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 135±6
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
315±29
to 424±25
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

a

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)

but nOt significantly.05 creases fluid index (Do. cholangitis 10 80 M Septic Ischemic colitis. CI. CI for independent extraction (Po.01). CaO. increased 100 200 300 602 FIGURE consumption 400 500 600 mi/mIn/m2 1.04) in the hypovolemic shock patients and from A-VdO.) following Cat). Downloaded From: http://journal.01). fluid challenge patients and was 66 ± II (NS).003 calibrated (OSM-2. Derived (CaO. index (mi/min/m’) was data included consumption 1) Do. saturation = was + 0. were and using Derived oxygen metabolic 2) Vo. the in MAP and 13o. in the in l3o.34 = (vol%) respiratory venous bowel level. (%) measured arterial (CO. venous oxygen content venous ratio. = data oxygen difference the 1.). Age Sex Features of shock Type Culture 24 Hours bleed Hospital 1 85 M Hypovolemic UGI 2 66 F Hypovolemic Hanging no no no 3 97 F Hypovolemic Cardiac no no yes no no no yes no arrest 4 87 F Hypovolemic Acute infarction 5 85 M Hypovolemic Dehydration 6 76 M Septic Perforated + blood cecum 7 83 M Septic Peritonitis yes no 8 82 M Septic Urinary tract + blood yes yes Septic infection Urinary tract + blood yes no no no yes no yes no yes no 9 88 M infection.. SVI. rising from 96±9 to 135±6 ml/min/m2 (p <0. were mean oxygen x and blood 134 ± 8 to 151 ± 7 mI/minim’ patients. challenge between SVI. t test 175 Differences All data are reported as (M). In the septic 315 ± 29 to 424 ± 24 from t * 1984 oxygen 337 .) on shock. Fluid resuscitation resulted in a significant increase in Do.chestnet. The #{149} Ba.) in five patients with delivery hypovolemic (bo. (vol%) 2) A-VdO. in both groups.) were no of PAWP. with hypovolemic and septic and HYPOVOLEMIC 200 SHOCK x 10 utilizing mean changes as follows: samples of the (p <0. oxygen mI/minim’ (p <0.Table 1-Summary of Patient Data Survived Case Clinical No.o1 50 from (p <0. the in- 2. The increase in 13o. iso E RESULTS The time 78 ± 18 mm to peak 13o. increased group Do. The individual are shown in Figures 1 and Radiometer). septic and Vo. 3) oxygen Blood extraction gases (ABL 2. in both patient groups. significant CI. differences LVSWI. (two the Student’s tailed). oxygen content calculated from 1) CO. peritonitis 11 73 F Septic Urinary tract + urine infection 12 75 M 77 13 F Septic Acute Septic abdomen Gangrenous small mixed blood. Comparison of baseline at peak Do.org/ on 08/28/2014 ± SEM P<O. 13o.05 P<0.01) shock 10 X accomplished dependent gas laboratory were delivery calculated = significant considered (Vo.). CHEST I 85 / 3 I MARCH. (mi/min/m’) analysis Statistical CI X (A-VdO. revealed signifi- 125 E 01 0 100 in PAWP.Iipe #{149} Peak 002 75 Mean and the oxygen extraction ratio decreased in both groups. was associated with a significant increase in Vo.publications.) Cat).) hourly. Effect of increases in oxygen (Vo. during in the hypovolemic mm in the septic group values to values obtained increases the septic cant both A-VdO. = oxyhemoglobin a hemoximeter and by an automated which arterial- CVO. ft)rmulae: x (% sat) - ratio Radiometer) concentration rectly (Hb) included content (A-VdO. In the hypovolemic shock 239 ± 25 to 386 ± 48 mI/minim’ shock group.) ± standard error at the There Hemoglobin measured di- 0. LVSWI and MAP in and hypovolemic group of patients.

7±1.0i * 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.2 NS NS +147.6±1.7 98.01 2.6±1.(mm PaCO.34±36 3.5±2. septic shock oxygen consumption was inversely related to arterial lactate level.1 .0 NS 142±19 171±25 +29.54±0.’3 of fluid In addition.2±19.1 -4±4 NS -9±8 NS NS 67.5±0.2 9.’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. inadequate is still unclear.6±3.0±29.cm’) }Ib(g/dl) PaO.4 + 17±4 .2 ‘o.7±25.2±3.1±0.4 +109.9 and Consumption -372 ± 166 93.1 NS NS 31.3 34.7±3.0±13.2±23.org/ on 08/28/2014 Oxygen 41.’ -9%±4% -19.4±1. patients #{149} Baa.6 11.(mm A-VdO.12 2.8 + 15±5 .200 SEPTIC 175 SHOCK severity // 01 E C of circulatory Interventions which be expected to increase al’3 noted E cardiac challenge E 01 125 0 .6±7.8±19.0 J3o. Hypovolemia The with Table after fluid hypovolemia.0 33.0 et their effects of fluid resuscitation in our five hypovolemic shock are consistent with resulted mands.2 NS 29±2 30±2 ±0.001 NS 1368 1167 NS 1207 NS NS 12. The oxygen consumption patients is inadequate to meet their mi/mIn/m’ in oxygen patients in eight 400 The with the findings challenge. 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.5 -0.01 NS -5%±4% NS 45%±5% 36%±2% NS NS NS 78. studies.7 NS 7.5±0.0% Lactate(mg/dl) 66.1±1.3±0.8±2.9±2. account for level or peritonitis cavity.7±2.7 423.6 NS NS 34.7±1.7± Delivery 1.(mm Pc’O.8±1.4±17.5 150.’#{176} The 2-Difference significant at the mitochondrial cannot be utiuized.5 NS 44.7 -0.3 52.0±14.3 +3.6±0. between patients (Table hypovolemic 2).01 NS +39. Rackow.publications.8±7.6±7.(ml/min/m’) 95.’ consumption.) 500 delivery 600 in shock delivery delivery with (bo.4±0.6±8. 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.” interstitial edema has intravascular also been volume Shock HS Hypovolemic Baseline HR(beats/min) MAP(mm Hg) PAWP(mmHg) CI IJmin/m’ SVR(dynes. (HS) ABaseline Septic p< Baseline Shock Peak bo.lipe #{149} Peak 75 00 Mean 50 100 200 300 602 2.) septic on oxygen shock.48±.01 56. output pathophysiology and flow. Felt) .2±3.6 .’ 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.26 + 1.9 5.8 -14.9 .9 .Ext(%) 42%±6.sec.01 NS 1.8 . shock in CI and 13o.0 +5. the development of anaerobic metabolism and consequent lactic acidosis serves as a metabolic marker of shock and a prognostic indicator in critically ill patients.1 -1.01 314.2±15 68.7±9. Indeed.1±7 10.0 during Fluid Resuscitation (Kaunan.02 NS 7..2±5.0±11.chestnet.’ et al’ documented in critically in oxygen consumption were in mortality.6 71.01 11. Baseline p< NS 85.6±2.0 NS NS 6.2 .(ml/min/m’ ± 281 835 ± 124 NS .8 13.5±26.4±.3 +6.4 4.5±28.8 +3. no At comparable increases significant difference Vo. theories to of a cellular be such occurs in fluid intake.0±0.1±1. blockade oxygen consumption is of the tissues.03 - 200 ± 84 10 vs SS Baseline 50.25 + 1.0±18 NS NS 386±48.0 +3.0 338 Downloaded From: http://journal.7±0. the increase in in and septic lary consumption metabolism.0 . who increased The groups.2±2.1 134.(Vol%) Hg) Hg) Hg) Peak Sh ock #{246}o.6 ± 136 111±8.4 .3±0.7% 37%±5.3 -2.0±5.6 -2.3±8.1 +16.56±0. Oxygen consumption decreases in hypovolemic shock as a result of a decrease in oxygen delivery. with sequestration may development Increases in have and Septic Hypovolemic septic insensible some within septic polyuria cellular of the shock.2 .0±0.5±7. Effect consumption of increases (Vo.9±0.1 238. would Mohr oxygen consumption had shock due to of these increases consumption was is docu- consumption.2±6.4±.1 O.8±5.02 7.> that increase patients oxygen oxygen patients index and usually sumption.1 ± 172 101± (SS) 89. ± SEN P<0.04 133.

S. Nevertheless. In septic shock oxygen venous of evidenced. The on oxygen resuscitation with septic study. oxygen consumption to increase further. LD. consumption The elevated oxygen and thus. of in our not be fluid patients the findings of Mohr’s in cardiac output and to volume body increase would effects loading signifi- reflected increased nutrient capillary blood flow. MacLean shock. associates#{176} demonstrated tients in septic shock sumption ever. Christensen critically in Oxygen M.org/ on 08/28/2014 be tissue oxygen in dogs injected with E coil endotoxin and Ibund that mixed venous oxygen remained in the normal range while tissue oxygen was decreased. genation blood these flow” flow Huller et al” decreased even though arterial oxygen and pressure were initially maintained.” They do not support the hypothesis that the patient in septic shock cannot consume oxygen due to mitochondrial blockade. Groves Defective Obstet during fluid consumption septic in shock.. oxygen and In: Hershey Brown ill surgical 3 DuffJH. McLean oxygen APH. expected on oxygen Mohr and hemodynamic improvement. anaerobic increases was no oxygen of cardiac significant consumption shock and septic shock patients the experimental findings of utilization of oxygen in septic shock. Abnormal vascular transport and myocardial failure in human Surg 1967.”7 To the contrary. profound may be state rate metabolic block to oxygen shock. In addition. sepsis of septic and Little. we conclude that increasing resuscitation oxygen increases with both delivery tissue oxygen hypovolemic and 1 Clowes GH. relationship between in patients a close low Furthercardiac Loeb atrial and plasma volume in septic shock patients. shunts blood increased cardiac creased capillary as would Since both during shock. 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. defective septic shock.chestnet. of an early state oxygen delivery sumption.” Since mixed venous oxygen represents the MacLean 85 I 3 / MARCH. pooling possibly of blood. patients. 1972. After inducing peritonitis by cecal perforation. related Thus. Several authors volume expansion means tissues.4”8 be in nutrient delivery with if other areas in areas of expected to be body’s maintained inadequate receive decreased tissue excessive nutrient decreased. JH. This in oxygen consumption indicative the in oxygenation index of the or normal a high even heart. authors ibund that there was no primary injury to hepatic mitochondria. gen hand.’7 plasma Nishijima volumes more.” and associates’#{176} documented decreases in right pressure despite normal blood volume in patients with septic output venous shock. hepatic tissue oxy- 2 Wilson can be distribution areas of the could measured Boston: be expected to result in as was true of the patients the deficit may result from flow. Ann McLean consumption ed. consumption L. of a more of volume representative loading. 1984 Regional 339 . 1969. RF. Del Guercio LRM. 85-106 C. In hypovolemic the deficit may result entirely from a decrease delivery and would venous desaturation. Alternatively.publications. Surg LD. 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. Gynecol 128:1051-60 Greenspan tone. that in oxy- On the dogs with other sepsis output was accompanied blood flow but decreased by inoxygen extraction. Oxygen Surg LPH. The most probable explanation for the differing response to volume loading in our septic shock patients versus those in Mohr’s series is that the initial oxygen consumption in our patients was only 134 mI/min/m’. 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. Ann MB. utilization but rather efficiency et al’ found Wright mitochondrial increased. 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. Duff 5 M5’ight & Co. oxygen consumption prior was oxygen that failed of Survival has who can inoutput’1 in few data are available on the effect of volume expansion consumption in patients with septic shock.’4’3’7”1 been reported to be improved in patients crease their stroke volume’s or cardiac response to fluid challenge. utilization 1971. 165:504-17 JH. consumption with both hypovolemic that Tissue patients whereas Mohr’s patients may have been during a later phase in which intracellular studied and of shock face metabolism oxygen consumption. Similar results were obtained by Fry et al” in a rat model of septic shock. in Septic fulminating shock in man.aPointe in septic in 176:801-04 R. 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. as oxygen An inefficient would effluents value REFERENCES fluid shock flow existed in both groups. Leblanc AC.depletion. LP. study. they et al” Ibund have documented with septic shock. the despite baseline challenge tive 200 of fluid challenge in pato increase oxygen con- mI/min/m’. peripheral cardiac the cardiac output is consistent with the relatively normal mixed venous oxygen in our septic shock patients. 4 Siegel transport shock. isted. CHEST I Downloaded From: http://journal.

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