Relationship between O2 Delivery and O2 Consumption in the Adult Respiratory Distress Syndrome

Table 2-Physiologic

Data

model

282)

account Mean

1SD

±

58.0

±21.0

PaCO2

38.0

±

7.0

14.8

±

2.4

32.0

±

5.0

10.3

±

1.9

44.0

±17.0

(mm

Hg)

pH

Arterial

CaO,

(mlldl)

PVO2

(mm

CVO2

(ml/dl)

Shunt

0.20

7.45±

Hg)

fraction

(%)

0.06

7.1

± 2.5 ±

1.4

9.2

±

4.0

02 delivery

(mI/mm/kg)

HGB

ml)

(g/100

Systolic

BP (mm

14.7

±

4.9

3.9

±

1.2

12.0

±

2.5

Diastolic BP

129.0

Hg)

(mm

5 Plus

x

fraction

=

FaCO2

ofinspired

arterial

content;

‘#{176}2

venous

oxygen

cardiac

index;

the

dioxide

tension;

CaO,

venous

oxygen

tension;

equation

CaO,

X Qt/body

The

Ana,

was arterial

least

inserted

obtained

from

standard Arterial measured

minutes

mixed using

C1 oxygen

=

(Radiometer, venous

artery

3 Mark

II,

At and

values Vo,

regression

Vo, =

analysis Vo,,

Qt,

+

x

from SVO,

+

calculated for 0,

per

delivery

kg body

x

Qt was FVO,

as were

weight

was

(C(a-v)O,)/weight

used

to assess

SVO2 and

the

C(a-v)O,.

SVO,)

were

measurements

parameters

were

obtained.

All

patients

percent.

had

21 mI/min/

All patients

exception

sponded pressor patients

Copenhagen).

for physiologic

hypoxemia despite a high F1o2; venous admixture was 44 ± 16

(systolic

using

of below

calculated

concentration

equation,

O delivery,

was

from

x SaO,

kgbodyweightwas

(normal

CO-

had significant arterial the mean calculated the

Laboratories,

(#{176}2 delivery -

status. Arterial

and

(Instrumentation

y=o.32 x

Simulsamples

minutes,

(SaO,

(CVO)

and

linear

values

exchange

in ventilator

made.

saturations

a CO-oximeter

artery. blood

10

by

A Teflon

in clinical

were

of

in duplicate

changes

within BMS

oxygen

(Edwards

radial

any

day

measured

catheter pulmonary

arterial

changes

per

were

n83

10-

mixed

output;

computer).’

the

after

spontaneous

gases

electrodes and

9520A

(kg)

the

a Coulter

was calculated concentration

mI/mm/kg)

Fick

between

per

by using

a

from

determined at approximately the same time in all patients are shown in Table 2. Seven to 18 sets of measurements were obtained in each patient; the mean values for each parameter represent the unweighted means of all values obtained in all patients. pH and Pco2 were either within or close to the normal limits in all patients. Body temperature was generally constant, at least at the times the reported hemodynamic and gas

pressure

measured

pulmonary

determinations

venous

was into

venous

30-40

observed

in the

(Edwards

mixed

at least

two-three

mixed

(Qt)

percutaneously

and

or any

placed

output

technique

obtained

settings

was

weight

to be 12.3-19.5

measured measured

hemoglobin

delivery

assumed

the

x

1.39

=

Oxygen

found

calculated

O content(CaO,) 02 content

oxygen

we

RESULTS

oxygen =

Vo,

thermodilution

CA)

cardiac

thermodilution

taneous

arterial

blood

PO,.

that was

into

oxygen

which

methods,

saturation

x hemoglobin

venous

CV02

x

relationship

nutrition. flow-directed

Santa

catheter

BP

Mixed

(k g). Least-square

tension;

#{176}I

pressure;

PaO,.

and

in

takes the

14.0

±

oxygen

cardiac

wedge

hemoglobin;

=

parenteral

thermodilution

pulmonary

HGB

patient.

were

Qt

=

A Swan-Ganz each

arterial

=

mixed Pl

Laboratories,

FaO1

carbon content;

consumption;

received

oxygen;

blood 1.39

on

samples

oxygen

curve

which

Pco,

of these

concentration

Arterial

0.003

Mean

FIo2

between

CaO,

and

venous

both

percent

dissociation

analyzer.

gas calculator pH

mixed by

Hemoglobin

equation

the

For

determined

±21.0

73.0

Hg)

oxygen

0.003

4.1

Vo, (mI/mm/kg)

of <3

the

CI (L/minlm2)

Hg)

difference oximeter.

Qt (Lfmin) FW(mm

was

blood

of temperature,

curve.6

saturation the

Severinghaus

effects

dissociation

Flo, (fraction) PaO, (mm Hg)

.72±

or the

the

of two,

pressure

<90

both

a normal

of whom mm

Hg).

cardiac

index

with

were

hypotensive

One

of

latter

re-

to fluid therapy, and the other required agents. Urine output was > 600 ml/24 hr in all except one who required peritoneal dialysis

kg)

0.53

r0.76 A

C

E

7.5

G

-

F B B B

C

0

D

5A

a E

FD

Cl)

C 0

F

B

-

2.5

D FE

0 c.1

0

G

0

268

JJ

U

1’

I

I

10

15

20

Oxygen

Delivery

(mi/mm/kg)

D I

25

1. The relationship between 0, delivery O consumption in patients with ARDS. Each patient is represented by aseparate symbol to show the relationship between 0, delivery and Vo, in individual patients. FIGURE

1

30

and

02

8fld Consumption

in ARDS (Mohsenlfaretal)

for renal failure. In our ten patients, when 0, delivery 21 ml/min/kg, Vo2 was linearly related 0.32

(V02

x

02

delivery-O.53;

cardiac

was less than to 02 delivery n

83;

=

r

tam metabolic

p <0.001)

nisms

mi/mm/kg,

may

(Fig 1). Ifwe include the data points above 21 the coefficient of correlation decreases significantly (r = 0.44). Although the number of samples

varied

among

patients,

correlation

coefficients

for

between between

0.67 Vo2

02 delivery

was

linear regression for each patient ranged to 0.99 and revealed a linear relationship

and 02 delivery

in each

patient

less than 21 ml/min/kg. higher than 21 mI/mm/kg,

when

However, there

at an 02 delivery was no correlation

between 02 delivery and Vo2. The correlation and 02 delivery is due to the relationship the combination of elements which comprise 02 delivery such as t, (C[a-v]O) and Ca02,

Vo,

presence

of

delivery

in both

t

the

did not delivery varied

=

between

PVO

0.09).

There and Vo2,

The adult respiratory associated with multisystem

distress syndrome abnormalities

is often in critically

ill patients.

ofthese

is therefbre

complicated improve

by the one

another.

fact

organ

Application

sary

in

arterial

oxygenation

supplementation. frequently decrease

ARDS

However, tissue

lead often

becomes maintain

levels

of PEEP

high

delivery

due

a,

of below

In

our

conflicting,7”4” in the underlying ten

in 0,, delivery,

Danek

et al4 who

between

declines patients.

of

are in a in

data

points

21 ml/min/kg

S

U)

S

20

25

30

35

pv02 FIGURE

venous

2. The relationship oxygenation (PVC),,).

between

(mm

U

40

45

higher

a linear

relationship

ofO,

delivery

above

Although

in which

(Fig 1),

the

0

delivery that

ex-

addition

0,

delivery

It is noteworthy

that

generated shock in

in two patients whom high O

(cases delivery

relatively

high

secondary to reduced and the variable o, degrees of vaso-regulatory

cardiac

vascular

due

created

the

relatively

would

be

have

which

we had

is unlikely

it

in

not

and

a linear

in this these

relation

of 0,,

range

data

points

were

4 and 6) with septic could be due to

output resistance

to varying with variable

blood

One

our the

flow

possible

results

be a difference

For example,

those underlying

authors

of

for

and

in the latter

to regions reason

the

of Danek disease

studied

more

I

50

mixed

the

higher

upper

limit

of 0,,

delivery

noted in their study compared to ours. It is possible that in patients with Gram-negative sepsis with very high cardiac output, Vo, and O delivery are well correlated

even

Although and

with

at an O delivery

Vo,,

Hg)

O consumption

of 0,,

linearly

data

consequence,

2.5-

U

levels

to

patients with Gram-negative sepsis (at least six patients) than we did (two patients), possibly resulting in the higher mean ()t (8.3 ± 3.2 Llmin) and, as a

5-

U

at

due

more

process.

I

a

between delivery.

et al4 could

U

value

high 02 requirements. discrepancy between

S

0

causes

between respiratory

in part process.4 fell

demonstrated

(nine)

0

C 0 C)

pressure demon-

also

ARDS,

or

0,, uptake

in calculated Vo, and 0,, delivery However, the latter authors did

ceeded

compensation

3

possibly disease

but

few

21 mI/mm/kg)

E

(anemia)

ofthe driving reports have

with

patients

to

E C

curve

that

below 21 mI/mm/kg,

delivery

in

7.5-

E

normal

indicating

in Qt in animals

not hold.

S C

were

a reduction

failure are differences

could n83 (02 delivery r-0.07

PVo hypoxia),

was independent of oxygen. Other

that

peripheral 10-

and

detect a threshold relationship did

of 0,

resulting to a reduction

which

dissociation

drop in Vo,.’ Reports on the relationship Vo, and 02 delivery in human beings with

ARDS

neces-

levels

normal mecha-

O extraction

0,,

in the

be

to main-

the body’s compensatory

in tissue

by shifts

may

in order

than 21 mI/mm/kg, there was no correlation with So,. These findings accord generally well with those of

adequate

nontoxic

by a fall in 02

designed

to deterioration

to

at relatively

complicated in

interventions may

of PEEP

with

patients

that

system

patients

(alveolar

reductions

DISCUSSION

Management

PaO,

reduced

strated

the

These

an increase

whether

by the tissues

of Vo2 and 02 SVO2 and (C[a-v]02)

or Vo2 (r

in 02 delivery

and/or local vasodilation9”#{176} and result in an increased arteriovenous O difference and, in consequence, a reduced PV02. On the other hand, Cain11 reported that in animals Vo, felilinearly when 0, delivery decreased below a critical level of 9.8 mI/mm/kg, regardless of

fur diffusion

correlate with 02 delivery at all levels of 0, (r = 0.26, 0.28 and 0. 26 respectively). t widely (3-15 liters) and did not correlate with P

vO, (r = 0. 17), SVO2 (r = 0.07) was no significant correlation r= -0.07 (Fig 2).

include be facilitated

between

calculation

PV02,

is inconsequential.

decreases

requirements.

between ‘O2 and and

Such

by various mechanisms a constant Vo, and fulfill

0.76;

=

output.

compensated

related this

it

at unusually high levels of 0, delivery. has not been proven that PVO is directly

to tissue

assumption.3-’6’7

oxygenation,

some

Moreover, CHEST

evidence

in studies

I 84 I 3 I SEPTEMBER,

supports of patients 1983

269

with a variety of cardiopulmonary Kasnitz et a!2 found that PVO2 was

disease the best

processes, predictor

hyperlactatemia

However,

PVO2

and

certain since

limitations is determined

it

from

a wide

have

a low

of

death.

as an indicator of tissue by the Po2 ofthe venous

variety ratio

of tissues,

of 02 uptake that under

tions

tissues

sepsis)

in which

ments may receive body perfusion.#{176} Changes in Vo2

in

our

any

evidence

base ters

changes

patients

in blood

In

Indeed,

of total

were

pH,

changes

directly (Fig 2). The were not associated with

metabolism plasma

as reflected

bicarbonate

excess, although the reliability as indicators of tissue hypoxia

We

factors

related

sepsis),

the

therapeutic may have lung,

following

to the

underlying

ment

severe at the

cellular

hypoxemia

could

result

disordered

and

the

alter

use

of PEEP

could low

02

our

level of ‘2 which found by Simmons occurence of tissue

Cain’s”

study

mean

PVO2 was

the driving

pressure

factor

since

associated

270

V02

decrease

pressure uptake

02

32

±

in limiting with

markedly

02

tatemia

associated with that measure-

ofLung

Diseases,

GL,

Yorra

JAMA

Alpas

uptake Am

Rev

Donoso

W,

Coulson

DP,

ments

ofcardiac

1971;

27:392-96

output JW.

gas

venous

cardio-

Hyperlacoutput,

or

dependence

respiratory

of distress

122:387-95

New

technique

by thermodilution

Blood

The

adult

1980;

HS.

A.

cardiac

DR.

with

Dis

Mixed

in severe

or reduced

delivery

R, Marcus

DH.

of

115:1071-78

236:570-74

Tashkin

Respir

1977;

survival

hypoxemia

on oxygen

Heart,

on mechanisms

F’, Simmons

1976;

AP,

to arterial

National

Conference report Am Rev Respir Dis

J

Am

Appl

Physiol

J

calculator.

for measure-

in man.

Cardiol 1966;

21:3-26 7 Lutch

JC, Murray on systemic Med

Powers

SR.

JE Continuous

oxygen

positive-pressure

transport

ventilation:

and tissue

oxygenation.

Ann

1972; 76:193-202 Mannal

R,

et al. Physiologic (PEEP) A, Cohen

Neclerio

M,

English

consequences

M,

Marr

of positive

ventilation.

Ann

J, Lichtman

MA,

Surg

1973;

Murphy

C,

Leather

end-expiratory 178:265-72

MS.

Schreiner

BC,

Shalt PM. The relationships among arterial oxygen flow rate, oxygen binding by hemoglobin, and oxygen utilization in chronic cardiac decompensation. J Lab Clin Med 1978; 94:635-49 10 Finch CA, Lenfant C. Oxygen transport in man. N Engl J Med 1972; 11

12

Cain

286:407-15

Oxygen

SM.

hypoxic

hypoxia.

Uzawa

T, Ashbaugh

in acute

delivery

and uptake

J AppI Physiol DC.

hemorrhagic

in dogs

1977;

during

Continuous

positive

pulmonary

anemic

and

42:228-34 pressure

J

edema.

AppI

breathing

Physiol

1969;

26:427-32 13

the in

Andersen

MN,

during Surg

PVO2

different

due

6 Severinghaus

a

uptake,

mechanism in our study.

low Vo2 were does not appear

it

Division

disease.

pressure

for 02 in our

ofO2 did not appear tissue

and

and hyperlactatemia,

DH,

9 Daniel

Hg,

and/or Vo2. Deeither by a fall in

02

Institute. failure.

P, Druger

pulmonary

W,

Qt

4 mm

ml/min/kg.

delivery accompanied

Staff,

tension

3 Simmons

8

to different

is greater than the critical et al3 to be associated with hypoxia in dogs.3 Moreover,

to be an important

low

and

Blood respiratory

Intern

result in shuntrequirements. In can

5

and

effects

blood flow disproportionaerobic metabolic needs.

It seems unlikely that low driving was a limiting factor for tissue since

in

Furthersubstances the systemic

of perfusion

rate of2l

Qt,

in were

REFERENCES

syndrome.

normal vaso-regulatory both total cardiac output of blood flow to tissues.24

in ARDS

distribution

organs,’ possibly reducing ately to organs with greater

patients,

decrease

metabolism. of vasoactive passage into

ARDS

we found and 1O2 PVO2 did not

oxygenation.

5 Ganz

in

with

tissue

oxygen

impair-

a reduction

for

vaso-regulation to organs with

the

thereby

widely

improve

respiratory

in a compensatory

the

the

with

with PEEP, 02 delivery

both. J Appl Physiol 1978; 45:195-202 4 Danek SJ, Lynch JP, WegJG, Dantzker

(eg,

and/or

seen

a reliable indicator of tissue oxygenaWe conclude that maximizing 02 be a major therapeutic goal in ARDS to

a

with ARDS other than

cause

level,E

may disturb that modulate redistribution

ing of blood

Patients in organs

Alternatively,

cellular 02 requirement more, in ARDS, formation (such as bradykinin) with circulation mechanisms and regional

process

mm from

ARDS. should

2 Kasnitz

to explain

itself

may

mitochondrial

02 utilization.

02 delivery

addition,

of PV02

Lung acute

delivery falls. by a number of

disease

(17-45

of patients

ventilation between

delivery

02

was

in a group

changes in Vo2

1 MurrayJF,

02

of ARDS

modalities employed. diffuse capillary injury

and

This

an

Vo2

PO2

PVO2 varied

tion in delivery

or blood

mechanisms

pathophysiology

disruption ing

the

low

by

of these paramehas been ques-

in Vo2 in our patients when V02 may be influenced

and

and

of PVO2.

mechanical relationship

oxygen

propose

patients

Since low 02 delivery a wide range of PVO2,

21

reduction In ARDS,

Hg)

ten

tissue oxygen demand as a compensatory or by tissue hypoxia not directly assessed

observed

with

mm

in our

conclusion,

reflect creases

02 require-

(23-99

Hg

levels

below

condi-

share

mm

receiving a direct

unreliable

low

did not correlate

of anaerobic

reduction

with

of Pa02 Similarly,

17-49

may

clinical

Hg).

varying

metabolic rates (stable body muscular activity due to drug-induced motor paral-

was measured in Vo2 we observed

decreases

certain

a disproportionate

despite apparently stable temperatures and reduced sedation with or without

ysis), and these in PVO2 which

of which is an

PVO2

has

hypoxia, effluent

to 02 delivery.

more recent data suggest indicator oftissue hypoxia (eg,

some

18.19

values of

14

15

Senning

extracorporeal

A.

Studies

circulation

in

with

oxygen

consumption

a pump-oxygenator.

Ann

1958; 148:59-65

McMahon

SM,

airway

pressure

1973;

108:526-35

King

EG,

Halprin

GM,

in severe

Jones

RL,

expiratory

pressure

syndrome.

Canad

02

Sieker

arterial

Patakas therapy

Anaesth

Delivery

DA. in

Soc

HO.

Positive

hypoxemia. Evaluation the

J

1973;

and Consumption

adult

end-expiratory

Am Rev

Respir

of positive respiratory

Dis end-

distress

20:546-58

in ARDS

(Mohsen!far et a!)

16 Mithoefer JC, administration tive pulmonary 17

Springer

patients 18 Tenney

venous 1974; 19

Brewis

RP,

FD,

on mixed

venous

disease.

Chest

Stevens

PM.

in respiratory

Keighley

A theoretical

blood

and mean

JE The effect

oxygenation

22 Rhodes GR, Newell JC, Shah D, Scovell RE, et al. Increased oxygen consumption creased oxygen delivery with hypertonic

of oxygen

in chronic

obstruc-

1974; 66: 122-32

The

influence

failure.

SM.

ofPEEP

Am J Med

analysis

tissue

of the

oxygen

1979;

on

survival

relationship

pressures.

respiratory

of

23 Robin

66:196-200 between

Respir

disease.

Physiol

24

20:283-96 BA.

hypoxia.

Br

Clinical

J

1979;

119:127

Jobsis

FF,

manifestations

measurements

Anaesth R,

1969; Wilson

tension

relevant

to the

assessment

of

Comparison

in endotoxic

of tissue

shock.

Am

Rev

and

mixed

Respir

Dis

(abstract) LaManna

cardiac

25 Tucker

41:742-50 F

26 JC.

ofrespiratory

In:

Robin

disease.

E, New

ed, York:

Extrapulmonary Marcel

Dekker,

distress ED,

ed

New

York:

oxygen

Marcel

HJ, blood

1973;

34:573-77

Am

J

JE

1979;

1978;

84:490-97

R, Hechtman

during

and

respiratory

1978:3

EE,

1973;

Effects

J, Dutton

accompanying inmannitol in adult

Guyton

its contribution

Physiol

in normal

flow and its distribution Surgery

and

flow

Tauber

W,

manifestations Dekker,

Murray

Justice

Surgery

HJ, Smith

delivery

output.

organ MannyJ,

syndrome. Extrapulmonary

AP, Granger

Shepherd oftissue

20 Hillir C, Bone venous oxygen 21

Holdford

AC.

Local

to the

diseased

HB.

of

pressure

on

225:747-55

of end-expiratory

and

control

regulation

dogs.

J Appi

Abnormalities

positive

end-expiratory

Physiol

in organ

blood

pressure.

85:425-32

1978:83

CHEST

I 84

I 3 I SEPTEMBER,

1983

271