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Townsend: Sabiston Textbook of Surgery, 16th ed., Copyright 2! ". #. $aunders Company
394
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e
r

3

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e
s
p
i
r
a
t
o
r
y

#
a
i
$
u
r
e
%a&id
T.
'arri
ngton
(.%.
)i$$ia
* +.
Cioffi
(.%.
The
diagno
stic
dilem
ma
posed
by
acute
respira
tory
failure
is
comm
on on
surgic
al
ser%ic
es,
with
up to
one
fourth
of
patient
s with
upper
abdom
inal
and
thorac
ic
incisio
ns
sufferi
ng
from
this
compl
ication
.
&urthe
rmore,
the
rate of
occurr
ence
may
increa
se as
the
popula
tion
ages
and as
the
elderl
y''
with
higher
rates
of
comor
bid
illness
es and
lower
physio
logic
reser%
e''
ma(e
up a
larger
propor
tion of
patient
s.
)*+

)!2+

Tachy
pnea,
tachyc
ardia,
and
the
use of
access
ory
muscl
es are
the
hallma
r(s of
respira
tory
dysfun
ction,
and
they
pose a
diagno
stic
dilem
ma for
the
physic
ian as
they
occur
in the
presen
ce of
failure
of
either
%entila
tion or
o,yge
nation.
Under
standi
ng the
differe
nce
betwe
en
these
two
proces
ses is
essenti
al to
deter
minin
g the
cause
of a
patient
-s
distres
s and
institu
ting
appro
priate
therap
y.
This
chapte
r
re%iew
s
norma
l gas
e,cha
nge
and
descri
bes
the
three
types
of
respira
tory
failure
. Type
/
0hypo
,emic
failure
1,
Type
//
0hyper
capnei
c1, and
Type
///
0posto
perati
%e1.
Mana
gemen
t of
these
pulmo
nary
dysfun
ctions
is
discus
sed in
both
the
nonint
ubated
and
the
intuba
ted
patient
.
&inall
y,
therap
eutic
option
s in
patient
s with
se%ere
or
refract
ory
respira
tory
failure
are
re%iew
ed.
,'-
.
Under
standi
ng
o,yge
n-s
journe
y from
atmos
pheric
air to
left
%entri
cular
blood
and
the
derang
ement
s that
lead to
syste
mic
hypo,
emia
begins
with
an
unders
tandin
g of
the
deter
minan
ts of
blood
o,yge
n
conten
t, the
charac
teristic
s of
the
o,yge
n'
hemog
lobin
dissoc
iation
cur%e,
and
the
princi
ples of
%entila
tion'
perfus
ion
matchi
ng.
2,yge
n
conten
t of
the
blood
is
deter
mined
predo
minan
tly by
the
ability
of
hemog
lobin
to
bind
to
o,yge
n.
Theref
ore, it
is
linearl
y
related
to
hemog
lobin
conce
ntratio
n
03gb1
and
percen
t
o,yge
n
saturat
ion
0$22 1.
4
minor
contri
butor
to
o,yge
n
conten
t is the
amoun
t of
o,yge
n
dissol
%ed in
plasm
a,
which
is
propor
tional
to the
partial
pressu
re of
o,yge
n in
plasm
a
0522 1.
2,yge
n
conten
t of
blood
0C22 1
is
calcul
ated.
C22 6
0!.78
9 :
$22 9
3gb1
;
0.7
9
5a22 1
/n
clinica
l
situati
ons,
522
and
o,yge
n
saturat
ion are
often
used
interc
hange
ably.
4ltho
ugh
related
, 522
and
o,yge
n
saturat
ion
ha%e a
compl
e,
relatio
nship,
as
descri
bed by
the
hemog
lobin'
o,yge
n
dissoc
iation
cur%e
0&ig.
27'!1 .
4t low
le%els
of
o,yge
n
tensio
n
0point
4 to
point
#1,
increa
ses in
522
transla
te into
only
small
increa
ses in
the
percen
tage of
o,yge
n
bound
to
hemog
lobin.
Durin
g mid'
range
o,yge
n
tensio
n
0point
# to
point
C1,
howe%
er, the
relatio
nship
of 522
to
o,yge
n'
hemog
lobin
bindin
g is
nearly
linear,
with
signifi
cant
increa
ses in
o,yge
n
saturat
ion
resulti
ng
from
increa
ses in
522 .
This
relatio
nship
is not
linear
at
higher
o,yge
n
tensio
n
0point
C to
point
D1,
such
that
contin
ued
increa
ses in
522
result
in
%ery
little
increa
se in
o,yge
n
saturat
ion of
hemog
lobin.
<entil
ation'
perfus
ion
matchi
ng 0 =
1 is
the
balanc
e
betwe
en
%entila
tion
and
perfus
ion at
the
al%eol
ar
le%el.
)7>+

)>7+
0
= 1
matchi
ng is a
contin
uum,
but
can
range
from
shunt,
where
an
al%eol
us has
no
%entila
tion
but
recei%
es
perfus
ion, to
dead
space,
where
an air
space
is
%entila
ted but
not
perfus
ed.
$hunt
?o
w =
@or
mal
=
3igh
=
Dea
d
space
4n
e,amp
le of
shunt
is
al%eol
ar
collap
se,
such
as
atelect
asis or
al%eol
ar
floodi
ng
with
fluid
and
inflam
mator
y
debris
0acute
respira
tory
distres
s
syndro
me, or
4AD$
1.
#lood
that
perfus
es
these
al%eoli
return
s to
the
left
atrium
with
low
o,yge
n
conten
t,
essenti
ally
the
same
conten
t as
that of
right
atrial
and
pulmo
nary
arteria
l
blood.
Dead
space
%entila
tion
occurs
in the
condu
cting
airway
s of
the
lung,
where,
in the
presen
ce of
abund
ant
%entila
tion,
perfus
ion is
limite
d and
essenti
ally no
gas
e,cha
nge
occurs
. /n
health
y
people
, the
%ast
majori
ty of
gas
e,cha
nge
occurs
in
al%eol
ar
units,
where
%entila
tion
and
perfus
ion are
well
match
ed
0norm
al =
1.
$mall
amoun
ts of
poorly
o,yge
nated
blood
do
return
to the
left
atrium
as a
result
of
right
to left
shunti
ng by
way of
the
corona
ry
sinuse
s and
the
presen
ce of
some
shunt
and
low
=
segme
nts.
$ignifi
cant
right
to left
shunti
ng can
occur
in
nonres
pirator
y
condit
ions
such
as
atrial
septal
defect
or
lung
arterio
%enou
s
malfor
matio
ns. /n
acute
and
chroni
c
diseas
e
states
rangin
g from
4AD$
to
chroni
c
obstru
cti%e
pulmo
nary
diseas
e
0C25
D1, a
greate
r
propor
tion of
perfus
ion
occurs
to
areas
of
abnor
mal
%entila
tion
and
there
is
greate
r
disper
sion of
perfus
ion
along
the
a,is of
= .
4n
increa
sed 4'
a22
gradie
nt
occurs
with
age
and
can be
estima
ted by
the
follow
ing
eBuati
on.
4'a
gradie
nt 6
2.C ;
.2! 9
4ge
There
are
genera
lly
four
mecha
nisms
that
predis
pose a
person
to
inadeB
uate
syste
mic
o,yge
nation
.
hypo%
entilat
ion,
%entila
tion'
perfus
ion
misma
tching,
shunt,
and
low
mi,ed
%enou
s
o,yge
n
saturat
ion.
3ypo,
emia
can
also
occur
from
low
conce
ntratio
ns of
inspire
d
o,yge
n,
such
as that
which
occurs
at high
altitud
es or
in fire
en%iro
nment
s.
4ltho
ugh
%entila
tion is
usuall
y
thoug
ht of
as a
proces
s to
elimin
ate
C2 2 ,
the
occurr
ence
of
hypo%
entilat
ion
resulti
ng in
the
accum
ulatio
n of
C2 2
in
al%eol
us,
which
decrea
ses the
al%eol
ar
o,yge
n
tensio
n, can
be
descri
bed by
the
al%eol
ar gas
eBuati
on.
5 4 22
6 &/22
054T
M '
53 2
21 '
05 4
C22
=AD1
39/
#igure
3!1
2,ygen
and
hemogl
obin
03gb1
dissocia
tion
cur%e.
4
sigmoid
'shaped
cur%e
shows
ma,ima
l
o,ygen
loading
in the
lung
and
unloadi
ng of 2
2 in the
periphe
ry
occurri
ng o%er
a %ery
narrow
range of
5a22 .
where
5a22
eBuals
partial
pressu
re of
2 2 in
the
al%eol
usE
&/22
the
conce
ntratio
n of
inspire
d airE
54TM
the
atmos
pheric
pressu
reE 53
2 2 the
%apor
pressu
re of
waterE
and 5
4 C22
the
partial
pressu
re of
al%eol
ar C2
2 ,
which
is
eBui%a
lent to
5aC22 ,
the
partial
pressu
re of
C2 2
in
syste
mic
arteria
l
blood.
F%en
in the
presen
ce of a
norma
l 4'a22
gradie
nt,
hypo%
entilat
ion
can
create
syste
mic
hypo,
emia.
3ypo,
emia
may
also
ensue
from
an
increa
sed 4'
a22
gradie
nt
arising
from
the =

misma
tches,
terme
d low
=
and
shunt.
To
unders
tand
shunt
and
low
= ,
consid
er the
lung
as
consis
ting of
two
al%eoli
with
differe
nt =
ratios
0&ig.
27'21
0&igur
e @ot
4%aila
ble1 .
/n this
two'
al%eol
us
model,
shunt
is
repres
ented
by one
al%eol
us,
which
is
perfus
ed but
not
%entila
ted as
a
result
of
al%eol
ar
floodi
ng,
and
the
other
al%eol
us,
which
has an
eBual
balanc
e of
%entila
tion
and
perfus
ion.
4ll
blood
comin
g from
the
shunt
al%eoli
has
poor
o,yge
n
conten
t, not
differe
nt
from
right
atrial
blood.
/ncrea
sing
&/22
has no
effect.
#lood
returni
ng
from
the
norma
l =
al%eol
us has
nearly
ma,i
mum
o,yge
n
conten
t
under
room
air
condit
ions.
/ncrea
sing
&/22
has
little
impact
on
o,yge
n
conten
t
becaus
e
o,yge
n
saturat
ion is
greate
r than
#igure
3!
0&igure
@ot
4%ailab
le1 4
model
of the
two'
al%eolu
s theory
of lung
functio
n. /n the
presenc
e of
al%eolar
collapse
or
al%eolar
floodin
g
0hatche
d area1,
nono,y
genated
%enous
blood
on the
right is
allowed
to shunt
pass the
al%eolu
s with
no
o,ygen
transfer,
yielding
a 5a2 2
of >
mm 3g
and
o,ygen
content
of !C
ml :.
Despite
a
normal
al%eolu
s on the
left and
normal
o,ygen
content
after
passing
by the
al%eolu
s 02 2
content
22 ml
:1, the
mi,ing
of right
and left
gi%es
the
systemi
c blood
a 52 2
of G
mm 3g
and a
low
o,ygen
content
of !*.C
ml :.
(From
Hall
JB,
Wood
LD:
Acute
hypoxe
mic
respirat
ory
failure.
I Hall
JB,
!chmid
t "A,
Wood
LDH
#eds$:
%ricip
les of
&ritical
&are.
'e(
)or*,
+c"ra
(,Hill,
-../,
(ith
permiss
io of
the
+c"ra
(,Hill
&ompa
ies.0
HC:.
The
increa
sed
dissol
%ed
o,yge
n in
plasm
a
increa
ses 2 2
conten
t
minim
ally.
Theref
ore,
syste
mic
hypo,
ia
resulti
ng
from
shunt
is a
reflect
ion of
the
relati%
e
percen
tages
of
blood
perfus
ing
shunt
and
norma
l =
areas
and is
poorly
respon
si%e to
increa
ses in
&/22 .
Consi
der a
two'
al%eol
us
model
of low
= ,
in
which
one
al%eol
us is
moder
ately
under
%entila
ted in
relatio
n to its
perfus
ion
and
the
other
al%eol
us has
balanc
ed =
. The
low
=
al%eol
us has
higher
5aC22
and
lower
5a22
as a
result
of
subopt
imal
%entila
tion
and
return
s
blood
to the
left
atrium
,
which
is
o,yge
nated
subopt
imally.
#lood
returni
ng
from
the
norma
l =
al%eol
us can
partial
ly
balanc
e this
decrea
sed
o,yge
n
conten
t and
the
syste
mic
hypo,
ia is
not as
profou
nd. /n
contra
st to
shunt
physio
logy,
increa
sing
inspire
d
o,yge
n
tensio
n in
condit
ions of
low
=
impro
%es
5a22 ,
increa
ses the
gradie
nt
betwe
en
al%eol
us and
pulmo
nary
capilla
ry
bed,
and
results
in
impro
%ed
o,yge
n
conten
t of
arteria
l
blood.
"here
as a
measu
rable
increa
se in
4'a22
gradie
nt still
e,ists
in this
low
=
model,
it is
less
than
that in
the
condit
ions of
pure
shunt,
and
syste
mic
hypo,
emia
is
attenu
ated.
4 final
cause
of
syste
mic
hypo,
ia is
the
result
of
syste
mic
factors
,
which
create
low
mi,ed
%enou
s
saturat
ions 0
22 1,
such
as
cardia
c
dysfun
ction
or
drama
tic
increa
ses in
o,yge
n
deman
d. /n
the
setting
of
norma
l = ,
a low
22
from
these
condit
ions
may
ha%e
little
impact
on
syste
mic
o,yge
nation,
but in
the
critica
lly ill
patient
with
areas
of =
misma
tching,
a low
22
can
result
in
syste
mic
hypo,
emia.
The
e,plan
ations
noted
earlier
accou
nt for
condit
ions of
syste
mic
hypo,
ia.
"here
as
deficie
nt
diffusi
on of
o,yge
n
throug
h
thic(e
ned
al%eol
ar'
capilla
ry
memb
ranes
was at
one
time
thoug
ht to
be the
primar
y
e,plan
ation
of
syste
mic
hypo,
ia, this
mecha
nism
has
little
clinica
l
signifi
cance.
C.
Carbo
n
dio,id
e is
produ
ced as
the
body
consu
mes
o,yge
n
0o,yg
enatio
n
consu
mptio
n 6
<22 1
and
fuel.
The
amoun
t of
C2 2
produ
ced
0<C22 1
depen
ds on
the
type
of fuel
burne
d. The
respira
tory
Buotie
nt 0AD
6 <C22
=<22 1
ranges
from
.8
when
fats
are
consu
med to
!.
when
carboh
ydrate
s are
burne
d. C2
2
produ
ced in
the
periph
ery
diffus
es out
of
cells
and is
transp
orted
to the
lungs
bound
to
hemog
lobin
or
dissol
%ed in
serum
as
bicarb
onate
03C2
7 1.
The
elimin
ation
of C2
2 in the
lungs
depen
ds,
first,
on the
ability
of
pulmo
nary
arteria
l C2 2
to
eBuili
brate
with
al%eol
ar gas
and,
secon
d, on
al%eol
ar
%entila
tion.
$imila
r to
o,yge
n,
there
is little
imped
iment
to
diffusi
on of
C2 2
from
capilla
ry to
al%eol
usE
howe%
er,
eBuili
bratio
n of
C2 2
betwe
en the
capilla
ry and
al%eol
us
depen
ds on
=
matchi
ng.
Dead
space'
'either
anato
mic
such
as in
the
trache
a and
other
condu
cting
airway
s, or
physio
logic
such
as
al%eol
ar
units
with
abund
ant
%entila
tion
and no
perfus
ion''is
usuall
y less
than
7C:
of
each
breath.
4 tidal
%olum
e 0<T1,
theref
ore,
has
both
al%eol
ar
%entila
tion
and
dead
space
%entila
tion.
<T 6
4l%eol
ar
%entila
tion ;
Dead
space
%entila
tion
"hen
dead
space
and
high
=
areas
recei%
e a
dispro
portio
nate
share
of
%entila
tion,
the
body-s
ability
to
clear
C2 2
is
limite
d.
F%en
in the
presen
ce of
norma
l =
matchi
ng,
adeBu
ate
%entila
tion
reBuir
es an
adeBu
ate
dri%e
to
breath
e
0origin
ating
in the
central
ner%o
us
syste
m1,
compe
tent
mecha
nics of
breath
ing,
and
the
lac( of
e,cess
i%e
respira
tory
load.
Aeduc
ed
dri%e
to
breath
e can
be the
result
of
sedati
%es
0narco
tics,
barbit
urates,
and
benIo
diaIep
ines1,
hypot
hyroid
ism,
central
sleep
apnea,
or
structu
ral or
ische
mic
lesion
s of
the
critica
l
respira
tory
tracts
of the
C@$.
@orm
al
mecha
nics of
breath
ing
reBuir
e
intact
periph
eral
neuro
muscu
lar
conne
ctions.
5hreni
c
ner%e
injury,
high
spinal
cord
lesion
s
caused
by
traum
a or
Juilla
in'
#arre
syndro
me,
myast
henia
gra%is,
and
physic
ian'
directe
d
pharm
acolog
ic
paraly
sis can
interfe
re
with
diaphr
agmati
c and
interc
ostal
muscl
e
ener%a
tion.
Muscu
lar
dystro
phies,
large
flail
segme
nts
follow
ing
traum
a,
shoc(
and
lac( of
adeBu
ate
blood
supply
, or
electro
lyte
distur
bances
0e.g.,
hypo(
alemia
,
hypoc
alcemi
a,
hypo
magne
semia,
and
hypop
hosph
atemia
1 can
impair
respira
tory
muscl
e
functi
on.
<entil
atory
failure
can
occur
e%en
in the
presen
ce of
396
norma
l
central
dri%e
and
norma
l
respira
tory
mecha
nics as
a
result
of
e,cess
i%e
respira
tory
load.
@orm
al
%entila
tion
in%ol%
es the
creatio
n of
negati
%e
intrapl
eural
pressu
re by
e,pan
sion of
the rib
cage
throug
h
interc
ostal
muscl
e
contra
ction
and
pushin
g
down
of the
intra'
abdom
inal
conten
ts
throug
h the
contra
ction
of the
diaphr
agm.
This
natura
l
%acuu
m
produ
ces the
gradie
nt for
the
flow
of air
into
the
lungs,
but it
is
oppos
ed by
resista
nce in
the
airway
s
0resisti
%e
load1
and by
the
elasta
nce of
the
lungs
and
chest
wall
0elasti
c
load1.
Aesisti
%e
load
0or
flow
resista
nce1
can be
caused
by
upper
airway
obstru
ction
0e.g.,
epiglo
ttitis,
foreig
n
bodies
,
laryng
eal
edema
, or
traum
a1,
asthm
a,
chroni
c
bronc
hitis,
or
airway
secreti
ons. /n
intuba
ted
patient
s,
increa
sed
resisti
%e
load
can be
the
result
of a
(in(ed
or
occlud
ed
endotr
acheal
tube
or
faulty
%entila
tor
circuit
s. 4n
increa
se in
elastic
load
may
be
caused
by
pleura
l or
chest
wall
diseas
e,
such
as rib
fractur
es or
circu
mfere
ntial
chest
burns,
or by
restric
tion of
diaphr
agmati
c
e,curs
ion
from
tense
ascites
, ileus,
abdom
inal
incisio
ns, or
obesit
y.
Flastic
load
can be
increa
sed in
patient
s with
airway
obstru
ction
resulti
ng
from
dynam
ic
airway
collap
se
0such
as that
which
occurs
in
bronc
hiecta
sis1
during
e,pira
tion,
which
leads
to air
trappi
ng and
high
le%els
of
intrins
ic
positi%
e end'
e,pira
tory
pressu
re
05FF5
1. This
hyperi
nflatio
n of
the
lungs
create
s a
mecha
nical
disad%
antage
for the
respira
tory
muscu
lature
0a
short
and
flat
diaphr
agm1
and
establi
shes
the
need
to
create
a
larger
pressu
re
gradie
nt
before
the
ne,t
cycle
of
inspira
tion
can
comm
ence.
)!+

&inall
y,
infiltra
ti%e
proces
ses
such
as
edema
,
fibrosi
s, or
infecti
on
in%ol%
ing the
al%eol
us can
increa
se
elastic
load.
/nsuffi
cient
al%eol
ar
%entila
tion
results
in
increa
sing
le%els
of C2
2 and a
decrea
se in
p3 of
the
blood,
as
descri
bed by
the
3ende
rson'
3assel
bach
eBuati
on.
p3 6
G.2 ;
log
0)3C
2 7 +=
).7 6
5C22 +1
3C27
is the
conce
ntratio
n of
bicarb
onate
in the
blood
and
5C22 is
the
partial
pressu
re of
C2 2 .
Aapid
accum
ulatio
n of
C2 2
results
in a
se%ere
acidos
is,
which
can
result
in
cellula
r
dysfun
ction
and, if
se%ere
, death
of the
patient
.
$lowe
r
accum
ulatio
n of
C2 2
allows
for
bicarb
onate
retenti
on by
the
(idney
and a
less
signifi
cant
decrea
se in
p3 of
the
blood.
@onco
mpens
ated or
compe
nsated
,
regard
less,
an
ele%at
ed C2
2
means
some
degree
of
%entila
tory
failure
.
0ung
Tidal
%olum
e is
only a
small
portio
n of
total
lung
capaci
ty
0T?C1
0&ig.
27'71
0&igur
e @ot
4%aila
ble1 .
@orm
al
inspira
tory
and
e,pira
tory
%olum
es
cycle
on top
of a
lung
%olum
e,
terme
d
fucti
oal
residu
al
capac
ity
0&AC1
. 4s
discus
sed
earlier
, &AC
is
stabili
Ied
and
recruit
ed in
the
postop
erati%e
patient
by
5FF5,
uprigh
t chest
positio
n,
incenti
%e
spiro
metry,
#igure
3!3
0&igure
@ot
4%ailab
le1
?ung
%olume
s.
$pirom
etry
data are
importa
nt to the
(nowle
dge of
functio
nal
residual
%olume
and its
relation
to
closing
%olume.
(From
West
JB:
1espira
tory
%hysiol
o2y,,
3he
4sseti
als, 5th
ed.
Baltimo
re,
William
s 6
Wil*is,
-..7.0
'' 5ulmonary &unction Tests
, forced e,piratory %olume in ! secondE A<, residual %olumeE T?C,
K5ulmo
nary
functio
n tests
showin
g
standar
d
paramet
ers for
an
a%erage
patient
and the
patterns
of
obstruct
i%e and
restricti
%e lung
disease.
#ase
d on
normal
spirome
try for
an
a%erage
'siIed
0C C
1 C'
year'
old
woman.
and
loss of
&AC
can
result
in
lung
collap
se,
atelect
asis,
and
hypo,
emia.
Aesid
ual
%olum
e is
the
remai
ning
lung
%olum
e
follow
ing a
ma,i
mal
e,hala
tion,
and
%ital
capaci
ty is
the
%olum
e
in%ol%
ed in a
ma,i
mal
e,pira
tory
effort
follow
ing a
ma,i
mal
inspira
tion.
Aate
of air
flow is
also a
comm
only
measu
red
respira
tory
param
eter
and
the
most
widely
used is
&F<
! ,
which
is the
ma,i
mum
%olum
e
e,pire
d
during
the
first
secon
d of a
forced
e,hala
tion.
The
hallma
r(s of
obstru
cti%e
lung
condit
ions
such
as
asthm
a,
bronc
hiecta
sis,
and
airway
collap
se are
a
depres
sed
&F< !
and
increa
sed
T?C
0Table
27'!1 .
The
hallma
r(s of
restric
ti%e
lung
diseas
e such
as
(ypho
scolio
sis or
morbi
d
obesit
y are
decrea
sed
T?C
and
residu
al
%olum
e and
relati%
ely
preser
%ed
&F<
! .
1ook*ar
k 2"0:
=das=boo(=
%iew=7>>7
C7*'
2=H2!=22C.
html=topU
se of this
content is
subject to
the Terms
and
Conditions
of the MD
Consult
web site.
Townse
nd:
Sabisto
n
Textbo
ok of
Surger
y, 16th
ed.,
Copyrig
ht
2!
". #.
$aunder
s
Compa
ny
C03
Type 4
Type /
respira
tory
failure
is
hypo,
emic
respira
tory
failure
.
#ecau
se this
type is
predo
minan
tly
caused
by
shunti
ng,
these
patient
s are
unresp
onsi%e
to
o,yge
n
therap
y and
ha%e
low
5a22
despit
e
recei%i
ng
supple
mental
o,yge
n.
Collap
sed or
floode
d
al%eoli
accou
nt for
the
shunt
of
Type /
respira
tory
failure
.
4l%eol
i are
collap
sed or
are
filled
with
either
purule
nt
materi
al
0pneu
monia
1,
blood
0pulm
onary
contus
ion,
al%eol
ar
hemor
rhage1
, or
fluid
0high'
or
low'
pressu
re
pulmo
nary
edema
1.
3igh'
pressu
re
pulmo
nary
edema
resulti
ng
from
cardia
c
dysfun
ction
is
often
accom
panied
by
clinica
l signs
of
fluid
o%erlo
ad,
such
as
jugula
r
%enou
s
distent
ion or
an $ 7
gallop,
and
can be
confir
med
by
in%asi
%e
monit
oring,
which
would
re%eal
pulmo
nary
artery
occlus
ion
pressu
res
genera
lly
greate
r than
!*
mm
3g.
?ow'
pressu
re
edema
04AD
$1
occurs
in the
absenc
e of
high
pulmo
nary
artery
occlus
ion
pressu
res
and
should
be
suspec
ted if
the
clinica
l
course
includ
es
incitin
g
e%ents
typical
ly
associ
ated
with
its
de%elo
pment
0e.g.,
sepsis,
aspirat
ion,
massi
%e
transf
usion,
shoc(,
pancre
atitis,
and
amnio
tic
fluid
and fat
embol
i
syndro
mes1.
)7+

4ltho
ugh
many
scorin
g
syste
ms
attemp
t to
Buanti
fy the
degree
of
lung
injury,
the
5a22 =
&/22
ratio
05=&1
is the
most
widely
used.
/n this
syste
m, a
5=&
less
than
7
and
greate
r than
2 is
consid
ered
an
acute
lung
injury
and a
5=&
less
than
2 is
consid
ered to
be
4AD$
.
)8+

)28+

/n
additi
on to
the
hypo,
ia of
Type /
respira
tory
failure
,
pulmo
nary
edema
'
induce
d
respira
tory
dysfun
ction
results
in
decrea
sed
lung
compl
iance,
which
drama
tically
increa
ses the
wor(
of
breath
ing for
the
patient
and
e,acer
bates
the
patient
-s
dyspn
ea and
tachyp
nea.
Type
The
hallma
r( of
Type
//
respira
tory
failure
is an
ele%at
ed
5C22 .
This
ele%ati
on is
caused
by
hypo%
entilat
ion
from
loss of
central
respira
tory
dri%e,
impair
ed
mecha
nics of
breath
ing, or
e,cess
i%e
load.
5atien
ts with
loss of
dri%e
will
ha%e
depres
sed
mentat
ion
and
may
lac(
the
typical
dyspn
ea and
tachyp
nea
presen
t in
most
types
of
respira
tory
failure
.
5atien
ts with
impair
ed
mecha
nics
ha%e a
depres
sed
negati
%e
inspira
tory
force
0@/&1
and
ma,i
mal
minut
e
%entila
tion
0MM
<1.
5atien
ts with
increa
sed
resisti
%e and
elastic
loads
ha%e a
decrea
sed
tidal
%olum
e
while
sponta
neousl
y
breath
ing
and
395
high
pea(
and
platea
u
airway
pressu
res
when
intuba
ted. 4
comm
on
presen
tation
of
Type
//
respira
tory
failure
is
terme
d
acute
o
chroi
c
respir
atory
failure
, in
which
a
patient
with
chroni
cally
compe
nsated
%entila
tory
dysfun
ction,
such
as
C25D
, has
an
additi
onal,
someti
mes
minor,
insult
such
as a
%iral
pneum
onia
or rib
fractur
es that
puts
them
into
uncom
pensat
ed
failure
.
)78+

Type
Type
///
respira
tory
failure
typical
ly
occurs
in
postop
erati%e
patient
s and
has
charac
teristic
s of
both
hypo,
emia
and
hypo%
entilat
ion.
4ltho
ugh
difficu
lt to
charac
teriIe,
this
type
of
failure
appear
s to be
the
result
of
worse
ning
atelect
asis,
possib
ly
from
diaphr
agmati
c
dysfun
ction
and
decrea
sed
abdom
inal
breath
ing,
and it
results
in
progre
ssi%e
respira
tory
distres
s.
)!!+

)77+

Jener
ally,
airway
s close
when
&AC''
norma
lly
C:
of
T?C''
goes
below
2C:.
4irwa
ys
close
at
&AC
at
greate
r than
2C:
of
T?C
in
elderl
y
patient
s,
patient
s with
a
smo(i
ng
history
, and
patient
s
e,peri
encing
pulmo
nary
edema
.
&urthe
rmore,
&AC
decrea
ses
with
supine
positio
ning,
abdom
inal
incisio
ns,
ileus,
and
ascites
, and
in
obese
patient
s. This
combi
nation
of
increa
sed
closin
g
%olum
e and
decrea
sing
&AC
puts
many
genera
l
surgic
al
patient
s at
ris(
for
postop
erati%e
respira
tory
failure
, and
the
subseB
uent
de%elo
pment
of
pneum
onia
and
the
need
for
endotr
acheal
intuba
tion.
1ook*ar
k 2"0:
=das=boo(=
%iew=7>>7
C7*'
2=H2!=22G.
html=topU
se of this
content is
subject to
the Terms
and
Conditions
of the MD
Consult
web site.
Townse
nd:
Sabisto
n
Textbo
ok of
Surger
y, 16th
ed.,
Copyrig
ht
2!
". #.
$aunder
s
Compa
ny
(36
1asi7
5re%e
ntion
of
respira
tory
decom
pensat
ion is
the
ideal
treatm
ent of
respira
tory
failure
. /n
the
postop
erati%e
patient
, early
assum
ption
of an
uprigh
t chest
positio
n and
mobili
Iation
preser
%e
&AC.
/ncent
i%e
spiro
metry
should
be
standa
rd for
all
surgic
al
patient
s and
should
begin
preope
rati%el
y with
patient
educat
ion.
The
use of
humid
ified
air and
early
remo%
al of
nasog
astric
tubes
aid in
the
cleara
nce of
secreti
ons.
Farly
remo%
al of
&oley
cathet
ers
and
chest
tubes
allows
for
easier
mobili
Iation.
5ain
contro
l
should
be
carefu
lly
adjust
ed to
pro%id
e
adeBu
ate
analge
sia for
coughi
ng,
deep
breath
ing,
and
mobili
Iation
yet not
suppre
ss
mentat
ion
and
central
respira
tory
dri%e.
5atien
t'
contro
lled
anesth
esia
de%ice
s and
epidur
al
cathet
ers are
ideal
metho
ds of
pain
contro
l to
achie%
e these
goals.
2nce
the
sympt
oms of
respira
tory
failure
de%elo
p, the
underl
ying
cause
should
be
pursue
d and
treated
. The
patient
-s
intra%
ascula
r
%olum
e
status
should
be
assess
ed by
clinica
l
criteri
a such
as
lung
auscul
tation,
urine
output
, daily
weight
s, and
inta(e
and
output
measu
remen
ts on
flow
sheets.
/f the
%olum
e
status
is still
unclea
r, a
central
monit
oring
cathet
er may
be
in%alu
able
for
detecti
ng
potent
ial
fluid
o%erlo
ad and
directi
ng a
diuere
sis.
/dentif
ied
infecti
ons
should
be
treated
with
appro
priate
antibi
otics.
/f
clinica
l
concer
ns of
infecti
on
remai
n e%en
in the
absenc
e of an
identif
iable
pathog
en,
empiri
cal
therap
y
should
be
consid
ered in
se%ere
ly ill
or
debilit
ated
patient
s. /n
patient
s who
do not
respon
d to
standa
rd
antibi
otic
regim
ens,
the
diagno
sis of
unusu
al
opport
unistic
infecti
ons,
such
as
with
mycob
acteria
, or
%iral
infecti
on
with
herpes
%irus
or
cytom
egalo%
irus,
should
be
enterta
ined.
#ronc
hospas
m is a
comm
on
cause
of
respira
tory
decom
pensat
ion.
The
first
line of
therap
y for
bronc
hospas
m is
deli%e
ry of
an
inhale
d beta'
agonis
t such
as
albute
rol.
Deli%e
ry of
selecti
%e
beta 2
agonis
ts by
inhalat
ion
appear
s to
ha%e
minim
al
syste
mic
effects
on
tachyc
ardia.
/n
more
se%ere
cases
of
bronc
hospas
m, the
intra%
enous
methy
l,anth
ine,
theoph
ylline,
may
ha%e a
synerg
istic
effect
when
used
in
conjun
ction
with
inhale
d beta'
agonis
ts and
may
impro
%e
diaphr
agmati
c
functi
on.
)H+

)2G+

#ronc
hospas
m,
which
is
refract
ory to
these
therap
ies,
should
be
treated
with
inhale
d or
intra%
enous
steroid
s
0meth
ylpred
nisolo
ne 2 to
7
mg=(g
=day
di%ide
d
e%ery
G
hours1
.
)!+

Une,p
lained
persist
ent
tachyc
ardia
or
episod
ic
hypo,
ia
should
lead to
e%alua
tion
for
pulmo
nary
embol
i.
F%en
thoug
h
pulmo
nary
effusi
ons do
not
routin
ely
deman
d
draina
ge,
worse
ning
respira
tory
failure
should
lead to
a
diagno
stic
and
potent
ially
therap
eutic
thorac
entesis
. The
airway
can be
the
cause
of
respira
tory
decom
pensat
ion in
patient
s with
an
obstru
cting
lesion
such
as
carcin
oma
or
trache
al
stenos
is
from
pre%io
us
intuba
tion.
The
sympt
oms of
upper
airway
obstru
ction
can be
tempo
riIed
by the
use of
helio,
until
the
underl
ying
proble
m is
treated
or a
definit
i%e
airway
is
secure
d. The
use of
a
8=7
heliu
m=o,y
genati
on
mi,tur
e
reduce
s
airflo
w
resista
nce by
a
densit
y'
depen
dent
mecha
nism
and
can
amelio
rate
the
sympt
oms of
respira
tory
distres
s.
)24+

#ecau
se the
e%alua
tion of
the
respira
tory
failure
is
ongoi
ng, all
patient
s
should
recei%
e
supple
mental
o,yge
n.
2,yge
n
therap
y can
re%ers
e
tissue
hypo,
ia,
thereb
y
impro
%ing
cellula
r and
organ
functi
on,
and
can
reduce
pulmo
nary
hypert
ension
by
amelio
rating
hypo,
ic
%asoc
onstric
tion.
4ltho
ugh
many
clinici
ans
are
concer
ned
that
orderi
ng
supple
mental
o,yge
n for a
patient
with
an
underl
ying
lung
diseas
e such
as
C25D
and
new
respira
tory
decom
pensat
ion
can
result
in
respira
tory
arrest
resulti
ng
from
loss of
the
Lhypo
,ic
dri%e
to
breath
e,L no
e%iden
ce
e,ists
to
substa
ntiate
this
allege
d
pheno
menon
.
Deli%e
ry of
supple
mental
o,yge
n may
increa
se C2
2 and
decrea
se p3,
but
these
effects
are
mainl
y due
to the
offloa
ding
of C2
2 from
hemog
lobin
03alda
ne
effect1
or
subtle
chang
es in
dead
space
%entila
tion.
$e%era
l
studie
s ha%e
shown
that
patient
s with
C25D
and
respira
tory
failure
ha%e a
supran
ormal
dri%e
to
breath
e,
which
is
minim
ally
suppre
ssed
by the
deli%e
ry of
supple
mental
o,yge
n.
)>+

)C+

)7G+

3owe
%er,
becaus
e the
condit
ion of
some
patient
s
deteri
orates
further
despit
e
o,yge
n
therap
y and
becaus
e an
ele%at
ed
5C22
that
may
secon
darily
suppre
ss
%entila
tion
de%elo
ps in
others,
the
institu
tion of
o,yge
n
therap
y, li(e
any
new
inter%
ention,
should
be
monit
ored
closel
y.
6onin
/f
attemp
ts to
arrest
the
progre
ssion
of
respira
tory
failure
are
unsuc
cessfu
l,
endotr
acheal
intuba
tion is
often
necess
ary.
There
are
se%era
l
nonin
%asi%e
inter%
ention
s that
can
suppor
t
o,yge
nation
and
%entila
tion,
and
possib
ly
elimin
ate the
need
for
endotr
acheal
intuba
tion
and
mecha
nical
%entila
tion.
/nterm
ittent
positi%
e
pressu
re
breath
ing
0/55#
1,
which
can be
perfor
med
e%ery
2 to >
hours,
aids in
cleara
nce of
secreti
ons
but is
labor
intensi
%e
and,
becaus
e it is
not
contin
uously
applie
d,
does
not
perma
nently
recruit
air
spaces
.
Contin
uous
positi%
e
airway
pressu
re
0C545
1
applie
d by a
tight'
fitting
mas(
can
mainta
in and
restore
&AC
and,
theref
ore,
pro%id
es a
tempo
rary
salutar
y
effect
on
o,yge
nation
as the
underl
ying
cause
of
hypo,
ia is
treated
. This
inter%
ention
has no
effect
on
%entila
tion
and
reBuir
es
nasog
astric
tube to
drain
the
aeroph
agia
associ
ated
with
this
treatm
ent.
#ile%e
l
positi%
e
airway
pressu
re
0#/54
51 also
uses a
tight'
fitting
mas(,
but it
also
reBuir
es a
%entila
tor to
deli%e
r a
baseli
ne
pressu
re
during
e,hala
tion
0li(e
5FF51
and
then a
higher
airway
pressu
re
during
sponta
neous
patient
'
initiat
ed
breath
s. This
deli%e
red
inspira
tory
pressu
re
pro%id
es a
small
%entila
tory
assist,
which
may
pre%en
t
respira
tory
fatigu
e and
the
need
for
endotr
acheal
intuba
tion.
?i(e
C545,
#/545
should
be
consid
ered a
short'
term
therap
y that
allows
for the
identif
ication
and
treatm
ent of
the
underl
ying
derang
ement.
Contin
ued
close
monit
oring
is
necess
ary for
patient
s on
C545
and
#/545
becaus
e their
condit
ion
may
deteri
orate
precip
itously
despit
e these
therap
ies.
(e7h
4ltho
ugh
se%era
l
labora
tory
criteri
a
strong
ly
sugges
t the
need
for
intuba
tion,
clinica
l
criteri
a and
clinica
l
judgm
ent
ultima
tely
should
guide
the
decisi
on
0see
Table
27'2 1.
Despit
e
accept
able
gas
e,cha
nge, a
patient
with a
sustai
ned
respira
tory
rate
greate
r than
7C and
a
subjec
ti%e
sense
of
tiring
should
be
consid
ered
for
intuba
tion
and
%entila
tion.
F%en
thoug
h
intuba
tion
and
contro
l of
the
airway
can be
life
sustai
ning,
artifici
al
airway
s are
not
witho
ut
compl
ication
.
@asotr
acheal
airway
s are
more
stable
and
less
suscep
tible
to
mo%e
ment
than
oral
trache
al
tubes
but
they
are
also
associ
ated
with
sinusit
is and
are
contra
indicat
ed in
patient
s with
a
bleedi
ng
diathe
sis.
2ral
trache
al
tubes
can
migrat
e 2 cm
or
more
with
head
398
mo%e
mentE
theref
ore,
tube
migrat
ion
and
tube
dislod
gment
are
more
comm
on.
Unpla
nned
e,tuba
tions
are
potent
ially
life'
threate
ning
and,
conse
Buentl
y,
freBue
nt
assess
ment
of
tube
positio
n and
use of
restrai
nts in
disorie
nted
or
comba
ti%e
patient
s on
mecha
nical
%entila
tion
should
be
standa
rd
practic
e.
@asotr
acheal
and
oral
trache
al
airway
s
imped
e the
coughi
ng
mecha
nism
and
allow
for the
accum
ulatio
n of
retaine
d
secreti
ons.
&inall
y,
e%en
thoug
h all
artifici
al
airway
s can
pre%en
t
large'
%olum
e
aspirat
ion,
they
do not
pre%en
t the
passag
e of
potent
ial
pathog
ens
into
the
airway
s from
the
phary
n,.
/f
respira
tory
failure
has
progre
ssed to
the
need
for
mecha
nical
%entila
tion,
most
patient
s
should
be
fully
suppor
ted on
a
%entila
tor for
the
first
2> to
>*
hours
after
intuba
tion.
This
suppor
t
allows
the
patient
to rest
and
pre%en
t
further
respira
tory
muscl
e
fatigu
e
while
the
underl
ying
causes
of the
patient
-s
deteri
oratio
n are
identif
ied
and
treated
.
$ucce
ssful
separa
tion of
the
patient
from
%entila
tory
suppor
t
necess
itates
aggres
si%e
treatm
ent of
the
underl
ying
cause
of
respira
tory
failure
.
$tanda
rd
initial
%entila
tor
setting
s are a
%entila
tor
rate of
* to
!G
breath
s per
minut
e, tidal
%olum
es of *
to !
ml=(g,
inspira
tory to
e,pira
tory
ratio
0/=F1
of !.>
to !.2,
flow
rates
of >
to !
?=min,
and
the
lowest
possib
le &/22
to
(eep
o,yge
n
saturat
ion
greate
r than
H:.
Most
patient
s are
comfo
rtable
and
adeBu
ately
suppor
ted at
these
setting
sE
howe%
er,
becaus
e of
differe
nces
in
lung
compl
iance,
o,yge
nation
gradie
nts,
and
metab
olic
rates,
some
patient
s need
carefu
l
adjust
ment
of
these
%entila
tor
setting
s.
5FF5,
first
ad%oc
ated in
!HG8
by
4shba
ugh
and
5etty,
can
drama
tically
impro
%e
o,yge
nation
and
should
be
used
for
nearly
all
patient
s
recei%i
ng
mecha
nical
%entila
tion.
5FF5
recruit
s &AC
by
openin
g
collap
sed
lung
units
resulti
ng
from
increa
sed
mean
airway
pressu
res,
and it
may
impro
%e
o,yge
nation
in
critica
lly ill
patient
s to
such a
degree
that
&/22
le%els
can be
reduce
d to
less
than
the
to,ic
le%el
of
o,yge
n
0MG:
1.
)7+
/n
condit
ions
such
as
4AD$
,
5FF5
redistr
ibutes
e,tra%
ascula
r lung
water
from
al%eoli
to
interst
itial
and
e,tra'
al%eol
ar
spaces
,
althou
gh it
has no
ability
to
pre%en
t
4AD$
.
)7!+

4ltho
ugh
5FF5,
&AC,
and
o,yge
nation
are
linearl
y
related
o%er a
certain
range,
abo%e
a
certain
le%el,
further
increa
ses in
5FF5
do not
recruit
additi
onal
air
spaces
and
offer
no
further
impro
%emen
t in
o,yge
nation.
3igh
le%els
of
5FF5
may
ha%e a
pernic
ious
effect
by
increa
sing
intrath
oracic
pressu
re,
inhibit
ing
%enou
s
return
to the
heart,
and
o%erdi
stendi
ng
norma
l
al%eoli
,
thereb
y
creatin
g
areas
of
high
<=D
and
dead
space.
)>!+

#ecau
se the
effect
of
5FF5
%aries
from
patient
to
patient
and
o%er
time
in the
same
patient
depen
ding
on
lung
and
chest
wall
compl
iance,
le%els
should
be
adjust
ed to
effect.
$ome
author
s
ad%oc
ate a
formal
iIed
5FF5
trial
where
5FF5
is
increa
sed in
7' to
C'cm
3 2 2
incre
ments
and
assess
ed
after
!C to
2
minut
es to
find
the
best
5a22
with
the
smalle
st
reduct
ion in
cardia
c
output
.
)2>+

4ltern
ati%ely
,
initial
5FF5
le%els
can be
set at
or just
abo%e
the
lower
inflect
ion
point
on the
pressu
re'
%olum
e
cur%e,
althou
gh this
metho
d may
still
undere
stimat
e
optim
al
5FF5.
)!H+

Moder
n
%entila
tors
are
compu
ter
eBuipp
ed
with
the
ability
to
%ary
nearly
e%ery
facet
of the
breath
cycle
from
breath
rate to
flow
rate,
as
well
as
sensiti
%ity,
%olum
e,
pressu
re, and
inspira
tory
time.
Most
patient
s,
howe%
er, can
be
%entila
ted
using
one of
three
standa
rd
%entila
tor
modes
. 0!1
assist'
contro
l
04=C1
and
021
synchr
oniIed
interm
ittent
manda
tory
%entila
tion
0$/M
<1,
which
are
%olum
e'
cycled
modes
, and
071
pressu
re'
suppor
t
%entila
tion
05$<1,
which
is a
pressu
re'
cycled
mode.
The
4=C
mode
includ
es a
set
sensiti
%ity,
tidal
%olum
e,
flow
rate,
flow
wa%ef
orm,
and
%entila
tory
rate.
"hen
the
patient
initiat
es a
breath
by
creatin
g a
negati
%e
inspira
tory
pressu
re in
the
%entila
tor
circuit
greate
r than
the
sensiti
%ity
thresh
old
0usuall
y '2
cm 3 2
21,
the
%entila
tor
deli%e
rs a
predet
ermin
ed
tidal
%olum
e at a
set
flow
rate
and
flow
wa%ef
orm.
4=C
mode
guaran
tees a
breath
rate
and
tidal
%olum
e.
Theref
ore,
e%en
minut
e
%entila
tion
trigger
s the
%entila
tor to
deli%e
r tidal
%olum
es in
the
absenc
e of
patient
effort,
for
e,amp
le, in
the
patient
under
hea%y
sedati
on. /t
does
allow
for
synchr
ony
with
the
patient
in that
patient
'
initiat
ed
breath
s
abo%e
the set
breath
rate
are
suppor
ted
with
the
predet
ermin
ed
tidal
%olum
e and
flow
rate.
5otent
ial
shortc
oming
s with
this
mode
includ
e
respira
tory
al(alo
sis, air
trappi
ng in
patient
s with
C25D
, and
dysyn
chron
y with
the
%entila
tor in
patient
s who
reBuir
e
higher
flow
rates.
$/M<
is
simila
r to
4=C in
that
sensiti
%ity,
tidal
%olum
e,
flow
rate,
flow
wa%ef
orm,
and
%entila
tory
rate
are
set.
$/M<,
li(e
4=C,
ensure
s a
minim
um
minut
e
%entila
tion,
but
unli(e
4=C, it
allows
for
unsup
ported
,
sponta
neous
%entila
tions
betwe
en the
set
%entila
tor
breath
s.
$/M<
is a
good
weani
ng
mode
and
can be
used
in
conjun
ction
with
5$<
to
allow
a
%ariab
le
le%el
of
%entila
tory
suppor
t for
the
non'
$/M<
breath
s. 5$<
is a
flow'
cycled
%entila
tory
mode
in
which
only
sensiti
%ity
and
pressu
re
le%el
are
set.
2nce
the
patient
create
s a
negati
%e
pressu
re
greate
r than
the
sensiti
%ity
thresh
old,
pressu
re is
rapidl
y
increa
sed in
the
circuit
for the
durati
on of
the
breath.
The
flow
rate is
deter
mined
by the
patient
,
which
impro
%es
patient
'
%entila
tor
synchr
ony,
and
pressu
re'
suppor
t stops
once a
flow
thresh
old on
the
decele
rating
phase
of
inspira
tion is
reache
d.
)7*+

#ecau
se this
mode
is
witho
ut a
set
breath
rate or
tidal
%olum
e and
does
not
ha%e
the
securit
y of
either
$/M<
or
4=C, it
should
not be
used
in
patient
s with
a
rapidl
y
e%ol%i
ng
clinica
l
course
or in
patient
s with
potent
ially
suppre
ssed
respira
tory
dri%e.
/t is
ideal
for
weani
ng.
5eriod
s of
prolon
ged
intuba
tion
usuall
y lead
to a
discus
sion
on the
need
for
trache
ostom
y.
Trache
ostom
y
decrea
ses
dead
space,
impro
%es
secreti
on
cleara
nce,
enhan
ces
patient
comfo
rt,
allows
for
patient
-s
%erbal
comm
unicati
on,
and
partial
ly
restore
s
glottic
functi
on.
Trache
al'
inomi
nate
fistula
and
trache
al
stenos
is,
howe%
er, are
two
signifi
cant
and
seriou
s
compl
ication
s of
trache
ostom
y. /n
the
absenc
e of
strong
data to
suppor
t %ery
early
trache
ostom
y 07 to
C
days1
in
critica
lly ill
patient
s,
most
practit
ioners
use a
deadli
ne of
2
wee(s,
such
that
patient
s who
are not
ma(in
g clear
progre
ss
towar
d
e,tuba
tion
under
go
trache
ostom
y.
Aecen
t
e%alua
tion of
trache
ostom
y
%alidat
es a
case'
by'
case
e%alua
tion of
patient
s and
confir
ms
that
clinici
ans
are
reason
ably
accura
te in
their
assess
ment
of
who
will
reBuir
e
prolon
ged
%entila
tion.
)2!+
)27+
4
few
rando
miIed
trials
ha%e
conclu
ded
that
early
trache
ostom
y
decrea
sed
infecti
on'
related
compl
ication
s.
)7C+

The
5atien
ts with
se%ere
lung
diseas
e are a
challe
nge to
o,yge
nate
and
%entila
te. 2n
standa
rd
%olum
e'
cycled
%entila
tor
modes
of 4=C
and
$/M<,
airway
pressu
res
may
climb.
2n
pressu
re'
cycled
modes
, the
deli%e
red
tidal
%olum
es
decrea
se.
4cute
lung
injury
is
charac
teriIed
by
stiff,
nonco
mplia
nt
lungs
that,
despit
e an
appare
nt
homo
genou
s
injury
patter
n on
plain
radiog
raphs,
ha%e
areas
of
collap
se and
areas
of
appare
ntly
norma
l lung.
The
consol
idated
areas
of the
lung
tend to
be the
depen
dent
areas
and
can
accou
nt for
C to
8:
of
norma
l lung
%olum
e.
)!7+

)!>+

This
lea%es
only
7 to
C:
of
lung
units
for
acti%e
%entila
tion
and
gas
e,cha
nge,
althou
gh it
appear
s that
these
remai
ning
open
units
ha%e
essenti
ally
norma
l
compl
iance.
)!7+

Deli%e
ry of
tidal
%olum
es of
! to
!C
ml=(g
to
these
norma
lly
compl
iant
but
small
%olum
e units
results
in
ele%at
ed
airway
pressu
res.
Multip
le
in%esti
gators
ha%e
shown
that
e%en
short'
term
%entila
tion
07 to
>C
minut
es1 of
norma
l lungs
with
high
airway
pressu
res
can
create
se%ere
lung
injury,
with
endoth
elial
fractur
e,
al%eol
ar
ruptur
e,
al%eol
ar
floodi
ng,
and
lymph
atic
lea(.
This
pheno
menon
appear
s most
depen
dent
on the
mecha
nical
o%erdi
stentio
n of
the
al%eoli
rather
than a
pure
pressu
re
effect.
)!8+

)2H+

)>2+

Despit
e great
ad%an
ces in
curren
t
unders
tandin
g of
the
pathop
hysiol
ogy of
acute
lung
injury,
definit
i%e
recom
menda
tions
for
optim
al
%entila
tor
strateg
ies
and
ma,i
mal
allowa
ble
airway
pressu
res are
not
a%aila
ble.
#ecau
se
al%eol
ar
damag
e
appear
s
related
to
al%eol
ar
pressu
re,
howe%
er,
limitin
g
mean
or
platea
u
airway
pressu
res,
which
closel
y
paralle
l
al%eol
ar
pressu
re, is
justifi
ed.
)22+

Curre
nt
recom
menda
tions
are to
(eep
platea
u
airway
pressu
res to
less
than
7C to
> cm
3 2 2.
)22+

)7*+
/n
se%ere
ly
compr
omise
d
lungs,
reduct
ion of
tidal
%olum
es to 7
to C
ml=(g
may
be
necess
ary to
adhere
to this
guidel
ine.
Aando
miIed
trials
e%alua
ting
such
lung'
protec
ti%e
strateg
ies of
low
tidal
%olum
es and
limite
d
airway
pressu
res
ha%e
shown
impro
%ed
succes
s at
weani
ng,
lower
rates
of
barotr
auma,
and
impro
%ed
short'
term
399
sur%i%
al
rates,
but
they
ha%e
not
shown
statisti
cally
impro
%ed
hospit
al
mortal
ity
rate.
)2+

)>+
This
is not
surpris
ing
becaus
e only
7:
of
patient
s with
respira
tory
failure
who
die
actuall
y
succu
mb
from
their
lung
dysfun
ction.
Mana
gemen
t of
the
difficu
lt'to'
%entila
te
patient
reBuir
es
(nowl
edge
of four
additi
onal
strateg
ies.
permis
si%e
hyperc
arbia,
in%ers
e'ratio
%entila
tion,
pharm
acolog
ic
paraly
sis,
and
prone
positio
ning.
Using
low'
%olum
e
%entila
tory
strateg
ies on
%olum
e or
pressu
re'
cycled
%entila
tors
create
s
ele%at
ed
5C22
0range
7* to
!C*1
and
low
p3
0G.8H
to
8.>C1,
but in
the
absenc
e of
head
injury
and
ele%at
ed
intracr
anial
pressu
re,
these
le%els
do not
appear
to
ha%e
ad%ers
e
seBuel
ae and
may
allow
for
enoug
h lung
protec
tion to
impro
%e
outco
mes in
patient
s with
4AD$
.
)!C+

)!*+

3yper
carbia
in and
of
itself
is not
a
proble
m and
a
syste
mic
p3 of
8.! is
well
tolerat
ed in
most
patient
s.
/n%ers
e ratio
%entila
tion
occurs
when
inspira
tory
time is
increa
sed to
greate
r than
C:
of the
respira
tory
cycle.
This
metho
d
increa
ses
mean
airway
pressu
re and
recruit
s air
spaces
by
auto'
5FF5
in a
manne
r
simila
r to
applie
d
5FF5.
)2+

/n%ers
e ratio
%entila
tion
should
be
used
with
cautio
n in
patient
s with
(nown
se%ere
C25D
and
asthm
a
resulti
ng
from
their
prope
nsity
for air
trappi
ng.
)>>+

5harm
acolog
ic
paraly
sis
rela,e
s the
chest
wall
muscu
lature
and
allows
for
synchr
oniIati
on of
%entila
tor
and
patient
while
decrea
sing
C2 2
produ
ction
of the
patient
-s
respira
tory
muscu
lature.
)7*+

F%en
thoug
h
paraly
sis
allows
for
deli%e
ry of
the
same
tidal
%olum
e at
lower
airway
pressu
res, it
is not
witho
ut
ris(.
5araly
sis
immo
biliIes
the
patient
and
allows
for the
retenti
on of
secreti
ons,
muscl
e
wastin
g, and
the
de%elo
pment
of
pressu
re
decubi
tus
ulcers.
/t can
also
be
catastr
ophic
if the
artifici
al
airway
becom
es
dislod
ged.
5rolon
ged
use of
pharm
acolog
ic
paraly
sis can
create
prolon
ged
neuro
muscu
lar
wea(n
ess
long
after
the
cessati
on of
the
medic
ations.
Theref
ore,
protoc
ols to
limit
the
deli%e
ry of
these
drugs,
such
as a
train'
of'
four
monit
oring
or
daily
cessati
on and
redosi
ng, is
desira
ble.
)!G+

/n
cases
of
refract
ory
hypo,
emia,
prone
positio
ning
of the
patient
may
allow
for
tempo
rary
impro
%ed
gas
e,cha
nge.
4ltho
ugh
this
may
limit
access
to the
patient
for
nursin
g care
and
physic
al
e,ami
nation,
the
impro
%emen
t in
o,yge
nation
throug
h
better
<=D
matchi
ng
occurr
ing in
G to
8:
of
patient
s can
be
drama
tic.
)2*+

&ailur
e of
standa
rd
therap
y in
the
most
refract
ory
cases
of
acute
lung
injury
has
led
some
intensi
%ists
to use
ad%an
ced
techni
Bues
of
trache
al gas
insuffl
ation,
inhale
d
nitric
o,ide,
high'
freBue
ncy
%entila
tion,
%ariou
s
e,trac
orpore
al
techni
Bues,
and
phase
//
e,peri
mental
trials
of
partial
liBuid
%entila
tion.
Using
flows
of 2 to
!
liters
of
!:
2 2
=minut
e
deli%e
red !
cm
abo%e
the
carina,
trache
al gas
insuffl
ation
decrea
ses
5aC22
by
dilutin
g
pro,i
mal
anato
mic
dead
space.
)72+

3igh'
freBue
ncy
%entila
tion
typical
ly
consis
ts of
<T of
! to 7
cc=(g
at
rates
of !
to
7
cycles
=minut
e and
allows
adjust
ment
of
mean
airway
pressu
res to
mainta
in
o,yge
nation.
)7H+
4
!H8H
@ation
al
/nstitu
tes of
3ealth
'
funde
d,
multi'
institu
tional
trial
blunte
d
enthus
iasm
for
using
e,trac
orpore
al
memb
rane
o,yge
nation
0FCM
21 in
adults
with
se%ere
lung
injury.
Aecen
tly,
howe%
er,
se%era
l
single'
center
e,peri
ences
with
FCM
2
ha%e
been
publis
hed
with
promi
sing
results
and
e,peri
ence
with
arteria
l
%enou
s C2 2
remo%
al
sugges
ts that
it may
offer
ma,i
mal
lung
protec
tion
witho
ut the
untow
ard
effects
of
FCM
2.
)2C+

)>C+
)>G+

Multip
le
animal
model
s of
acute
lung
injury
ha%e
shown
that
partial
liBuid
%entila
tion''
in
which
the
lung is
filled
to
&AC
with
perflu
orocar
bon
and
then
subjec
ted to
standa
rd
mecha
nical
%entila
tion''
is
efficac
ious in
preser
%ing
lung
histolo
gy,
lung
compl
iance,
and
syste
mic
o,yge
nation.
5hase
/ and
//
human
trials
ha%e
shown
this
therap
y to be
safe
and
well,
tolerat
ed.
4necd
otal
succes
s has
been
report
ed for
each
of
these
inno%a
tions
but it
is
unli(e
ly that
any
one of
them
will be
a
panac
ea for
the
treatm
ent of
se%ere
respira
tory
failure
.
4ppro
priate
treatm
ent of
these
patient
s will
reBuir
e an
arsena
l of
se%era
l of
these
techni
Bues.
)eani
4
distinc
tion
betwe
en
rapid
withdr
awal
of
%entila
tory
suppor
t after
major
surger
y and
a brief
period
of
%entila
tion
should
be
disting
uished
'' Criteria for /ntubation
5a2
5aC2
p3 M 8.2C
AA N 7C breaths=min
<e N !2 ?=min
AA, respiratory rateE <e, minute %entilation.
K4lthou
gh the
decisio
n to
intubate
should
primaril
y be a
clinical
decisio
n,
se%eral
laborato
ry
%alues
and
pulmon
ary tests
can
help
guide
therapy.
from
liberat
ion of
the
patient
from
the
%entila
tor
o%er a
period
of a
wee(
or
more.
F,tub
ation
in the
first
scenar
io can
ta(e
place
rapidl
y, with
the
patient
Buic(l
y
placed
on a
T'
piece
or
small
amoun
t of
5$<
0C to G
cm 3 2
T'
piece
or
5$<
and
mainte
nance
of
o,yge
nation
should
lead to
promp
t
e,tuba
tion if
there
is no
e%iden
ce of
upper
airway
obstru
ction.
The
secon
d
scenar
io
reBuir
es a
gradua
l
declin
e in
%entila
tor
suppor
t while
obser%
ing the
patient
for
signs
of
respira
tory
fatigu
e.
tachyp
nea
0AA N
71,
agitati
on,
diapho
resis,
and
tachyc
ardia.
The
best
metho
d of
weani
ng''by
decrea
sing
the
rate of
$/M<,
increa
sing
inter%
als of
T'
piece,
or
decrea
sing
5$<
suppor
t''has
not
been
pro%e
n.
5$<
weans
ha%e
been
benefi
cial in
rando
miIed
trials
only
in
Buadri
plegic
patient
s.
Tolera
nce of
weani
ng and
succes
s of
e,tuba
tion
depen
d on
many
factors
. The
patient
should
not
ha%e
an
acti%e
pulmo
nary
infecti
on or
copiou
s thic(
secreti
ons.
The
patient
should
ha%e
an
accept
able,
stable
mental
status
that, at
the
%ery
least,
allows
for
protec
tion of
the
airway
and
cooper
ation
with
medic
al
treatm
ent,
such
as
pulmo
nary
toilet
and
mobili
Iation.
4ccep
table
o,yge
nation
with a
5=&
ratio
greate
r than
7
and
suffici
ent
pulmo
nary
mecha
nics to
meet
the
minim
um
standa
rds of
@/&
greate
r than
'2C
cm 3 2
2 in
liters1
less
than
! is
recom
mende
d
before
attemp
ting
e,tuba
tion. /f
liberat
ion
from
the
%entila
tor is
unsuc
cessfu
l
despit
e
meetin
g
these
criteri
a,
other
potent
ial
causes
should
be
enterta
ined.
F,ces
si%e
load
from
small'
diamet
er
endotr
acheal
tubes,
bronc
hospas
m,
pulmo
nary
floodi
ng
0high'
or
low'
pressu
re
pulmo
nary
edema
1
leadin
g to
decrea
sed
lung
compl
iance,
e,cess
i%e
secreti
ons,
o%erfe
eding
and
high
C2 2
produ
ction,
or
high
minut
e
%entila
tion
resulti
ng
from
sepsis
should
be
sought
. 5oor
%entila
tory
mecha
nics
such
as
delaye
d
effects
of
pharm
acolog
ic
paraly
sis,
electro
lyte
imbala
nce
052 > ,
Mg
2;
1,
malnu
trition,
or
diaphr
agmati
c
paraly
sis
0e.g.,
from
surger
y,
tumor,
traum
a1
should
be
consid
ered.
Aespir
atory
muscl
e
atroph
y is an
o%erus
ed
diagno
sis to
e,plai
n
dimini
shed
%entila
tory
mecha
nics as
a
cause
of
weani
ng
failure
and
should
be a
diagno
sis of
e,clus
ion.
@onpu
lmona
ry
factors
such
as
myoca
rdial
ische
mia or
an,iet
y
should
be
assess
ed.
/dentif
ication
of any
of
these
factors
should
lead to
a
tempo
rary
aband
onmen
t of
weani
ng
until
the
abnor
mality
is
correc
ted.
1ook*ar
k 2"0:
=das=boo(=
%iew=7>>7
C7*'
2=H2!=228.
html=topU
se of this
content is
subject to
the Terms
and
Conditions
of the MD
Consult
web site.
Townse
nd:
Sabisto
n
Textbo
ok of
Surger
y, 16th
ed.,
Copyrig
ht
2!
". #.
$aunder
s
Compa
ny
C.6
A 89,
year,
old
(hite,
sli2htl
y
o:ese
femal
e (ho
rarely
see*s
medic
al
care
has a
teder
,
pulsat
ile
a:do
mial
mass
ad a
:lood
pressu
re of
.7;<7.
A
rapid
operat
i=e
iter=
al
care.
1ook*ar
k 2"0:
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%iew=7>>7
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