shock

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shock

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• ??Introduction
• 1. 1731. Le Dran French
• He first used shock to describe
  the severe condition of
• the patient of hurt.

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• 2. 1895 Warren
• describe the clinical manifestations
• of shock

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• the face is pale or cyanosis
• cold and clammy skin
• rapid and thready pulse
• oliguria
• apathy
• ?hypotension (Crile)

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• Mechanism
• peripheral circulatory failure
• Vascular center paralysis
• Treatment pressor

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• 1960s
• The theory of microcirculation
  Sympathetic-adrenal medulla hypersympathetic
• 70s Cellular metabolic disturbance
• 80s septic shock

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• ??Concept
• Causes disturbance blood flow of
  microcirculation functional and
  metabolic disorders of the vital organs
• Inadequate tissue perfusion

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• ??Etiology and classification of shock
• ? Etiology
• 1. Blood loss and body fluid loss
• SIHR/SBP
• SI Blood Loss
• 0.5 10 compensation
• 1.0 20 30 shock
• 1.5 50 death
  

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• fluid loss vomit. diarrhea
• collapse
• 2.Burn/trauma pain, plasma loss burn
  shock, infection shock(late)

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• 4. Infection infectious shock
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• ?endotoxicshockLPS,
• 
  pseudosympathetic
• septic shock
• hypodynamic shock low-output,cold shock
• hyperdynamicshockhigh-output,warm shock
  (pink,dry), NO,PGI,PGE

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• 5. Anaphylaxis anaphylaxic shock
• 6. Cardiogenic shock
• 7. Neurogenic shock
• ? classification of shock
• 2. 1. According to the cause of shock

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• According to the start problem
• 1) Hypovolemic shock
• CVP,CO,artery blood pressure PR
• 2) Vasogenic shock 1/5 cap opening
• Cardiogenic shock CO CIlt2.2L/min.m2
  myoardiumgenic shock
• non myoardiumgenic shock

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• ??  Periods and pathogenesis
• ? early phase of shock (ischemic phase,
  compensatory stage, ?phase)

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• 1.changes of the microcirculation and its
  mechanism
• 1)Microcirculation

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• contraction
• micro-artery
• Metarteriole
• precapillary sphincter
• Micro-vein

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• ?Axial flow particles flow
• ? a. Capillaries were closed,
• b.thoroughfare channel and Arteriovenous
  shunts are open
• ß-receptor
• ? perfusion flow perfusion lt flow

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• 2) mechanism
• Sympathetic-adrenal-medullary system
• Renin-angiotensin system

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• (1)BP sympathetic contraction of
  the
• pain nerve
  artery and vein
• Endotoxin
• (2)sympathetic renal blood flow
  angiotesin
• 
  
• nervous system catecholamine

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• (3) endothelin (ET)
• tissue impairment
• (4)TXA2
• lecithoid (??)

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• Opposite effectTNF,NO,lactic acid
• 3) compensatory meaning
• Bp self-transfusion
• self-blood transfusion
• CO
• HR
• redistribution of blood flow

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2. Manifestations

• ? mental status dysphoria, anxiety,
• consciousness
• ?skin cold and clammy, paleness of
• complexion
• ?cardiovascular system
• rapid and thready pulse,
• BP,
• pulse pressure
• ?urine oliguria

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• ? shock phase (stage of stagnant anoxia, ? phase)

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• 1. changes of microcirculation and its mechanism
• 1)Microcirculation
• Dilation
• micro-artery.
• Metarteriole.
• precapillary sphincter
• perfusion flow perfusion gt flow

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• Hemorheology
• RBC acetylneuraminate(???) COOH
• bring negative charge
• sulfate(endothelium) negative charge
  
• stack(??), sludge

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• 2) mechanism
• Hypoxia
• Histamine vasodilation congestion
  
• post-capillary resistance gt pre-capillary
  resistance
• Kinin(??) permeability blood
• Histamine of capillaries volume
• hypoxia of brain and heart

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• LPS,TNF,IL-1
• P-selectin\E- selectin
• ICAM-1,VCAM( endothelium )
• WBC adhesion to endothelium cell

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• perfusion flow perfusion gt flow
• 3)effects on body
• a. Bp
• b. Peripherial resistance coronary artery

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• 2. manifestations
• ?mental status faint coma
• ?skin cyanosis ,veined marble
• ?BP heart sound slight pulse(septic
• shock full pulse)
• ?urine oliguria or anuria

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• ? Terminal shock (phase of DIC, ? stage,
• refractory shock stage,irreversible stage,)
• microcirculatory failure stage)
• VSMC in wall of vessel of micromirculation(
  paralysis)

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• 1.Formation of DIC
• 1)concentration fibrinogen
• of blood velocity of blood flow
• 2) acidosis damage of intrinsic blood
• endotoxin endothelium coagulation

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• 3)traumatic factor ? extrinsic
  blood
• shock (TF)
  coagulation
• Common pathway ?

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intrinsic blood coagulation
extrinsic blood coagulation
Cascade trigger Dominoes push over
coagulation
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• 4)progressive decrease of vessel reaction
• Vessel to CA
• H , NO VSMC KATP open Kout
  Ca2in
• PGI

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• 2.changes of microcirculation
• no perfusion , no flow , no-reflow(, WBC
  sequestration
• 3.Effects on body
• a.venous return to heart
• b.Coagulation bleeding
• c. Thrombosis and embolism

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• 4. Manifestations
• Cogulation bleeding

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• ??Cellular metabolism alteration
• (?) Dysfunction of Cellular metabolism
• a. hypoxia glycolysis
  lactic acidosis
• b. ATP Na-K pump cellular edema
• c. metabolic acidosis

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Cells damage


mitochondria
hypaoxia acidosis
free radical
lysosome
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• Experiment
• The function of WBC leucocyte deficiency
• Copy shock model of Rat
• Test group 40mmHg all alive
• Control 36 death
• Test group 30mmHg all alive
• Control 100 death

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(?)Injury and apoptosis of cells 2002
WHO You ,he or she
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• apoptosis of cells gene regulation
  procedure death
• Physiologic
• pathologic

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.
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Activating Endonuclease degrade DNA
180-200bp oligonucleotide
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• (?)inflammatory mediator
• TNF \ IL-1,2,6,8 \ TXA2
• Anti- inflammatory mediator
• IL-4, 10\ NO\ PGI2
• (?)signal transduction
• 1.NF-?B
• 2.MAPK

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• ?systemic inflammatory response syndrome(SIRS)
• 1.Introduction inflammatory medium release
• body reaction
• 38? lt T lt36?
• HRgt 90?/min
• Rgt 20?/min or PaCO2 lt4.0kPa
• 4109/L gt WBC gt12109/L
• two points of above SIRS

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• 2. Etiology and classification
• Etiology
• a.an-infective agent trauma,operation
• 
  ischemia-reperfusion
• b. Infective agent microorganism 70
• second hit

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• 3.period of SIRS
• 1) Inflammatory cells activity
• 2) Inflammatory mediator spillover
• local whole body,
• 3) SIRS/CARS imbalance
• inflammatory mediator overflow
• 
  mixed antagonist
• compensatory anti- inflammation response
  syndrom(CARS)
• response syndrom(CARS)

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Pathogenesis
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multiple organ dysfunction
symdromeMODS

• Multiple organ dysfunction syndrome
• 1975? multiple organ failure(MOF)
• 1991? multiple organ dysfunction
• symdrome(MODS)

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?????? Sequential system failure Tilney 1973
?????????????? Multiple progressive or sequential systems failure Baue 1975
??????? multiple organ failure Eiseman 1977
?????? remote organ failure Polk 1977
??????? multiple systems organ failure Fry 1980
???????? acute organ-system failure Knaus 1985
?????????? multiple organ dysfunction syndrome ACCP/SCCM 1991
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• 1. Concept of MODS
• Organ function in normal ,shock ,large operation
  dysfunction /failure of two or more than
  two organs occur at the same time or one after
  another (36hs) .

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• 2. classification
• a. rapid single-phase 12-36h
• Causes dysfunction of two organs
• b. delayed two-phase after 1-3week
• inflammative factor second hit

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3.important organ failure

• 1)Acute renal failure(shock kidney)
• early stage renal blood flow
• functional renal failure GFR
  oliguria
• late stage acute tubular necrosis(ATN
  )
• parenchymal renal
  failure
• (?????)

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• Grade of renal failure
• Endogenous creatinine clearance rate
• Pcr(plasma creatinine)
• ? Pcr gt1.8mg/dl
• ? Pcr gt2.5mg/dl
• ? Pcr gt5.0mg/dl, hemodialysis(????)

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• 2)Acute respiratory failure(shock lung)
• congestion
• edema
• thrombosis
• atelectasis
• formation of hyaline membrane
• lung bleeding

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Korea,Vietnam?? war hemodialysis
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• Grade of respiratory dysfunction
• ? PaCO2 lt 33mmHg, PaO2 gt 60mmHg
• ? PaO2 lt 60mmHg ,cyanosis
• ? O2 50 ,breathing apparatus assist,
• PaO2 lt 50mmHg , PaCO2

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3)Cardiac functional diaturbance(shock
heart)

• early stage compensation
• late stage
• coronary blood flow
• acidosis?ATP
• hyperkalemia heart
  failure
• MDF
• DIC of myocardium

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• Grade of cardial dysfunction
• CI(cardiac index) 3.0-3.5L/min/ m2
• ?CIlt3.0 L/min/ m2
• ?CIlt2.0 L/min/ m2
• ?CIlt1.5L/min/ m2 , drugs

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• 4) Brain function disturbance(shock brain)
• early stage consciousness
• late stage ischemia hypoxia
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• brain edema faint?coma

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• 5) Hepatic dysfunction
• a.Kupffers cell IL-8 PMN
  sequestration
• b.xanthine oxidase release O2 -
• c.liver function acidosis,endotoxemia
• icterus

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• Grade of liver dysfunction
• Bilirubin
• ?gt 2.0 mg/dl icterus
• ? gt 4.0 mg/dl
• ? gt 8.0 mg/dl

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• 6) Digestive tract
• stomach ischemia, DIC, congestion
  
• 
  stress ulcer
• intestine perfusion barrier
  function
• microthrombus
• bacteria\toxin get
  into blood

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• ?? Principle of treatment
• 1. Restore blood volume
• Volume of transfuse 5 times lose
• CVP (right heart)
• PAWP (left heart)
• 2. Treatment of acidosis

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• What will be transfused?
• Blood
• crystalloid 0.9NaCl (sodium chloride)Saline,isot
  onic solution)
• water 10 glucose glycogen
• colloid plasma ,to keep osmotic pressure

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• 3. Application of vasoactive drugs
• pressors drugs mortality
• vasodilation drugs?(blood volume,CVP,Bp)
• From Lab to bedside, from bedside to Lab
• 4. Protection of cells hormone
• 5. Antagonists of humoral factor
• Benzantin histamine
• SOD O2 -

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Case 1

• A 62-year-old man was brought to the emergency
  room by his son,who reported that the
  man(documented diabetes) had been eating poorly
  for 2 days and difficult to arouse that morning.
• On exam
• The patient would open his eyes and mumble
  incoherently in response to pain.T38.6?
  BP75/40mmHg, HR 124/min,his skin was warm.
• Lab data
• WBC 19.5103/mm3,oliguria, cloudy urine. Blood
  was sent for culture.

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Treatment

• Volume
• Antibiotics
• Pressors PRN

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Case 2

• A 67-year-old-femal arrived in the emergency room
  complaining of chest pain and severe weakness
  present for 12 hours.These symptoms had been
  preceded by several days of poor appetite,
  nausea( ??)and vomiting.
• On exam
• P 110/min,Bp85/50mmHg.ECG suggesting an evolving
  inferior myocardial infarction

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Treatment

• 1?Venodilator nitroglycerin???? (further reduces
  preload)
• 2?Transfusion filling pressure

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Referrence

• 1.???????,?????
• 2.Textbook of medical physiology ,tenth
  edition,Arthur C,Guyton,M.D.
• 3.Pathophysiology,Kong Xianshou
• 4.??????????,?????
• 5. Pathophysiology,Chen guoqiang,Wang jianzhi

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