07 shock

Dept. of PathologyDept. of PathologyMedical CollegeMedical College

Hunan Normal UniversityHunan Normal University(( 湖南师范大学医学院病理学教研室湖南师范大学医学院病理学教研室 )) 1

Chapter 7Chapter 7

ShockShock（休克）（休克）

ShockShock

①① IntroductionIntroduction②② Pathogenesis of ShockPathogenesis of Shock③③ Alterations of Metabolism Alterations of Metabolism

and Functionand Function④④ Pathophysiological Basis of Pathophysiological Basis of

TreatmentTreatment

Apoptosis Oxygen Society Education Program Tome & Briehl 4

Introduction of Shock

I: Definition of ShockI: Definition of Shock

II: Classification of ShockII: Classification of Shock

Definition

A dangerous systemic pathologic process

under the effect of various drastic etiological

factors, characterized by acute circulatory

failure, leading to inadequate tissue

perfusion, cellular metabolism impediment

and dysfunction of multiple organs.

Etiological factorsEtiological factors

Microcirculation failureMicrocirculation failure

Cell injury and organ dysfunctionsCell injury and organ dysfunctions

Effective circulatory volume Effective circulatory volume ↓↓

Blood volume

Three Factors Determining Effective circulatory

volumeHeart function

Blood vessel tone

Introduction of Shock

I: Definition of ShockI: Definition of Shock

II: Classification of ShockII: Classification of Shock

↓↓Blood volume Blood volume

Heart failureHeart failure

↑↑Blood vessel Blood vessel capacitycapacity

HypovolemHypovolemicic

CardiogeCardiogenicnic

VasogeniVasogenicc

Effective Effective

circulatory circulatory

volume↓volume↓

ShocShockk

General Categories of General Categories of ShockShock

Classification According to CausesClassification According to Causes

Loss of Loss of blood and blood and

fluidfluidBurnBurn

TraumaTrauma

InfectionInfection

AnaphylaAnaphylaxisxis

(Allergy)(Allergy)

Nerve Nerve stimulatiostimulatio

nnHeart Heart failurefailure

HypovoleHypovolemicmic

VasogeVasogenicnic

CardiogeCardiogenicnic

①①Hemorrhagic shockHemorrhagic shock②②Burn shockBurn shock③③Traumatic shockTraumatic shock④④Anaphylactic shockAnaphylactic shock⑤⑤Infectious shock Infectious shock

(Septic shock)(Septic shock)⑥⑥Neurogenic shockNeurogenic shock⑦⑦Cardiogenic shockCardiogenic shock

ShockShock

TreatmentTreatment

1. 1. Sympathetic activationSympathetic activation rather than rather than sympathetic failure during shocksympathetic failure during shock

2. Essential issue of shock 2. Essential issue of shock - - Not: Not: BP↓BP↓- - But: But: Blood flow↓ → Tissue perfusion↓Blood flow↓ → Tissue perfusion↓

Microcirculation TheoryMicrocirculation Theory

The circulation between arterioles and venules.The circulation between arterioles and venules.

The location The location where fluids, gasses, nutrients, anwhere fluids, gasses, nutrients, an

d wastes are exchanged between the blood and d wastes are exchanged between the blood and

body cells.body cells.

Microcirculation (MC)

①① ArterioleArteriole②② Post-arteriolePost-arteriole③③ Pre-capillary Pre-capillary

sphinterssphinters④④ True capillaries; True capillaries;

Straight pathStraight path⑤⑤ VenuleVenule⑥⑥ A-V shunt A-V shunt

Pre-cap sphincter & Pre-cap sphincter & arteriole constrictionarteriole constriction → Capillary

perfusion → Local metabolites& histamine

↓VSM response to constrictive substance

Pre-cap sphincter & Pre-cap sphincter & arteriole dilationarteriole dilation

Capillary perfusion ←←

Local Feedback Regulation of Capillary Perfusion

Local metabolites& histamine

VSM response to constrictive substance

Pathogenesis of Shock

Microcirculation Changes

Cellular Mechanisms

Humoral Mechanisms

Three Stages of Microcirculation Changes

Stage I: Ischemic hypoxia stageStage I: Ischemic hypoxia stage

Stage II: Stagnant hypoxia stageStage II: Stagnant hypoxia stage

Stage III: Refractory stageStage III: Refractory stage

Compensatory stage

Stage of vasoconstriction

1. Ischemic Hypoxia Stage

Main driver:

Excitation of sympathetic nerve-

adrenomedullary system ++

Mechanism of microcirculatory changesActivation of sympathetic nerve-

adrenomedullary system

Vasoconstrictive substances ↑ ↑(Catecholamines, angiotension , vasopressin, endothelin)Ⅱ

α -receptors

Constriction of microvessel

β -receptors

Opening of A-V shunts

Ischemic Hypoxia Stage

Redistribution of Blood Flow During Redistribution of Blood Flow During Stage IStage I

α-receptorα-receptor

Catecholamines

Sympathetic-adrenal system

excited

β-receptorβ-receptor

Normal Ischemic hypoxia stage

Microcirculatory changes

Arteriole +++Sphincter ++++

Venule +

Inflow ↓ ↓ & outflow ↓

Characteristics of MC perfusionArteriole +++Sphincter ++++

Venule +

Inflow < outflow

↓ Opening of true capillaries

Compensatory significance

①①Maintenance of blood volumeMaintenance of blood volume•Auto Auto bloodblood transfusion transfusion•Auto Auto fluidfluid transfusion transfusion

②②Maintenance of BPMaintenance of BP•↑ ↑ returned bloodreturned blood•↑ ↑ cardiac outputcardiac output•↑ ↑ peripheral resistance peripheral resistance

③③Blood supply to heart and brainBlood supply to heart and brain - Redistribution of blood flow- Redistribution of blood flow

Ischemic hypoxia stage

Auto Auto BloodBlood Transfusion During Stage I Transfusion During Stage I

The “first defense line” in shockThe “first defense line” in shock

Capillary hydrostatic pressure ↓Capillary hydrostatic pressure ↓

Absorption of fluid into blood vessels ↑Absorption of fluid into blood vessels ↑

Auto Auto FluidFluid Transfusion Transfusion

Auto Auto FluidFluid Transfusion During Stage ITransfusion During Stage I

↓ ↓ Opening of true capillariesOpening of true capillaries

The “second defense line” in shockThe “second defense line” in shock

Excitation of sympathetic-adrenomedullay system

Catecholamines ↑

Vasoconstriction

Renal ischemia

Skin ischemia

Urine↓ Pallor faceCool limbs

Sweat gland secretion ↑

Sweating

Excitation of CNS

AgitationRestless

Heart rate ↑Contractility ↑

Peripheral resistances↑

BP(-)Thread pulse

Ischemic hypoxia stageClinical Manifestations

2. Stagnant Hypoxia Stage

Decompensatory stage

Stage of shock

Main driver:Main driver:

Over excitation of sympathetic Over excitation of sympathetic

nerve-adrenomedulla system nerve-adrenomedulla system ++++++++

Change of microcirculation

Normal Stagnant hypoxia stage

Stagnant Hypoxia Stage

Arteriole +Sphincter -

Venule +++

Precapillary vessel and sphincter dilation

Mechanism of Microcirculatory Stasis

Acidosis:Acidosis: Anaerobic glycolysis ↑Anaerobic glycolysis ↑ →lactate ↑→lactate ↑

↓ ↓ blood perfusion → COblood perfusion → CO22 removal ↓ → H removal ↓ → H22COCO33 ↑ ↑

Effects of humoral factorsEffects of humoral factors Nitric oxide (NO), histamine, kinin, etcNitric oxide (NO), histamine, kinin, etc

↓ response of SMC to catecholaminesresponse of SMC to catecholamines

Constriction Constriction of Arteriolesof Arterioles

Constriction Constriction of Venulesof Venules

DilationDilation of of ArteriolesArterioles

ConstrictionConstriction of Venulesof Venules

Stage IIStage IIStage IStage I

Cell Adhesion Molecules

Calcium-dependentCalcium-dependentIntegrinsIntegrinsCadherinsCadherinsSelectinsSelectins

Calcium-independentCalcium-independentImmunoglobulin superfamily (IgSF) CAMsImmunoglobulin superfamily (IgSF) CAMsLymphocyte homing receptorsLymphocyte homing receptors

Families of Cell Adhesion Molecules (CAMs)

Inflow ↑ & outflow ↓

Characteristics of MC perfusionVenule +++ ↑ CAMs

Inflow > outflow

↑ Opening of capillary

Arteriole +Sphincter -

Vicious cycleVicious cycle

Opening of CapillariesOpening of Capillaries

Returned bloodReturned blood↓↓

CO, BP CO, BP ↓↓

Tissue perfusionTissue perfusion↓↓

Ischemia, Hypoxia, AcidosisIschemia, Hypoxia, Acidosis

Consequences of MC Consequences of MC Changes Changes

Sympathetic nerve +Sympathetic nerve +

Microcirculation stasis

Cardiac output ↓

Renal blood flow ↓

Returned blood volume ↓

Oliguria or anuria

Blood pressure ↓↓

Brain ischemia

Dull or coma

Stasis in kidney

Cyanosis or maculation

Stasis in skin

Clinical ManifestationsStagnant Hypoxia Stage

Treatment principlesTreat microcirculatory stasis

②. Volume replacement “ Infusion as much as required”

①. Acidosis correction

③. Vasoactive drugs Vasodilators vs. Vasoconstrictors

Terminal stage of shock

Microcirculatory failure stage

Irreversible stage

3. Refractory stage

Also called:

Damage of EC + HemoconcentrationDamage of EC + Hemoconcentration

Aggregation of RBCs, platelets → CoagulationAggregation of RBCs, platelets → Coagulation

Consumption of coagulation factors → Consumption of coagulation factors → Bleeding, hemolysisBleeding, hemolysis

Congestion, Hypoxia, AcidosisCongestion, Hypoxia, Acidosis

Disseminated Intravascular Coagulation Disseminated Intravascular Coagulation (DIC)(DIC)

Refractory Stage

Blood volume Blood volume ↓↓ ↓↓

Changes of MicrocirculationChanges of Microcirculation

Paralytic dilation of microvesselsParalytic dilation of microvessels

Microthrombosis Microthrombosis → → DICDIC

Characteristics of MC PerfusionCharacteristics of MC Perfusionno inflow and no outflowno inflow and no outflow

Refractory Stage

Microcirculatory Changes - paralyzed and collapsed

Normal Stage III

Refractory Stage

Extracellular [K+] ↑

Refractory phase

Membrane hyperpolarization

K+ Channel activationNO↑

Vasoconstrictive response ↓

Mechanism for Progressive Hypotension

Ischemia, Hypoxia → ATP↓

cGMP↑

Intracellular H+↑

H+-Ca2+

compete

Calcium influx ↓

Mechanism for DIC Development

1) Increased blood viscosity

2) Coagulation system activated

3) Platelet aggregation and adhesion

1) MC blocked by microthrombi1) MC blocked by microthrombi

2) Hemorrhage2) Hemorrhage

3) Increased capillary permeability3) Increased capillary permeability

4) Organ infarction (and failure)4) Organ infarction (and failure)

Consequences of DIC

Refractory Stage

1) Circulatory collapse1) Circulatory collapse

Progressive refractory BP Progressive refractory BP ↓↓

2) Development of DIC2) Development of DIC

3) Failure of vital organs3) Failure of vital organs

Lung, kidney, liver, heart and brainLung, kidney, liver, heart and brain

Caused by hypoperfusionCaused by hypoperfusion

Clinical Manifestations

Refractory Stage

Refractory Mechanisms

1) DIC1) DIC

2) Failure of vital organs2) Failure of vital organs

3) No-reflow phenomenon3) No-reflow phenomenon

Refractory Stage

No-Reflow Phenomenon

The failure of blood to reperfuse an ischemic area after the The failure of blood to reperfuse an ischemic area after the

physical obstruction has been removed.physical obstruction has been removed.

Following treatment of shock with blood transfusion or Following treatment of shock with blood transfusion or

fluid infusion:fluid infusion:BP could be restored temporally;BP could be restored temporally;Microcirculatory perfusion is not improved obviously;Microcirculatory perfusion is not improved obviously;Blood flow in capillary is not recovered. Blood flow in capillary is not recovered.

No-Reflow Phenomenon

A: Microvascular injury A: Microvascular injury B: Interstitial edemaB: Interstitial edemaC: RBC lineup C: RBC lineup D: WBC adhesion on endothelial cellsD: WBC adhesion on endothelial cellsE: Capillary narrowing E: Capillary narrowing F: Platelets F: Platelets G: ThrombosisG: Thrombosis

Initial Cause

Effective Circulatory Volume ↓

MC Ischemia

MC Stasis

MC Failure

Cell damage

Organ failure

Compensatory

Decompensatory

Refractory MODS

Stage I Stage II Stage III

Shock Pathogenesis - Summary

NormalNormal Stage IStage I

Stage IIIStage IIIStage IIStage II

Cellular Mechanisms

Humoral Mechanisms

Cell Damage

1) Cell membrane damage1) Cell membrane damage

2) Mitochondrial swelling2) Mitochondrial swelling

3) Lysosome swelling and vacuole 3) Lysosome swelling and vacuole formationformation→→ Cell necrosisCell necrosis

Cell DamageCell Damage

Cell Membrane DamageCell Membrane DamageNaNa++/Ca/Ca2+2+ pump dysfunctionpump dysfunctionNaNa++/Ca/Ca2+2+ inflowinflow ，， KK++ outflowoutflowCellular edemaCellular edema

Lysosomal DamageSwelling and vacuole formationLysosomal enzyme releaseCell autolysis

Mitochondrial DamageMitochondrial DamageAcidosisAcidosis→→Respiratory enzymes Respiratory enzymes ↓ ↓ HypoxiaHypoxia→→ATPATP↓↓

Cellular Mechanisms

Humoral Mechanisms

Vasoactive Substances

Inappropriate Inflammatory Response

Vasoactive SubstancesVasoactive SubstancesVasoconstrictorsVasoconstrictors VasodilatorsVasodilators

Endothelin

Angiotensin

ADH (Vasopressin)

Histamine

5-Hydroxytryptamine

PGE2PGI2TXA2

Bradykinin

-endorphin

Humoral Mechanisms

Vasoactive Substances

Inappropriate Inflammatory Response- Systemic Inflammatory Response Syndrome

An inflammatory state affecting the whole body, An inflammatory state affecting the whole body,

frequently a response of the immune system to an frequently a response of the immune system to an

infectious or noninfectious insult. infectious or noninfectious insult.

Key IssuesKey Issues

▲ ▲ Disseminated activation of inflammatory cellsDisseminated activation of inflammatory cells

▲ ▲ Inflammatory mediator spilloverInflammatory mediator spillover

Systemic Inflammatory Response Systemic Inflammatory Response SyndromeSyndrome

(SIRS)(SIRS)

Development of SIRS

Causative Factor

Inflammatory Cells

Inflammatory mediators

Cascade

Pro-inflammatory mediatorsPro-inflammatory mediatorsTNFαTNFα 、、 IL-1IL-1 、、 IL-2IL-2 、、 IL-6IL-6 、、 IL-8IL-8 、、 IFNIFN 、、 LTsLTs 、、 PAFPAF 、、 TXATXA22

Anti-inflammatory mediatorsAnti-inflammatory mediatorsIL-4IL-4 、、 IL-10IL-10 、、 IL-13IL-13 、、 PGEPGE22 、、 PGIPGI22

Inflammatory MediatorsInflammatory Mediators

Inflammatory CellsInflammatory Cells

MacrophagesMacrophagesTNFTNFαα 、、 IL-1IL-1 、、 IL-6IL-6 、、 IL-8IL-8 、、 IFNIFN 、、

IL-10IL-10 、、 IL-4IL-4

NeutrophilsNeutrophilsLTsLTs （（ LeukotrieneLeukotriene

ss ））PlateletsPlatelets

PGGPGG22 、、 PGHPGH22 、、 TXATXA22 （（ Thromboxane AThromboxane A22 ））Endothelial cellsEndothelial cells

IL-1IL-1 、、 GM-CSFGM-CSF 、、 ROSROS 、、 PGIPGI22

Compensatory Anti-inflammatory Compensatory Anti-inflammatory Response Syndrome (CARS)Response Syndrome (CARS)

With the increase of pro-inflammatory With the increase of pro-inflammatory mediators during SIRS, anti-inflammatory mediators during SIRS, anti-inflammatory factors begin to emerge. Overload of these factors begin to emerge. Overload of these anti-inflammatory factors will inhibit immune anti-inflammatory factors will inhibit immune system increase the chance of infection. system increase the chance of infection.

This is called Compensatory Anti-This is called Compensatory Anti-inflammatory Response Syndrome (CARS).inflammatory Response Syndrome (CARS).

SIRS vs. CARSSIRS vs. CARS

• SIRS > CARS:

Cell death, Organ dysfunction

• CARS > SIRS:

Immunosuppression, increase of infection

• SIRS ↑CARS↑:

- Disturbance of inflammation and immunity

- Mixed antagonist response syndrome

(MARS)

ShockShock

TreatmentTreatment

Alterations of Metabolism and

FunctionMetabolic Disorders

Water, Electrolytes and Acid-Base Disturbance

Multiple Organ Dysfunction Syndrome

Organ Dysfunction During Shock

0102030405060708090

Lung Liver Kidney GI Heart

Multiple Organ Dysfunction Multiple Organ Dysfunction Syndrome (MODS)Syndrome (MODS)

Pathogenesis of MODS:Pathogenesis of MODS: Ischemia Ischemia HypoxiaHypoxia Acidosis Acidosis Uncontrolled inflammatory responseUncontrolled inflammatory response

- SIRS- SIRS

ShockShock

TreatmentTreatment

Etiology control

Eliminate or control the Eliminate or control the primary cause (disease) of primary cause (disease) of the shockthe shock

2) Prevent cell damage and protect cell function

3) Block the effect of inflammatory mediators

4) Prevent onset of DIC and MOSF

1) Improve MC

Prevention & treatment according to Pathogenesis

Treatment principlesTreat microcirculatory stasis

②. Volume replacement “Infusion as much as required”

①. Acidosis correction

③. Vasoactive drugs (Vasodilators vs. Vasoconstrictors)

07 shock

Education

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