Its
Relation
REJANE
Pulmonary
Circulation:
to
and
Normal
HARVEY,
M.
M.D. and M. IRENE
York, New York
New
Although
circulations
the anatomic
have
been
differences
between
performance
of
differences
recognized
these
the
pulmonary
two
reviewed
observed
in
The
point
through
disease
ventricle,
the
venous
The
become
animals,
output.
The
dynamically
pulmonary
in
during
which
the
some
states
past
of
in
of
pressure
normal
in
man
a
patterns
resistance
remaining
receiving
one-half
the
and
remaining
furthermore
lung,
which
approximately
the
cardiac
normal
will
For
output,
flow
of
without
example,
three
of
is
it
flow
the
mean,
about
one-
capillaries
that
the
Is
also
blood
through
necessarily
above
Is
circulation
the
total
The
artery
blood
times
man
circula-
dissimilar.
result
In
the
blood
pneumonectomy
per
is trebled
*From
the Department
of Medicine,
and Surgeons,
and the Cardiopulmonary
Chest
Services
(Columbia
University
normal
systemic
That
flow,
pulmonary
readily
the
pulentailing
through
resting
the
level,
liters
per
minute
per
square
meter
of
pulmonary
hypertension.
Considered
of one
lung
and
hence
doubling
the
the
liters
blood
In the pulmonary
These
facts
Indicate
lung,
does
not
not
do so until
before
1.5
quite
system.
that
the
accelerated
increased
in
the
pulmonary
the pressure
capillaries.
arteries.
be
the
anatomic
artery
add
the
markedly
of the bronchiolar
than
1 per
cent
are
In
low
through
less
however,
reaching
values
between
8 and
11
body
surface
area,
without
producing
from
another
point
of view,
removal
flow
In
tension
flows
small
contribution
circulation
these
may
decade,
the
pulmonary
circulation
which
by the
fact
be greatly
the
Influences
pulmonary
pressure
is
controls
latter
the aorta
and
of the systemic
is shown
arteries
can
a rise
lungs
the
that
pressures,
circulation
distensible
monary
the
as
effective,
seen
that
measure
through
the
systemic
the
abnormal
projected.
large
same
disregards
to the
tenth
that
is one-sixth
or
apparent
against
because
the
if one
adds
in
atrium
outflow.
blood
flow
cardiac
or
have
be
in
and
systemic
functional
until
technics
became
available
which
of pulmonary
blood
flow
and
blood
presimportant
features
of the
normal
human
background
may
which
left
quantitatively
tion,
which
a
known
normal
and
the
pulmonary
circulation
could
logically
be defined
from
an
of view
as including
all the
structures
from
the
pulmonary
the
pulmonary
veins.
However,
dynamically
one
must
right
and
which
as
In
M.D.
pulmonary
some
of
were
circulation
Dynamics*
FERRER,
the
and
circulations
pulmonary
circulation
be
between
years
for
In man
was
not
clearly
defined
permitted
direct
measurements
sures.
In this
paper
some
of the
will
Altered
square
as
pulmonary
hyperflow
through
the
was
meter
of
body
It may
be
during
accustomed
surface
to
area,
exercise.
Columbia
University
College
of Physicians
Laboratory
of the First
Medical
and
Division),
Bellevue
Hospital,
New York City.
247
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017
248
HARVEY
As
has
been
circulations
left
mentioned,
is the
and
right
arterial
exist
where
right
least
stability
ventricular
under
of
distensibility
of
designed
still in
is
finding
has
the
to
an
some
action
arteries,
pulmonary
is
of
upon
largely
Extensive
the
hypertension.
rupture
thinning
ever,
has
flow
indicated
and
before
severe
of
pulmonary
the
fashion
by
lumen
scribed
congenital
the
mitral
other
factors,
must
malformations
congenital
stenosis.
may
as
anomalies
very
just
it
the
In
the
pressures
blood
flow
tree
and
in
hence
produce
in
size
chronic
of
the
upon
the
diminished
in
upon,
the
increased
lesions
hand,
the
a somewhat
and
hence
blood
flow
discussed,
pulmonary
not
only
reduce
size
different
reduce
the
pathologic
lesion
has
been
for pulmonary
hypertension
pulmonary
by
sole
emphyhow-
anatomic
other
re-
bed
as
hypercapnia,
On
a
pulmonary
these
patients
in
the
pulmonary
indicted
anoxia,
and
interference
formerly
their
elasticity.
would
favor
lesions
have
high
artery
site
of
yet,
dein
Is Increased,
and
patent
ductus
arterlosus.
the
effects
of a decreased
distensibility
The
sclerotic
lesions
observed
in the
may
alter
dilatation,
arterial
The
vascular
of
and
artery
no
superimposed
be
the
blood
although
least
presumably
encroach
where
defect
consider
pressures.
at
is
exists.
which
of
musculature
pulmonary
e.g.
be
hypertension
bed
identified,
pulmonary
there
was
of
levels
pulmonary
the
mode
the
curtailment
vessels.
This
type
be In part
responsible
of the vessels
but also
limiting
mechanical
hypertension.
Extensive
of
could
arterial
tree,
a changing
capacity
and
unresolved.
rise
in patients
with
pulmonary
hypertension
of
lesions
Interatrial
septal
Finally,
one must
pulmonary
vascular
with
anatomic
capillaries
vascular
e.g.
in
bed
pulmonary
of, individual
In, and
may
certain
pulmonary
the
hypervolemia,
vascular
as
the
this
because
at
been
between
actual
that
level
of
permit
the
Pharmacologic
bed
implicated,
long
of
of such
a pressure
The
reversibility
blood
so
the
yet
is still
a balance
systemic
the
pulmonary
vascular
suggested
recently
that
upon
directly
of
capacity
Indeed,
and
cause
sema.
of
capacity,
outflow.
The
of
capillaries.
of
been
to raise
However,
not
the
of
which
pulmonary
action
problem
be
lesser
outputs
man.
hypertension
have
pressures,
destruction
in
the
topical
entire
resultant
vascular
venous
duction
normal
and
be insufficient
normal
man.
bed
a
and
1954
stroke
output
and
heart
rate
overall
change
In arterial
blood
not
been
conclusively
shown
to
control
it has
in
would
In
cannot
circuit
the
greater
stroke
mechanisms
pulmonary
the
has
This
lesser
pulmonary
pulmonary
tree
levels
vasomotricity
control
in
reflex
activity
anoxia
vessels.
Since
identical
reflex
However,
produces
anoxia
that
the
average
“arterioles”
demonstrate
early
stage.
anoxia
of
be
through
the
regulatory
vasomotor
that
may
also
March,
normal
circumstances
in the
pulmonary
the
pulmonary
artery
pressure
in face
output
Is chiefly
a reflection
of the
great
flow
which
of themselves
pressures
to abnormal
of
flow
to changes
in left
ventricular
that
there
may
not
be an
reflex
mechanisms
have
at
there
blood
FERRER
presumably
are
however,
adjust
a way
Such
studies
bed are
and
ventricles
tree
bed to
in such
pressure.
the
same
AND
the
upon
arterial
lumen
A reduction
in distensibility,
the
production
of pulmonary
also been
described
in patients
artery
pressures
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017
seen
in
250
HARVEY
between
pulmonary
Hg.)
hydrostatic
phasized
capillary
pressures.
when
one
(30 mm.
oncotic
Hg.)
and
in the
pressure
systemic
of similar
capillaries,
increasing
as is seen
transudation
into
evidence
of considerable
the
pulmonary
edema.
accounts
stenosis
pulmonary
brief
obvious
producing
fact
have
summary
explains
that
In
the
favor
of
the
why
this
an
and
the
with
pulmonary
increment
pulmonary
of
expect
trans-
with
clinical
if ever,
pulmonary
left
mm.
em-
between
than
one
may
without
disease,
1954
pressure
system
is seldom,
within
pulmonary
frank
capillaries
ventricular
hypertension
failure
or
without
circulation
of
the
may
with
mitral
on this
instances,
signs
actually
attributed
to
be misleading
stenosis,
of
In a short
progress
where
this
review
concerning
has
to
interesting
be
omitted.
area
between
moses
pulmonary
have
not
shown
to
mitral
stenosis,
occur
of
pressures
such
as
escape
to
occur
in
clinical
to-
the individual
separately,
it
is
is involved
of pulmonary
advanced
clinical
stage.
criteria
in
Unfor
its
recognition
surprising
therefore
early
notice.
a loud
been
hypertension
be absent
hypertension
attempted
of these
diagnosis
in the
reliable
e.g.
recently
pulmonary
to
left
ventricular
Furthermore
pulmonic
found
in
diagnosed
when
measured
was
present
in
second
patients
clinically
directly.
when
there
In
other
was
no
sound.
it is impossible
the
lesser
to comment
circulation
However,
a word
investigation,
and
bronchial
definitely
in
a
wide
of
These
level
affecting
is yet
in
to
be added
here
the
existence
diseases
lnfarcts,
anastomoses
these
gas
be
adequately
and
perforce
circulations.
proved
in normal
pulmonary
conditions.
in
should
namely
variety
pneumonia,
or precapillary
importance
Although
treated
which
permit
phase.
It is not
hypertension,
as has
been
cardiac
so disastrous.
have
been
disorder,
treated
hypertension,
emphysema,
basis
was
found
severe
pulmonary
accentuation
be
has
may
be involved,
singly
or
hypertension.
This
circulatory
consequences,
right
ventricular
states
more
than
one
status.
The
clinical
this
hemodynamic
hence
more
easily
and
some
sound,
pulmonary
oncotic
differential
capillary
when
systemic
in
made
without
difficulty
as yet
no constant
or
lesser
degrees
of
and
pulmonary
arterial
tional
capillary
(25
is further
plasma
there
safety
edema,
can
hypertension
most
clinical
final
physiologic
is often
there
are
diagnosing
the mild
congenital
the
fact
pericarditis,
systemic
tissues
congestion,
that
patients
moderate
of
pulmonary
which
hypertension
fortunately
in
constrictive
Into
the
margin
the
may
this
example,
to both
attention
on the
mechanisms
which
in the
production
of pulmonary
has
been
emphasized
because
its
failure
and
mechanisms
that
failure
for
to
for
added
systemic
This
of
Is a greater
pressure
in the
pulmonary
Thus,
is
This
systemic
and
pressures
chronic
of fluid
alveoli.
March,
rales.
This
focus
gether,
disorder
these
in
FERRER
mm.
Hg.)
importance
that
there
pressure
capillaries.
magnitude
udation
also
mitral
(5
The
relates
and notes
hydrostatic
AND
various
exchange,
Although
man
including
on all
some
concerning
of anastomoses
occur
states.
However,
pulmonary
one
these
anastothey
have
been
bronchiectasis,
emphysema
may
the work
material
and
certain
the
venous,
their
funcflow
or
at
blood
defined.
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017
250
HARVEY
between
pulmonary
Hg.)
hydrostatic
phasized
capillary
pressures.
when
one
(30 mm.
oncotic
Hg.)
and
in the
pressure
systemic
of similar
capillaries,
increasing
as is seen
transudation
into
evidence
of considerable
the
pulmonary
edema.
accounts
stenosis
pulmonary
brief
obvious
producing
fact
have
summary
explains
that
In
the
favor
of
the
why
this
an
and
the
with
pulmonary
increment
pulmonary
of
expect
trans-
with
clinical
if ever,
pulmonary
left
mm.
em-
between
than
one
may
without
disease,
1954
pressure
system
is seldom,
within
pulmonary
frank
capillaries
ventricular
hypertension
failure
or
without
circulation
of
the
may
with
mitral
on this
instances,
signs
actually
attributed
to
be misleading
stenosis,
of
In a short
progress
where
this
review
concerning
has
to
interesting
be
omitted.
area
between
moses
pulmonary
have
not
shown
to
mitral
stenosis,
occur
of
pressures
such
as
escape
to
occur
in
clinical
to-
the individual
separately,
it
is
is involved
of pulmonary
advanced
clinical
stage.
criteria
in
Unfor
its
recognition
surprising
therefore
early
notice.
a loud
been
hypertension
be absent
hypertension
attempted
of these
diagnosis
in the
reliable
e.g.
recently
pulmonary
to
left
ventricular
Furthermore
pulmonic
found
in
diagnosed
when
measured
was
present
in
second
patients
clinically
directly.
when
there
In
other
was
no
sound.
it is impossible
the
lesser
to comment
circulation
However,
a word
investigation,
and
bronchial
definitely
in
a
wide
of
These
level
affecting
is yet
in
to
be added
here
the
existence
diseases
lnfarcts,
anastomoses
these
gas
be
adequately
and
perforce
circulations.
proved
in normal
pulmonary
conditions.
in
should
namely
variety
pneumonia,
or precapillary
importance
Although
treated
which
permit
phase.
It is not
hypertension,
as has
been
cardiac
so disastrous.
have
been
disorder,
treated
hypertension,
emphysema,
basis
was
found
severe
pulmonary
accentuation
be
has
may
be involved,
singly
or
hypertension.
This
circulatory
consequences,
right
ventricular
states
more
than
one
status.
The
clinical
this
hemodynamic
hence
more
easily
and
some
sound,
pulmonary
oncotic
differential
capillary
when
systemic
in
made
without
difficulty
as yet
no constant
or
lesser
degrees
of
and
pulmonary
arterial
tional
capillary
(25
is further
plasma
there
safety
edema,
can
hypertension
most
clinical
final
physiologic
is often
there
are
diagnosing
the mild
congenital
the
fact
pericarditis,
systemic
tissues
congestion,
that
patients
moderate
of
pulmonary
which
hypertension
fortunately
in
constrictive
Into
the
margin
the
may
this
example,
to both
attention
on the
mechanisms
which
in the
production
of pulmonary
has
been
emphasized
because
its
failure
and
mechanisms
that
failure
for
to
for
added
systemic
This
of
Is a greater
pressure
in the
pulmonary
Thus,
is
This
systemic
and
pressures
chronic
of fluid
alveoli.
March,
rales.
This
focus
gether,
disorder
these
in
FERRER
mm.
Hg.)
importance
that
there
pressure
capillaries.
magnitude
udation
also
mitral
(5
The
relates
and notes
hydrostatic
AND
various
exchange,
Although
man
including
on all
some
concerning
of anastomoses
occur
states.
However,
pulmonary
one
these
anastothey
have
been
bronchiectasis,
emphysema
may
the work
material
and
certain
the
venous,
their
funcflow
or
at
blood
defined.
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017
vol.
xxv
PULMONARY
CIRCULATION
251
SUMMARY
Some
of
circulation
have
been
anisms
the
physiologic
which
reviewed.
are
producing
and
important
Particular
pulmonary
anatomic
characteristics
to the
emphasis
understanding
has
been
of
the
pulmonary
of disease
upon
the
placed
states
mech-
hypertension.
RESUMEN
Se
cas
revisan
algunos
de la circulaciOn
aspectos
pulmonar,
de
de enfermedad.
Result#{225}ndose
producir
hipertensiOn
pulmonar.
los caracterlsticas
Importantes
para
especialmente
anatOmicas
comprender
los
y fisiolOgilos estados
mecanismos
capaces
de
RESUME
Quelques
characteristiques
lation
pulmonaire
present#{233}es. On
l’hypertension
qui
souligner
physlologiques
et
anatomiques
servent
#{233}clairer certaines
partlculierement
les mechanisms
de
maladies,
qui
la
circu-
ont
produisent
#{233}te
pulmonaire.
PHYSIOLOGIC
ASPECTS
REFERENCES
OF THE PULMONARY
CIRCULATION
Ankeney,
J. L.: “Further
Experimental
Evidence
that
Pulmonary
Capillary
Venous
Pressures
Do Not Reflect
Cyclic
Change
in Left Atrial
Pressure
(Mitral
Lesions
and Pulmonary
Embolism)
Circulation
Research,
1:58, 1953.
Burwell,
C. S.: “Some
Effects
of Pericardial
Disease
on the Pulmonary
Circulation,”
Trans.
of the Assn.
of Am.
Phys.,
64:74,
1951.
Cournand,
A., Riley,
R. L., Himmelstein,
A. and Austrian,
H.: “Pulmonary
Circulation and Alveolar
Ventilation-Perfusion
Relationships
After
Pneumonectomy,”
J. Thoracic
Surg.,
19:80, 1950.
Dexter,
L., Dow, J. W., Haynes,
F. W., Whittenberger,
J. L., Ferris,
B. G., Goodale.
W. T. and Hellems,
H. K.: “Studies
of the Pulmonary
Circulation
In Man
at
Rest.
Normal
Variations
and
the Interrelation
Between
Increased
Pulmonary
Blood
Flow, Elevated
Pulmonary
Arterial
Pressure,
and High Pulmonary
‘Capillary’ Pressures,”
J. Clin.
Invest.,
29:602,
1950.
Ferrer,
M. I., Harvey,
H. M., Cathcart,
R. T., Cournand,
A. and Richards,
D. W.:
“Hemodynamic
Studies
in Rheumatic
Heart
Disease,”
Circulation,
6:688,
1952.
Ferrer,
M. I., Harvey,
R. M., Cathcart,
R. T., Webster,
C. A., Richards,
D. W. and
Cournand,
A.: “Some
Effects
of Digoxin
Upon
the Heart
and
Circulation
in
Man. Digoxin
in Chronic
Cor Pulmonale,”
CirculatIon,
1:161, 1950.
Hamilton,
W. F.: The Lewis
A. Conner
Memorial
Lecture,
“The
Physiology
of the
Cardiac
Output,”
CIrculation,
8:527,
1953.
Harvey,
R. M., Ferrer,
M. I., Cathcart,
R. T., Richards,
D. W. and Cournand,
A.:
“Mechanical
and
Myocardial
Factors
In Chronic
Constrictive
Pericarditis,”
Circulation,
to be published.
Hickam,
J. B. and Cargill,
W. H.: “Effect
of Exercise
on Cardiac
Output
and Pulmonary
Arterial
Pressure
in Normal
Persons
and
in Patients
with
Cardiovascular
Disease
and Pulmonary
Emphysema,”
J. Clin.
Invest.,
27:10,
1948.
Motley,
H. L., Cournand,
A., Werko,
L., Himmelstein,
A. and Dresdale,
D.: “The
Influence
of Short
Periods
of Induced
Acute
Anoxla
Upon
Pulmonary
Artery
Pressure
in Man,”
Am.
J. Physiol.,
150:315,
1947.
Nisell,
0.: “The
Influence
of Blood
Gases
on the Pulmonary
Vessels
of the Cat,’
Acta.
Physiol.
Scand.,
23:85,
1951.
Opdyke,
D. F., Duomarco,
J., Dillon,
W. H., Schreiber,
H., Little,
R. C. and Seely.
H. D.: “Study
of Simultaneous
Right
and
Left
Atrial
Pressure
Pulses
Under
Normal
and Experimentally
Altered
Conditions,”
Am.
J. Physiol.,
154:258,
1948.
Wade,
G., Werko,
L., Eliasch,
H., Gidlund,
A. and Lagerlof,
H.: “The Hemodynamic
Basis
of the Symptoms
and Signs
In Mitral
Valvular
Disease,”
Quart.
J. Med.,
21:361,
1952.
,“
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017
252
HARVEY
AND
FERRER
March,
Werko,
L., Varnauskas,
E., Eliasch,
H., Lagerlof,
H., Senning,
“Further
Evidence
that
the Pulmonary
Capillary
Venous
Reflects
Cyclic
Pressure
Changes
in the Left
Atrium,”
1:337, 1953.
ANATOMIC
ASPECTS
OF
THE
PULMONARY
A. and
Pressure
1954
Thomasson,
B.:
Pulse
in Man
Circulation
Research,
CIRCULATION
Cudkowicz,
L. and Armstrong,
J. B.: “Injection
of the
Bronchial
Circulation
In a
Case
of Transposition,”
Brit.
Ht. i., 14:374,
1952.
Daman,
J. F. Jr. and
Muller,
W. H. Jr.:
“The
Role
of the Pulmonary
Vascular
Bed
in Congenital
Heart
Disease,”
Pediatrics,
12:307,
1953.
Edwards,
J. E. and
Chamberlin,
W. L. Jr.:
“Pathology
of the Pulmonary
Vascular
Tree.
III.
The
Structure
of the
Intrapulmonary
Arteries
in Cor
Triloculare
Blatriatum
with
Subaortic
Stenosis,”
Circulation,
3:524,
1951.
Kinney,
T. and Welch,
K.: “The
Effe#{243}t of Patent
Ductus
auricular
and Interventricular
Septal
Defects
on the
ary Vascular
Lesions,”
Am.
.1. Path.,
24:729,
1948.
Larrabee,
ary
W.
Arteries
F.,
Parker,
R. L. and
and
Arterioles
in
24:316,
1949.
Liebow,
A. A.: “The
Reference
Bronchopulmonary
to Emphysema,”
Am.
Edwards,
Mitral
J. E.:
Stenosis,”
Venous
J. Path.,
Liebow,
A. A., Hales,
M. R. and Lindskog,
Arteries,
and Their
Anastomoses
with
tasis,”
Am.
J. Path.,
25:211,
1949.
Collateral
29:251,
G.
the
“Pathology
Proc.
Arteriosus
and
Development
of
Staff
of
Inter-
of Pulmon-
the IntrapulmonMeet.,
Mayo
Clin.,
Circulation
with
Special
1953.
E.: “Enlargement
of the Bronchial
Pulmonary
Arteries
in Bronchiec-
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21245/ on 06/16/2017