The Relationship

Between Oxygen Delivery

and Consumption
during Fluid
Resuscitation
of Hypovolemic
and
Septic Shock*
Brian

The

S. Kaufman,

effects

of

M.D.;

increasing

Eric

C. Rackow,

oxygen

delivery

and Jay L. Falk,

M.D.;

(l)o,)

on

386 48 mI/minim
(p <0.01) and Vo, increased
from 96 9
to 1356
mI/min/m
(p <0.Ofl
There
was
no significant
difference
in either the increase
in Do, or Vo, between
the
septic shock and hypovolemic
shock patients.
We conclude
that increasing
Do, by fluid resuscitation
increases
Vo,
during both hypovolemic
and septic shock.

oxygen

(o,) in eight patients

with
septic
shock
and
five patients
with hypovolemic
shock
were
studied
during
fluid resuscitation.
In the septic shock group, Do, increased
from
31529
to 42425
mI/min/m
(p <0.01)
and Vo,
increased
from
134 8 to 151 7 mI/min/m
(p <0.01).
In the
hypovolemic
shock
group,
Do,
increased
from
239 26 to
consumption

ecovery
from
restoration
oxygen
utilization
respiratory
Decreases
circulatory

circulatory
shock is dependent
on the
of oxygen
delivery
and subsequent
for oxidative
phosphorylation
by the

controversial.
Some authors
believe
shunting
with a resultant
deficiency
lary flow occurs,
whereas
others
cellular
utilize
This

in a terminal

function
delivered

with an
oxygen.

All patients

prospective

study

was designed

catheterization

with

continuous

pulmonary

ing in order

to guide

fluid

challenge.

volume
Data
dynamic

mean

and

arterial

the

supine

and septic

shock.

volume

loading

patients

ranged

(38 percent)
percent)
Patients
tions

oxygen

in age from
of the

blood

culture

revealed:

into

1) a cardiac

systolic

intra-arterial

lactate

greater

septic
the
index

pressure
than

pressure

(PAWP)

less

the study

if they

were:

(CI)

of less

18 mg/dl,
than

and

15 mm

1) less

than

shock.

Sepsis

less

than

3) a pulmonary
Hg.

Patients

18 years

verified

Ellis

Hospital

and

The

Division

pulmonary
output

with

ar(CO),

patient

in

Bell

and

zeroed

to atmosphere
All

monitor

Derived

were

(SOLO,

was taken

10 ml of 5 percent

and

pressures

Mennen
as the

dextrose

mean

in water

hemodynamic

stroke
volume
(UVSWI),
and

from the following

index
systemic

data

(SVI),
left
vascular

formulae:

BSA
2)

by

SVI

(mi/rn)

L/min/m

or a

3)

LVSWI

4)

SVR(dynes.sec.cm)

(g-m/m2)

CO
x BSA
(SVI) (MAP-PAWP)

x 0.0136

80

2) an arterial
excluded

of age,

2) considered

of Critical

Care

Lactate

wedge

samples

from

preservative

to be

measured

within

Medicine,

is less

of Health
SciencesfFhe
Chicago
Medical School,
North
Illinois.
Manuscript
received
May 20; revision
accepted
September
13.
Reprint
requests:
Dr Rackow,
UHS/CMS,
3333 Green
Bay Road,
North
Chicago,
Illinois
60064
University

Downloaded From: http://journal.publications.chestnet.org/ on 08/28/2014

arterial
blood
saturation

Oxygen

Delivery

drawn

tube
The

from

that

20 minutes

Abbott).
than

was

with

normal

the

arterial

line

immediately
an automated

arterial

lactate

into

placed

a sodium
on ice,

and

spectrophotometer
level

in our

laboratory

7 mg/dl.

Primary

Chicago,

336

were

fluoride
(ABA-SO,

5From

mean

the

output

10 C.

hemopressure

cardiac

standard.

(C),
index

calculated

HR

artery

were

(SVR)

(62

determinaHg,

resistance

than

hemo-

(720!,

position,

cardiac

less

clinical,

transducers

microprocessor

index
work

1) CI (Limin/m)

Five

site.
2.2

90 mm

to

cardiac
stroke

during

intra-arterial

recorded

gauge

using

delivery

The
Eight

was

if pretreatment
than

1.

whom

81 years).

of an infected
study

in

investigated.

(median

shock.

in Table

shock

in hypovolemic

or identification

entered

is given

were

years

were
had

data

cooled

included
ventricular

mean

were

Thermodilution

meaduring

Primary

(VP),

mercury

a bedside

of

thermodilution

mid-chest

known

measurements

injectate

circulatory

delivery

661097

patients

patients

were

patient

with

patients

increased

of the

positive

individual

oxygen

inlbrmation.

strain

un-

and metabolic
30 minutes

consisted

(HR),

All pressures

monitor-

15 minutes

to baseline.

pressure

utilizing
to the

to

of triplicate
METHODS

venous

lactate.

leveled

rate

(PAW!),

position

Howell)

patient

Laboratories)
pressure

ml every

of maximum

heart

pressure

with

of the

artery

of 250

respiratory

(cardiac
loading.

Becton-Dick-

Edwards

for comparison

each

central

wedge

point

and

data included

(iXP),

how

on

metabolic

mc).

consecutive

challenge

was chosen

collected

dynamic,

tery

The

loading

Medical,

A summary

a fluid

delivery

to volume

(Longdwell,

(Swan-Ganz,

recorded

Thirteen

artery

artery

calibrated

AND

femora!

underwent

increases
in oxygen
delivery
during
volume
loading
affect oxygen
utilization
in patients
with hypovolemic

MATERIALS

oxygen

in response

pulmonary

the

to

to evaluate

to increase

content)

til the PAWP reached

15mm
Hg. Hemodynarnic
surements
were obtained
at baseline
and every

shock
is a reThe etiology
of
in septic
shock is

of mitochondria

or 3) fliled
oxygen

and

inson)

that arteriovenous
in nutrient
capilimplicate
impaired

inability

state,

x arterial

output

enzymes
of the mitochondria.
of oxygen
consumption
in patients
with
shock correlate
with mortality.2
The decline

in oxygen
consumption
in hypovolemic
sult of a decrease
in oxygen
delivery.3
the decrease
of oxygen
consumption

M.D.

respiratory

blood
(PO,),

(Pat),),
arterial

of arterial

and Consumption

data included
the

partial
hemoglobin

blood,

during

the partial

pressure

pressure

of oxygen
(Hb),

and percentage
Fluid Resuscitation

of oxygen

in mixed

percentage
of oxygen

(Kaufrs,an,

of

in

venous
oxygen

saturation

Rackow,

of

Felt)

Table

1-Summary

of

Patient

Data

Survived

Case

Clinical

No.

Age

Sex

Features

of shock

Type

Culture

24 Hours

bleed

Hospital

85

Hypovolemic

UGI

66

Hypovolemic

Hanging

no

no

no

97

Hypovolemic

Cardiac

no

no

yes

no

no

no

yes

no

arrest
4

87

Hypovolemic

Acute
infarction

85

Hypovolemic

Dehydration

76

Septic

Perforated

+ blood

cecum
7

83

Septic

Peritonitis

yes

no

82

Septic

Urinary

tract

+ blood

yes

yes

Septic

infection
Urinary

tract

+ blood

yes

no

no

no

yes

no

yes

no

yes

no

88

infection,
cholangitis
10

80

Septic

Ischemic
colitis,
peritonitis

11

73

Septic

Urinary

tract

+ urine

infection
12

75

77

13

Septic

Acute

Septic

abdomen
Gangrenous

small
mixed

blood.

venous

oxygen

content

venous
ratio,

Derived

(CaO,),

oxygen

content

calculated

from

1) CO,

(vol%)

2) A-VdO,
3) oxygen
Blood

extraction

gases

(ABL

2,

were
and

using

Derived
oxygen

metabolic

2) Vo,

(mi/min/m)

analysis

Statistical

CI

(A-VdO,)

standard

error

at

the

There

Hemoglobin
measured

di-

0.05

creases
fluid

index

(Do,)

were

no

of PAWP,
challenge

between

SVI,

septic
and

Vo,

the

in-

2.

significant

CI,

in the
in l3o,

differences
LVSWI,

the

in

MAP

and

13o, with

hypovolemic

and

septic

and

HYPOVOLEMIC

200

SHOCK

x 10
utilizing

mean

changes

as follows:

samples

of the

(p <0.01)

shock

10

accomplished

dependent

gas laboratory

were
delivery

calculated

significant

considered

(Vo,)

Cat),

were
mean

oxygen

and

blood

134 8 to 151 7 mI/minim

patients.
The individual
are shown
in Figures
1 and

Radiometer).

CI

for independent

extraction

(Po,)

hourly.

saturation

was

+ 0.003

calibrated

(OSM-2,

index

(mi/min/m)

was

data included

consumption

1) Do,

oxygen

mI/minim
(p <0.01).
The increase
in 13o, was associated with a significant
increase
in Vo, in both patient
groups,
rising
from
969
to 1356
ml/min/m2
(p <0.04)
in the hypovolemic
shock patients
and from

A-VdO,
CaO,

oxyhemoglobin

a hemoximeter

and

by an automated

which

arterial-

CVO,

(%)

measured

arterial

(CO,),

ft)rmulae:

x (% sat)
-

ratio

Radiometer)

concentration

rectly

(Hb)

included

content

(A-VdO,)

following

Cat),

data

oxygen

difference
the
1.34

(vol%)

respiratory

venous

bowel

level.

(two

the

Students

tailed).

t test

175

Differences

All data are reported

as

(M).

iso
E

RESULTS

The

time
78 18 mm

to peak
13o, during
in the hypovolemic

mm in the septic
group
values
to values
obtained
increases
the septic

cant

both
A-VdO,

fluid challenge
patients
and

was
66 II

(NS). Comparison
of baseline
at peak Do, revealed
signifi-

125
E
01

0
100

in PAWP, CI, SVI, LVSWI

and MAP in
and hypovolemic
group of patients.
The

#{149}
Ba..Iipe
#{149}
Peak 002
75
Mean

and

the oxygen
extraction
ratio decreased
in
both
groups,
but nOt significantly.
Fluid
resuscitation
resulted
in a significant
increase
in Do, in both groups.
In

the

hypovolemic

shock

239 25 to 386 48 mI/minim

shock

group,

13o,

increased

group

Do,

increased

100

200

300

602
FIGURE

consumption

400

500

600

mi/mIn/m2

1. Effect
of increases
in oxygen
(Vo,) in five patients
with

delivery
hypovolemic

(bo,)

on
shock.

CHEST I 85 / 3 I MARCH,

Downloaded From: http://journal.publications.chestnet.org/ on 08/28/2014

SEM

P<O.05
P<0.o1

50

from

(p <0.01).
In the septic
315 29 to 424 24

from

t
*

1984

oxygen

337

200

SEPTIC

175

SHOCK

severity

//

01

E
C

of circulatory

Interventions

which

be expected

to increase

al3 noted

cardiac
challenge

E
01

125

0
.>

that

increase

patients

oxygen

oxygen

patients

index
and
usually

sumption.
patients

#{149}
Baa.lipe
#{149}
Peak

75

00

Mean

50
100

200

300
602

2. Effect

consumption

of increases

(Vo,)

500

delivery

600

in shock

delivery

delivery

with

(bo,)

septic

on oxygen

shock.

who

increased

The

groups.
no

At comparable
increases
significant
difference

Vo,
between
patients
(Table

hypovolemic
2).

shock

in CI and 13o,;
the increase
in

in

and

septic

lary
consumption

metabolism.
determined
Wilson
decreases
increases

by

is an overall

The
optimal
the metabolic

index

oxygen
needs

of total

body

ill patients
that
associated
with
that in patients

between

in patients
with
in cardiac
output
in oxygen
con-

During

of

or the

in

loss,

inadequate

is still unclear.
theories
to

of a cellular

be

such

occurs

in

fluid

intake,

with

sequestration

may

development
Increases

in

have

and Septic

Hypovolemic

septic

insensible

some

within

septic

polyuria

cellular
of the

shock.3

of fluid

In addition,

of a hyperdynamic
capillary
permeability

delivered

to pre-existing

increased

an inappropriate

fluid accumulation
and
postulated
as a cause

the
this

metabolic

that

secondary

decreased

patients

oxygen
of a lactic

At present,
account
for

level

or peritonitis

cavity.4

shock
de-

the redistribution
of blood
decrease
in nutrient
capil-

commonly

the peritoneal

oxygen

in septic
metabolic

development

development

may

fluid
oxygen

and

increases

subsequent

hypovolemia

illness,

septic
shock
oxygen
consumption
was inversely
related
to arterial
lactate
level.
Indeed,
the development
of anaerobic
metabolism
and consequent
lactic
acidosis
serves
as a metabolic
marker
of shock
and a
prognostic
indicator
in critically
ill patients.#{176} The
2-Difference

significant

at the mitochondrial
cannot
be utiuized.

Hypovolemia
The

with

Table

after
fluid
hypovolemia.

studies.
output

pathophysiology
and

flow,

blockade
oxygen

consumption
is
of the tissues.

et al documented
in critically
in oxygen
consumption
were
in mortality.
Duff et al noted

in

debt
are either
with consequent

oxygen

DIScUssIoN

Oxygen

previous
in cardiac

acidosis
in septic
shock
most
widely
accepted

shock

shock

due

renal

with

to the

circulation.
interstitial

edema
has
intravascular

also been
volume

Shock
HS

Hypovolemic
Baseline
HR(beats/min)
MAP(mm

Hg)

PAWP(mmHg)
CI

IJmin/m

SVR(dynes.sec.cm)
}Ib(g/dl)

PaO,(mm
PaCO,(mm
PcO,(mm
A-VdO,(Vol%)

Hg)
Hg)
Hg)

Peak

Sh ock
#{246}o,

(HS)
ABaseline

Septic
p<

Baseline

Shock

Peak

bo,

Baseline

p<

NS

85.67.1

-44

NS

-98

NS

NS

67.05.4

+ 174

.01

56.52.6

71.73.8

+ 155

.02

NS

7.17

10.61.3

+3.50.9

.02

7.40.8

13.61.3

+6.11.4

.01

NS

1.560.12

2.540.26

+ 1.00.2

.01

2.3436

3.48.25

+ 1.10.2

.001

NS

1368

1167

NS

1207

NS
NS

12.30.6

11.70.7

-0.60.1

.01

11.41.2

9.30.6

-2.00.7

98.819.0

+5.67.0

NS

14219

17125

+29.014.6

NS

NS

34.92.0

33.23.1

-1.72.2

NS

292

302

0.71.1

NS

NS

31.23.3

34.81.8

+3.62.5

NS

44.82.0

+3.22.0

NS

NS

6.4.9

5.50.5

-0.90.7

NS

7.11.4

4.4.3

-2.71.2

NS

NS

+147.029.9

.01

314.528.7

423.725.4

+109.223.6

.01

NS

+39.013.0

.04

133.87.5

150.57.1

+16.63.8

.01

NS

-5%4%

NS

45%5%

36%2%

NS

NS

NS

78.215

68.018

NS

NS

38648.1

238.526.2

o,(ml/min/m)

95.79.1

O,Ext(%)

42%6.7%

37%5.0%

Lactate(mg/dl)

66.417.3

52.011.1

134.85.8

-14.38.0

338

Downloaded From: http://journal.publications.chestnet.org/ on 08/28/2014

Oxygen

41.7

Delivery

1.9

and Consumption

-372

166

93.219.0

J3o,(ml/min/m

281

835 124

NS
.03

200 84

10

vs SS

Baseline

50.25.1

172

101

(SS)

89.68.6

136

1118.0

et

their

effects
of fluid resuscitation
in our five
hypovolemic
shock
are consistent
with

resulted

mands.

would
Mohr

oxygen
consumption
had
shock
due
to

of these
increases

consumption
was

is docu-

consumption.

consumption.
The oxygen
consumption
patients
is inadequate
to meet
their

mi/mIn/m

in oxygen

patients

in eight

400

The

with

the findings
challenge,

SEN

P<0.0i

shock
there

in our

Siegel
and
associates4
noted
that
hypovolemic
shock small increments
were associated
with
large increments

100

FIGURE

shock

mented
by the profound
lactic acidosis.
Oxygen
consumption
decreases
in hypovolemic
shock
as a result
of a decrease
in oxygen
delivery.

-9%4%
-19.26.0

during

Fluid Resuscitation

(Kaunan.

Rackow.

Felt)

depletion.7
plasma

Nishijima
volumes

more,

they

et

al

Ibund

have

documented

with

septic shock.
relationship
between

in patients

a close

low
Furthercardiac

Loeb
atrial

and plasma
volume
in septic
shock patients.
and associates#{176} documented
decreases
in right
pressure
despite
normal blood volume
in patients

with

septic

output

venous

shock,

pooling

possibly

of blood.

related

Thus,

in patients
with septic
shock
venous
return
and therefore
the

to

the initial

weighted

may be a function
of the
the preload
presented
to

have stressed
the beneficial
effects
in patients
with either
hypodynamic

or hyperdynamic
septic
shock.4371
been reported
to be improved
in patients
crease
their
stroke
volumes
or cardiac
response
to fluid challenge.
Nevertheless,

associates#{176} demonstrated
tients
in septic
shock
sumption
ever, the

despite
baseline

challenge
tive

200

of

fluid challenge
in pato increase
oxygen
con-

mI/min/m.

consumption

The

elevated

oxygen

and thus,
oxygen
consumption
to increase
further.
The
on oxygen

resuscitation

with

septic
study.
We
oxygen

shock
found

delivery

cantly

increased
that

suggests

consumption

do not support
that increases
in response
total

the

Howto fluid
level

of

patients
may be indicadelivery
prior
to volume

in these

adequate

loading,
expected

on oxygen
Mohr
and

hemodynamic
improvement.
oxygen
consumption
prior

was

oxygen

that
failed

of

Survival
has
who can inoutput1
in
few data are

available
on the effect of volume
expansion
consumption
in patients
with septic
shock.

of

in our

not be
fluid

patients

the findings
of Mohrs
in cardiac
output
and

to volume

body
increase

would

effects

loading

signifi-

reflected
increased
nutrient
capillary
blood
flow. The
most probable
explanation
for the differing
response
to
volume
loading
in our septic
shock
patients
versus
those
in Mohrs
series
is that the initial
oxygen
consumption
in our patients
was only
134 mI/min/m,
of a more

of volume
representative

loading.
Alternatively,
of an early
state

oxygen

delivery

sumption,

profound

may

be

state

rate

metabolic

block

to oxygen

shock,
oxygen
mixed

in our

time

our patients
may be
of septic
shock where
limiting

utilization

The
increase
of oxygen
resuscitation
in patients
with
capillary

at the

to oxygen

con-

septic

shock

suggests

was

a deficit

a redistribution
of blood
normal
or increased.48

be

in nutrient

delivery

with

if other
areas
in areas
of

expected

to

be

bodys

maintained

inadequate

receive
decreased

tissue

excessive
nutrient

decreased.

genation
blood
these

flow
flow

Huller

et

al

decreased

even

though

arterial

oxygen

and

pressure
were initially
maintained.
In addition,
authors
ibund that there was no primary
injury to

hepatic

mitochondria,

gen
hand,

utilization

but

rather

efficiency
et al found

Wright

mitochondrial

increased.
that in

oxy-

On the
dogs
with

other
sepsis

output
was accompanied
blood
flow but decreased

by inoxygen

extraction.
Finley
et al documented
similar
that increases
in cardiac
output
were
not
with decreases
in capillary
blood
flow in

results
in
associated
septic
pa-

tients,
isted.

shunts
blood

increased

cardiac

creased

capillary

as would
Since both

during
shock,
flow

be expected
if anatomic
studies
evaluated
capillary

the hyperdynamic
they do not exclude
as the

mechanism
during

septic

septic state
a decreased

Our findings
that at comparable
index
and oxygen
delivery
there
difference

in

the

increase

between
hypovolemic
are consistent
with
unaltered
mitochondrial

in

exflow

but not in septic

capillary
blood

leading
to increased
shock.

anaerobic

increases
was no
oxygen

of cardiac
significant

consumption

shock and septic

shock patients
the experimental
findings
of
utilization
of oxygen
in septic

shock.
They do not support
the hypothesis
that the
patient
in septic shock cannot
consume
oxygen
due to
mitochondrial
blockade.7
To the contrary,
we conclude

that

increasing

resuscitation

oxygen

increases
with

both

delivery

tissue

oxygen

hypovolemic

and

1 Clowes

GH.

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of

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Little,

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1969;
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APH,

CHEST I

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be

tissue
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in dogs injected
with E coil
endotoxin
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venous
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oxygen
was
decreased.
Similar
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by Fry et al
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of septic
shock.
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oxy-

2 Wilson

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areas

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be expected
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in
as was true of the patients
the deficit
may result
from

flow, as oxygen
An inefficient

would

effluents

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