Chapter 7 Shock

Department of Basic Medicine

Du Jing
How much do you know about “shock”?

Shock?

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Shock-----
A Life Threatening Emergency
 Circulatory system failure
 Inadequate blood flow to vital organ
of the body
 A MAJOR CAUSE OF DEATH !

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Content
Introduction
Etiology and classification
Pathogenesis of shock
Alterations of metabolism and function
Features of several common types of shock
Pathophysiological basis of treatment

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Section Ⅰ

Introduction

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 Introduction
The History of Shock
1. Symptom description（19 century）
shock syndrome:
--Pale and cold clammy skin,
--tachycardia with a thready pulse,
--hypotension with a narrowed pulse pressure,
--dulled sensorium and oliguria
2. acute circulation failure（in the Word War ⅠandⅡ)
Paralysis of SN,vasodilation,low BP--epinephrine
3. Microcirculation theory (since 1960s)
Disorder of MC caused by excessive excitation of SN, ECBV↓
----expanding blood volume,vasoactive drugs, vasodilaters
4. Present to the future: the level of cell and molecular
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 Introduction
Concept of shock
Shock refers to a dangerous systemic
pathophysiological process under the
effect of various drastic etiological factors
(massive hemorrhage, severe infection,
trauma etc.), characterized by sharply
decreased effective circulatory blood
volume, inadequate tissue perfusion, and
results in cellular metabolic disorder and,
dysfunction of multiple organs.

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Section Ⅱ

Etiology and classification of shock

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Etiology
 Loss of blood or body fluid
 Trauma
 Infection
 Anaphylaxis (hypersensitivity reaction)
 Heart failure
 Neurogenic stimulus (e.g.high level spinal injury,
over does of depressants)

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Classification of shock
1. Classification of etiology
(1) Loss of blood or body fluid---hypovolemic shock
e.g. blood loss---hemorrhagic shock
fluid loss---dehydration shock
burn---burn shock
(2) Trauma---Traumatic shock
(3) Infection ---Infectious shock
(4) Anaphylaxis ---Anaphylactic shock
(5) Heart failure---cardiogenic shock
(6)Neurogenic stimulus --Neurogenic shock

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Normal blood circulation depens on three basic links.

Sufficient blood
volume

Normorl circulation
Normal cardiac
pump function

Normal vasomotor
function
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The three initial links of shock

Blood volume


Effective
Inadequate
Dysfunction of circulatory
shock
tissue
cardiac pump blood volume
perfusion
↓↓

Vasodilation 

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2. Classification of initial link

Hypovolemic shock (blood volume ↓)

 Cardiogenic shock (cardiac output ↓)
 Vasogenic shock (vasodilation ↑)

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Section Ⅲ

Pathogenesis of shock

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Microcirculatory mechanisms
Microcirculation ——From arteriole to veinule

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Stages according to changes in microcirculation

 Ischemic hypoxia stage (compensatory stage)

 Stagnant hypoxia stage
(decompensatory/progressive stage)
 Refractory Stage
(microcirculatory failure /irreversible stage)

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 venule
preferential channel

arteriov
True capillary
enous
shunt
Normal
pre-capillary
arteriole
sphincter
preferential channel

venule
Stage Ⅰ：
arteriov
True capillary enous Ischemic
shunt
hypoxia
pre-capillary
arteriole
stage
sphincter

persistent peripheral vasoconstriction

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sympathetic-adrenal-system(+)—catecholamine
 Ischemic hypoxia stage
1. Changes in microcirculation
(1) General strong constriction of arteriole and pre-capillary
sphincter (entrance of blood inflow)
(2) Mild constriction of venules (exit of blood outflow)
Precapillary resistance  > > postcapillary resistance 
inflow<<outflow
(3) Arteriovenous shunts open
Important areas of capillary exchange are bypassed,
resulting in ischemic hypoxia

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 Ischemic hypoxia stage
2. Mechanism:

• activation of sympathetic-adrenal system；

Catecholamine（CA）↑
-Rvasoconstriction
-R vasodilation、AV shunt opening

• Other vasoconstricting agent:

Angiotensin II (ATⅡ), vasopressin (ADH),
Thromboxane A2 (TXA2), Endothelin (ET),
myocardial depressant factor (MDF), Leukotrienes (LTs)

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 Ischemic hypoxia stage

3.Compensatory significance ：
(1) Auto blood transfusion ；

(2) Auto fluid transfusion .

(3) Blood redistribution ；

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 (1) Auto blood transfusion

Venous constriction increase venous

return to the heart

maintain blood
pressure

Venous constriction may mobilize the stored blood return to

the circulation—— The first defense line against decrease in
venous return and so called “auto blood transfusion”．
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 (2)Auto fluid transfusion
increase
Blood pressure in the capillaries plasma
volume
EFP is decreased
Interstitial fluids

The second defense line against decrease in venous return and

so called “auto fluid transfusion "．
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(3)Blood redistribution

Vessels in Skin, skeletal muscle and abdominal organs constrict;

Vessels in the heart and the brain dilate;

 Mechanism
-----unbalanced response to
sympathetic excitation .
periphery vessels constriction
(more α-receptors);
coronary and cerebral vessels are
less sensitive to the sympathetic
nevers .

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(3)Blood redistribution

Reduce blood flow in skin, skeletal muscle

abdominal organs and kidneys

Maintain adequate blood

supplying to brain and heart

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Compensatory significance of Ischemic hypoxia stage

 Contributes to blood supply to the heart and brain

---by blood redistribution
 Blood volume
---by auto blood transfusion, auto fluid transfusion
 Maintenance of BP
---CO (heart rate and strength)
---blood volume
---peripheral resistance

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 Clinical manifestation in stage Ⅰ

pathogenic factor

sympathoadrenal system⊕

CA secreted ⊕
Heart rate ⊕
mycoardial Renal vessel Sweat gland ⊕ CNS ⊕
contractility ⊕ constricted

TPR Pulse
Ischemia of skin
pressure↓ Urinary anxiety
BP↓or output↓ sweat
normal Pale, cool
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28
Review

History
Definition
Etiological factors
Classification
Initial links
Shock
Ischemic hypoxia
Vasoconstriction, inflow<<outflow,
Ateriolevenous shunts open
Three stages Stagnant hypoxia
Vasodilation, inflow>>outflow,
Microcirculation stasis
Refractory
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 Stage II： Stagnant hypoxia stage
thorughfare channel

venule

arteriov
True capillary enous
Ischemic
shunt hypoxia
stage
pre-capillary
arteriole
sphincter
Microcirculatory Stasis:
Arterioles dilate, and blood begins to
pour into the microcirculation.
blood flow slows down at the end of
thorughfare channel

microcirculation.
venule
arteriov
True capillary enous
shunt Stagnant
hypoxia
pre-capillary stage
arteriole
sphincter
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 Stagnant hypoxia stage
1. Alteration of microcirculation

 Vasodilation
 precapillary resistance   >> postcapillary resistance 
inflow >> outflow
 Stagnation in capillaries (blood cell aggregation and
adhesion) → blood viscosity , capillary permeability 
→ stagnant anoxia.

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 Stagnant hypoxia stage
2.Mechanism of microcirculatory stasis
(1) acidosis→ responses to CA  → vasodilation
→ precapillary resistance ；

(2) Local accumulation of substances (such as: K+,

adenosine, histamine, kinins, complements, endorphin,
NO, PAF, …) to bring about vasodilation；

(3) changes of hemorheology : blood cell aggregation

and adhesion, blood viscosity (result in sludged blood)

(4)the effect of endotoxin ：NO

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blood cell aggregation and adhesion, blood
viscosity (result in sludged blood)
3.Decompensatory effects of microcirculation
changes

 Blood volume:
capillary flow stagnates, venous return declines ，
fluid transferred from circulation to interstitial space ,
auto blood and fluid transfusion stop ,
extravasating of fluid
 BP progressively
blood volume
heart function
peripheral resistance
 Vicious cycle is formed

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 Vicious cycle in the stagnant hypoxia stage

(1) venous return↓ → ECBV↓

(2) more blood inflow →aggravates mircrocirculation stasis

→ ECBV↓

(3) venous return↓ and ECBV↓ →progressive BP↓

→ blood perfusion to heart and brain↓

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 Clinical manifestation in stage Ⅱ

mircocirculation stasis

Returning blood
Stagnation of kidney
Stagnation of skin

Cardiac output

Renal blood flow BP Ischemia of brain

Coldness,
Impaired
Low urinary output 36
cyanosis
consciousness
Stage III Refractory stage (microcirculation failure stage)
thorughfare channel

venule
arterio
True capillary
venous
shunt

pre-capillary
sphincter arteriole

paralytic vasodilation,
No responses to vasoactive substances,
blood flow stops,
damage of vessels and deficiency of oxygen and nutrition
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 Refractory stage
1.Alteration of microcirculation

 No responses to vasoactive substances

 Paralytic vasodilation,
 Blood flow stops,
 no-reflow phenomenon
 DIC (disseminated intravascular
coagulation )

Changes of microcirculation may result in MODS

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 SHOCK
● concentrated blood, blood flow
slow down,high viscosity----
hypercoagulable state
●acidosis severely damage
vascular endothelium.
TF is released and than activate
external coagulation.
● imbalance of TXA2 and PGI2
DIC
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●The microthrombus blocked
microcirculation and lead to
decreasing of blood return to heart
●FDP is increased and than enhance
vascular permeability, aggravating
microcirculation disorder.
●extensive bleeding furtherly
decreases the effective circulation
blood volume.
●embolism and infarction of organs
aggravate acute organ failure.
FDP:fibrinogen degradation product
 Clinical manifestation in stage Ⅲ

Microcirculation stasis,Diminished perfusion

low perfusion in tissues

BP CVP  microthrombus

MODS
no-reflow phenomena

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MSOF
 About pathogenesis of shock:

Cellular and molecular mechanisms

Several facts was found recently, which suggest the

primary causes of shock may also damage cells directly.
These primary or secondary alterations in cells and
molecules (cell injury and apoptosis)may induce or
aggravate microcirculation disorder or organ dysfunction
Afterwards, the understanding for shock has been involved
to the cellular and molecular levels.

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Section Ⅳ

Alterations of metabolism
and function

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1.Metabolic imbalance and disorder

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 1.Metabolic imbalance and disorder

Secretion of catecholamines ,
growth factors, glucocorticoid High metabolic status
hormones and glucagons

Catabolism of fat Ketone bodies

Enhanced glycolysis
Temporal hyperglycemia
Glucosuria

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2. Water ,electrolytes and acid-base
disturbance

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Cell injury Intracellular sodium and water
Na+-K+-ATPase
and lack of
dysfunction Extracellular potassium
ATP
Cell swelling and hyperkalemia

Widespread and prolonged Mitochondria dysfunction

tissue ischemia and Aerobic respiration is
hypoxia replaced by anaerobic glycolysis

Poor renal ATP

Excretion of
perfusion acid products Metabolic acidosis

Ventilation PaCO2 Respiratory alkalosis

Shock lung ,respiratory failure Respiratory acidosis 50

3. Organ dysfunction

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Organ dysfunction
Prolonged and severe ischemia and hypoxia
Acidosis and uncontrolled inflammatory response

Organs injury
Lung , kidney, liver, gastrointestinal tract , heart and brain

ARDS Jaundice Cardiac

Enzymes dysfunction
Bleeding
Acute increase Dull
Endotoxin
renal failure coma
translocation

Dysfunctions of more than two organs occur

successively in patients leads to MODS.
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multiple organ dysfunction syndrome (MODS):

dysfunctions of more than two organs occur

successively in patients without pre-exist
organ dysfunction.
MODS MSOF

The most frequent cause of death in shock.

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Section Ⅴ
Features of several common
types of shock
Hypovolemic shock
Septic(infectious) shock
Anaphylactic shock
Neurogenic shock
Cardiogenic shock
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Hypovolemic shock
Characterized by: Diminished blood volume
Acute loss of >15%-20% of circulating blood volume
Loss of whole blood (hemorrhage)
Loss of plasma (severe burns)
Loss of extracellular fluid (vomiting or diarrhea)
Internal hemorrhage
Fluid shifted from the vessels to the interstitial space
Shock caused by hemorrhage → acute renal failure (shock kidney)

Compensatory blood redistribution Severe ischemia of kidney

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Septic shock Gram-negative bacteria infection.
Systemic response to infection.
a high mortality rate of >50%.
Most common cause of death in ICU
Release of capillary permeability ↑,
Microorganism plasma extravasation →blood volume ↓;
and toxin inflammatory Vasodilation;
mediator Damage myocardial cells

Effective circulation Septic

blood volume↓ shock

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Anaphylactic shock Severe allergic reaction

The CO and arterial pressure decrease drastically.

Antigen-antibody reaction

Histamine or a histamine-like substance release

Venous Vascular Venous

dilatation capacity return Effective circulation
Capillary Fluid and protein into blood volume ↓
permeability the tissue spaces

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 Brain or spinal cord injury
Deep general anesthesia
Neurogenic shock Drug intoxication
Hypoxia
Mental strike
disfunction in vasomotor center in the brain stem

Inhibit sympathetic control of blood vessel constriction

Vasodilation and pooling of blood in the veins

Venous return

Cardiac output

ECBV
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Cardiogenic shock

Extensive infarction of the left ventricle(AMI)

Primary myocardial disease
Severe arrhythmia
Valvular dysfunction
Blood flow to tissue is no
Dysfunction of cardiac pump longer adequate to meet
metabolic demands

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Section Ⅵ

Pathophysiological basis of
prevention and treatment

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1、Basic life support

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2. Etiologic treatment
Correction of initial etiological factors
3. Pathogenesis treatment
(1) Expanding blood volume ；
(2) Correction of acidosis ；
(3) Application of vasoactive drugs;

4. Cell protection
5. Block or eliminate inflammatory
mediator and organ protection

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 KEY POINTS
 Grasp the concept of shock
 Grasp etiological classification of shock

 Grasp the initial links of shock

 Grasp the three stages of shock(names, typical

changes of microcirculation, compensatory
significance or decompensatory effects)
 Grasp concept of MODS

 Be familiar with the features of several common

types of shock
 Be familiar with Pathophysiological basis of
prevention and treatment
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