Cardiovascular
negative-pressure
responses of man during
breathing’
E. Y. TING,2
S. K. HONG3 AND H. RAHN
of Physiology,
The University
of Buffalo,
Bufalo,
Debartment
1
TING,
E. Y., S.
sponses of man during
K.
HONG
AND
negative-pressure
H.
RAHN.
breathing.
.Lw
York
rg6o.-Blood
pressures, heart rate and finger
I5 (4) : 557-560.
volumes were recorded while supine subjects submitted to
various degrees of continuous negative-pressure
breathing.
The lowest pressure was -30 cm I&O. Systolic and diastolic
arterial pressures as well as heart rate remained essentially
venous
pressure estimated by an
unchangkd. The peripheral
indirect method was slightly lowered .. Finger plethysmography
indicated a peripheral vasoconstriction
to the same degree as
observed during positive-pressure
breathing.
Various considerations suggest that during negative-pressure breathing the
veins entering the thoraci,c cavity collapse and effectively divide
the circulation into the thoracic one which operates at a considerably reduced pressure, and the nonthoracic circulation
which is maintained
at normal pressures. The pressure difference between these two circulations is maintained
by the
METHODS
Arterial
bloodpressure
and heart rate. Eight subjects served
in these experiments.
The pressure differential
was applied by having the subject completely
enclosed in a
body box which could be pressurized
to +30 cm HZO,
while the airway was connected
to the outside and the
lungs remained
at atmospheric
pressure, i.e. continuous
negative-pressure
breathing.
Before the subject entered
the box a blood pressure cuff and a stethoscope
drum
were placed over the right upper arm and the cubital
region, respectively.
The rubber tubes from the pressure
cuff and the stethoscope were led through
two pipes in
the wall to be reconnected
to a sphygmomanometer
and stethoscope ear pieces on the outside. Each subject
rested for 20-30 minutes in the body box, for recording
the normal pulse rate and arterial
blood pressure. This
was followed
by pressurizing
the chamber
to + 15 and
later to +30 cm H20. Measurements
were made hetween 2-3 and between 4-6 minutes following
pressure
exposure as well as after recovery. A I o-minute rest period
was provided
between
each pressure exposure.
Three
determinations
each were made of heart rate, systolic
and diastolic pressure and averaged. The blood pressure
values were corrected
by subtracting
the positive pressure inside the box.
Peripheral
vasomotor
activity.
In these experiments
five
subjects lay on a comfortable
mattress and breathed
air
through
inspiratory
and expiratory
tubes connected
to
the body box. In this case the body box was partially
evacuated to pressures of IO, 20 and 30 cm Hz0 below
negativeatmospheric
pressure in order to simulate
pressure breathing
(this method is illustrated
in fig. I B
of the preceding
communication
(I ).
In these experiments
the finger volume was recorded
under various degrees of negative- and positive-pressure
left ventricle.
negative-pressure
breathing
the
URING
CONTINUOUS
pressure within
the lung is maintained
at a lower value
than that in the rest of the body. This condition
is realized to some degree whenever
the body is submerged
with the head above the water, but particularly
when
the body is more deeply submerged
and the airway is
connected
by rigid tubes to the atmosphere
as in the
popular
watersport
of ‘snorkeling.’
These underwater
conditions
can in part be simulated
by differential
air
pressurization
as discussed in the foregoing
communication (I).
This transthoracic
pressure difference
is expected to
have a profound
effect on the circulation,
since the intrathoracic veins, the pulmonary
circulation
and the heart
are maintained
at a considerably
lower absolute pressure than the rest of the circulation.
At the small resting
lung volumes
maintained
by this negative-pressure
breathing
the recoil of the lung tissue is probably
less
Received
for publication
February
8, 1960.
1 This
study
was supported
in part
by the Air
Research
and
Development
Command,
Wright-Patterson
Air Force
Base, Ohio.
2 Present
address:
Albert
Einstein
College
of Medicine,
New
York
City
61.
3 Present
address:
Dept.
of Physiology,
Yonsei
University
School
of Medicine,
Seoul,
Korea.
557
Downloaded from http://jap.physiology.org/ by 10.220.33.5 on September 17, 2016
than 1-2 cm H20 and, theref’ore,
the total pressure
differential
is transmitted
to the intrathoracic
(intrapleural)
space.
In this study subjects were submitted
to continuous
negative-pressure
breathing
in order to record the arterial blood pressure, heart rate and finger volume and
to determine
by indirect means the venous blood pressure.
Cardiovascular
reJ. Appl. Physiol.
55 8
E. Y.
RESULTS
AND
DISCUSSION
Artkal
blood pressure and pulse rate. The mean values
obtained
from 12 measurements
on 8 subjects are shown
in table I. It is evident from this table that there is no
significant
change in either blood pressures or the pulse
rates during negative-pressure
breathing.
Only the heart
rate appears to increase very slightly
at 30 cm Hz0
pressure differential.
Furthermore,
the estimations
of
peripheral
venous pressures (discussed below) show only
a slight change from 12 to 5 cm HZO. Thus, it would
appear that the whole body, with the exception
of the
thoracic cavity, has blood pressures which
remain
essentially stable during negative-pressure
breathing.
This
may at first seem surprising
since the vessels in the thoratic cavity, including
the large veins, heart and pulmonary
circulation,
are subjected to negative pressures as much
mm Hg. That nearly all of
as -30 cm H20 or -22
this pressure (intrapulmonary
pressure which is applied
TABLE
I. Blood Pressures and Heart Rate at - r5 and -30
Pressure Breathing in Supine Posture
-15
S. K.
HONG
AND
H.
l<.JIH,U
minus lung tension of the normal resting lung volume)
is transmitted
to the intrathoracic
space has been demonstrated recently bvs Lenfant and Howell
(2).
The observations
of relative
stabilitv I of the arterial
blood pressures during
negative
pressure differ from
those previously described by Dern and Fenn (3). These
authors demonstrated
a fall of about 8 mm Hg in both
diastolic
and SYstolic pressu res whe n a supi ne subject
was exposed to a negative pressure of -30
cm HZO.
The onlv apparent
difference
in their
exp erime ntal
procedure
was the fact that in their studies the head and
neck were outside of the body box, which would expose
the carotid sinus to the negative pressure. Such a procedure might result in a slight mechanical
dilation
of
the carotid
sinus complex
and thus bring
about reflexlv , a fall in arterial pressure.
The relative
stabilitv , of the t>lood pressures in the
nonthoracic
blood vessels when in trapulmona
rv and
intrathoracic
pressures were maintained
at very much
lower levels led to further explorations
of vascular pressures in anesthetized
dogs. Six animals were anesthetized
with
Nembutal
and catheterized
under
fluoroscopic
control. These animals breathed spontaneously
and were
intermittently
subjected to - 20 cm Hz0 intrapulmonary
pressure bv, rebreathing
from a large box maintained
at
the a ppropria te pressure. Catheters were placed in the
right atrium,
artery, inferior
and superior
P ulmonarv
vena cava and by retrograde
catheterization
into the
pulmonary
vein, and in order to follow the pressure
change when the intrapulmonary
pressure was reduced.
Figure I indicates a typical response to negative-pressure breathing.
While the pulmonary
vein and the right
atrium pressure fell immediately
by approximately
half
the value applied
to the intrapulmonary
space, the
peripheral
vein showed only a small and temporary
fall.
The latter catheter was in the inferior vena cava onlv
a few centimeters
below the diaphragm.
When catheters
were in the superior
vena cava, but just beyond the
chest, the peripheral
venous response was similar. Frequently, no change at all was observed. Yet, as soon as
the catheters
were advanced
toward
the heart and
entered
the thoracic
cavity, the venous pressures responded similarly
to those recorded in the right atrium.
The overshoot
of intrathoracic
vascular pressure after
release of pressure breathing
was always evident.
It
cm Hz0
Continuous
--_____--30
cm
cm
Recovery
2-3 Min.
Syst.
Diast.
Pulse
Pulse
pr.
pr.
pr.
rate
II5h2.5
76~12.3
39+2*4
74*3
-8
II6a.g
72&3.0
44*2*9
79*4*6
113h2.1
73h2.6
4oh2.7
79*4*5
I r3*3-5
74*3
*7
39*3*5
813~4.4
4-6 Min.
114k2.8
75zt3.2
39*3
*5
82dz4.5
,
I 16~t4.5
1
77+4*7
39*5-o
72&a.
I
Downloaded from http://jap.physiology.org/ by 10.220.33.5 on September 17, 2016
breathing.
In another test the changes in finger volume
were recorded following
various degrees of venous blood
flow obstruction
and compared
to similar changes during
negative-pressure
breathing.
From such data it is possible to assess the changes in peripheral
venous pressure.
The finger plethysmograph
was made of a tapered glass
tube open at both ends. The finger (usually index or
middle finger) was placed into the wider end of the tube
and sealed with plasticene.
The narrow end of the tube
was connected
to a strain gauge pressure transducer
connected
to a Sanborn
recorder.
At the end of each
experiment
the finger plethysmograph
was calibrated
by
injecting
a known
amount
of air into the tube. The
normal finger volume was estimated
by measuring
the
volume of water displaced in a graduated
cylinder.
The
changes in finger volume were all expressed as percentage of change of the normal finger volume. The venous
occlusion was produced
by inflating
a small cuff encircling the first finger joint. It was situated far enough from
the plethysmograph
so that the tissue displacement
following
cuff inflation did not distort the volume changes
recorded from the distal joints of the finger. Pressure of
20-60 cm Hz0 was applied
to the first finger joint at
various intervals during the experiment
and the changes
in finger volume recorded.
TING,
VASCULAR
RESPONSES
DURING
PKESSUKE
BREATHING
cm
HP
IO
Per. V.
5
0
-5
-10
min.0
3
6
Pressures
in the right
atrium
(Rt. A4.), pulmonary
vein
(Pd.
V.) and peripheral
vein (Per. V.) in an anesthetized
dog when
subjected
to 3 min.
of negative-pressure
breathing
(NPB)
of -20
cm H?O.
Peripheral
vein catheters
were in the inferior
vena cava a
few centimeters
below
diaphragm
and
pressure
remained
independent
of that found
in right
atrium.
FIG.
I.
0A-30
06
1.5 I
Intrapulmonory
-20
-IO
I
I
Pressure
0
40
I
I
cm H,O
420
I
+30
I
1
IO
20
Venous
30
40
Occlusion
50
60
cm H,O
FIG. 2. A, average
finger
volume
decrease
and S.E. in 8 subjects
when
subjected
to positiveand negative-intrapulmonary
pressures.
Finger
volumes
are expressed
as ‘,;; changes
of total
finger
volume
inside
plethysmograph.
B, changes
in finger
volume
when
v-enous
outflow
is obstructed
by a cuff at base of finger.
Cuff
pressure
is
indicated
on abscissa.
Lower
line represents
average
values
and S.E.s
under
normal
conditions
while
Z&W line is an average
of all v*alucs
found
when
subjects
were subjected
to IO, 20 and 30 cm of negative-pressure
breathing.
pressure breathing,
either positive or negative, the finger
volume was invariably
decreased. This decrease in finger
volume
was usually
maintained
for the duration
of
pressure breathing.
The percentage
of reduction
in finger volume during
the application
of various pressures
of
is shown in figure 2. The pattern and the magnitude
this reduction
in finger volume
are very similar
for
positive- and negative-pressure
breathing.
The averages
indicate that the reduction
in finger volume approaches
a plateau at 20 cm Hz0 during both positive- and ne,gative-pressure
breathing.
Since a change in finger volume
is the net result of the rate of inflow and drainage
of
blood, it is dificult
to interpret
the change as due to a
peripheral
vasoconstriction,
which would decrease the
inflow of arterial
blood, or a venomotor
reflex, which
would facilitate the drainage of blood in peripheral
veins.
In order to dissociate these two factors, the same experiments were carried out after the venous blood flow from
the finger was partially occluded by a finger cuff inflated
to a pressure of 60 cm HZO. With this occlusion
the
finger volume still decreased immediately
after the onset
of pressure breathing
(both positive and negative). This
suggests that the observed reduction
in finger volume
during
pressure breathings
is most likely due to a decreased arterial
inflow, triggered
by a peripheral
vasoconstriction.
Venous compliance and pressure. With various degrees of
negative pressure in the lung, finger-cuff
pressures of
20-60 cm H20 were successively applied
to the base of
Downloaded from http://jap.physiology.org/ by 10.220.33.5 on September 17, 2016
required
several minutes for complete recovery and suggests a gradual
loss of vasoconstrictor
tone induced
by
this maneuver.
These observations
confirm the venous-pressure
measurements made by Holt in dogs (4) and man (5). With
negative-pressure
breathing
the central venous pressures
decrease to about half of the pressure change applied to
the lung, while peripheral
venous pressure remains unaltered. Holt (4) and, more recently,
Brecher (6) concluded that the veins collapse just before entering
the
chest. Thus, a large resistance is provided
which effectively separates the thoracic from the nonthoracic
circulation, each operating
now from its own pressure base
line. All the intrathoracic
vessel pressures including
the
left atrium are maintained
at very much lower pressures
during negative-pressure
breathing
(3). The left ventricle
must now make up for this pressure loss in the thoracic
vascular
compartments
if it is to deliver
the normal
pressure to the nonthoracic
parts of the body. This happens in man where we find no significant
change in
arterial
blood pressure. It would, therefore, appear that
the circulatory
strain of negative-pressure
breathing
is
placed on the left ventricle
and that the right heart and
the pulmonary
circulation
are protected
from over-congestion by the mechanical
collapse of the peripheral
veins as they enter the thorax.
Finger volume changks. Immediately
after the onset of
E. Y. TING,
560
a finger and the increase in finger volume
recorded.
Figure 2 shows a linear increase in finger volume as the
cuff pressures are increased.
The increases in finger
volume during
- IO, - 20 and -30 cm Hz0 negativepressure
breathing
were indistinguishable
from each
other and were averaged to comiare
with the normal
values. By definition,
the slope of these lines represents
the compliance
of the (venous)
vessels in the finger.
Since these two lines are virtually
parallel,
it implies
that the pressure-volume
characteristics
of the veins
did not change
during
negative-pressure
breathing,
that is to say that no change in venomotor
tone was discernible
by this method.
When one extrapolates
the
S. K.
HONG
AND
H.
KAHN
line back to zero per cent change in finger volume, the
intercept
represents
the estimated
peripheral
venous
pressure. According
to this method
of estimation,
the
venous pressure is 12 cm Hz0 in the control period and
reduced to approximately
5 cm Hz0 during
negativepressure breathing.
A measurable
decrease in the peripheral
blood flow
during
both positiveand negative-pressure
breathing
has previously
been reported
by DeLalla
(7) and Fenn
and Chadwick
(8). The mechanism
which elicits this
peripheral
vasoconstriction
is not demonstrated,
although it may conceivably
be due to the baroreceptors
in the carotid and aortic sinus.
REFERENCES
I. HONG,
S. K.,
E. Y. TING
AND H. RAHN.
J. App/.
Physiol.
1960.
2. LENFANT, C. AND B. HOWELL.
J. ‘4ppZ. Physiol.
3. DERN, R. J. AND W. 0. FENN. J. CZin. Inv. 26:
4. HOLT, J. P. Am. J. Physiol.
142 : 594, I 944.
15: 425, 1960.
460, 1947.
15:
5. HOLT, J. P. Am. J. Physiol.
139: 208, 1943.
6. BRECHER,
G. A. Venous Return.
New York:
7. DELALLA,
V., JR. Am. J. Physiol.
152 : 122,
8. FENN, W. 0. AND L. E. CHADWICK.
Am.
1947.
Grune,
1948.
J. Physiol.
1956.
151 : 270,
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550,