Title: SHOCK
1SHOCK
- Department of Surgery Ruijin Hospital,
- Medical College, Shanghai Jiaotong University
2I. Historical Aspect
Initial records of shock
- Western record
- violent impact or blow, 1743
- physiologic instability, 1815
- Eastern record
- ??,????
3Initial Explanation of shock
- Western
- Thomas Latta, 1831
- Patients with Cholera
- Infusion of fluids
- ? improvement
- Eastern
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Hypovolemia
4with 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
5with 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
6Antedate 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
7Controversy 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
8II. 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
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10Explanation
- 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
11Explanation
- Tissue hypoperfusion
- tissue hypoxia
- anaerobic metabolism, acidosis
- inflammatory mediaters
- circulatory redistribution
- early involvement of splanchnic circulation
- cellular injury
- septic complications
- MODS
12Explanation
- 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)
13Circulatory 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
14The 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
15III. 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.
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19IV. Pathophysiologic staging of shock
- Secondary visceral impairement
20- Microcirculatory constrictive phase
- Microcirculatory dilatation phase
- Microcirculatory failure phase
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Microcirculatory Structure
22- energy metabolic abnormality
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- metabolic acidosis
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- barrier function defects of membrane
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23 Secondary Visceral Impairment
- Heart
- Kidney
- Lung
- Brain
- Gastrointestinal tract
- Liver
24Clinical 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.
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27V. 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
28VI. Measurement of Shock
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- Urgent measurement
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- Resuscitation
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- Treat inciting cause of shock
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- Control electrolytes, and acid base derangement
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- Inotropic agent
- ??DIC,?????
- Treat DIC, improve microcirculation
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- Corticosteroids
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29i. 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
30Optimize 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
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32ii. Current Strategy for Shock Solution
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Effort Effect
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? Timing Strategy
33Prevention, early Identification, early and
specific treatment for Shock and MODS
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(24h)
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SIRS
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MODS
MODS
Primary
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Secondary
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341. 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
352. 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
384. 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
395. 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
40VII. Solution of Shock
- A. E. Baue, the Expert on shock
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- 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 ?
42VIII. 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