shock(休克) - zhejiang universitya young man is brought to the emergency department by ......
TRANSCRIPT
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Shock(休克)
Hu Xiaolan(胡晓兰), MD, Associate Professor of
Pathophysiology, Zhejiang University School of Medicine
Email: [email protected]
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Clinical Manifestation
Hypotension
Narrowed pulse pressure
Cold and clammy skin
Oliguria
Dulled sensorium
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Case presentation
A young man is brought to the emergency department by ambulance on the
next day after a severe traffic accident. He is unconscious.his blood pressure is
78/48mm Hg, heart rate is 130 beats per minute. There is no evidence of head
trauma. The pupils are 2 mm and reactive. He withdraws to pain. Cardiac
examination reveals no murmurs, gallops, or rubs. The lungs are clear to
auscultation. The abdomen is tense, with decreased bowel sounds. The patient
shows cyanosis, with thready pulses.
Question:
What are the three major pathophysiologic causes of shock? Which was likely
in this patient? Why?
What are the three general stages of shock according to the different changes in
microcirculation? Which was likely in this patient? Why?
What pathogenetic mechanism accounts for this patient’s unresponsiveness and
cyanosis?
What therapeutic measures are essential for this patient?
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What is shock ?
Shock refers to a dangerous systemic
pathological process under the effect of
various drastic etiological factors,
characterized by acute circulatory failure
including decreased effective circulatory
volume,inadequate tissue perfusion,cellular
metabolism impediment and multiple organs.
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Four stages of shock research
Describing symptom
Acute circulatory failure
Microcirculation theory
Cellular and molecular levels
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Teaching contents
Etiology and classification of shock
Pathogenesis of shock
Alterations of metabolism and function
Features of several common types of shock
Pathophysiologic basis of prevention and
treatment
Case presentation
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Etiology and classification
1.Classification according to cause
① Loss of blood or fluid:
Blood loss: hemorrhagic shock; Fluid loss: dehydration shock
(collapse); Burn: burn shock
② Trauma: traumatic shock
③ Infection: infectious shock; endotoxic shock; septic shock
④ Anaphylaxis: anaphylactic shock
⑤ Heart failure: cardiogenic shock
⑥ Strong stimulation on nerve system: nerogenic shock
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2.Classification according to the initial changes
①Hypovolemic shock
②Vasogenic shock
③Cardiogenic shock
Etiology and classification
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Etiology and classification
3.Classification by hemodynamic characteristics
① Hyperdynamic shock: warm shock
high cardiac output, low vascular resistance,warm skin
② Hypodynamic shock:cold shock
low cardiac output, high vascular resistance,cold skin
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Pathogenesis of shock
Ischemic hypoxia stage
Stagnant hypoxia stage
Refractory stage
Microcirculatory mechanisms
Cellular and molecular mechanisms
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Microcirculation Theory
0 1 2 3 4 5 6 7 8 9 10
BP
PR
CA
BF
Presented by Lillehei in 1964.
Shock is a syndrome mainly of
microcirculation impairment.
The sympathetic-adrenal system
is consecutive excited all time
during shock development,
leading to decreased tissue
perfusion by vasoconstriction.
Blood loss Blood transfusion
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microcirculation impairment caused by
intensive excitation of sympathetic-adrenal system
blood flow rather than blood pressure
intensive excitation rather than
failure or numbness of sympathetic-adrenal system
Shock
The common pathogenic link is
The pathogenic key point is
The mechanism is
“Microcirculation Theory”of
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Microcirculation
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Microcirculatory mechanisms
Microcirculatory changes
Mechanism of microcirculatory changes
Compensatory significances
Clinical manifestations
1. Ischemic hypoxia stage (compensatory stage)
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Microcirculatory changes
Normal Ischemic hypoxia stage
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Microcirculatory changes
Small blood vessel constriction.
Precapillary resistance↑↑ > postcapillary resistance↑
Closed capillary↑.
Blood inflows vein by straightforward pathway and
A-V shunt.
Characteristics of inflow and outflow: inflow and
outflow↓↓; inflow < outflow.
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Mechanism of microcirculatory changes
Blood lose、Traumar etc.
Activation of sympathetic-adrenal system
vasoconstrictive substance ↑ ↑
(catecholamine,angiotensionⅡ, vasopressin, TAX2, endothelin)
Activation of α -receptors Activation of β -receptors
Opening of A-V shuntsConstriction of micrangium
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① Venous constriction → stored blood return
to circulation (self blood transfusion) (60~70%) Maintain
② Capillary pressure → fluid transfer from interstitial arterial
space to circulation (self fluid infusion) (1500ml) pressure
Catecholamines , AII → cardiac contractility
peripheral vascular resistance
③ Redistribution of blood → Decrease blood flow to the skin,
skeletal muscle, kidneys and abdominal organs
maintain blood supplying to heart and brain
①
②
③
→
Compensatory significances
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heart rate thready pulse and
cardiac contractility narrowing of pulse pressure
sympatho-
adrenal vasoconstriction and ischemia urine
medulla of abdominal organs anus temperatureexcitation
ischemia of skin pale face, cool limbs
catecho-
lamines sweat gland secretion sweating, clamminess
excitation of agitate, restless
senior region of CNS (awake but somewhat anxious)
Clinical manifestations
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Microcirculatory mechanisms
Microcirculatory changes
Mechanism of microcirculatory stasis
Effect of microcirculatory stasis
Clinical manifestations
2. Stagnant hypoxia stage (reversible decompensated stage)
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Microcirculatory changes
Normal Stagnant hypoxia stage
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Microcirculatory changes
Precapillary resistance↓↓ > postcapillary
resistance(-) or ↓.
Opened capillary↑.
Characteristics of inflow and outflow: inflow↑
and outflow↓; inflow > outflow.
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Mechanism of microcirculatory stasis
Acidosis
Local accumulation of metabolic products
Alteration of hemorheology
Endotoxin
Effects of humoral factors
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Effect of microcirculatory stasis
Effective circulating blood volume ↓↓
Blood flow resistance ↑↑
Blood presure ↓↓
Blood supply for vitals ↓↓ and dysfunctional
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Clinical manifestations
Cardiac output ↓
Microcirculation stasis
Renal blood flow ↓
Returned blood volume ↓
Blood pressure ↓
Brain ischemia
Dull or coma
Stasis in kidney
Cyanosis or maculation
Stasis in skin
Oliguria or anuria
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Microcirculatory mechanisms
Microcirculatory changes
Mechanism of microcirculatory failure
Effect of microcirculatory failure
Clinical manifestations
3. Refractory stage (microcirculatory failure stage)
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Microcirculatory changes
Normal DIC stage
Characteristic : neither inflow or outflow; inflow = outflow
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Disseminated intravascular coagulation formation
The mechanisms of DIC in this stage:
1) blood concentrated, fibrinogen↑, RBC and platelet aggregation,
blood viscosity↑→ blood flow slow down
2) Severe acidosis → vascular ECs injury.
3) Septic Shock: bacteria and toxin→ mono/macrophage secreting
cytokines → monocyte and endothelium releasing tissue factor
4) Traumatic shock: tissue factor release
→ initiating the extrinsic clotting pathway
5) Hetero-type blood transfusion → hemolysis
→ erythrocytin release
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The consequences of DIC:
1) The microcirculation pathway completely blocked by
microthrombi → blood return to heart reduced sharply
2) Fibrinopeptide, fibrin degradation product (FDP) and
complement↑→vascular permeability↑
→ aggravating microcirculation impairment
3) Bleeding → ECBV further decreased.
4) Embolism and infarction of organs
→ aggravating acute organ failure
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Cellular and molecular mechanisms
Vasoactive amines
Endothelium-derived vasoactive mediators
Regulation peptides
Alteration of cellular metabolism
Cell injury and apoptosis
Humoral factors
Inflammatory mediator and inappropriate
inflammatory response
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TF
CFR
Integrin
ICA
Cadherin
PSTK-RT
NR
TGFR
SmadSmad
Proteolysis
Endonuclease
PCD
Caspase
NF-kB
STAT
MAPK
PKA
FasNF-kB
IkB
IKK
STAT
JAK
MAPK
CaM-K
PKA
MAPKK
Golgi
CaMcAMP
Rab
MAPKKK
PKC
Ca2+
GPCR
AC
Ras
DAC
PLC
Stressheat、H2O2
EGF
RTK
GSK3
PI3K
PKB
Rho
FAKSrc
Mit
G
Vit A, D & steroid hormone
TNF-R
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In the microcirculation impairment theory, impairment
of cell metabolism is thought to be secondly to the
microcirculation impairment and is caused by hypoxia and
acidosis.
However, several facts was found recently, which suggest
the primary cause of shock may also damage cells directly.
Afterwards, the understanding for shock has been
involved to the cellular and molecular levels.
Alteration of Cell Metabolism and Multiple
Organ Dysfunction
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1. Impairment of cell metabolism
(1) Oxygen deficiency and glycolysis enhancement
ATP↓, Lactic acid↑
(2) Energy deficient, sodium pump dysfunction and Na+,
H2O inflow Cellular edema, Hyperkalemia
(3) Lactic acid and CO2↑ Local acidosis
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(1) Cell Injury
1) Cell membrane damage
2) Mitochondria damage
3) Lysosome damage
2. Cell injury and apoptosis
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secrete or release
attack
2
1
3
(2) Cell apoptosis
The activated inflammatory cells
cytokines, inflammatory mediators and oxygen free radicals
vascular endotheliums,PMNs, mono/ macrophages,
lymphocytes and parenchymal cells of various organs.
denaturing , apoptosis or necrosis
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3. Multiple organ dysfunction syndrome
MODS: More than 2 organs dysfunction occur successively in
patients without pre-exit organ dysfunction
(1) Causes and category
1) Causes
① Infectious causes (severe infection in abdominal cavity, bile duct)
② Non-infectious cause (severe trauma, operation, shock)
2) Clinical types
① Rapid single-phase (directly caused by injurious factors)
1~3 weeks② Delayed two-phase (first hit second hit)
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1
(2) Common MODS
1) Pulmonary dysfunction (83%~100%)
Acute lung injury (ALI)
→ acute respiratory distress syndrome (ARDS)
Clinical manifestation:
Acute respiratory failure characterized by
progressive dyspnea,
hypoxia, cyanosis,
pulmonary edema,
decreased pulmonary compliance.
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1
23
4
Pathogenesis:
Activated PMN→cytokines→Mf→inflammatory cascade, OFR
Pulmonary stasis,
edema, bleeding Diffusion
EC injury Transparent disorder
membrane formationpulmonary
microcirculation Embolism or thrombosis Ventilationdysfunction in micro circulation /perfusion
Local atelectasis肺不张
mismatching
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1
2
3
4
Clinical manifestation:
Jaundice occurred in 5 days, bilirubin↑.
2) Hepatic dysfunction (95%)
Bacteria and toxin from intestine
Kupffer’s cells activated Hepatic
→IL8 →PMN attracted and adhesion cells
→TNF, IL-1, OFR injury
Xanthine Oxydase (rich in liver)→OFR
黄疸 胆红素
黄嘌呤氧化酶
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3) Renal dysfunction (40%-55%)
Acute renal failure (shock kidney)
Sympathetic, Ang II
→Renal vasoconstriction, RBF↓→ Functional renal failure
ALD, ADH↑ ↗ (early stage)
→ Tubular reabsorption of H2O and Na+↑
Persistent ischemia, toxin, OFR, microthrombosis
→ acute tubular necrosis → parenchymal renal failure
(ATN)
(persistent shock)
1
2
3
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4) Gastrointestinal dysfunction
Mucosa edema, stress ulcer, intestinal ischemia
→ necrosis, bleeding
5) Cardial dysfunction
Heart dysfunction may occur at late stage.
6) Others
Immune inhibition, coagulation dysfunction, CNS dysfunction
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4. Systemic inflammatory response syndrome
SIRS is defined as auto-magnified and destroyed inflammation,
characterized by disseminated activation of inflammatory cells
and inflammatory mediator spillover.
(1) Causes
1) Severe infection (septicemia)
2) Non- infectious hit (necrosis, ischemia, trauma, burn)
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(2) Pathogenesis
1) Activation and diffusion of inflammatory cells
Mf, PMN, EC and platelet
2) Proinflammatory mediators spillover
TNF, ILs(1,2,6,8), IFN, LTB4, PAF, TXA2
3) Compensatory anti-inflammatory response syndrome (CARS)
sTNFR, IL-1ra, IL-4, IL-10, IL-13, PGE2, PGI2,
Shock & multiple organ dysfunction
Immune inhibition
1
2
3
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Alterations of metabolism and function
Disturbance of microcirculation Inappropriate inflammatory response
Metabolic alteration Multiple organ dysfunction
Negative
Nitrogen
balance
Anaerobic
glycolysislung liver heart brainkidney
ATP↓ Metabolic
acidosis
ARDS
Na+-K+-ATPase ↓
Cell swelling vasodilation
Respiratory
acidosis
Acute renal
failure
Jundice
enzymes↑
Cardiac
dysfunction
Bleeding
endotoxin
translocation
Dull
coma
GI
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Cardiogenic shock
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Neurogenic shock
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Hypovolemic shock
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Anaphylactic shock
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1. Etiological prevention and treatment
2. Pathogenetic treatment
(1) Correction of acidosis.
(2) Expansion of blood volume
(3) Application of vasoactive drugs reasonably
(4) Treatment of cell damage
(5)Application of proinflammatory mediator antagonists.
(6) Prevention of organ function failure
Pathophysiologic basis of shock
prevention and treatment
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summary
Shock is a dangerous general pathogenic process caused by various drastic etiological factors, characterized by acute circulatory failure including microcirculation impairment, inadequate perfusion of vital organs, cellular metabolism impediment and dysfunction of organs.
Microcirculation impairment caused by intensive excitation of sympathetic-adrenal system is the common pathogenic link of shock.
According to the different changes of microcirculation, shock can divided into 3 stages:
Ischemic hypoxia phase (compensatory stage)Stagnant hypoxia phase (reversible decompensatory stage) Refractory phase (microcirculatory failure stage ).
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summary
The compensatory effects in ischemic hypoxia stage include: Auto-blood transfusion (venous constriction), auto-fluid infusion (capillary pressure), peripheral resistance and redistribution of blood
The mechanisms for microcirculation stasis in stagnant hypoxia stage are vasodilation (mainly by prolonged tissue ischemia and hypoxia) and changes of hemorheology.
The mechanisms of DIC in refractory stage include blood flow slow down, vascular ECs injury (severe acidosis) and TF release (septic or traumatic shock and hemolysis). Its consequences are blood return to heart reduced sharply, ECBV further decreased, aggravating microcirculation impairment and acute organ failure.
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Besides microcirculation impairment, the primary cause of
shock may also damage cells directly, Including impairment of
cell metabolism, cell injury(membrane,mitochondria, lysosome)
and apoptosis.
Infectious or non-infectious causes may leading to MODS. The
common multiple organ dysfunction syndrome include:
summary
Pulmomary dysfunction-- Adult Respiratory Distress Syndrome
Hepatic dysfunction– hepatocyte injury and jaundice
Renal dysfunction -- Acute Renal Failure
Gastrointestinal dysfunction--mucosa edema, stress ulcer, etc.
Cardiac dysfunction and others( immune, coagulation ,CNS)
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Case presentation
A young man is brought to the emergency department by ambulance on the
next day after a severe traffic accident. He is unconscious.his blood pressure is
78/48mm Hg, heart rate is 130 beats per minute. There is no evidence of head
trauma. The pupils are 2 mm and reactive. He withdraws to pain. Cardiac
examination reveals no murmurs, gallops, or rubs. The lungs are clear to
auscultation. The abdomen is tense, with decreased bowel sounds. The patient
shows cyanosis, with thready pulses.
Question:
What are the three major pathophysiologic causes of shock? Which was likely
in this patient? Why?
What are the three general stages of shock according to the different changes in
microcirculation? Which was likely in this patient? Why?
What pathogenetic mechanism accounts for this patient’s unresponsiveness and
cyanosis?
What therapeutic measures are essential for this patient?