Hypoxemia

Yann Huet, M.D.;* Christian Bernard Didier

in Acute Pulmonary
Francots
Lemaire,

Embolism

M.D.;* A. Knaus, M.D.;*t M.D.;* and

Brun-Buisson, M.D.;* Teisseire, Ph.D.;1: Didier Mathieu, M.D.

William Payen,

Most have roles

patients
arterial

with

severe,

acute

pulmonary

embolism

(PE)

hypoxemia.

of ventilation shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean Pa08, 6711 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVt/QT 16.6 5.1 percent) was present in all patients. The relative contributions of VA/() mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study,
trapulmonary

To further define the respective to perfusion (VA/Q) mismatch and in-

all patients had some degree of VA/(I mismatch, the two patients studied early (ie, <48 hours following acute FE) had normal chest x-ray film findings and no significant shunt; VA/ mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute FE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.
Although

cute

pulmonary common

embolism diagnoses

(PE) of

remains acutely frequent for

one ill,

of the hospi-

after

the

PE.

In one

of these,

Wilson

et al#{176} suggested for most of the the major role to the investigators relative contributimes oxygen of ininferred gives an cardiac by of VA/ oxygen to the

more

talized patients tions to occur ders.2 clinical feature

and one of the more during hospitalization is of PE significance established. impaired as well been unclear. a Its consistent

complicaother disorimportant and pre-

Hypoxemia

and

that atelectasis and shunt accounted hypoxemia, whereas Kafer2 attributed VA/Q mismatching. In these studies were unable to examine directly the tions after method trapulmonary of the
A/a

pathophysiology

cise clinical been clearly abnormalities,45 ary shunting, remains shunts,467 of each Although

in man, however, have not Ventilation/perfusion (VA/a) diffusion,3 and intrapulmonas right-to-left but related intracardiac the exact role implicated,

mismatching embolus. Both shunting

vs shunt at different studies also used the and not the degree but was measured

to assess

hypoxemia,

all have hypoxemia

using the alveolar-arterial oxygen difference. Today, bedside right heart catheterization accurate evaluation of the contribution factors Wagner technique distributions method In this to the et hypoxemia. al2 of the The multiple precise possible these recent, aim was recent inert gas

of

has been

to the

degree

introduction elimination

of pulmonary vascular obstruction reports of massive PE with normal tension (Pa02).#{176}No clear relationship clinical characteristics and the PaO, Variations in the timing and methods hypoxemia in previous studies may gas long, this confusion. humans were
*SeMce de

(PVO),8 there are arterial oxygen between other

allows a more than was alone. study,

evaluation using the

has been
used

found. to assess to

we combined patients with acute PE. Our

two techniques
angiographically to determine the chest gas

have

contributed

The major performed

exchange frequently

studies in months,
Mondor and

study seven documented

Reanimation

M#{233}dicale, H#{244}pital Henri

mechanism of their of our investigation abnormalities study. to the

hypoxemia and each results

by relating patients of their

timing x-ray

Universit#{233} Paris-Val de Mane, France. tICU Research Unit, The George Washington University Medical Center, Washington, DC. Laboratoire des echanges gazeux (INSERM U 138), H#{244}pitalHenri Mondor and Universit#{233} Paris-Val de Mane. Service de Radiologie, H#{244}pital Henri Mondor and Universit#{233} Paris-Val de Marne. This work was supported in part by a grant from the D#{233}partement de Pharmacologie Clinique, H#{244}pital Henri Mondor, Creteil. Presented at the Annual Meeting of the American Thoracic Society, Anaheim, Calif, May, 1985. Manuscript received April 2; revision accepted July 15.

exchange

PATIENTS

AND

METHODS

Patients
Seven (ICU) studied. had any consecutive for hemodynamic Their individual significant patients clinical admitted and to our treatment Intensive of acute Care Unit monitoring preexisting PE were 1. None One pa-

characteristics cardiopulmonary

are in Table
disease.

CHEST

/ 88 / 6 I DECEMBER,

1985

829

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Table

1-Clinical

Features
Clinical

and
Features
.

Chest

X-ray

Findings

in 7 Patients

with

Acute

Pulmonary

Embolism

X-ray
.

Fi ndings

at Time
.

of Studyl

Hours Patient No. 1 2 3 4 5 6

7
*

Since Precipitating Cause Immobilization Pelvic surgery limb Lower fracture

Pulmonary Vascular Obstructiont 58 60 65 cancer limb 56 35 65 surgery 50

Age, yr/Sex 4IJF 41/M 40/F 69/F

Occurrence of PE 24 48 84 102 128 192 216

Elevated Diaphragm + 0 + + 0
+ +

Platelike Atelectasis 0 0
+ +

Infiltrates 0 0 0 +
+ +

Immobilization Hepatic Lower fracture

+
+

50/M
61/M

Immobilization Neurosurgery Immobilization Abdominal Lower fracture limb

+ + ++

+ +

+ +

50/M
according to time vascular 0 sign

++

++

*Numbering tIn

elapsed

since

initial
according

symptoms to index
+ +

of embolism. described marked and/or by Tibutt multiple et al.#{176} changes.

% of pulmonary as follows:

bed,
absent;

estimated
+

Notation

minimal

changes;

tient had suffered a pulmonary embolism five yeas before but had no residual effects. The diagnosis of PE was made on clinical history and the results of a pulmonary angiogram perfurmed within a few hours of ICU admission. The degree of PVO was determined using the index described by Tibutt et al.#{176} A Swan-Ganz catheter and radial artery line were already in place. The gas exchange study was perfbrmed on the first day in the ICU, approximately two hours after the pulmonary angiogram. The delay between the first symptom of PE (acute chest pain and/or dyspnea) and the inert gas study was carefully determined and ranged between one and nine days (Table 1). The patients were receiving only heparin therapy at the time of the study. No vasoactive drug was used. After the study, we gave urokinase to all except patient 5, who was recovering from recent
neurosurgery.

method
physiologic dioxide Anatomic instrumental the

and computed dead space

calculated dead inert space dead

with the standard equation of Berggren; (8) assessed by the Bohr dead space for carbon
expired)
from body

as (arterial-mixed was assumed space

divided weight of.&/( as described follows.

by ratios

PaCO,. plus using

(1 mI/Ib)

(80 ml); (9) distribution technique, technique in 15-mI blood

multiple

gas elimination
of this [SF61, were intravenously simultaneous last

by Evans gases

and Wagner.4 A brief summary

(sulfur ether, solution hexafluoride and acetone) Then,

Six inert
halopropane,

ethane, equilibrated

cyclopropane, a 5 percent rate samples (IV) at a constant

dextrose of 5 mI/mm were drawn of the gas was in a

and infused

for 25 minutes.

from the pulmonary inert gas concentrations.

sampled. heated The for SF6 Instrument detector The equilibrated by an Co) and blood

artery

and a systemic At the same time,

were the five equilibrated expired detector other gases

artery for analysis 50 ml of expired with nitrogen were 429;

Methods The gas exchange study was done with patients in a semirecumposition. All were breathing spontaneously via a face mask with humidified room air or supplemental oxygen (patients 3 and 7) as required to maintain an adequate oxygen arterial partial pressure. The masks were tightly fitted to the patients face so that no air leaks occurred. Patients breathed through a circuit consisting of an 0, blender, a humidifier, and a specially designed heated mixing box via a one-way valve. The expiratory tubing was also heated to prevent condensation and extraction of the more soluble gas, ie, acetone.
bent In each patient, (1) minute Wright gas and in the the following ventilation inspiratory arterial
recorder);

samples blood and the

bath for 45 minutes. gas samples

(Packard by analyzed Packard ionization electron for capture

a flame

(Packard). The blood solubility coefficient of each gas was determined for each patient. The relative concentrations of the inert gases in arterial and mixed venous samples were derived from the equilibrated samples and the measured solubilities. The error of
measurement of SF6 determined in our laboratory was 1.3 percent.

and less than

constructed. perfusion technique.4 ing ram
VA/Q

1.8 percent and these,

was

for the the residual the best

other

five

gases.S curves of the the was curves of the ridge and the were ventilationregression then

measurements
WE)

and volume

calculations (VT) using 0, (Flo,)

atrial,

Retention-solubility a by From
distributions

excretion-solubility approximation using of square determined, sum distribution analysis

were made:
calibrated sampling pulmonary, ducer cardiac
perfurmed

and tidal
of the

spirometer; systemic (CO)

(2) fraction line pressures (4) cardiac by computer

of inspired circuit; (Statham index (CI), thermodilution 9520, A. Edwards

(3) right derived

The

mean between

3.2 2.0, distribution

indicatinert gas of the

and
output

P23 DB transfrom

compatibility data.4

Honeywell in triplicate

A computer-assisted

measured (CO mixed PO,, saturation

the

technique Laborato-

ries); dioxide

(5)

arterial
tension and (6) total arterial wedge most (7)

and
(PaO,, 0,

venous
PaCO,) (SaC),

oxygen
(ABL

tension
30,

and carbon
Radiometer

ratios allowed the determination of shunt (Qs/Qt); ie, Y..JQ <0.005; low VA/Q; ie, 0.005<VA/Q<0.1; high VA/Q; je, 10<VA/Q <100; and dead space (Vu/VT); ie, VA/Q<100. The mean peak values flow and (log ventilation. with in the pressure SD), ventilation which The the is taken ventilation mixed venous distribution calculated to
as an index

of blood the and in abcissa combined

were

determined, log scale distributions

as well of blood output,

as

Copenhagen)

ometer);
pulmonary

pulmonary

pressure
pressure likely venous

resistance (PAP) divided

measurements

and SO,) (OSMII; Radi(TPR) calculated as mean

by cardiac were index possible the (pulmoonly arterial oxygen

SD of the

distribution

with a natural
of dispersion perfusion

for the flow were

VE,

nary capillary two patients,

obstruction);

because
admixture

of extensive
(QVAJQT)

pulmonary using

and PaO,
partial

50-compartment
of oxygen.

blood gases, cardiac model4 to predict

the arterial

830

Hypoxemla

In Acute

Pulmonary

Embolism

(Huet

of a!)

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Table 2-Hemodynamic
Patient No. 1 2 3 4 5 6 7 Mean SD *HR cardiac
=

Data*
SAP CI, Hg Limin#{149}m 4.76 1.91 mm TPR, Hgfmin/m/L 4.2 12.5 11.2 12.6 10.7 7.5 5.9 9.2 3.3
arterial

HR, beats/mm 105 110

RAP mm 2 12 15 10 2 3 3 7 5 Hg

PAP mm 20 24 29 32 24 20 19 24 5 pressure;
=

Hg

mm

100
70 60 87 76

145
90 103 84 110 107 20 heat index; rate;

103 106
86 18
arterial

2.58 2.54 2.25 2.65

3.2

2.84 0.94
=

XP
=

=
total

mean

right

atrial

mean

pulmonary

pressure;

mean

systemic

pressure;

CI

TPR
chest

pulmonary was also

resistance. obtained on the day of the to (2) were

+ +

A standard

x-ray

film

moderately

low

(2.840.96

L/minm)

and

notably

study. Analysis of the films was who did not know the patients Fleischner, ing: (1) elevated atelectasis 0 for and/or the data two are no platelike they described hemidiaphragm
and

made by two independent clinical characteristics. film were with marked slight There
SD.

observers According on the followor absent; and

each areas

emphasis present opacities, was close

depressed in patient 2 (1.91 L/min#{149}m). Total pulmonary resistance was markedly elevated (9.2 3.2 mmHg/L.min.m). The hemodynamic impact of PE
was further evidenced by the increased arteriovenous

of consolidation
+ for

(infiltrates)

scored
marked between

abnormality, multiple observers expressed

for

opacities. on all films. as mean

agreement

All the

oxygen difference (mean 5.7 1.5) with a calculated mean oxygen consumption of 16539 mllminm. No patient, however, had a systolic blood pressure less than 90 mm Hg.

RESULTS

Standard gas exchanges mild hypoxemia (mean 67 patients are listed from 1 all patients. The enlarged, monary venous patient, output

are presented in Table 11mm Hg) was recorded 02 difference

3. A in

In all tables

and

figures

the

alveolar-arterial

was

to 7 corresponding symptoms of PE
x-ray findings are

to the time elapsed from initial to the gas exchange study. The chest
recorded in Table 1. The

two patients
had Localized common obstruction
55 percent

but did not correlate to the degree of pulvascular obstruction or to the PaO,. Calculated admixture (0, method) was elevated in each and ranged (mean, 16.6

studied parenchymal

within

two

days

of initial

symptoms

no in

radiographic

abnormalities.

from 10.5 to 25.6 percent of cardiac 5.1). Mixed venous oxygen partial

atelectasis and/or small infiltrates were patients studied later. Pulmonary arterial was substantial in all patients (mean value, of the obvious findings The pulmonary arterial vascular bed). between data geographic relationship and site of embolus. standard hemodynamic

pressure and saturation were low (mean, 27 5 mm Hg and 52 10 percent, respectively), as could be expected from the decreased cardiac index. The Bohr dead space was markedly high, ranging from 44 to 75 percent of minute ventilation. All of the patients had an arterial hypocarbia, and respiratory alkalosis was noted in five of seven patients (mean pH, 7.470.04). The inert gas study revealed different patterns of VA/Q distribution in relation to the timing of the study and the with presence Acute of x-ray
Pulmonary
PO,, Hg 42 55 88 53 43 44 112
-

There

was radiologic

no

are shown

in Table

2. Right atrial pressure ranged from 2 to 15 mm Hg. Mean pulmonary arterial pressure was only moderately increased (24
5

mm

Hg).

Cardiac

index

was

abnormalities. Embolism
SO,, (>VA/(>r, Hg 65 45 43 44 45 57 65 52 10 % 19.3 15.8 10.5 15.3 15.8

Shunt,

ie,

Table 3-Standard
Patient Weight, Height, PaO,,*

Gas Exchange
SaO,,

in 7 Patients

PaCO,, mm 34 27 29 26 31 37 26 30 4 Hg pH 7.45 7.52 7.40 7.49 7.49 7.42 7.51 7.47

P(A-a)0,, mm

VD/VT (Bohr), 57.6 66 75 62 47 62 44 59 10 SaO, PO,

-

No. 1 2 3 4 5 6 7 Mean SD *4.ll patients

kg 45 73 71 62 68 72 80 67.3 10 breathing saturation; pressure

cm 162 180 170 157 180 170 171 170 8 room air, PaCO, of oxygen;

mm 66 60 90 62 65 57 70 67 11 except
=

Hg

% 94 93.5 95 92.5 92.5 89.5

mm 34 25 25 21 25 29 32 27 5

Hg

mm

25.6
18.5 16.6 5.1 of oxygen; difference; (oxygen

93.5
93 2 3 and 7 (FIo,=
carbon

0.04
Abbreviations: P(A-a)O, saturation;

0.30).

PaO,
=

arterial

partial
oxygen
=

pressure tension admixture

arterial
=

oxyhemoglobin venous
partial

arterial
=

dioxide venous

tension;

alveolar-arterial QVA/QT

mixed

Sco,

Mixed

oxyhemoglobin

venous

method);

VD/VT

dead

space

(Bohr). 831

CHEST

I 88 I 6

DECEMBER,

1985

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Table 4-Inert

Gas

Data#{176}
Perfusion Distribution, Ventilation Distribution,

%CO Perfusion Pa02/PaO,, VE, Limn 1 2 3 4 5 6 7 11 20 31 21 14 13 17 18 7

VT,

%VE
. . ,

to

Ventilation to Unperfused Lung,1 %

Anatomic Dead Space,* % Mean Ratio VAJQ

Unventilated Lung,t % 0 0.3 4.6 3.2 4.2 8.8 16.9 5.4 5.9 VT

Log SD of
Blood Flow Mean Ratio 1.58 5.45 5.01 2.19 VA/Q Distribution 0.838

Log SD of
Ventilation Distribution 1.129 0.877
1.031

CO, L/mn 5.3 3 4.4 5.7 6.1 5.4 6.3 5.2 1.1

Meas/Pred, mm Hg

ml 730 910 910 820 700 650 770 784 101 iTE

66/72
60/56 90/106 62168 65/63

56.8
53

63.4 55.1
40.5

23.3 24.8 24.4 24.5

30.8 32.5 31.2

0.58 1.65 1.22

1.39 1.03 0.89

1.235 1.163
1.142

0.877

0.842
0.815 0.691

1.96
1.26

0.723
0.494 0.676

57/66 70/66
67/71 11/15 ventilation;

58.4 35.4
51.8 10.1 tidal volume; CO

1.66
1.20 0.40

2.68
2.88 1.67

Mean
SD

0.950
0.210

0.83 0.22

#{176}Abbreviations:
t7A/(

expired

cardiac

output.

0.005. A/() 100. Anatomic dead space

assumed

from

weight

(1 ml/lb)

plus

instrumental

dead

space.

perfusion patients part

to the unventilated 1 and 2 but accounted output (3.2

lung, was negligible for a low but significant to 8.8 percent) in patients

in 3

each

patient not

and shows

a normal that

control. the mean different

Analysis peak from 1 (1.2

of the of blood

\TA/

distribution

flow, had part

A/(

of cardiac

although

markedly

0.4),

to 6, and to as much as 17 percent of cardiac patient 7 (Table 4). There was no relationship venous admixture measured with the Qs/t (six inert gases method). Figure 1 correlates the shunt ties, when

output in between

a large dispersion of perfusion was

(0.95 0.21). Thus, distributed to lung

a significant units with

02 method x-ray abnormali-

and

to the shunt

ratios lower than 1 (between 1 and 0.1), despite absence of a definite zone of very low VAJQ ratios. measured PaO, values were closely related to the values predicted from the PiIO, to the and unperfused the distributions (Table 4). In all patients, ventilation

the The PaO,

VA/

and

shows

that

a significant infiltrates the 2 shows

occurred seen distribution

only radiofor

atelectasis Figure

and/or

were VAJQ

graphically.

areas

Atelectasis a
Sc

o
Infiltrat#{149}s

0 0

++

++

++

++

1+

++

.15

[
.10
-

.fl.ii.fl
I I

0
FIGURE

Days

1. Association between shunt measured with the six inert gas technique and x-ray findings in relation to time elapsed since the occurrence of PE. X-ray changes scored as: 0 = no abnormality; + = slight opacities; + + = marked and/or multiple opacities. It is clear that a significant shunt is present only when chest x-ray is abnormal. Conversely, normal chest films were obtained in patients with no detectable shunt and studied within 48 hours after embolism.

832

Hypoxemla

In Acute

Pulmonary

Embolism

(Huot

of a!)

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I.8

CO

4.4

SHUNT
1.4

YE DEAD

74 SPACE
1.4

1.1%

26.5%

CO 5.3
YE SHuNT
0.0% DEAD 56.8%

11
SPACE

1.0

I
S
0
/.

0.6

0 0 0

0.2

1/
ii
001 0.1

/ / \\..__J
10 100 VE DEAD 31 SPACE 63.4%

z
4 1.4

0,01

01

10
IA

I
1.4

C03 SHUNT 0.3%

1.0

VE DEAD
I

20

CO

4.4

SPACE 53.0% 1.0

SHUNT
4.6%

0.6

o.e

/
OI OI

0.2

0.2

001

0.1

1O

tOO

10

500

VENTILATION CO
3i%

PERFUSION
1.4

PATIO
YE 14 SPACE

5.7

()

VE DEAD
55.5%

21 SPACE
SHUNT 4.2% DEAD

SHUNT

40.5%

1.0

to

E 0.6 08

I
S
0 0 0 0

0.2
W. 0 I 0.1 I 1 I 10 I 100

0.2

0.01

z
4

1.4

CO

5.4

1.4

YE

CO 13 SHUNT

6.3 DEAD

YE

I? SPACE

SHUNT
8.8% 1.0

DEAD SPACE 58.4%

1.0

16.9%

35.4%

A
0.8 0.2

0.6

-V

#{149}#{149}t I 0.01 0.1

II

1/
10

0.2

0:01 100
VENTILATION-PERFUSION RATIO

i#{243}o

FIGURE 2 (A, upper, and B, lower). Distribution of ventilation and perfusion, according to the ventilation! perfusion ratios in a normal subject (0) and 7 patients with acute PE (ito 7). Co = cardiac output (Llmin); VE = minute ventilation (Limmn). Normally, perfusion and ventilation are distributed to VA1Q around 1, with tall and narrow unique peak. No shunt exists. By contrast, patients 1 and 2, studied within the 48 first hours, have no shunt but a marked enlargement of the perfusion peak. Thus, a significant part of perfusion is distributed to VA/Q between land 0.1. The ventilation peak is shifted to the right. Dead space is markedly increased. Patients 6 and 7, studied later, have a normal mode of VAJQ ratio distribution, with a narrowed perfusion peak around 1 and a shunt of 9 and 17 percent, respectively.

(dead space) was markedly high (5210 percent) and accounted for as much as 63 percent of YE in patient 3 (Table 4). Anatomic dead space assumed from body

weight

was markedly

smaller

than

inert

gas dead

space

(27 percent vs 52 percent, respectively). quence of the increased dead space, minute
CHEST I 88 I 6 I DECEMBER,

As a conseventilation
1985

833

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(E)

was consistently

increased

(mean

VE 177

L/min)

following ity across to perfusion at to in either

acute the the

PE:

(1) a decreased

0,

diffusing

capac-

and was above 20 IJmin in patient ventilation was also consistently

VA/

2. The shifted with

mean peak of to the high dispersion

pulmonary mismatching;46 intracardiac

membrane;38 (2) ventilation and (3) shunting of blood, or the intrapulmonary cause a the surface available for

ratios

(mean,

2.88

1.67),

a large

of the The contrast and to patient embolic ings,

distribution (.83 .22). VA/Q diagrams in Figure these different compare them 1, who event was and had

2 make
VA/

it possible
distribution example, hours film

patterns of to normal. studied normal within chest

level.7#{176} An embolus could theoretically decrease in diffusing capacity by reducing area of the alveolar capillary membrane gas exchange flow through the measured PaO, values distributions. not a cause or by decreasing the a reduced pulmonary PaO, values predicted This suggests for hypoxemia several

For 24

of the find-

transit time of blood vascular bed. But identical actual diffusion a finding and clinito the
,A/

x-ray

peak
the

there is substantial dispersion of the perfusion but no shunt. In patient 6, studied one week after onset of symptoms and presenting with atelectasis a shunt of 9 is close to
VA/Q

were nearly from the that in our recent impaired patients, experimental

was in

and infiltrates percent. His normal,

approximately

chest x-ray film, VA/Q distribution, a mean 1.

DIscUssIoN

we found however, on a

agreement with cal studies.

with

value

centered

ratio

of

In contrast, in most of our patients an increased venous admixture (0, method) in the absence of a parallel increase in Qs/t (inert gases method) indicated that VAIQ of their studied was the found
VA/

mismatching hypoxemia. early, eg, despite

accounted

for a substanapparent virtually of 19 gas study

Hypoxemia has been acute PE,345#{176}but its believed cause was that part related to

consistently demonstrated etiology remains unclear. difficulty in in discovering the selection and variations

in We its of to the clinical inin

tial portion in patients no shunt and confirmed documenting out a definite VA/ ratios increased the conclusion

This was most 1 and 2, in whom a venous admixture inert The

of the

16 percent

of cardiac increased zone may

output.

patients or in the severity of the embolism long delay between initial symptoms investigation.5 In terpreted hypoxemia P(A-a)0, cance mine, and venous addition, in regard past studies to associated

and

mismatching dispersion

in these patients by of perfusion, withon (Fig 2). The low the basis of an lung. This computer was

have changes

of very low be explained to the nonembolic a recent

admixture.#{176} The

clinical

signifi-

perfusion from

of these measurements are since they are influenced diffusion.7 a group

difficult to deterby shunt, VAJ of patients percent) shortly with but

automated

mismatching, and impaired In this study, we examined

analysis of ventilation-perfusion lung scans in II patients with acute pulmonary emboli and normal chest x-ray findings. In each of these patients the analysis showed emboli perfusion It has could areas fused. canine lung areas remote that had an abnormal with also be caused contiguous This has relative been suggested by selective to the embolic been and from those matching that this affected by the of ventilation to
\TA/

large (mean vascular obstruction 55 nonlethal acute pulmonary embolism their first symptoms. All were 67 II), and each had moderate sion from vasoactive zation nique shunt, factors the acute embolism, drugs. We combined inert relative

after

hypoxemic (mean PaO,, hemodynamic depresbut right none heart required catheteri-

overperfusion. mismatch in perpneumoconstriction lung that remain in experimental is attributed to reflex Bronshown in

with the multiple to determine the

sA/Q

gas elimination techimpact of pulmonary and their cardiac hypox-

demonstrated

thromboembolism has

mismatch, on the hypoxemia.

impaired diffusion, We found that pulmonary findings and studied due

bronchoconstriction choconstriction

or pneumoconstriction.4 also been consistently

emia was depending elapsed

caused by different on chest x-ray since the PE. hypoxemia with without through 2). 1 and volume

mechanisms, on the time early followVA/

In patients low VA/C a significant

human pulmonary embolism,4 and a shift of ventilation away from the unperfused lung has been demonstrated in man after the temporary occlusion of one pulmonary

ing embolism, of lung units mismatching), perfusion shunting contributor (Fig of lung

was mainly

to perfusion from ie,

artery.
tion lung Our

This

bronchoconstriction for lung.9 such

or pneumoconstricsubsequent volume loss loss occurs, of

ratios (ie, contribution lung became if atelectasis In

may then be responsible volume in the embolic data suggest that when

of blood

unventilated Shunt only loss

units,

a significant or other our studied proposed hypoxemia series 48 to

to hypoxemia

shunt enters the discoid atelectasis has already been studies, usually autopsy. porarily

clinical picture. The high incidence of in patients with measurable shunts emphasized.#{176} In experimental PE is at temwere
of a!)

causes

developed.

these characteristics were found in patients hours or more after the initial symptoms. Three major mechanisms have been explain
834

shunt as a major reported when Wilson lower et their

Hypoxemla

contributor to hypoxemia alveolar collapse is seen that P(A-a)O,

Pulmonary

al#{176} found patients

in Acute

they

could if they

the

pulmonary

contribution

to the

Embolism

(Huet

Downloaded From: http://journal.publications.chestnet.org/ on 08/10/2013

encouraged

to

breathe

80

to

ifi

percent

of

their

ventilation 2.88. CO, (Bohr,

shifted 59

to the dead 10

right,

with using and

a mean both the the

value expired

of of

predicted inspiratory capacity, thus decreasing the amount of focal alveolar collapse. Similarly, no shunt was demonstrated in the study by Caldini6 when mechanical ventilation with periodic sighs was used. In the patients we studied, clinically significant shunting was found only in those with atelectasis and infiltrates (Fig 1). It may be that significant loss of lung volume and alveolar early collapse to those developed of pulmonary in lung vascular of these from alteration zones of areas corresponding and that shunting. Pulmonary obstruction produced pulmonary

Measured

space, percent)

excretion

soluble gases (inert gas dead was higher than the predicted (27 4 percent), corresponding unperfused lung. In addition

space, 5210 percent) anatomic dead space to the to the ventilation of dead space, PE high et al of that

patients studied within the first 48 hours following had a supplemental mode of ventilation, with VA/Q ratios (Fig 2). In dog experiments, Dantzker have such already demonstrated a high mode, with VA/Q the early between occurrence 10 and 100,

reperfusion edema

alveolar-capillary permeability flow to the still-perfused lung tion for shunting in acute PE, repeatedly However, pulmonary are distinctly been shown in convincing clinical edema rare. in patients None

or from increased blood is an alternative explanaand animal reports free of our alveolar edema has experiments.67 of PE with acute of left heart patients had disease x-ray

disappeared after a few hours. The major limitation to our findings number of patients studied and that, reasons, within shunt have the inert gas study could not individuals over time. permitted the Repeated patient the

is the small for practical be repeated

to document changes in VA/Q and A larger number of patients would use of stronger statistical testing to and in the relationship determinations would have between the results that hypoxemia atelectasis between further atelectasis of gas exchange supported

demonstrate shunting. the same

evidence of acute lung. Subclinical cannot be Remaining acute PE

edema in nonembolic areas of the focal pulmonary edema, however, in the areas of for right-to-left shunts from the consolidation. shunting opening shunts opening ruled in of a from of a out in

excluded explanations are intracardiac

observations made less, we believe that firm enough to suggest PE, initial Only when has acute mismatch.

individuals. Neverthein these individuals are an acutely ill patient is caused by VA/Q or other indications

when

patent foramen ovale67 or intrapulmonary the opening of precapillary shunts.3 The patent foramen ovale cannot be entirely

our patients, but their right atrial pressures were in the normal range, especially in those with the largest shunts. The opening of precapillary shunts never has been demonstrated in patients tal studies, and no relationship shunt and PAP in our patients. As already
A/

of lung volume attributed to therefore increasing ing on the should the

loss develop should the hypoxemia be shunting. Initial therapeutic measures be aimed functional function at preserving residual may also rapid

or, if possible,
Dependsupport part of initial

capacity. be a critical

or in recent experimenwas found between the moderate magnitude and of V dispro-

clinical

circumstances,

of cardiovascular management.

mentioned, and shunt

however, were

mismatching

CONCLUSION

portionate patients. worsen patients

to the degree This suggests the hypoxemia. suffered from

of hypoxemia recorded in our that an additional factor may Except patient 1, all of our hemodynamic changes associBecause of their low cardiac (27 5 mm Hg), and this no hypoxemia. of shunt Dantzker would by The or low and potential
VA/

The pulmonary tern sion

primary

cause embolism

of the appears

initial

hypoxemia a disturbed Simultaneous contributes

in acute patdepresto hypoxbecome of lung

to be

of ventilation to perfusion. of cardiac function further intrapulmonary until atelectasis develop.

ated with their acute PE. output, they had low PO, doubt role recently Assuming contributed of a low PO, been that to their

emia, but important volume loss

shunting does not or another cause

for any level emphasized

VA/

has unACKNOWLEDGMENT: Francoise Veyssi#{232}re for Mrs. Fiorella Delcampe manuscript. We are indebted to Robert Herigault and her excellent technical assistance, and to and Maryse Gu#{233}rinfor preparation of the

Bower.6

distributions

remain

changed, these authors crease in predicted PaO,

calculated that a marked inwould result from an increase

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