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SHOCK. Department of Surgery Ruijin Hospital, Medical College, Shanghai Jiaotong University. I. Historical Aspect . Initial records of shock. Western record violent impact or blow, 1743 physiologic instability, 1815 Eastern record 厥脱,内闭外脱. Initial Explanation of shock. Western

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shock

SHOCK

Department of Surgery Ruijin Hospital,

Medical College, Shanghai Jiaotong University

i historical aspect
I. Historical Aspect

Initial records of shock

  • Western record
    • violent impact or blow, 1743
    • physiologic instability, 1815
  • Eastern record
    • 厥脱,内闭外脱
initial explanation of shock
Initial Explanation of shock
  • Western
    • Thomas Latta, 1831
      • Patients with Cholera
      • Infusion of fluids

→ improvement

  • Eastern
    • 邪毒内陷
    • 气随血脱
    • 阴亏气脱
    • 气机郁闭
    • 阴绝阳脱

Hypovolemia

with the rise of physiology
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
with the combination of physiology and biochemistry
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

antedate the era of critical care medicine
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
controversy on lung kidney
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

ii definition of shock
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 hypoxiadue to hypoperfusion
    • Defects
    • Injury
slide9

休克的根本问题是:

A. 组织低灌注所致细胞缺氧B. 低血压C. 酸中毒D. 心功能不全E. 以上都不对

slide10

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
slide11

Explanation

  • Tissue hypoperfusion
    • tissue hypoxia
    • anaerobic metabolism, acidosis
    • inflammatory mediaters
    • circulatory redistribution
      • early involvement of splanchnic circulation
    • cellular injury
    • septic complications
    • MODS
slide12

Explanation

  • O2 Debt
    • Whether DO2crit is increasedin 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)

circulatory redistribution

Explanation

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
the changes in microcirculatary level

Explanation

The changes in MicrocirculataryLevel
  • 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
iii classificaion of shock
III. Classificaion of Shock
  • Hypovolemic Shock
    • Hemorrhage -
    • Plasma losses -
  • Cardiogenic Shock
    • Intrinsic -
    • Extrinsic
      • Compressive -
      • Obstructive -

Surgical Shock 1

GI Bleeding

Trauma

Ruptured aneurysms

Burn

Bowel obstruction

Cardiac Rhythm disturbance

Valvular Heart Disease

Cardiomyopathy

Myocardial infarction

Myocardial depression

Tension pneumothorax

Pericardial tamponade

High level of positive-pressure ventilation

Pulmonary embolism

slide16
Neurogenic Shock
    • e.g.
  • Vasogenic Shock
    • SIRS, toxin
    • Septic despite adequate fluid resucitation
    • Traumatic
    • Anaphylactic and Anaphylactoid
    • Hypoadrenal

Severe head injury

Spinal cord anesthesia

Spinal cord injury

Surgical Shock 2

slide17
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.
slide18
各型休克的共同特点是:

A. 血压下降B. 中心静脉压下降C. 脉压缩小D. 尿量减少E. 有效循环血量锐减

iv pathophysiologic staging of shock
IV. Pathophysiologic staging of shock
  • Secondary visceral impairement
  • Microcirculatory changes
  • Metabolic changes
slide20

Microcirculatory Staging

  • Microcirculatory constrictive phase
  • Microcirculatory dilatation phase
  • Microcirculatory failure phase
slide21

加重过程——

只出不进/只过不进只进不出/进多出少

A-V吻合支

微静脉

微动脉

微V

后微A

前括约肌

Microcirculatory Structure

slide22

Metabolic Changes

  • energy metabolic abnormality
    • 无氧糖酵解,产能减少
  • metabolic acidosis
    • 引起微血管扩张,等
  • barrier function defects of membrane
    • 累及基底膜,细胞膜,溶酶体膜
secondary visceral impairment
Secondary Visceral Impairment
  • Heart
  • Kidney
  • Lung
  • Brain
  • Gastrointestinal tract
  • Liver
clinical staging
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 <20% ,<800ml
slide25

Shock inhibiting stage

    • faint, dullness, confusion, coma
    • cyanosis, dyspnea
    • extremities cold and wet, pulse fast and weak
    • oliguria, anuria
    • BP decreased
    • Blood loss>20% ,>800ml
slide26
关于休克代偿期微循环改变, 下列那一项是错误的:

A. 动静脉短路开放B. 直捷通道开放C. 微动脉收缩D. 微静脉收缩E. 毛细血管内血液淤积

v diagnosis and patient monitoring
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 (<5, 5~10cmH2O, >15, >20)
    • Blood routine test/Arterial blood gas analysis/Electrolytes
    • PCWP(6~15mmHg)
    • CO CI
    • Serum lactate concentration
    • Arterial blood gas analysis
    • DIC: PLT/FDP
vi measurement of shock
VI. Measurement of Shock
  • 一般紧急处理
    • Urgent measurement
  • 补充血容量
    • Resuscitation
  • 积极处理原发病
    • Treat inciting cause of shock
  • 纠正酸碱平衡失调
    • Control electrolytes, and acid base derangement
  • 血管活性药物的应用
    • Inotropic agent
  • 治疗DIC,改善微循环
    • Treat DIC, improve microcirculation
  • 皮质类固醇和其它药物的应用
    • Corticosteroids
  • 心理支持与呵护
slide29

PCWP

CVP

<15, Volume expansion

<10cmH2O

<18, Consider volume

< 14

>18 Diurese

>14

i. Volume Resuscitation & Initial end-points

  • 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

Fluid resuscitation

End-point reaching

slide30

Optimize Oxygen Delivery

Keep SaO2>90% Optimize Cardiac IndexOptimize Hb

Supply supplemental O2 Early hemodynamic monitoring 11-13 g/dl

Ventilator, if necessary

Assess volume status(preload)

PCWP

<15, Volume expansion

<18, Consider volume;

>18 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

slide31

休克病人经补液后,血压仍低。5 ~ 10 min内经静脉注入等渗盐水250ml,如血压上升,而中心静脉压不变,提示:

A. 心功能不全

B. 血容量不足

C. 血容量过多

D. 血管张力升高

E. 以上都不是

slide32

Disturbance

Shock

MODS

Death

ii. Current Strategy for Shock Solution

!

Effort & Effect

!

!

? Timing & Strategy

prevention early identification early and specific treatment for shock and mods
Prevention, early Identification, early and specific treatment for Shock and MODS

复苏失败

死亡

(24h)

感染

创伤

烧伤

SAP

代谢

紊乱低氧

乏氧代谢

痊愈

休克

SIRS

好转

MODS

MODS

Primary

Secondary

低血容量

心源性、神经源性因素

(感染)

1 hypovolemic shock

Specific

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

    • CVP decrease
  • Treatment
    • Resuscitation & Control the inciting cause of shock
2 traumatic shock

Specific

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
3 septic shock

Specific

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
treatment of septic shock

Specific

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

Specific

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
      • 缩血管
    • Aminophylline
    • Corticosteroids
    • Antihistamine

Immunologically Mediated: byIgE antibody

  • Not Immunologically Mediated: Radiographic contrast dyes, narcotics
5 cardiogenic shock
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
vii solution of shock
VII. Solution of Shock
  • A. E. Baue, the Expert on shock: 链子的牢固程度是由最薄弱的环节所决定的。当前一个弱点加固之后,又会出现新的易断点。
  • 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
slide41

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 ?
slide42

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
slide43
Pivotal Factor of shock?
    • Extrinsic or Intrinsic
  • Solution?
    • Eastern or western

The END