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SHOCK

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SHOCK Department of Surgery Ruijin Hospital, Medical College, Shanghai Jiaotong University I. Historical Aspect Western record violent impact or blow, 1743 ... – PowerPoint PPT presentation

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Title: SHOCK


1
SHOCK
  • Department of Surgery Ruijin Hospital,
  • Medical College, Shanghai Jiaotong University

2
I. Historical Aspect
Initial records of shock
  • Western record
  • violent impact or blow, 1743
  • physiologic instability, 1815
  • Eastern record
  • ??,????

3
Initial Explanation of shock
  • Western
  • Thomas Latta, 1831
  • Patients with Cholera
  • Infusion of fluids
  • ? improvement
  • Eastern
  • ????
  • ????
  • ????
  • ????
  • ????

Hypovolemia
4
with the Rise of Physiology
  • Burgeoning of Cardiovascular physiology in the
    end of 19CN, Crile
  • CVP dropped after hemorrhage
  • Animal survival was increased after the infusion
    of saline
  • the Use of Cardiac Catheterization
  • Blood volume loss ?fall in Cardiac Output

5
with the Combination of Physiology and
Biochemistry
  • Toxin theory of shock, Cannon Bayliss
  • impairment of oxygen transport
  • development of acidosis
  • toxin in severe muscle injury
  • ?loss of vasomotor tone
  • ?venous sequestration of blood
  • ?hypotension

6
Antedate the Era of Critical Care Medicine
  • Extensive physiologic research of Wigger, in
    early 1940s
  • integrating the Concepts of
  • impaired oxygen delivery
  • oxygen debt
  • tissue injury / death
  • the concept of irreversible shock
  • progressive systemic circulatory decompensation

7
Controversy on Lung Kidney
  • ARDS
  • Introduction of the flow directed pulmonary
    artery catheter, in 1970
  • Noncardiogenic nature Not due to volume
    overload
  • ARF
  • More prompt and aggressive resuscitation
  • Incidence ?

Hypovolemia / Toxin /Cytokine
Defects in Cell Membrane Function and
Vascular Permeability
ARDS happens
Hypoxia
ARDS
ATN happens hypoperfusion
8
II. Definition of shock
  • A syndrome that results from inadequate perfusion
    of tissues
  • insufficient to meet metabolic demand
  • lead to cellular dysfunction, elaboration of
    inflammatory mediators, and celluar injury
  • which may be limited, or widespread
  • A continuum, ranging from subclinical deficits
    in perfusion to MODS or frank organ failure.
  • Tissue hypoxia due to hypoperfusion
  • Defects
  • Injury

9
????????
  • A. ???????????B. ???C. ???D. ?????E. ?????

10
Explanation
  • Impaired tissue perfusion
  • Wider spectrum of shock presentations
  • Ranging from occult tissue hypoxia to full-blown
    cardiovascular collapse or Multiple organ
    dysfunction
  • Implication
  • alarm earlier
  • treat earlier

11
Explanation
  • Tissue hypoperfusion
  • tissue hypoxia
  • anaerobic metabolism, acidosis
  • inflammatory mediaters
  • circulatory redistribution
  • early involvement of splanchnic circulation
  • cellular injury
  • septic complications
  • MODS

12
Explanation
  • O2 Debt
  • Whether DO2crit is increased in ARDS, or sepsis ?
  • Delivery -dependent oxygen uptake Hypoxia
  • cause MODS
  • supranormal levels supply of O2
  • prevent the progression of MODS ?
  • Providing opportunity for intervention
  • Providing time for the disease to subsider

2
Oxygen consumption(vO )
O2 Debt
Oxygen delivery(DO2)
13
Circulatory redistribution
Explanation
  • Concept
  • Homeostatic response to hypoperfusion to preserve
    oxygen delivery to heart and brain by selective
    diverting blood
  • Mechanism
  • catechols, angiotension II, Vasopressin,
    endothelin,TXA2
  • Consequence
  • Cellular and organ derangement ? MODS
  • Breakdown of the intestinal epithelial barrier
  • bacterial and toxin translocation? SIRS?MODS

14
The changes in Microcirculatary Level
Explanation
  • intrinsic obstruction of cap. Bed
  • low-flow states, hypothermia, and increased
    viscosity
  • cap. Sludging intravascular coagulation,
    platelet aggregation, other intraluminal debris
  • preventing RBC from reaching the tissues
  • extrinsic obstruction of cap. Bed
  • local tissue inflammation, edema, or hemorrhage,
    ACS
  • vessel wall permeability deficit

15
III. Classificaion of Shock
  • Hypovolemic Shock
  • Hemorrhage -
  • Plasma losses -
  • Cardiogenic Shock
  • Intrinsic -
  • Extrinsic
  • Compressive -
  • Obstructive -

Surgical Shock 1
Trauma
GI Bleeding
Ruptured aneurysms
Burn
Bowel obstruction
Myocardial infarction
Cardiomyopathy
Valvular Heart Disease
Cardiac Rhythm disturbance
Myocardial depression
Tension pneumothorax
Pericardial tamponade
High level of positive-pressure ventilation
Pulmonary embolism
16
  • Neurogenic Shock
  • e.g.
  • Vasogenic Shock
  • SIRS, toxin
  • Septic despite adequate fluid
    resucitation
  • Traumatic
  • Anaphylactic and Anaphylactoid
  • Hypoadrenal

Spinal cord injury
Severe head injury
Spinal cord anesthesia
Surgical Shock 2
17
  • The others
  • There may be a to be filled.
  • but cellular shock, such as poisoning,
    hypoxia, hypoglycemia, is not the syndrome,
    continuum, or tissue hypoxia due to
    hypoperfusion, may be excluded from the category
    of shock.

18
??????????
  • A. ????B. ???????C. ????D. ????E. ????????

19
IV. Pathophysiologic staging of shock
  • Microcirculatory changes
  • Metabolic changes
  • Secondary visceral impairement

20
  • Microcirculatory Staging
  • Microcirculatory constrictive phase
  • Microcirculatory dilatation phase
  • Microcirculatory failure phase

21
???? ????/?????????/????
A-V???
???
???
?V
??A
????
Microcirculatory Structure
22
  • Metabolic Changes
  • energy metabolic abnormality
  • ?????,????
  • metabolic acidosis
  • ???????,?
  • barrier function defects of membrane
  • ?????,???,????

23
Secondary Visceral Impairment
  • Heart
  • Kidney
  • Lung
  • Brain
  • Gastrointestinal tract
  • Liver

24
Clinical Staging
  • Shock compensatory stage
  • nervous, restless, agitation,
  • cool, pale, thirsty,
  • tachycardia, short of breath
  • BP normal or increased, pulse pressure decreased,
    urinary output normal or decreased
  • Blood loss lt20 ,lt800ml

25
  • Shock inhibiting stage
  • faint, dullness, confusion, coma
  • cyanosis, dyspnea
  • extremities cold and wet, pulse fast and weak
  • oliguria, anuria
  • BP decreased
  • Blood lossgt20 ,gt800ml

26
????????????, ?????????
  • A. ???????B. ??????C. ?????D. ?????E.
    ?????????

27
V. Diagnosis and patient monitoring
  • Causes and Prediction
  • Conventional monitoring
  • Mental status
  • Skin temperature
  • Blood pressure, Pulse rate
  • Urinary output (30ml/hr)
  • Special monitoring
  • CVP (lt5, 510cmH2O, gt15, gt20)
  • Blood routine test/Arterial blood gas
    analysis/Electrolytes
  • PCWP(615mmHg)
  • CO CI
  • Serum lactate concentration
  • Arterial blood gas analysis
  • DIC PLT/FDP

28
VI. Measurement of Shock
  • ??????
  • Urgent measurement
  • ?????
  • Resuscitation
  • ???????
  • Treat inciting cause of shock
  • ????????
  • Control electrolytes, and acid base derangement
  • ?????????
  • Inotropic agent
  • ??DIC,?????
  • Treat DIC, improve microcirculation
  • ?????????????
  • Corticosteroids
  • ???????

29
i. Volume Resuscitation Initial end-points
Fluid resuscitation
End-point reaching
  • Reestablishment of urinary output
  • to a rate of 0.5-1.0ml per kg. Per hour
  • A normal heart rate and blood pressure
  • Adequate capillary refill
  • Normal sensorium
  • Normal CVP and PWCP

30
Optimize Oxygen Delivery
Keep SaO2gt90 Optimize Cardiac Index
Optimize Hb Supply supplemental O2
Early hemodynamic monitoring
11-13 g/dl Ventilator, if necessary
Assess volume status(preload)
PCWP
lt15, Volume expansion
lt18, Consider volume
gt18 Diurese
Reassess
Keep PCWP15-18 mmHg, MAP 60-80mmHg, Delivery
independent O2 consumption
Goal meet Goal not meet
Treat inciting cause of shock Control
SIRS Nutritional support
Inotropic support beta agonism
Goal meet
Goal not meet
Consider Vasodilator, alpha agonist
Initial resuscitation of patients in Shock
31

????????,?????5 10 min??????????250ml,????
?,????????,??
  • A. ?????
  • B. ?????
  • C. ?????
  • D. ??????
  • E. ?????

32
ii. Current Strategy for Shock Solution
!
Effort Effect
!
!
? Timing Strategy
33
Prevention, early Identification, early and
specific treatment for Shock and MODS
????
??
(24h)
?? ?? ?? SAP
?? ???? ????
? ? ? ?
??
??
SIRS
??
MODS
MODS
Primary
? ? ? ? ?
Secondary
????
??????????
(??)
34
1. Hypovolemic shock
Specific
  • Symptom
  • a decrease in pulse pressure
  • tachycarida and hypotension
  • urine output falls
  • normal skin turgor is lost
  • mental status changes - in a progressive fashion
  • apprehension, anxiety, complete obtundation
  • CVP decrease
  • Treatment
  • Resuscitation Control the inciting cause of
    shock

35
2. Traumatic shock
Specific
  • Type
  • Vasogenic shock that begins as hypovolemic shock
  • Character - refractory to fluid replacement
    therapy
  • Larger volume losses, greater fluid sequestration
  • More intense activation of inflammatory mediators
  • Development of SIRS
  • Devastating soft tissue injuries
  • Machanism
  • increasing microvascular permeability, Excessive
    fluid requirement
  • Frequently Require
  • mechanical ventilation, Pulmonary artery catheter
    monitoring
  • Cardiovascular support
  • Operation

36
3. Septic shock
Specific
  • Type
  • Vasogenic shock, Refractory to fluid replacement
    therapy
  • Definition
  • Sepsis with hypotension despite adequate fluid
    resuscitation
  • along with the presence of manifestations of
    hypoperfution
  • such as lactic acidosis, obliguria, or acute
    alteration in mental status
  • Mechanism
  • Cytokines
  • Vasodilatation, Increasing microvascular
    permeability, Excessive fluid requirement

37
Treatment of Septic shock
Specific
  • Resuscitation
  • Control infection
  • Normalization of electrolytes, acid base
    dearangement
  • Inotropic agent
  • Corticosteroids
  • Nutritional support, deal with DIC, organ
    function support

38
4. Anaphylactic and Anaphylactoid shock
Specific
  • Mechanism
  • Inflammatory mediators
  • C3a, C5a, Histamine, Kinnins, Prostaglandins
  • symptoms
  • Vasodilatation, increased capillary permeability
  • bronchospasm, airway edema, circulatory collapse
  • Treatment
  • Epinephrine 0.3-0.5ml s.c. / 0.5-5ug/min / bolus
    0.1-0.2ml
  • ???
  • Aminophylline
  • Corticosteroids
  • Antihistamine

Immunologically Mediated byIgE antibody
Not Immunologically Mediated Radiographic
contrast dyes, narcotics
39
5. Cardiogenic Shock
  • Symptom
  • Weak or slow pulse rate
  • tachycarida or bradycardia
  • urine output falls
  • Cough, pink foamy phlegm, dyspnea, cyanosis
  • mental status changes
  • fatigue, apathia
  • BP decrease CVP normal or increase
  • Treatment
  • Resuscitation cardiac stimulant, diuretics,
    vesodialators

40
VII. Solution of Shock
  • A. E. Baue, the Expert on shock
    ??????????????????????????????,??????????
  • Chain Ring
  • Heart, Lung, Kidney, Liver, Brain
  • Dilema Option
  • Extended or limited?
  • Early or delayed?
  • Intervention and Care
  • Balance Adjust
  • Volume, osmotic pressure, composition
  • Special agent

41
  • Cytokine and Mediators
  • Activated after severe injury, ischemia, or
    sepsis
  • Mechanism of SIRS, MODS
  • Parameter of Severity
  • Prevention of irreversible shock, and MODS
  • timing of intervention
  • Manipulation possible ?
  • One dose therapy ?

42
VIII. Before closing, can we draw a
conclusion?
  • What is shock? What is surgical shock?
  • Recommendation
  • Specialist, books and references
  • Recognition
  • Confusing, busy
  • Deny, neglect
  • Aggressive, defensive
  • Affected / affecting
  • Exploration / clarifying

43
  • Pivotal Factor of shock?
  • Extrinsic or Intrinsic
  • Solution?
  • Eastern or western

The END
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