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SHOCK

Shen Hong

Zhejiang University School of Medicine.
Historical Aspects

The concept of shock has evolved over the centuries from the earliest
description in antiquity of traumatic wounds and hemorrhage.

Hippocratic facies (460~380 B.C.): tourniguet. Bloodletting

Galen (A.D. 130~200): erroneous knowledge of anatomy. Ligation of
bleeding vessels

Vesalius. William Harvey (16 centuries): anatomy and circulation of
the cardiovascular system

A French military surgeon: the use of simple bandages

Thomas Latta: in 1831. infusion of intravenous fluids into hypovolemic patients inflicted with cholera caused clinical improvent.
Pathogenesis:

a. vasomotor exhaustion: neurogenic theory

b. traumatic toxemia: cannon. Bay(World War I)

c. hypovolemia: Keith, Blalock(experiments on dogs)

d. fat embolism;

e. acidosis

f. adrenal dysfunction
Pathogenesis:

resuscitation, individual argan dysfunction, cellular
derangements(Korean, Vietnam conflict).

Shock lung. ARDS

molecular biology, inflammatory mediator,

metabolic support, oxygen delivery, organ
ischemia, sepsis.
II. Definition of shock


A syndrome results from inadequate perfusion
of tissues alterations in cellular metabolism,
cellular dysfunction and cellular injury, MODS
due to tissue hyperfusion, hypoxia.
Oxygen delivery; oxygen debt; oxygen
demand exceeds the oxygen supply.
III. Cause, classification of shock
1. hypovolemic shock

1) hemorrhagic losses: trauma, gastrointestinal
bleeding ruptured aneurysm.

2) plasma volume losses: extravascular fluid
sequestration, pancreatitis, burns, bowel
obstruction.
2. cardiogenic shock

dinminished cardiac output
intrinsic cause
 extrinsic cause





myocardial infarction
cardiac rhythm disturbances.
Tension pneumothorax
pericardial tamponade
3. neurogenic shock

failure of the sympathetic nervous system to
maintain normal vascular tone.

Spinal cord injury, severe head injury. Spinal
anesthesia
4. vasogenic


endogenous or exogenous vaso-active mediators
systemic inflammatory response syndrome(SIRS)
sepsis (infectious)
 noninfectious




Anaphylactic
Hypoadrenal
traumatic
IV. Pathophysiology of shock
Impaired tissue perfusion
Tissue hypoxia
Anaerobic
metabolism
Inflammatory
Mediators
Circulatory
redistribution
Ischemia/
Reperfusion
Acidosis
Cellular dysfunction
SIRS / Sepsis
Multiple organ dysfunction syndrome
Pathophysiology:
Role of hypoxia
 Anaerobic metabolism and acidosis
 Hyperlactatemia
 Circulatory redistribution
 Impairment of gut perfusion

Anaerobic metabolism and acidosis
Glycogen
Anaerobic
glycolysis
Aerobic
glycolysis
Glucose
Pyruvate
lactate
cytosol
mitochondria
Acetyl CoA
Citric
Acid
cycle
Circulatory redistribution
Vaso-constrictive factors:
 Catechol, angiotensin II, vasopressin,
endothelin, thromboxan A2
 Vaso-dilatory:
 Nitric oxide, prostaglandin E2,
prostacyclin, interleukin-2, bradykinin.

Impairment of gut perfusion:

Subsequent bacterial or toxin translocation

Systemic inflammatory response, MODS
I. baroreceptors





Vasomotor center(medulla)
Sympathetic neural output
Increased systemic vascular resistance
Increased venous return to the heart
Arteriolar vasoconstriction(cutaneous tissue.
Skeletal muscle. Renal and splanchnic
vascular beds)
II. adrenal medullary output↑
tachycardia, enhanced
cardiac contractility

III. Antidiuretic
hormone(posterior pituitary)
 Vasoconstriction
 Water
reabsorption in the distal
tubule of the kidney
IV. rennin(kidney)
Angiotensin I (liver)
 Angiotensin II (lungs)

 vasoconstrictor
 aldosterone(adrenal
of sodium
cortex) →reabsorption
V. microcirculatory autoregulation
Mediator of shock and sepsis



Endotoxin
Complement fragments
Eicosanoids


Cytokines:


Leukotrienes, Prostaglandins, Throbomxanes
Interleukins(IL1, IL2, IL6); TNF-a; CSF,
GCSF,GM-CSF; IFN-r
Neuroendocrine mediators:

catechols, cortisol, glucagons
V. diagosis and management of
shock: General approach
Keep SaO2> 90%
Optimize cardiac index
supply supplemental
O2 mechanical
ventilation, if
necessary
May need early
hemodynamic monitoring
Optimize Hb
11-13g/dl
Assess volume status(preload)
PCWP<15 volume expansion PCWP>15 consider volume if
PCWP<18 diureses if PCWP>18
Reassess to keep:
PCWP 15-18 mmHg
MAP 60-80 mmHg
SvO2 >65-70%
Delivery independent O2
consumption
Goals not met
Goals met
Inotropic support (b agonism)
Treat inciting cause of shock
Dobutamine
control inflammatory response
Dopamine
nutritional support
Epinephrine
Reassess
Goals met
Treat inciting cause
of shock control
inflammatory
response nutritional
support
Goals not met
Consider vasodilators
Nitroglycenin
Nitroprusside
Consider a agonist
Norepinephrine
Epinephrine
Neosynephrine
Plus
Dopamine
SPECIFIC SHOCK
SYNDROMES
al signs and symptoms of hemorrhagic shock based on severity
loss
Percent loss of circulating blood
volume(volume loss for 70kg
male)
Pulse rate
Systolic pressure
Pulse pressure
Capillary
refi
ll
Respirations
Central
nervo
us
syste
m
Urine output
<15%(<750ml)
15%-30%(7501500ml)
30%-40%(15002000ml)
>40%(>2000ml)
normal
>100
>120
>140
nonpalpab
le
normal
normal
weak decreased
marked
decreased
normal
decreased
decreased
marked
decreased
normal
delaye
d
delaye
d
absent
Normal
Mild tachypnea
Marked
tachypnea
Marked
tachypnea
normal
anxious
confused
lathargic
normal
2030ml
/hr
20ml/hr
negligible
Traumatic shock

Hypovolemic shock with
 1.
larger volume losses
 2. greater fluid sequestration in the
extravascular compartments
 3. more intense activation of inflammatory
mediators development of SIRS
 4. microcirculatory derangements
 5. MODS frequently occur
Traumatic shock
 treatment
 1.
excessive fluid requirements
 2. mechanical ventilation
 3. pulmonary artery catheter monitoring
 4. cardiovascular support
Shock Associated with SIRS,
Sepsis, and MODS

SIRS: two or more of following
 1.
temperature greater than 38℃ or less than
36℃
 2. heart rate greater than 90 beats per minute
 3. respiratory rate greater than 20 breaths per
minute or PaCO2 less than 32mmHg
 4. white blood cell count greater than 12,000
per cu mm, less than 4000 per cu mm or
greater than 10% band forms
VII. Diagnosis of hypovolemic shock



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1. clinical history;
2. physical findings;
3. blood tests.
4. characteristic hemodynamics
1. low right and left sided filling pressures(low
central venous pressure, low PCWP)
 2. decreased cardiac output, decreased SvO2
 3. increased systemic vascular resistance

VIII. Treatment


Patients airway; adequate ventilation, oxygenation
Fluid replacement isotonic electrolyte solutions
Crystalloid --- Ringer’s lactate solution
 Blood transfusion --- type-specific type O packed red
blood cells


Guide treatment

If absent
monitor the central venous pressure
 Place a pulmonary artery catheter



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Then: urinary output rate of 0.5 to 1.0 ml/kg/hour
The pneumatic anti-shock garment
Colloid solution; hyper-tonic saline(controversy)
SEPSIS


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Sepsis: the presence of SIRS in association with
culture-proven infection
Septic shock: sepsis with hypotension despite
adequate fluid resuscitation, along with the
presence of manifestations of hypoperfusion,
including, but not limited to, lactic acidosis,
oliguria, or an acute alteration in mental status.
Mutiple organ dysfunction syndrome (MODS):
the presence of altered organ function in an
acutely ill patient such that homeostasis cannot
be maintained without intervention.
Mortality rate
26% SIRS→Sepsis
Mortality rate: 7%→16%
 4%Sepsis→Septic shock
Mortality rate: 7%→46%
 MODS mortality range from 20% to
100% depending on the number of failed
organs severity of illness scoring systems

MODS
Primary MODS
 Ischemic
 Reperfussion
 direct insult
 Secondary MODS(two-hit model)
 exaggerated uncontrolled systemic
 inflammatory response

clinical features:


fever, tachycardia, hypotension, oliguria
(obtundation, coma)altered mental status.
Leukocytosis or leukopenia increased or decreased
systemic vascular resistance.
Positive microbial cultures
gram-negative bacteria
 escherichia coli, klebsiella
 pseudomonas
 staphylococcus streptococcus spices,fungal, viral ,
protozoal


pneumonia, gastrointestinal perforation biliary tract
infection, urinary tract infection burn wounds
The Two-hit Theory of MODS
First
Hit
Systemic
Inflammatory
response
1°
MODS
Death
Amplified
Systemic
Inflammation
response
Second
Hit
Recovery
2°
MODS
Recovery
Death
1. Pulmonary failure ARDS
 Mortality
exceeds 50%
 ventilation
perfusion abnormalities
 pulmonary edema
 hypoxemia
 decreased functional residual capacity
 decreased infiltrates on chest X-rays
2. Gastrointestinal dysfunction
 Gastritis.
Ulcerations. Pancreatitis;
cholesystitis, mal-absorption, mucosal
atrophy, translocation of bacteria or toxins.
3. Renal dysfunction
Tissue hypoperfusion
 Tissue damage by activated
infalammatory cells and their mediators
 Uremia electrolyte disturbances dialysis

4. Cardiac dysfunction
1 depreesed coronary blood flow
 2 direct endotoxin toxicity
 3 myocardia depressant factor(TNF)

5. CNS manifestation of MODS
 GCS
scoring; mental status the
patients’ best eye opening, verbal and
motor responses
Treatment


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To prevent the progression to MODS. To improve
oxygen delivery and oxygen comsumption
Oxygen delivery: Volume expansion;Provision of
red blood cell mass;Use of pharmacologic
agents:Beta agonists & Vasodilators
For monitoring: e.g. pulmonary artery catheter
For hemodynamic and other physiologic evaluation
Antibiotics: to detect possible sources of
infection(culture)
 Surgical debridement
 Drainage
 Nutritional support

The End