Download The Effect of PEEP on Cardiac Output

The Effect of PEEP on Cardiac Output*
Paul
M.
Dorinsky,
M.D.;t
and
Michael
sitive
end-expiratory
pressure
ventilation
(PEEP)
is
well established
as an integral part ofthe management
of
patients
with the adult respiratory
distress syndrome.
While
PEEP improves
pulmonary
gas exchange
in the majority
of
patients,
it may also decrease
cardiac
output.’5
As a result,
oxygen
transport
(cardiac
output
x arterial
oxygen content)
may not increase
and tissue oxygenation,
a critical determinant of normal
organ
function,
may be impaired.’#{176}
In 1948, Cournand
et al#{176}
proposed
that PEEP decreased
CO by increasing
intrathoracic
pressure
thus impeding
venous
return
to the heart.
Since Coumand’s
study, basic
concepts
of cardiac
physiology
have been refined
and expanded.
Within
this context,
more recent
studies’22
of the
effect of PEEP
on cardiac
function
have suggested
that
impairment
ofvenous
return
does not adequately
explain
the
decrease
in cardiac output
produced
by PEEP.
Understanding the mechanisms
by which PEEP reduces
cardiac output
may have important
therapeutic
implications
for the management ofpatients
with acute respiratory
failure. Therefore,
in
this article we summarize
the results of recent studies
that
have addressed
this issue.
DETERMINANTS
It
is
important
cardiac
OF
to
physiology
ventricular
physiologic
nant
of
reflexly
in
Stroke
volume
PEEP
may
is the product
is the
heart
changes
in
to
is influenced
ventricular
filling,
tncular
distensibility
or
their
effects
on
and
the
afterload
preload;
influence
3)
Drive,
210
1)
2) yenventricular
Preload
volume
diastole,
and
by
while
stroke
Cardiac
muscle
tion of cardiac
muscle
also
crease
in sarcomere
length
in
less
than
filaments
contraction
Hall,
ofa
number
increases.
beyond
of partially
overlap
However,
2.2 microns
between
sarcomere
decreases.
These
initial
volume
muscle
length.
(VEDV)
(ie,
the
two
are
Since
preload)
major
and
force
relationlaw which
shortening
to
ventricular
determines
it
factors
thick
of muscle
ultrastructural
comere
length
at end-diastole,
determinant
of stroke
volume.
There
an inresults
the thin
so that
ships form the basis for the Frank-Starling
relates
the extent
of cardiac
muscle
end-diastolic
resting
saris
which
an
important
influence
yen-
tricular
preload-venous
return
and
ventricular
distensibility.
Since
ventricular
distensibility
will be
discussed
in detail
in the succeeding
section,
only the
effects
ofvenous
return
will be discussed
at this time.
Venous
volume
during
return
to the
of blood
diastole
amount
and
into the
increase
thorax
determines
the
that is available
to fill the
(ie, preload).
Venous
tone
distribution
of total
thorax,
affects
venous
in mean
intrathoracic
venous
return
rate,
ventricular
cally
to the
ences
thorax
by altering
filling
augmenting
blood
and
return.
pressure
and
the
thus
time
atrial
diastolic
ventricular
Department
actual
ventricle
and the
volume
have
For example,
an
may decrease
decrease
available
contraction,
ventricular
preload.
fur diastolic
by mechanifilling,
also influ-
preload.
1655
Upham
Distensibility
Ventricular
ance)
distensibility
is a diastolic
is defined
Means
optimal
of the
Ventricular
N-325
is composed
overlapping
thin and thick filaments
arranged
in units
known
as sarcomeres.
As resting
sarcomere
length
increases,
the extent
of shortening
and force of contrac-
volume
Instructor.
of Medicine.
requests:
Dt
Dorinsky,
Columbus,
Ohio 43210
FC.C.P1
Preload
Heart
systole.
*Fmm the Ohio State University
College ofMedicine,
of Medicine,
Pulmonary
Disease
Division,
Columbus.
tClinical
tProfessor
Reprint
factors:
M.D.,
obvious
influence
on venous
return
and therefore
preload. Similarly,
intrathoracic
pressure,
by influencing
the pressure
gradient
for blood flow from the abdomen
volume.
termed
during
pathodetermichanges
stroke
major
heart
cardiac
rate and
major
rate
by four
compliance;
of
potential
most
and 4) ventricular
afterload.
distensibility
influence
stroke
contractility
during
In
volume
while
diastolic
contractility;
ventricular
aspects
the
decrease
ofheart
volume.
stroke
output,
response
certain
to appreciate
stroke
states,
cardiac
OUTPUT
understand
in order
mechanisms
by which
output.
Cardiac
output
left
CARDIAC
E. Whitcomb,
property
by relating
changes
(is,
of the
intact
in ventricular
changes
in pressure.#{176}3’
Since
the heart
may vary independently
Effect of PEEP on Card)ac
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
ventricular
the
compliventricle
that
volume
to
pressure
around
of the measured
Output
(Doilnsky,
Whltcomb)
ventricular
filling
pressure,
rate to measure
ventricular
pressure
and
(the
pressure
outside
of the
in assessing
heart
difference
ventricle
the
ventricle
nize that
and
VEDPTM
and
VEDP
circumstances,
between
structed
the
there
for
be nearly
will
any
of the
equal.
Under
not be significant
by
an
VEDV,
in
in
the heart
(ie, increased
intrathoracic
pressure),
and VEDP
may be markedly
different
for any
VEDV.
Under
these
circumstances,
these
pres-
VEDPTM
given
measurements
comparing
Ventricular
sibility
thickness
cannot
ventricular
is a function
of the ventricular
and
geometry
muscle
of the
of the
the
ventricle.
will
result
A decrease
in ventricular
in a decrease
results
in a decrease
mined
by the
in stroke
in VEDV.
by
of
distensibility
Since
interrelationship
detected
curve
volume
only
VEDV
if it
return
and
ventricular
distensibility,
a decrease
in distensibility
will result
in a decrease
in stroke
volume
only if venous
return
does not increase
proportionately.
Ventricular
distensibility
is altered
primarily
by
pathologic
infiltrate)
changes
or changes
an increase
in intrathoracic
be accompanied
volume
curve
The
likely
or pencardial
precise
distensibility
intrathoracic
ever, as will
a
cause
that
or pencardial
be discussed
that
muscle
thickness.
(is, scar and
In addition,
pressure
may
accompanies
number
of
factors
in
increases
including
their
given
in
Howit is
altered
myocardial
blood
the alterations
in ventricular
distensibility
trathoracic
Ventricular
that
accompany
increases
in
and pericardial
pressures.
distensibility
is not altered
by changes
that
onset
Ventricular
The
effects
expected
to
alter
afterload
or
to the
a function
of the
inotropic
state
ventricular
of the
peak
force.27
ventricular
of these
factors
lies
in
and
wall
systole.
aortic
as the
of the
and
law of LaPlace,
is
ventricular
size.
myocardial
radius.
the
afterload
tension
of intracavitary
ventricular
or tenafter
Ventricular
pressure
product
force
ventricle
is
ventricular
Thus,
for
a given
aortic
pressure,
ventricular
afterload
will increase
as
ventricular
volume
increases.
Likewise,
at a constant
ventricular
volume,
ventricular
afterload
will increase
as aortic
been
pressure
mural
the
increases.
suggested
that
pressure
wall
tracavitary
changes
(LVTM) may
ventricular
In addition,
it has recently
in left ventricular
transeffect
tension
pressure.’
decreases;
likewise,
afterload
necessary
Thus,
Stroke
by altering
to generate
as LV,
as LVTM increases,
volume
is
in-
decreases,
afterafterload
inversely
related
to
ventricular
afterload.
As other
determinants
of stroke
volume
remain
constant,
an increase
in afterload
will
decrease
will
stroke
increase
volume
stroke
During
in-
while
a decrease
in afterload
volume.
OF PEEP
or dobuta-
past
CARDIAC
ON
decade,
studies
lished.
parameters,
individual
the
determinants
determined.
The
in the
results
of clinical
to define
the
CO have
a number
effect
of
of stroke
following
OUTPUT
a number
attempting
by which
PEEP
decreases
By carefully
monitoring
nisms
in
the
experimental
of these
been
pubof hemo-
PEEP
volume
studies
and
mecha-
on
have
are
the
been
summa-
paragraphs.
ventricular
Decreased
and
ejection
of altering
is defined
in the
According
EFFECT
Contractility
volume
deforce
(dp/dt),
to develop
capable
ANIMAL
contractile
stroke
be
be
parameters-peak
importance
develops
on
rized
not
accom-
can
Afterload
dependent
Thus,
mine
would
distensibility.
The
of ventricular
dynamic
as dopamine
that
in
in the
to modify
ventricular
performance
at any
of ventricular
distensibility,
preload
and
Ventricular
sion
the contractile
state ofthe
ventricle.
This is supported
by the fact that the ventricular
pressure-volume
curve
does not shift when
ventricular
contractility
changes.27
such
relationships
contractility
necessary
is
a decrease
Changes
development
are
that
altered
geometry
to produce
agents
time
ability
level
and
ventricular
flow interact
inotropic
while
various
of factors
increases.
for the alteration
pressure
is unknown.
in a subsequent
section,
and
contractility.
load
by a shift in the ventricular
pressureindicating
an alteration
in ventricular
distensibility.
ventricular
in ventricular
in muscle
fraction
of the
other
deterin contrac-
volume.
in ventricular
of force
It is
state
in a manner
stroke
by measuring
pressure
is deter-
of venous
force-velocity
Ventricular
disten-
itself,
as well as the
ventricular
walls.27
Changes
in ventricular
distensibility
are
shifts in the normal
diastolic
pressure-volume
volume
volume
myocardial
rate
contractile
that occur
in the
Thus,
an increase
stroke
decreases
changes
relationships.
the
afterload.
be used
interchangeably
pressure-volume
curves.
distensibility
increases
A variety
pressure
stroke
contractility
developed,
con-
However,
increase
tility
tected
differences
curves
effects
that
independent
of changes
minants
ofstroke
volume.
pany
these
force-velocity
to recognize
ventricle
to recogoutside
the
pressure-volume
VEDP
or VEDPTM.
characterized
inside
given
myocardial
important
(VEDPTM)
relationship
thus
will
ventricular
using either
situations
sure
when
between
at end-diastole)
pressure-volume
altering
more
accutransmural
(ie, distensibility).
It is important
under
most conditions,
pressure
is negligible
outside
it is probably
end-diastolic
It
ventricle
performance
by
is
trathoracic
Venous
widely
STUDIES
Return
accepted
pressure
that
that
occurs
CHEST
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
the
increase
in
during
PEEP
impedes
I 84 I 2 I AUGUST,
1983
in-
211
venous
return
right ventricular
may
to the heart
fi1ling.
decrease
during
and results
Therefore,
PEEP
even
changes
in ventricular
tractility.
However,
Culver
to the
et al2#{176}
suggest
decrease
in
that additional
cardiac
output
PEEP
When
investigators
these
which
produces
and
lung
an
increased.
increase
greater
both
and
PEEP,
pleural
pressure
atrial
pressures
left
creased.
If PEEP
decreasing
decreased
venous
output
ments.
should
These
of venous
must
the
output
also
have
determinants
output
explanation
produced
an effect
by
in cardiac
Scharf
PEEP
tion
Ringer’s
solution
Ventricular
A number
lar
Wood
studied
effect of PEEP
on ventricular
contractility.
et al’3 used a high fidelity
transducer-tipped
left
measure
line
period
significant
state
in left ventricular
after
10 cm
ventricular
contractility
PEEP
Haynes
diastolic
et al’4 measured
area and the area
the
(ie,
difference
PEEP
had
not
between
area
decreased
during
ofthe
dogs
area
is an index
area and
15 cm H2O
end-diastolic
doing,
Haynes
between
on PEEP
contractility
Qvist
two
function
transmural
diastolic
pressure
212
groups
had not
et al’6 studied
ventricular
plotting
right
and
left
would
PEEP
of
changed.
the effect
in their
infused
dexend-diastolic
be equivalent
areas
of the dogs on no
et al found
no difference
these
endat the
area which
End-diastolic
end-diastolic
to represent
stroke
fiber shortening.
dogs
ofl2
to the
PEEP
In so
in stroke
area
indicating
cm H2O
PEEP
in dogs. This was accomplished
right
and
left ventricular
against
ventricle
the
(ie,
stroke
Starling
work
indices
curves).
and ejec-
volume
period
and
Ringer’s
solution
into
The infusion
of lactated
dogs
on PEEP
enabled
the
the
end-
in which
contractility
volume
altered
Since
rameters
of
decrease
However,
Prewitt
volumes
and
the
directly
ventricular
ventricular
in CO
right
and
measuring
left
pa-
shown
that
have
contractility,
contractility
caused
patheir
In addition,
that PEEP
possibility
distensibility
of the
other
investigators
contractility
and
nor
based
no
PEEP
impairs
that impaired
changing
in ventricu-
ofassumptions.
to exclude
the
ventricle.
without
directly
a number
unable
in dogs.
increases
a decrease
ventricular
contractility
on
had
PEEP
neither
of
were
indicating
during
measured
they
the
on ventricular
function
concluded
that PEEP
end-systolic
Elevated
They
took
and onset-
area).
cm
These
it is unlikely
contributes
to
by PEEP
that
during
both left ventricular
of the left ventricle
study.
However,
these
investigators
then
tran into the dogs on PEEP
so that the
areas
the
indicating
changed
onset-diastolic
between
diastolic
area
of ventricular
stroke
during
a baseThey found
no
dp/dt
H2O
to
of 15-20
dogs.
a baseline
a situation
afterload
Ventricular
It has
of diastole
onset
Robotham
catheter
ventricular
dp/dt
in dogs
and after 10 cm H2O PEEP
change
baseline
the
the
H2O PEEP
investigators
ventricular
of the
have
into
12
fraction
between
the control
state and PEEP
indicating
that
ventricular
contractility
had
not changed
during
PEEP
Finally,
Prewitt
and Wood’5 investigated
the effect of
rameters
of investigators’’624
in
after
ventricuPEEP
diastolic
volume
ofthe
left ventricle
was nearly
identical in the control
state and after 15-20 cm H2O PEEP
In so doing,
Scharfet
al found
no difference
in ejection
Thus,
Contractility
effect
during
to create
conclusions
Decreased
the
end-diastolic
dogs
and
that
during
function
following
the infusion
oflactated
dogs on 15-20 cm H2O PEEP
PEEP
volume.
studied
function
state
indicating
changed
ventricular
in
ventricular
baseline
identical
had
not
measured
ventricular
the
the
the
et aP
on
fraction
or more
by
on one
for
Likewise,
20 cm
These
in these
experithat an impairment
sole
of stroke
solely
differences
observed
suggest
is not
in cardiac
PEEP
no
have been
observations
return
decrease
cardiac
return,
lar
were
investigators
Furthermore,
they found
that despite
the
in right atrial pressure,
cardiac
output
fell to a
degree
when
lung
volume
was allowed
to
than
when
pleural
pressure
alone
was in-
increase
other
vena
applied
in both
right
the
during
H2O PEEP
contractility
cm
that
demonstrated
obtained
investigators
re-
lung volume)
raisleft atrial
pressure
they
results
curves
H2O
venous
occluding
when
increase
volume,
by
factors
contribute
observed
during
(constant
and
contrast,
study
reduced
right
no
or con-
of a recent
cava or by isovolumically
ing pleural
pressure,
In
are
afterload
results
by partially
decreased.
if there
distensibility,
the
experimentally
turn
in a decrease
in
cardiac
output
that
on
by
end-
been
ventricular
Afterload
clearly
shown
afterload
Collapse
resistance.37’
increased
alveolar
capillary
arterioles
that
PEEP
by increasing
increases
right
pulmonary
of pulmonary
pressure
and
by lung
inflation
vascular
capillaries
compression
by
of pre-
are responsible
for
the increase
in pulmonary
vascular
resistance
that occurs with PEEP
Since abnormalities
in left ventricular
function
have been
observed
in other
conditions
in
which
right ventricular
afterload
is increased,3’
the
results
of
studies
tween
right
ventricular
examined.
Various
investigating
ventricular
afterload
function
during
PEEP
experimental
studies#{176}’4’ have
progressive
increases
in mean
sure produced
by constricting
result
in increases
volume
(RVEDV)
of the
creases
in
Their
(LVEDV)
the relationship
beand decreased
left
must
be carefully
in
right
and
shown
ventricular
pressure
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
of PEEP
on Cardiac
Output
presartery
end-diastolic
(RVEDP)
left
ventricular
end-diastolic
and pressure
(LVEDP).
It has
EffeCt
that
pulmonary
artery
the pulmonary
and
de-
volume
been
sug-
(Dorlnsky,
Whltcomb)
gested
that
are
these
caused
septum
by
into
in
changes
changes
in left
displacement
the
left
ventricular
of the
ventricular
function
noted
interventricular
cavity
by the
increase
Although
this sequence
of physiologic
might
also occur
during
PEEP,
there
are
number
of differences
when
right ventricular
Several
LVEDP
in the hemodynamics
afterload
is increased
investigators’4’6
and RVEDP
transmural
have
increase
a
that
PEEP
both
while
ventricular
end-diastolic
and
diastolic
pressure
one investigator
transmural
right
ventricular
endfall. Although
at least
that RVEDV
decreases
during
PEEP,’
ventricular
(RVEDPTM)
has
reported
is possible
it
afterload
increase
RVEDV
contributes
to
altering
left
that the increase
that
under
the
occurs
some
during
in right
PEEP
circumstances
decrease
ventricular
pressure
in
and
cardiac
distensibility
is
no evidence
afterload.
The
is little
sure
there
changed
is a decrease
changes
left
would
increases
arterial
left
pres-
The
effects
Furthermore,
Neither
of these
an adverse
during
effect
on
which
on the
quite
pressure
very
consistent.
Scharf
are
viewed
have
Despite
disvolume
separately,
volume
the
and
distensibility)
aP
found
obtained
1-Effect
trans-
that
LVEDV
for any given
left
was less on PEEP
during
OJPEEP
the
on
when
were
baseline
Ventricular
atrial
than
pressurecompared
state,
Year-Investigator(Ref.
and
Contractility
No.)
Contractility
Distensibility
sibility
were
lungs
cardiac
the
In
during
-
1980-Robotham’3
-*
1980-Haynes’4
-
1981-Prewitt4
-+
Definition
not
ofsymbols:
measured
and
t
or unable
increase,
I
to be determined
contact
between
of a decrease
in
suggest
during
airway
that
ventricu-
PEEP
by
to the
pressure
the
heart
the
contribute
observed
results
a decrease
the
to
PEEP
during
the
of
diastolic
sibility
that
experiments
decrease
distensibility
in
cardiac
Many
factors
pressure-volume
the left ventricle.
It is likely
ventricular
interdependence
flow and
to produce
animal
in left ventricular
that
a number
altered
,
output
are capable
relationship
of
of
ofthese
(ie,
m yocardial
increased
juxtacardiac
pressure)
inthe decrease
in ventricular
disten-
occurs
during
PEEP79”4’”42’
STUDIES
In the
past
three
years,
the
certain
degree
by the
techniques
results
offour
important
the effects
of PEEP
on
subjects
have been
pubhave been
limited
to a
inherent
in humans
problems
and
of utilizing
by the variability
of
-
:
-+
aW’
lungs.
invasive
I
1981-Calvin’7
et
and LVEDPTM
the pericardium
of actual
production
PEEP
disten-
by physically
holdThese
observations
heart.
clinical
studies
investigating
cardiac
function
in human
lished.’’7”8”
These
studies
I
I
1981-Jardin’2
or contractility,
-
1980-Fewell21
Human
Studies
1979-Cassidy”
during
of signifi-
Fewell
LVEDPTM
the
of positive
that
blood
teract
expancardiac
In addition,
these
the effect ofPEEP
on
is impaired
summary,
must
in-
in ventricular
removed.
to abolish
and
from
distensibility
via
afterload
the importance
and lungs in the
transmission
these
and
Furthermore,
totally
able
LVEDV
away
output
in
volume
volume
a decrease
PEEP
or
decrease
ventricular
in transmural
during
stroke
also
curve
of
decrease
addition,
decreases
in both
LVEDV
PEEP
regardless
of whether
emphasize
the heart
-
1979-Scharf’
presdata
levels.
These
changes
coupled
with the absence
with
intact
lar
pressure
return
in ventricular
during
observed
during
In
that
left
and
their
increase
HUMAN
:
1979-Prewitt’5
=
consistent
PEEP
filling
to
Studies
1975-Qvist”
-
changes
are
altering
was
it
in left
during
ventricular
from
a significant
to pre-PEEP
expansion,
cant
has been
Distensibility
Animal
output
volume
was
during
noted
suggest
the baseline
state.
In addition,
curves
obtained
during
PEEP
those
and
ventricle
ventricular
ventricular
pressure,
during
volume
when
(ie, ventricular
et
transmural
volume
right
variable.’3’4’24
are present
between
mural
end-diastolic
left and
pressure
relationship
pressure
ing the
ofthe
to be
filling
vestigators
investigators
PEEP
Left
et al’3 observed
a significant
volume
and transmural
left
decreasing
ofPEEP
transmural
Table
PEEP
to have
volume
pressure
crepancies
to
PEEP’3’5
in LVTM with
stroke
shown
or
PEEP
systemic
Robotham
both
stroke
sufficient
Distensibility
transmural
been
during
be expected
ventricular
Ventricular
that
mean
area.
constructed
were
a decrease
taken
place
revealed
a leftward
shift of the pressure-area
the left ventricle
during
PEEP
indicative
ofa
in left ventricular
distensibility
during
PEEP
ventricular
terdependence).
There
ventricular
end-diastolic
curves
sion
by
that
PEEP
had
left
in-
during
et al’4 demonstrated
in both LVEDPTM
thus
output
obtained
Similarly,
Haynes
results
in a reduction
does
(ventricular
curves
PEEP
PEEP
sure-area
left
(LVEDPTM)
the
ventricular
observed
by PEEP
observed
during
that
shifted
to the left indicating
ventricular
distensibility
decrease,
from
-*
the
I
the
clinical
I
I
ment
of respiratory
the results
ofthese
no change,
tion
study
experiments.
data.
which
conditions
that
failure
studies
complements
Since
contribute
obtained
results
CHEST
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
develop-
in patients.
Nevertheless,
provide
important
informathat
the
to the
from
of these
I 84
I 2 I AUGUST,
animal
studies
1983
are
213
particularly
relevant
dynamic
effects
be considered
Jardin
respiratory
to
in clinical
LVEDP
measured
directly
Left
area
from
and interventricular
two-dimensional
during
expansion
left
from
wedge
pressure
juxtacardiac
pressure
surements.
Left
determined
from
was
calculated
stroke
from
volume
fraction.
During
the
H2O),
left ventricular
and
wedge
pressure
finding
in the remainder
Prewitt
et aP’ studied
LVEDV
or left ventricular
ventricular
was
was
of PEEP
Despite
was
and
(10-15
increased
cm
while
there
was no evidence
contractility
during
transmural
pulmonary
evidence
of a de-
in two patients.
was the major
patients.
oflO cm H20
extensive
cardiology
technique.
H2O
while
significant
left ventricular
nary
There
PEEP,
both
capillary
was
wedge
no evidence
contractility
during
LVEDV
decreased
During
in
invasive
man,
techniques
studies
conclusions
which
PEEP
gies
PEEP
respira-
Swan-Ganz
can
least
that
oflO
cm
reviewed
the
Assuming,
pressure
tended
output
increased
distensibility
Finally,
decreased
during
PEEP
Cassidy
et al’8 studied
the
suggests
that
to
increase.
in left ventricular
the fact that
capillary
wedge
left
effects
ventricular
of 10 cm
sure
cardiac
function
cardiac
gaps
physiology
existing
in our
in this
paper,
reasonable
due
decrease
in an
however,
may
effects
or
be
that
PEEP
increased
ofPEEP
by
contribute
by
to
of
the
PEEP-
(right
ventricular
filling),
afterload
and decreased
left
Since the decrease
in venous
to
the
increase
in
by PEEP,
mean
in cardiac
conventional
must
only
presoutput.
positive-pres-
be employed,
by
correcting
determinants
loading
mean
ventilatory
intrathoracic
increase
on other
volume
by
strate-
effects
produced
produced
result
with
hemodynamic
probably
which
ventilation
verse
of PEEP
be resolved
in the
on the results
of
output
pressure
would
in LVEDV
occurred
fraction
and pulmo-
effect
will
based
adverse
primarily
techniques
decreases
ejection
the
time
be formulated.
three
factors
is
sure
application
the
can be drawn
about
the mechanisms
decreases
CO and thus reasonable
for correcting
PEEP
At
the
PEEP
However,
while
pulmonary
left
has not been
totally
inherent
limitations
in
to study
it is unlikely
published
intrathoracic
for a decrease
that
impaired.
physiology
there
are
knowledge
at the present
near
future.
Nevertheless,
ejection
fraction
and
an equilibrium
nuclear
pressure
214
acute
from
it
in all
appeared
could
be
evidence
investigation,
cardiac
Because
return
obtained
decreased
CONCLUSION
pressure
Left
ventricular
were measured
using
impaired
and
venous
return
right ventricular
distensibility.
measurements
ventricle.
of these
clinical
studies
of animal
experiments.
no consistent
decreased
increased
ventricular
catheters.
LVEDV
in
of
measured,
function
were
dimensions
contractility
using
with
left
and ventricular
distensibility
in those
studies
in which
There
assessed.
of ther-
patients
echocar-
were not
ventricular
function
results
findings
tory insufficiency
of noncardiac
origin.
Estimates
of
LVEDP
were made
using pulmonary
capillary
wedge
in nine
of the
ventricular
in
function
addition,
LVEDPTM
that right
decrease
on cardiac
In
revealed
a slight increase
diameter
and velocity
shortening
the
the
of the studies
to be decreased
ejection
of their
the effect
left
In summary,
largely
confirm
measurements
crease
in left ventricular
distensibility
A decrease
in left ventricular
preload
Right
and
M-mode
from
PEEP
left ventricular
revealed
fiber
LVEDP
and
et al’8 concluded
mea-
fraction
fraction
superior
estimated
was
measurements.
were derived
increased.
circumferential
on human
defined.
LVEDV
decreased.
Although
for a decrease
in left ventricular
PEEP,
plots
of LVEDV
and
pressure
During
the application
oflO cm H2O
atrial pressure
and right atrial trans-
right
possibly
ten normal
pressure
was
in the
positioned
pressure
diameters
pressure
Although
Cassidy
in
pul-
angiography
application
ejection
mural
during
cross-
pressure
ejection
radionuclide
juxtacardiac
diographic
measurements
right ventricular
end-diastolic
and
disten-
measurements
esophageal
a catheter
and
echocardiograms.
PEEP,
both
deat 30
ventricular
using
cava
un-
LVEDPTM
balloon-occluded
ventricular
with
capillary
remained
volume
LVEDP
capillary
LVEDV
RVEDPTM
study,
Calvin
et al’7 studied
15 patients
edema
ofcardiac
or noncardiac
origin.
estimated
modilution
that as PEEP
left ventricular
and
that
pres-
were derived
Using
these
was a large increase
in
increase
in left ventricular
area suggesting
was decreased.
of
cross-sectional
contractility
In addition,
In a similar
with pulmonary
on cardiac
performance
In this study,
right
atrial
from
esophageal
left ventricular
either
esophageal
found
H2O,
LVEDPTM
ventricular
cm H2O PEEP,
there
with only a moderate
H2O PEEP
volunteers.
vena
ventricular
septal
motion
echocardiograms.
area,
while
monary
from
ventricular
these
investigators
from 5 to 30 cm
cross-sectional
a left
from measurements
pressures
were
or estimated
measurements.
techniques,
was increased
with
RVEDP
Pleural
sure
They
will
patients
with
the adult
. These
investigators
directly
catheter
and estimated
right
atrial
pressure.
sectional
sibility
hemothey
measured
al” studied
ten
distress
syndrome
measured
changed.
the
situations,
separately.
et
creased
understanding
ofPEEP
to
cardiac
the
ad-
of cardiac
augment
venous
return.
As mentioned
previously,
volume
loading
may
have deleterious
effects
on pulmonary
gas exchange.
There
is little
that can be done
therapeutically
to
decrease
pulmonary
vascular
resistance
during
conEffect of PEEP
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
on Cardiac
Output
(Dorinsky, Whitcomb)
ventional
PEEP
intuitively,
pressure
ventilation.
pulmonary
ventricular
vascular
afterload.
vasodilator
drugs
resistance
Although
may
or mediator-induced
these agents
have
beneficial
with
PEEP45’
However,
and
the
the
oflung
to which
they
may
increase
decrease
pulmonary
have
gas exchange
and
should
in left ventricular
a decrease
in
cardiac
creased
and
increase
cardiac
proportionately.
output
of a decrease
sibility
may
or
ejection
the
volume
thus
left
expansion
creased
ventricular
produce
resistance
As
though
cardiac
in
not
in
return
the
face
volume
may
be further
impaired
may occur.
Left
tion
be
fraction
may
increased
and
by a decreased
without
LVEDV,
increasing
series
toring
output
during
PEEP
step,
a trial
crystalloid
should
crease
in pulmonary
cautious
volume
Nevertheless,
of acute
volume
be
undertaken.
capillary
wedge
expansion
should
concern,
this
approach
should
unless
accompanied
by deterioration
exchange.
volume
in-
increase
If cardiac
expansion,
output
inotropic
does
not
not
agents
a logical
while monitension.
As
expansion
distress
with
insti-
Neclerio
above,
since
of pulmonary
they have
on
end-expiratory
pres-
147:518-24
M,
Isenberg
English
MD.
M,
Optimum
with acute
CJ,
JS,
Am
Murray
JF.
Marr
C,
Lea-
Dehart
P, Lynch
in
end-expiratory
pulmonary
the
failure.
JP, Weg
adult
N EngI
JG.
Ventila-
respiratory
distress
MannyJ,
Justice
Rev
Surgery
1979;
Respir
Dis
1980;
122:387-95
Continuous
positive-pressure
oxygen transport
76:193-202
and tissue
oxygenation.
Abnormalities
in organ
R, Hechtman
flow and its distribution
HB.
during
positive
ventilation:
end-expiratory
Ann
blood
pressure.
85:425-32
10 Tucker
HJ, Murray
JE Effects of end-expiratory
organ blood flow in normal and diseased
dogs.
pressure
on
Physiol
J
AppI
34:573-77
11 Cournand
studies of
on cardiac
12 Jarclin F,
A, Motley HL, Werko L, Richards
DW. Physiologic
the effect of intermittent
positive pressure
breathing
output
in man. Am J Physiol 1948; 125:162-74
Farcot J, Boisante
L, Curien
N, Margairaz
A, Bourdarias
J. Influence
of positive
end-expiratory
pressure
on left
ventricular
performance.
N EngI J Med 1981; 304:387-92
13 Robotham
JL, Lixfeld W, Holland
L, MacGregor
D, BromB, Permutt
expiratory
pressure
5, et al. The
on right
effects
of positive
and left ventricular
end-
performance.
Am Rev Respir Dis 1980; 121:677-83
14 Haynes
JB, Carson
SD, Whitney
WP, Zerbe
GO, Hyers TM,
Steele P. Positive end-expiratory
pressure
shifts left ventricular
diastolic
pressure-area
curves. J Appl Physiol 1980; 48:670-76
15 Prewitt RM, Wood LD. Effect of positive end-expiratory
prossure on ventricular
function
in dogs.
Am J Physiol
1979;
236:H534-H44
17
to acute
Brook
on systemic
Med 1972;
be abandoned
in pulmonary
gas
be
HB,
effects
Intern
16 Qvist
should
R,
syndrome.
8 Lutch
Although
an inpressure
during
be noted
with
respond
as stated
great caution
of positive
1978;
distributions
berger-Barnea
can be undertaken
and arterial
oxygen
in
vasodilator
Am Rev Respir Dis 1979; 120:1039-52
SJ, Lynch JP, WegJG,
Dantzker
DR. The dependence
of
uptake
on oxygen
delivery
in the adult respiratory
syndrome.
1973;
is no way to predict
in a given patient
approach
may be best to optimize
of interventions
cardiac
output
first
will
DR,
tion-perfusion
LVEDP
Clearly,
there
which
therapeutic
cardiac
output
However,
with
effects
and Obst
Mannal
Fairley
6 Dantzker
pulmonary
fraction
caused
harmful
pressure
in patients
1975; 292:284-89
J Med
across
by administering
cardiac
PM,
airway
9
and no increase
ventricular
ejec-
in ejection
stroke
volume
SR,
oxygen
As a result,
increase,
gas exchange
may
in oxygen
transport
otropic
agents.
If the increase
compensates
for the decreased
5 Suter
of de-
of fluid
increase
R, et al Physiologic
consequences
of positive end-expiratory pressure
(PEEP) ventilation.
Ann Surg 1973; 178:265-71
4 Kanarek
DJ, Shannon
DC. Adverse
effect of positive
endexpiratory
pressure
on pulmonary
perfusion
and arterial
oxygenation.
Am Rev Respir Dis 1975; 112:457-59
expansion
in LVEDP
and
Surg Gynecol
7 Danek
LVEDV
venous
not
ther
previously,
movement
output
beneficial
is de-
increasing
does
on cardiac
measures,
used
if it is
only
effect
1 Kumar A, Falke KJ, Geffin B, Aldredge
CF, Layer
MB, Lowenstein E, et al. Continuous
positive-pressure
ventilation
in acute
respiratory
failure.
N Engl J Med 1970; 283:1430-36
2 Toung
TJ, Saharia
P, Mitzner
WA, Permutt
S, Cameron
JL. The
the effects
on
ventricular
disten-
augment
favoring
results
mentioned
increase
on
great
does
output
therapeutic
may be employed.
agents
should
be
3 Powers
and
effect
with
continued
a beneficial
if cardiac
to these
sure.
pulmonary
microvasculature
into the interstitial
alveolar
spaces
may be markedly
increased.
Thus,
even
the
though
fraction
distensibility,
forces
even
if LVEDV
However,
a marked
hydrostatic
only
by either
LVEDV.
limited
be used
ejection
may
been
an adverse
Therefore,
in left
fraction.
increase
may
ventricular
be overcome
fraction
distensibility
output
drugs
these
be
have
REFERENCES
decreased
had
vascular
may
caution.
A decrease
shunt
vasodilators,
output,
Finally,
response
should
they
they are likely
to cause
a deterioration
gas exchange
and thus negate
any effect
cardiac
output.
distress
tension
perfusion
pulmonary
cardiac
output.
right
that
studies,
apparently
due
blood
flow to nonventi-
Thus,
agents
that
shown
to increase
animals
during
oxygen
drug infusion
in these
increase
in pulmonary
by vasoconstnction.
the
and
been
and
These
determined
hypoxic
respiratory
intrapulmonary
arterial
tuted.
vasoconstriction,
to be therapeutically
the adult
Nitroprusside
has
output
in patients
areas
in reversing
pulmonary
not been shown
increased
lated
agents,
induced
increase
and thus increase
one might
expect
be effective
in patients
syndrome.
cardiac
during
to an
Pharmacologic
should
have no effect on the PEEP
relationships
within
the lung which
J,
Pontoppidan
Hemodynamic
The effect
Calvin
pressure
patients
H,
responses
Driedger
RS,
Lowenstein
to mechanical
of hypervolemia.
JE,
Wilson
AA,
Anesthesiology
Sibbald
E,
ventilation
WJ.
Layer
with
MB.
PEEP:
1975; 42:45-55
Positive
end-expiratory
(PEEP)
does not depress
with pulmonary
edema.
left ventricular
Am Rev Respir
SS,
Robertson
function
in
Dis 1981;
124:121-28
18 Cassidy
Eschenbacher
WL,
CHEST
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
I 84
CH,
I 2 I AUGUST,
Nixon
1983
JV,
215
Blomqvist
G, Johnson
pressure
RL.
ventilation
in
Cardiovascular
normal
effects
J AppI
subjects.
its contractile
of positive-
Physiol
1979;
47:453-61
19 Craven
KD
sures
20
Wood
with
LD.
positive
Physiol
1981;
51:798-805
Culver
BH,
Marini
pressure
effects
and
Extrapericardial
end-expiratory
on
esophageal
pressure
JJ, Butler
in
J. Lung
ventricular
volume
and pleural
Physiol
1981;
J Appl
function.
pres-
J Appl
dogs.
JJ, Culver
distention
with
Respir
22
Dis 1981;
Wise
BA,
BH,
J.
Butler
positive
pressure
Mechanical
on
effect
cardiac
function.
of
lung
Am
Rev
124:382-86
Robotham
JL,
Bromberger-Barnea
B,
Permutt
S.
Effects
of PEEP
on left ventricular
function
in right-heartbypassed
dogs. J AppI Physiol 1981; 51:541-46
23 Fewell JE, Abendschein
DR. Carlson CJ, Rapaport
E, Murray
JE Mechanism
of decreased
right and left ventricular
enddiastolic
tion
24
volumes
in dogs.
SM,
Scharf
Changes
positive
25
26
27
Res
Brown
in canine
continuous
1980;
Physiol
positive-pressure
N, Green
ventricular
size
pressure.
Circ
Res
Ingram
configuration
1979;
Braunwald
E. Contraction
ofthe
normal
heart.
In: Braunwald
Disease:
A textbook
of cardiovascular
W. B. Saunders,
1980
West
Blood
E.
Regulation
of the
circulation
(first
of two
parts).
compliance:
mechanisms
and
clinical
implications.
Am J Cardiol 1976; 38:645-53
31 Diamond
G, Forrester
JS, Hargis J, Parinley
WW,
Danzig R,
Swan
HJ. Diastolic
pressure-volume
relationship
of the canine
left ventricle.
Circ Res 1971; 29:267-75
32 Parker JO, Case RB. Normal left ventricular
function.
Circulation 1974; 60:4-12
33 Braunwald
E. On the difference
between
the heart’s output and
216
41
42
N
J Med
ventricular
40
43
1974; 290:1124-29
29 Braunwald
E. Regulation
ofthe circulation
(second oftwo parts).
N EngI J Med 1974; 290: 1420-25
30 Gaasch
WH, Levine
HJ, Quinones
MA, Alexander
JK. Left
EngI
JB.
flow.
In:
West
JB.
Respiratory
physiology.
Baltimore:
Waverly Press,
1976
38 Whittenberger
JL, McGregor
M, Berglund
E, Borst HC.
Influence
ofstate
ofinflation
ofthe
lungs on pulmonary
vascular
resistance.
J Appl Physiol 1960; 15:878-82
39 Baum GL, Schwartz
A, Llamas R, Castillo C. Left ventricular
E,
medicine.
233:H635-H641
37
44:672-78
Robertson
CH, Pierce
AK, Johnson
RL. Cardiovascular
effects
of positive end-expiratory
pressure
in dogs. J
Appl Physiol
1978; 44:743-50
Rushmer
RE Cardiac control.
Factors affecting
cardiac
output.
In: Rushmer
RF, ed. Cardiovascular
dynamics.
Philadelphia:
WB. Saunders,
1976
43: 171-74
Binion JT, Morgan WL, Sarnoff SJ. Alterations
in
central
blood volume
and cardiac
output
induced
by positive
pressure
breathing
and counteracted
by metaraminol
(Aramine).
Circ Res 1957; 5:670-75
with
55,
Braunwald
1977;
function
RH.
1971;
E,
ventila-
LH,
and
Circulation
Braunwald
47:467-72
R, Saunders
left
end-expiratory
Cassidy
ed Heart
Philadelphia:
28
during
Circ
(editorial).
36
50:630-35
21 Marini
state
Buda AJ, Pinsky MR, Ingels NB, Daughters
GT, Stinson
EB,
Alderman
EL. Effect ofintrathoracic
pressure
on left ventricular
performance.
N EngI J Med 1979; 301:453-59
35 Scharf
SM, Ingram
RH. Effects of decreasing
lung compliance
with oleic acid on the cardiovascular
response
to PEEP. Am J
34
in chronic
obstructive
lung
disease.
N EnglJ
Med
1971;
285;361-65
Kelly DT, Spotnitz
HM,
Beiser
GD,
Pierce
JE, Epstein
SE.
Effects ofchronic
right ventricular
volume
and pressure
loading
on left ventricular
performance.
Circulation
1971; 44:403-12
Stool EW, Mullins
CB, Leshin SJ, Mitchell
JH. Dimensional
changes
of the left ventricle
during
acute pulmonary
arterial
hypertension
in dogs. Am J Cardiol
1974; 33:868-75
Glantz SA, Misbach
GA, Moores WY, Mathey
DG, Lekven J,
Stowe DF, et al. The pericardium
substantially
affects the left
ventricular
diastolic
pressure-volume
relationship
in the dog.
Circ Res 1978; 42:433-41
Reddy PS, Curtiss
El, O’Toole JD, Shaver JA. Cardiac tamponade: hemodynamic
observations
in man. Circulation
1978;
58:265-72
44
RM, Oppenheimer
Prewitt
ofpositive
end-expiratory
in patients
1981;
with
L, Sutherland
pressure
hypoxemic
JB, Wood
on left
respiratory
ventricular
failure.
LD.
Effect
mechanics
Anesthesiology
55:409-15
Prewitt
RM, Oppenheimer
L, Sutherland
JB, Wood LD. Acute
effects
of nitroprusside
(NP) on hemodynamics
and oxygen
exchange
in patient
with hypoxemic
respiratory
failure
(HRF)
(abstract).
Am Rev Respir Dis 1980; 121:179
46 Prewitt
RM, McCarthy
J, Wood LD. Treatment
of acute low
pressure
pulmonary
edema in dogs. Relative
effects of hydro-
45
static
expiratory
and
oncotic
pressure,
nitroprusside,
J Clin Invest
pressure.
EffeCt
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21373/ on 06/16/2017
of PEEP
and
positive
end-
1981; 67:409-18
on Cardiac
Output
(Doiinsky, Whitcomb)