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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• 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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