Transcript SHOCK - Stanford University

SHOCK
History
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First used as a term to denote physiologic
instability in 1815 by then English surgeon,
George James Guthrie
Before then a variety of more colorful terms
were used to denote shock states:
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“final sinking of vitality”
“great nervous depression”
“sudden vital depression”
Modern Working Definition
 The
reduction of effective
tissue perfusion leading first to
reversible, then to irreversible
cellular injury
Traditionally catagorized
 Hypovolemic
 Cardiogenic
 Vasogenic
(Distributive)
 Obstructive
Alternatively…..
 Failure
of Cardiac Output
 Failure of Peripheral
Resistance
???? This is the time for audience
participation.....WAKE UP
CO
= ____ x ____
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CO
= SV x HR
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Failure of Cardiac Output

Heart Rate
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Too slow
Too fast
No flexibility to adjust to
need
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Stroke Volume
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Failure to receive
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Hypovolemia
MS
Tampannade
Failure to eject
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CHF
PE
Outflow obstruction
Ohm’s Law of the Heart???
again, this is YOUR turn to talk..
MAP
= ___ X ___
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MAP
= CO x SVR
systemic vascular resistance
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Failure of Peripheral Resistance
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Anaphylaxis
Sepsis
Loss of vasomotor tone
Spinal Shock
Vasodilatory Shock
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SO……practically
speaking how does this
help you care for
patients?

You are called to the ED at the Valley.
There is a 2 year old, hit by a car.
His VS: 66/48 180 28 92% (on
oxygen) You are IT. The trauma team is
busy with is mother who is in full arrest.
The PICU attending is 30 minutes away.
What do you do??? There was no LOC.
He is moaning and localizing to painful
stimuli. There is a noticeable tire mark
across his pelvis which is unstable on
exam.
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The Proxy Measure
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Blood Pressure
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Ohm’s Law: V=IR (MAP=CO x SVR)
Measureable since the early 1900’s
Hypotension is late for most patients
Still..it is the proxy measure
Interventions
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ABC’s
Volume
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Salt
More salt
Colloid
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Albumin or Starch
Vasoactive medications
Diagnostic Labs
Volume
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Saline
Ringers
Albumin
Starch solutions
Hypertonic salt
How much?? When to say when
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Positive fluid balance infers or confers morbidity
Vasoactive Medications
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Which one?
How much? When to say when or when
to say ECMO?
Dopamine..Why? Why not??
Vasopressin.. Why?? Why not??
The other interventions
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Central Access?
Arterial Access?
Antibiotics?
Corticosteroids?
Blood products?
In parallel to exogenous
support....the response of the body
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Catacholamine release
Vasopressin surge
Aldosterone and ADH
defend intravascular
volume
Corticosteroid levels rise
Insulin in suppressed,
GH increases
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 And
yet, even when we execute
the perfect resuscitation and the
body defends itself without limit,
the irreversible nature of the
initial insult often prevails. The
patient develops MODS (MSOF)
and dies....
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What is on the horizon?
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The Aquatic Turtle?

Has the capacity
to downregulate
metabolic pathways
during hypoxia and
upregulate that
activity when O2
is available...
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Inducing hypoxia tolerance
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Closer to the bedside
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Hydrogen Sulfide
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Third gaseous transmitter (NO, CO)
Dose dependent pro or anti-inflammatory
Dose dependent pro or anti-apoptotic
**Inhibits cytochrome c oxidase
Protects animals from MODS after
hemorrhagic shock and profound
hypoxemia
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Matches supply and demand
October 10, 2006 | 1 comments
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 Suspended
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