerebral ischemia
                                ↓                  ↓  
     Oliguria              Bp ↓          coma

3. Organ Dysfunction  Stage

severe hypoxia in tissue level
Cell injury, Blood vessel injury ,Collagen exposure
Blood coagulation  factors activation Acidosis 
(disseminated intravascular coagulation)

   DIC is an acquired hemorrhagic syndrome 
in which both clotting and bleeding occur 
simultaneously. Widespread clotting in small 
vessels leads to consumption of the clotting
 factors and platelets, which in turn leads
 to bleeding.

DIC  <::::::::>   shock

MSOF----multiple system organ failure

    MODS is the progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury.


Ischemic hypoxia Stage
Stagnant hypoxia Stage 
Organic failure Stage

IV. Organ dysfunction

1. Shock lung 

  Shock lung or the adult respiratory distress syndrome (ARDS) is a form of respiratory failure that can follow severe shock. Alveolar capillary permeability is increased and interstitial edema develops, the lung becomes engorged and gas exchange is impaired, hyaline membrane develops.

Shock lung

Rapid and labored respiration 

Diffusion impairment
Ventilation-perfusion imbalance

2. Acute renal failure

  Renal failure 

  • Oliguria

  • Azotemia 

  • Hyperkalemia 

  • Metabolic acidosis

Functional renal failure 

Parenchymal  renal failure 

3. Heart failure

Heart failure

  • Acidosis 
  • Hyperkalemia
  • Decreased PO2
  • DIC
  • Endotoxin 

4. Gastrointestinal dysfunction

ischemic injury
redistribution of blood flow 
Gastric mucosal damage, intestinal ischemia and stress ulcer
Clinical manifestation: 
     Abdominal pain 
     Vomiting blood
     Blood in stool

V. Treatment:

   Shock is easier to prevent than to cure.      
 Don’t wait for symptoms to develop before beginning the treatment for shock. 
         prevention first

1. Blood and Plasma transfusion:

The amount is based on how much patients do

2. Vasoactive Drugs:

Note: a precondition
expansion of blood volume

Vasodilator substance.
Vasoconstrictive substance.e.g;
neurogenic shock
anaphylactic shock

3-Other treatment measures:

-Oxygen therapy
-treatment on acidosis 
-treatment by the head-down position
-treatment with glucocorticoids

Questions just for review!
1. What is the concept of shock?
2. What are the major causes of shock?
3. How many stages are there in hypovolemic shock? What are they?
4. What are the compensatory mechanisms and significance in first stage of hypovolemic shock?

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