Professional Documents
Culture Documents
Michael L. Cheatham, MD
Ernest F.J. Block, MD
Howard G. Smith, MD
John T. Promes, MD
Surgical Critical Care Service
Department of Surgical Education
Orlando Regional Medical Center
Orlando, Florida
is
one
yet
of
the
poorly
most
frequently
understood
clinical
The
"shock"
in
to
very
definition
critical
of
care
what
constitutes
management,
patients
who
tissue
hypoxia,
anaerobic
metabolism,
improve
patient
outcome
following
the
development of shock.
identification
DEFINITION
Although early definitions of shock lack
scientific terminology and reveal the inadequate
understanding of pathophysiology prevalent at
the time, they compensate for it in simplicity and
accuracy. John Collins Warren described shock
of
the
The ultimate
hypoperfused
state,
This chapter
PHYSIOLOGY
Over the past decade, significant progress
the
improved
physiologic
cascade.
predisposes
tissues
inadequate
machinery
of
tissue
life.
perfusion
With
and
cellular
Cellular
to
"reperfusion
hypoxia
injury"
activation
of
neutrophils
of
tumor
death.
proinflammatory
cytokines
and
such
release
as
lesions,
or
increased
intracranial
pressure.
shock
must
resuscitation,
available.
the
intensivist
physical
measurements.
findings
and
shock.
physiologic
worsening
of
advanced
techniques.
hemodynamic
cardiac
dysfunction
and
self-
Secondary cardiac
monitoring
well known.
Hypovolemic Shock
Hypovolemic shock
is
often
the
hypoperfusion.
first
Physical
activation)
(shunting
blood
topic.
physical
findings
Hinshaw
and
Cox
(proposed
peripheral
volume
stem
hypoperfusion
centrally).
from
the
These
various
Other
cardiac
right
tamponade),
c)
cardiogenic
(shock
sympathetic
atrium
and
responses
activation
of
include
the
renin-
angiotensin system.
myocardial
myocardial
recently
the
contractility
been
increasingly
after
recognized
and
cardiovascular
responses
Vasopressin,
are
almost
instantaneous (3).
is
placed,
the
intensivist
must
for
30%.
body
patient
who
can
compensate
well
fluid
volume
depletion
occurs
Total
as
shock
may
be
further
resuscitation.
aneurysms).
hypovolemic shock.
high
despite
intravascular
hypovolemia.
CLASS I
up to 750
CLASS II
750-1500
CLASS III
1500-2000
CLASS IV
2000 or more
up to 15%
15-30%
30-40%
40% or more
<100
>100
>120
140 or higher
Blood Pressure
Normal
Normal
Decreased
Decreased
Pulse Pressure
Normal/Increased
Decreased
Decreased
Decreased
Capillary Refill
Normal
Decreased
Decreased
Decreased
14-20
20-30
30-40
>35
30 or more
20-30
5-15
Negligible
CNS-Mental Status
Slightly anxious
Anxious
Fluid Replacement
Crystalloid
Crystalloid
Pulse Rate
Respiratory Rate
Urine Output (mL/hr)
Crystalloid + blood
(Modified from: Committee on Trauma of the American College of Surgeons. Advanced Trauma Life Support for Doctors.
loss.
participating
perfusion.
bowel obstruction.
development.
in
end-organ
of
shock-induced
"capillary
leak"
must
be
nonburned tissue.
severely
burned
patient.
Significant
sensitivity
Obstructive Shock
Obstructive forms of shock are those in which
the
underlying
pathology
is
mechanical
and
rapid
performance
Recent
of
the
examination (7).
Pulmonary
thromboembolus
may
Cardiac
shock.
debate (5,6).
pressure (PAOP).
This vascular
myocardium,
(aortic
thromboembolic disease.
Although numerous
regurgitation),
air
myocardial infarction.
embolism
is
diagnosed
clinically
by
reduced
valvular
stenosis,
cardiac
contractility
aortic
dissection),
dysrhythmias
and
catheter.
Unless a lesion
peripheral
vasoconstriction
are
evident
and
oliguria is common.
decreased,
and
not
chest
radiography.
Needle
although
pulmonary
peripheral
examination
and
physical
intravascular
edema,
volume
and
reliably
status.
is
in
occlusion
suggests
mitral
The term
ventricular
dysfunction
as
hemodynamic picture.
may
major
because
their
If inotropes are
output (14).
differences
shock
significant
by
septic
management.
suggested
of
right
of
be
management
in
challenge
to
the
intensivist.
The
In addition to malignant
myocardial disease.
left
cardiac
dilation.
Cardiac
function
Distributive Shock
shock
ventricular
Despite
output
and
systemic
Such hyperdynamic
Conflicting
include
urticaria,
processes.
depression.
24).
dermatologic
etc.)
and
reaction
(erythema,
respiratory
obstructive
parameters
to
cardiac output.
A complex immunologic sequence initiates
septic shock. A variety of potentially inciting toxic
stimuli
are
especially
currently
the
under
role
of
investigation,
endotoxin,
Neurogenic
shock,
another
type
of
The
septic shock.
hemodynamic
hemorrhage,
instability,
should
be
such
as
occult
excluded
before
performance
myocardial
depression
related
cardiac
to
direct
ischemia
shock
stems
from
the
fall
in
Although euvolemic,
space
through
vasodilatation.
If
envenomation (28).
Anaphylactic reactions
In
thyroid
hormone
replacement.
Secondary
evidence of hypogonadism.
Endocrine Shock
In
the
outpatient
hypothyroidism
setting,
Myxedema
coma
is
an
uncommon
patients
and
(34).
manifest
by
with
laboratory
may
demonstrable
patients
respiratory
The
may
reversible condition.
(32).
hypothyroidism
and
accelerated
in
also
present
with
shock.
The
hyperthyroidism (33).
myocardial ischemia.
sign.
In such
panhypopituitarism
patients,
consideration
should be given.
of
Tachyarrhythmias,
including
atrial
The
insufficiency
exists,
concomitant
empiric
treatment
with
development
in
of
relative
response
to
adrenal
certain
10
mortality
to normal ranges.
despite
seemingly
adequate
administration
of
titrated
levels
of
Shock is
PHYSIOLOGIC MONITORING
Perhaps more than for any other disease
Heart Rate
artery catheters.
VITAL SIGNS
The diagnosis of shock was originally based
considered
synonymous
with
shock.
As
and
urinary
output
was
not
Its presence in a
11
titrate
cardioactive
infusions
and
other
Temperature
Patient temperature, although not indicative
of either the presence or absence of shock, may
help define the etiology and can have significant
prognostic value. (40-42) Temperature is most
accurately
measured
thermistor
(i.e.,
by
from
an
intravascular
pulmonary
artery
Blood Pressure
Hypertension is an uncommon finding in
appropriate
(43).
of
anaerobic
shock.
metabolism
Normotension
should
and
be
The
presence
Axillary
of
temperatures
hypothermia
(core
perfusion.
patients.
as
it
suggests
severe
physiologic
pressure
noninvasively
by
may
be
measured
sphygmomanometry
or
Hypothermia
places
for
the
patient
at
risk
cardiac
Both
and
(41,42).
(SBP)
consumption.
and
are
subject to
diastolic blood
mechanical
pressure (DBP)
one
measurements
may
vary
widely
from
12
Pulse Oximetry
process.
hypothermia
perfusion
during
the
should
be
rewarming
avoided
or
rapidly
the
It may
principles
of
spectrophotometry
and
plethysmography,
and
radiologic
commonly
of infection.
and
laboratory
tests
this
technique
deoxyhemoglobin
to
uses
calculate
the
the
For
Of the four
directed
pulmonary
artery
catheter
allowing
thermodilution technique.
multisystem organ
tubular dysfunction).
In 1972, addition of a
This revolutionary
dysfunction
or
refractory
13
right
ventricular
volumes
became
available
critically
ill.
pulmonary
Recently,
artery
fourth-generation
catheters
to
esophageal
Doppler,
echocardiography),
and
designed
These
transesophageal
pulmonary
artery
appropriate
resuscitative
Combining these
therapy.
These
in shock.
MPAP
RVSWI
PULMONARY
RIGHT
VENTRICLE
PAOP
LEFT
VENTRICLE
CVP
LVSWI
MAP
SYSTEMIC
SVRI
FIGURE 1: Measured and calculated hemodynamic variables in the assessment of vascular resistance and cardiac work. MAP
- mean arterial pressure; MPAP - mean pulmonary artery pressure; PAOP - pulmonary artery occlusion pressure; CVP - central
venous pressure; SVRI - systemic vascular resistance index; PVRI - pulmonary vascular resistance index; LVSWI - left
ventricular stroke work index; RVSWI - right ventricular stroke work index
14
Unit
Torr
Torr
Torr
Torr
Torr
Torr
beats/min
L/min
(fraction)
Normal Range
90-140
60-90
15-30
4-12
2-12
0-8
(varies by patient)
(varies by patient)
0.40-0.60
Calculated Variables
Variable (abbreviation)
Unit
Mean Arterial Pressure (MAP)
Torr
Mean Pulmonary Artery Pressure (MPAP)
Torr
Cardiac Index (CI)
L/min/m2
Stroke Volume (SV)
mL/beat
Stroke Volume Index (SVI)
mL/beat/m2
Systemic Vascular Resistance Index (SVRI)
dyneseccm-5
Pulmonary Vascular Resistance Index (PVRI)
dyneseccm-5
Left Ventricular Stroke Work Index (LVSWI)
gmm/m2
Right Ventricular Stroke Work Index (RVSWI)
gmm/m2
Coronary Perfusion Pressure (Coronary PP)
Torr
Cerebral Perfusion Pressure (Cerebral PP)
Torr
Abdominal Perfusion Pressure (Abdominal PP)
Torr
Right Ventricular End-Diastolic Volume Index (RVEDVI) mL/m2
Body Surface Area (BSA)
m2
Normal Range
70-105
9-16
2.8-4.2
(varies by patient)
30-65
1600-2400
250-340
43-62
7-12
>60
>60
>50
60-100
(varies by patient)
decision
making
and
resuscitative
therapy
Preload augmentation is an
Changing
ventricular
compliance
Mitral
valve
disease
15
(LAP).
equal to LAP.
ventricular
compliance
caused
by
state
caused
by
inotropes,
PAOP
reflect
critically
ill
patients
Catheter position
Elevated intrathoracic
or intra-abdominal pressure
FIGURE 2: POTENTIAL CAUSES FOR ERROR IN PAOP MEASUREMENTS
LVEDV - left ventricular end-diastolic volume, LVEDP - left ventricular end-diastolic pressure, LAP left atrial pressure, PAOP - pulmonary artery occlusion pressure
16
PAOP
In fact, reliance
measurements
for
preload
Coronary
perfusion
pressure
should
be
patients (55).
Thus, every
perfusion is compromised.
important
in
the
head-injured
patient
with
increased ICP.
patient in shock.
brain:
Coronary perfusion
myocardial
myocardial
perfusion.
wall
tension
PAOP
and
estimates
resistance
to
17
athletes.
Flow-related
In order to
18
Increased
obstructive,
SVRI
is
hypovolemic,
commonly
late
seen
septic,
in
and
rise
as
increased
in
non-shock
pheochromocytoma
states
(secondary
such
to
increased
intra-abdominal
pressure
LVSWI = (MAP-PAOP)(SVI)(0.0136)
(gm/m2)
RVSWI = (MPAP-CVP)(SVI)(0.0136)
(gm/m2)
The
stenosis,
myocardial
depression/ischemia/infarction,
pulmonary
hypertension,
occur
despite
normal
systemic
perfusion
pressure.
advanced
age.
When
and
As
(increased
MAP
or
MPAP)
or
Volumetric Variables
19
increases
in
artifactually
intrathoracic
increase
pressure
PAOP
and
may
CVP
measurements (71-73).
changes
specialized
cardiac
to
With
A combination of
the
catheter
output
computer
and
allow
recognition
of
the
limitations
of
over
the
safety
of
right
heart
fraction
volumetric
(RVEF),
providing
an
online
preload
assessment
have
been
developed.
status.
This
intrathoracic
blood
volume
(ITBV).
This
via
volume
cardiac
Esophageal
also
(70,71).
mechanical
end-
techniques
has
been
efficacious
nor
do
increased
ventilation
with
intraabdominal
positive
pressure
where
pulmonary
artery
catheter
measurement,
output
been
pulmonary
Doppler
(74).
requirement
artery
for
found
they
made
catheters.
ultrasonography
advocated
The
and
hemodynamic
to
allow
Although
be
more
continuous
20
discussed below.
Oxygen Transport
delivery
and
consumption
in
the
two forms.
Oxygen transport
When
regional
acidosis,
Left
shock-induced
and
cellular
systemic
death
or
result.
PULMONARY
RIGHT
VENTRICLE
CvO2
PvO 2
SvO 2
CcO2
PAO2
LEFT
VENTRICLE
Ca-vO2
OUC
SYSTEMIC
CaO2
PaO2
SaO 2
FIGURE 3: The vascular circuit of the body: oxygen content, tension, and saturation can be defined at any point in the body.
CcO2 - pulmonary capillary oxygen content; CaO2 - arterial oxygen content; CvO2 - venous oxygen content; Ca-vO2 - arteriovenous oxygen content difference; PAO2 - alveolar oxygen tension; PaO2 - arterial oxygen tension; PvO2 - venous oxygen
tension; SaO2 - arterial oxygen saturation; SvO2 - mixed venous oxygen saturation; OUC - oxygen utilization coefficient.
21
aerated
alveoli.
In
normal
patient,
law:
CaO2
PAO2 = alveolar oxygen tension =
FiO2(PB-PH20)-(PaCO2/RQ)
where:
plasma
blood
due
to
the
introduction
of
The venous
22
The
arterial-venous
oxygen
600 mL O2/min/m2
content
= CaO2 - CvO2
5 mL O2/dL blood
= (Ca-vO2)(CI)(10 dL/L)
150 mL O2/min/m2
tissue
oxygen
delivery
concentration.
The
is
optimal
hemoglobin
hemoglobin
critically ill.
controversy,
balance
Values indexed to
while
the
optimal
minimizing
hemoglobin
the
potentially
Judicious
23
approximated as 1- SvO2.
perfused tissues.
unloading of oxygen.
Once these variables have been derived,
Two
additional
variables
delivery
and
(supply"
versus
"demand):
utilization
oxygen
oxygenation
consumption
the
oxygen
follows:
= VO2 / DO2
0.25
dedicated
resulting
computer
blood
system
temperature
measures
the
changes
and
Normal Range
70-100
35-50
0.93-0.98
0.70-0.78
36-42
13-17
Calculated Variables
Variable (abbreviation)
Unit
Oxygen delivery index (DO2)
mL/min/m2
Oxygen consumption index (VO2)
mL/min/m2
Arterial oxygen content (CaO2)
mL O2/dL blood
Mixed venous oxygen content (CvO2)
mL O2/dL blood
Arterial-venous oxygen content difference (Ca-vO2)
mL O2/dL blood
Oxygen utilization coefficient (OUC)
(fraction)
Respiratory quotient (RQ)
(fraction)
Intrapulmonary shunt (Qsp/Qt)
(fraction)
Normal Range
500-650
110-150
16-22
12-17
3.5-5.5
0.22-0.30
0.7-1.0
0.03-0.08
24
Continuous cardiac
advantages
ill
patient
exhibits
significant
previous
of
measurements
the
determination
assessment
intermittent
over
critically
thermodilution
of
continuous
cardiac
output
intensivist
of
with
minute-to-minute
hemodynamic
function
and
oxygen
available.
thermodilution
Second,
methods
(84).
transport
These
balance
not
capabilities
previously
allow
earlier
7
6
5
4
3
2
1
0
0:00
3:00
6:00
9:00
12:00
Time (hours)
FIGURE 4: Continuous cardiac output monitoring allows detection of hemodynamic changes missed by use of
conventional intermittent cardiac output techniques (diamonds).
25
bed.
process.
It
requires
constant
to interpret.
otherwise
result.
may be utilized.
hemodynamics
generally
excess
the
allowing
technique
and inflammation.
to
pulmonary
of
artery
reflectance
catheter
spectrophotometry.
of
consumption.
This
state
of
oxygen
hemoglobin
VO2.
saturation
concentration,
and
cardiac
tension,
output,
and
Continuous
hemoglobin
such errors.
increase
oxygen
delivery
(SaO2,
the
SvO2
measurement.
Proper
26
and
artery
catheter
derived
hemodynamic
before
clinically
using
randomized
otherwise go unnoticed.
physiologic
deterioration
is
goal-directed
study
of
prospective,
Oxygen Consumption
supranormalization
protocol
(92).
supranormal
oxygen
Yu et al. performed a
randomized
in
trial
a
of
combined
post-operative
lower
complications
(89).
They
mortality
rate
(94).
Both
Yu
and
cannot
interventions
survivors
that
some
(90).
They
hypothesized
mL/min/m .
be
optimized,
and
despite
are
able
to
patients
never
spontaneously
all
achieve
achieve
larger
physiologic
reserve
and
27
liver
accumulate
Thus, although
resuscitation
false
endpoints
per
se,
they
are
and/or
kidneys.
in
Third,
tissues
impression
of
during
lactate
periods
may
of
Fourth, excessive
perfusion
inadequacy.
critical illness.
Arterial Lactate
Shock
is
(i.e.,
shock
resulting
in
hepatic
hypoperfusion).
hypoperfusion
resulting
in
The
anaerobic
metabolism
triphosphate
resuscitation
oxygen
pathologic process.
improved
anaerobic
by
adenosine
and
albeit
make
grossly
continued
(ATP),
to
the
tissue
conditions,
Under
however,
respectively (100).
101).
28
Base Deficit
The treatment of
allowing
spontaneous
resolution
of
with
Serial
(104,105).
measurements
of
lactate
during
the
presence
It
and
The normal
severity
predicts
fluid
of
shock
resuscitation
lactic
aggressive
acidosis
occurring
during
Further, it
Base deficit
resuscitation adequacy.
Several
authors
have
documented
the
morbidity
Often
of
mmol/L.
central
be
the ICU.
following
venous
aggressive
lactate
restoration
levels
should
and
mortality
in
trauma
patients
29
<7.32
correlated
with
mortality
and
the
(109,115,116)
unclear (117).
tissue
less
perfusion
has
therefore
become
than
widespread
utilization
of
gastric
widespread.
Further
brain
shock.
and
heart
at
the
expense
of
the
studies
are
needed
to
prove
the
elevated
(118).
called
intra-abdominal
pressures
in
the
hypertension"
and
well-documented (71,73,118).
applied
to
measure
malperfusion
of
the
The significant
afforded
techniques
practiced (71,118).
through
is
now
use
widely
of
abdominal
recognized
and
tissues
(107,108).
Intramucosal
114).
Calculated as the
30
Preload
in
patients
pressures
with
as
elevated
result
of
intra-abdominal
intra-abdominal
exists.
(73).
Therefore,
the
initial
therapeutic
mortality
profound hypotension.
in
surgical
and
trauma
patients.
Additional crystalloid
to
reduction
be
useful
endpoint
in
guiding
the
in
tachycardia,
restoration
of
abdominal pressures.
output,
return
of
improvement in
TREATMENT PRINCIPLES
normal
oxygen
mentation,
transport
and
variables.
catheters.
significantly
of end-organ failure.
Since
Optimal access is
resistance
reduce
resistance
is
to
inversely
flow
of
sites
shock
hemodynamic
catheter
states.
Utilizing
the
are
unavailable,
placement
as
central
compared
venous
to
the
to
optimize
the
patient's
end-organ
The
continues
crystalloid
to
be
versus
waged
colloid
despite
debate
abundant
31
Recent meta-
historically
with
colloids
being
restricted
indications (120-122).
to
specific
No survival benefit is
touted
to
treat
shock
prior
to
Recently, this
studies
circulation (126).
(124).
Large
volume
crystalloid
fail
to
demonstrate
consistent
Contractility
Resuscitative
therapy
aimed
to
alter
hypothermia.
of
output.
Cardiac
is
at
risk
for
iatrogenic
dysrhythmias
may
present
with
supraventricular
tachyarrhythmias
in
the
stimulation
resuscitation
of
from
shock.
Prevention
may
help
ameliorate
the
32
will
frequently
benefit
from
resetting
their
overall.
made.
Dopamine,
naturally
occurring
Norepinephrine
is
naturally
both
alpha
occurring
catecholamine
considered
dopamine
appropriately
(127,128)
renal
dose
in
that
with
volume
repleted
and
beta
patient
who
beta
effects.
receptors.
High
dose
therapy
(10
phosphodiesterase
(133).
hypotension.
In
some
III
inhibitor,
raising
In patients with
patients,
its
vasodilatory
Afterload
dopamine,
does
norepinephrine.
not
directly
release
persistently
hypotensive
patient
cannot
The
be
33
resuscitation,
especially
in
patients
with
decreased contractility.
In this
perfusion
by
reducing
coronary
perfusion pressure.
Oxygen Transport
Nitroprusside
myocardial
Alternatively,
primarily
capacitance,
ischemia
affecting
exist.
venous
Angiotensin
Further
function.
Restitution of adequate levels of hemoglobin
Afterload may also be reduced mechanically
IABP is
the
after
immediate
postoperative
period
significantly
improve
oxygen
transport.
IABP demonstrates
unchanged.
afterload
reduction
may
be
34
When hemoglobin
may
oxygenation.
further
decrease
Further
tissue
compounding
the
have
tended
to
Such studies,
exclude
certain
therapy.
Inadequate
tissue
complication
of
end-organ
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