SHOCK

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SHOCK

• Department of Surgery Ruijin Hospital
• Shanghai Second Medical University

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How to Learn Shock
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Timing, sequence of selected items, and its
meaning
The ART bring with JOY
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I. Historical Aspect
Ancient term about shock
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• First use the word shock
• to refer to violent impact or blow, 1743
• to refer to physiologic instability, 1815
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Initial Recognition of shock
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• Thomas Latta, 1831
• Patients with Cholera
• Infusion of intravenous fluids ? improvement

Hypovolemia
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the Rise of Physiology in 19 CN
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• Burgeoning of Cardiovascular physiology in the
  end of 19CN, Crile
• CVP dropped after hemorrhage
• Animal survival was increased after the infusion
  of saline

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with the Combination of Biochemistry and
Physiology

• Toxin theory of shock, Cannon Bayliss,
  Physiology
• impairment of oxygen transport
• development of acidosis
• toxin in severe muscle injury
• ?loss of vasomotor tone
• ?venous sequestration of blood
• ?hypotension
• the Use of Cardiac Catheterization
• Blood volume loss ?fall in Cardiac Output

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Antedate the Era of Critical Care Medicine

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

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Organ Failure

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

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ATN
Why it happens
shock - Hypovolemia / Toxin /Cytokine
Defects in Cell Membrane Function and
Vascular Permeability
Hypoxia
ARDS
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II. Summary - Definition of shock
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• 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
• Oxygen less available
• increased organ demands

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III. Classificaion of Shock (i)

• Hypovolemic Shock
• Hemorrhage -
• Plasma losses -
• Cardiogenic Shock
• Intrinsic -
• Extrinsic
• Compressive -
• Obstructive -

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
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III. Classificaion of Shock (ii)

• 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
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IV. Pathophysiology of shock

• 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

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

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Role of Hypoxia

• O2Extraction RatioVO2/ DO2
• in resting state 1/4, 1/3
• under the condition of either increased energy
  expenditure or decreased DO2

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Oxygen consumption(vO )
DO2crit DO2ERcrit
Oxygen delivery(DO2)
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• 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

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Oxygen consumption(vO )
O2 Debt
Oxygen delivery(DO2)
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• A Decrease in O2ER in Septic patients
• Microcirculatory derangement
• A-V shunting
• maldistribution
• defective oxygen utilization at the cellular
  level
• late sepsis, hemorrhage, or traumatic shock
• early shock with inadequate volume resuscitation
  
• down-regulation of oxidative metabolism
• endotoxin may cause a decrease in oxidative
  metabolism in skeletal muscle

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Circulatory redistribution

• 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

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The changes in Microcirculatary Level

• 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
• Damage to EC

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V. Diagnosis and patient mornitoring

• Conventional monitoring
• Mental status
• Skin temperature
• Blood pressure, Pulse rate
• Urinary output (30ml/hr)
• Special monitoring
• CVP (lt5, 510cmH2O, gt15, gt20)
• PCWP(615mmHg)
• CO CI
• Serum lactate concentration
• Arterial blood gas analysis
• DIC

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VI. 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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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 resucsitation of patients in Shock
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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)
CVP lt 6 cmH2O, Volume expansion lt12, Consider
volume gt12 Diurese
Reassess
Keep CVP 6-12cmH2O, 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 resucsitation of patients in Shock
(Modified)
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1. Hypovolemic shock

• 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
• Treatment
• Resuscitation Control the inciting cause of
  shock

Aggressive fluid resucitation before
surgical control of hemorrhage may lead to
disruption of thrombus, increased bleeding, and
decreased survival.
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• Initial end-points volume resuscitation
• 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

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2. Traumatic shock

• 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

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3. Septic shock

• 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

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Treatment of Septic shock

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

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4. Anaphylactic and Anaphylactoid shock

• 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
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VI. Further Development Mediators,
Cytokines

• 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 ?

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Modern Surgery, Intensive Care Medicine

• Integrate the concept of intensive care medicine
• Identification and Manipulation Metabolic
  derangement
• glucose, electrolytes, etc.
• utilization of nutrition
• Oxygen Supply and consumption
• Supportive therapy for Organ dysfunction
• Prevention, early Identification of Shock and MODS

We can perform operation safer, with fewer
limitation, And therefore surgery has been
developing rapidly.
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How to Learn Shock
???? ???? ????
? ? ????,????
? ? ????,????
? ? ????,????
?????
????????
Timing, sequence of selected items, and its
meaning
The ART bring with JOY
37
How to Learn Shock
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Shock and MODS Prevention, early Identification,
prompt and proper treatment, passive
treatmentCOST-EFFECTIVE?
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Become aProvide the
Specialized
Service Surgeon Clinician
Educated
Under Mal Partial Absolute

• Morality, make us to be complete, help us to get
  a best perception.
• Theory, help us to think and practice
  rationally.
• Technique, help us to realize, or achieve our
  goal.