(Chest. 2002;121:566-572.)
© 2002
American College of Chest Physicians
Effects of Partial Liquid Ventilation on Unilateral Lung Injury in Dogs*
Shigeki Sawada, MD;
Kenichi Matsuda, MD;
John G. Younger, MD;
Kent J. Johnson, MD;
Robert H. Bartlett, MD, FCCP and
Ronald B. Hirschl, MD, FCCP
*
From the Departments of Surgery (Drs. Sawada, Matsuda, Bartlett, and Hirschl), Emergency Medicine (Dr. Younger), and Pathology (Dr. Johnson), University of Michigan Medical Center, Ann Arbor, MI.
Correspondence to: Ronald B. Hirschl, MD, FCCP, F3970 Mott Hospital Box 0245, University of Michigan Medical Center, Ann Arbor, MI 48109-0245; e-mail: rhirschl{at}umich.edu
 |
Abstract
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Study objective: The overall physiologic effect of
partial liquid ventilation (PLV) in the setting of unilateral lung
injury remains unclear. Therefore, we evaluated the effect of PLV on
gas exchange in unilateral lung injury.
Design and
methods: Left unilateral lung injury was induced in 14 adult dogs
by oleic acid instillation into a left pulmonary artery. The animals
were divided into two groups: gas ventilation (GV) and PLV. During both
GV and PLV, systemic blood gas levels were analyzed. Oxygen consumption
(
O2), carbon dioxide production
(CO2) and pulmonary blood flow (Q) of
both the right lung (uninjured lung) and left lung (injured lung) were
measured.
Results: During PLV,
O2 of the injured left lung
(o2-injured),
CO2 of the injured left lung
(CO2-injured), and Q of the injured left
lung (Q-injured) were greater than those in GV
(O2-injured, 41.6 mL/min vs 23.4 mL/min,
p = 0.006; CO2-injured, 34.4 mL/min vs
25.5 mL/min, p = 0.026; and Q-injured, 0.47 L/min vs 0.22 L/min,
p = 0.002, respectively). However, overall
PaO2 during PLV was less than that during GV,
likely due to either a redistribution of Q toward the injured lung (PLV
Q-injured, 0.47 L/min vs GV Q-injured, 0.22 L/min; p = 0.002) or
reduced gas exchange efficiency in the healthy lung.
Conclusions: We conclude that in our model, PLV increases
O2 and VCO2 in
the injured lung. However, over all gas exchange efficiency is
reduced.
Key Words: carbon dioxide production • oleic acid • partial liquid ventilation • perflubron • unilateral lung injury
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Introduction
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Many
animal and human studies1
2
3
4
5
have demonstrated the ability
of partial liquid ventilation (PLV) to support or improve gas exchange
in the setting of respiratory failure. However, it has also been
observed that PLV results in a deterioration in gas exchange in normal
lungs.6
7
8
9
10
Syndromes associated with asymmetrical or
unilateral lung injury caused by aspiration pneumonia, pulmonary
hemorrhage, and pulmonary edema are occasionally observed clinically.
In addition, the use of PLV for lavaging the unilaterally injured lung
has been considered. However, the overall physiologic effect of PLV on
gas transport in such a setting with one injured lung and one healthy
lung remains unclear. In fact, there is concern that administration of
perflubron in such patients may actually diminish gas exchange. With
this study, therefore, we intended to evaluate the effect of PLV on gas
exchange in the setting of unilateral lung injury. We developed the
following hypotheses prior to performing the experiments: (1) gas
exchange is improved overall during PLV in the setting of unilateral
lung injury, (2) gas exchange is enhanced in the injured lung and
reduced in the healthy lung, and (3) pulmonary blood flow (Q) is
redistributed from the healthy to the injured lung during PLV in the
setting of unilateral lung injury.
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Materials and Methods
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Animal Preparation
A cohort of 14 adult healthy heartworm-free dogs weighing
20.8 ± 0.6 kg (mean ± SE) were anesthetized with a 25
mg/kg IV pentobarbital sodium injection. A midline neck incision and a
tracheotomy were performed. A 35F double-lumen Carlens endotracheal
tube (Rusch; Duluth, GA) was placed. After intubation, mechanical
ventilation was performed with a fraction of inspired oxygen
(FIO2) of 1.0, a tidal volume of 15
mL/kg (right lung, 8 mL/kg; left lung, 7 mL/kg), and positive
end-expiratory pressure of 5 cm H2O using a
double-piston ventilator (model 818; Harvard Apparatus; South Natick,
MA). The PaCO2 was maintained between
34 mm Hg and 46 mm Hg by adjusting the respiratory rate. Anesthesia was
maintained by intermittent bolus injections of pentobarbital sodium,
130 mg, when tachycardia and hypertension were observed. Pancuronium
bromide, 0.1 mg/kg, was administered every hour to maintain paralysis.
After induction of anesthesia, a 7F pulmonary arterial catheter was
advanced through the external jugular vein to measure pulmonary
arterial pressures, for administration of medications, and for mixed
venous blood gas measurements. An arterial line was placed in the
carotid artery to measure arterial pressure and for arterial blood gas
assessment. After placement of catheters, a left thoracotomy was
performed. Both left and right pulmonary arteries were isolated, and 6
mm and 12 mm in diameter flow probes (Transonic Systems; Ithaca, NY)
were placed around the left and right pulmonary arteries, respectively.
The right pulmonary flow (Q of the uninjured right lung
[Q-uninjured]) and the left pulmonary flow (Q of the injured left
lung [Q-injured]) were recorded. Cardiac output (Qt) was calculated
as the sum of right and left pulmonary flows. The left mainstem
bronchus was isolated, and the tip of the double-lumen endotracheal
tube was advanced into the left mainstem bronchus by manual palpation.
The tip was secured in position by tying an umbilical tape externally
around the bronchus and endotracheal tube tip. The left lung was
inflated to make sure that the left upper bronchus was not obstructed
by the tube. The left thoracotomy was then closed with a chest tube
placed to 10 cm H2O of suction.
Thirty minutes following closure of the thoracotomy, the baseline data
indicated below were recorded. Heparin, 1,500 U, was administered
systemically along with 200 mL of lactated Ringer’s solution.
Unilateral lung injury was induced by administration of oleic acid,
0.08 mL/kg, into the left pulmonary artery, while the right pulmonary
artery was clamped via temporary reopening of the anterolateral
thoracotomy incision. Prior to administration, oleic acid, 0.08 mL/kg,
was diluted with 20 mL of blood and 500 U of heparin and then injected
slowly with continuous shaking of the syringe via the proximal port of
the pulmonary artery catheter over 10 min. The right pulmonary artery
was maintained clamped for 2 min after completion of the oleic acid
administration. The left thoracotomy was then closed as a thoracostomy
tube was placed. Lactated Ringer’s solution was infused at a constant
rate of 100 mL/h via the proximal port of the pulmonary artery catheter
throughout the study period.
Experimental Design
Following data collection at the point of lung injury, the
animals were divided into two groups. In the first group (n = 7), gas
ventilation (GV) was performed for 2 h. In the second group
(n = 7), PLV was performed in both the right and left lungs for
2 h. The 2-h time period was chosen to follow a 90-min period of
lung injury development since, in our experience, it is adequate to
evaluate a stable effect of ventilation strategy in the acute oleic
acid lung injury model.
GV was performed using a Harvard double-piston ventilator with each
limb of the double-lumen tube connected to one of the pistons. The
ventilator was set as described above throughout the experiment. PLV
was performed by introducing perflubron (LiquiVent; Alliance
Pharmaceutical Corporation; San Diego, CA) via both the right and left
endotracheal tubes during temporary endotracheal tube disconnect.
Perflubron was administered until a meniscus was observed in the both
endotracheal tubes at the anterior chest level. The total volume of
perflubron administered was 439 ± 9 mL (250 ± 9 mL in the right
lung and 188 ± 6 mL in the left lung) initially
(mean ± SEM). PLV with gas ventilation was then performed in
similar fashion to the GV-treated animals. Additional perflubron was
administrated every hour to maintain a similar liquid meniscus present.
PLV was performed in both lungs simultaneously in order to simulate the
clinical application of PLV in the setting of a unilateral lung injury.
Data were obtained at the following time points: baseline, 90 min
following administration of oleic acid (injury), and every hour for the
duration of the 2-h study (post 1 and post 2). At the conclusion of the
experiment, all animals were killed with an overdose of pentobarbital
sodium. Postmortem examination was performed on all dogs to confirm the
presence of unilateral lung injury. A lung specimen was obtained from
the anterior, middle, and dependent lung segments of both the right and
left lungs, and fixed with 10% formaldehyde for histologic analysis.
Outcome Measures
Spirometric measurements of individual lung oxygen consumption
(O2) were accomplished at each
data point by intermittently connecting a device (Fig 1
) to the distal tip (left injured lung) or side port lumen (right
uninjured lung) of the endotracheal tube. The device circuit and
spirometer were flushed with 100% oxygen, and the entire system was
pressurized by placing a 500-g weight on the top of the spirometer in
order to demonstrate that the system was leak free. The device was then
connected to one lumen of the endotracheal tube, and ventilation of
that lung was initiated using a bellows in a box connected to the
Harvard ventilator. A NaHCO3 scrubber was placed
in the circuit to remove expired carbon dioxide.
O2 was evaluated by
measurement of the volume loss from the spirometer in the closed
circuit. The average volume loss per minute was measured over a 5-min
period.
Individual lung carbon dioxide production
(CO2) was assessed by
collecting expired gas from each lung into a spirometer that allowed
assessment of minute ventilation volume. The average minute ventilation
volume was determined over a 2-min period. A capnometer (HP-47210A;
Hewlett Packard; Waltham, MA) was placed between the mixing chamber and
the spirometer and used to determine the mixed expiratory carbon
dioxide level. The capnometer was calibrated before each preparation.
CO2 for each lung was
calculated based on the following equation:
CO2 and
O2 were corrected to standard
temperature and pressure, dry and for the vapor pressure of perflubron
at 37°C.
At each data point, mean arterial pressure, mean pulmonary artery
pressure, individual peak inspiratory pressures, along with ventilator
rate and FIO2 were assessed with a
pressure monitor (HP-78901A; Hewlett-Packard). Right and left pulmonary
artery flow rates were recorded by the flow probes. Arterial and mixed
venous blood samples were analyzed by an ABL-520 blood gas analyzer and
OSM-3 Co-oximeter (Radiometer Copenhagen; Copenhagen, Denmark). Core
body temperature was recorded via the pulmonary artery catheter
thermistor. Intrapulmonary shunt (Qs/Qt) was calculated by the
following equation:
where Qps = physiologic shut;
CaO2 = oxygen content of arterial
blood; CvO2 = oxygen content of
mixed venous blood; and
CiO2 = oxygen content of the blood
draining from the ideal alveolus ventilated with gas
(FIO2 = 1.0) as derived from the
alveolar gas equation and the oxygen dissociation curve.
Data Analysis
The within-group effect of oleic acid administration was
compared between the data points of baseline and injury with paired
t tests. The effect of PLV in the setting of unilateral lung
injury was compared between the GV-treated and PLV-treated groups using
a two-way repeated analysis of variance across the post-1 and post-2
data points. Comparisons were considered to be significant when the p
values were < 0.05. Data are demonstrated as mean ± SEM.
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Results
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All dogs survived the duration of the experiment. Postmortem
examinations confirmed that the left lungs of all dogs demonstrated
external evidence of lung edema, hemorrhage, and dependent atelectasis,
while the right lungs appeared pink and well inflated. Representative
biopsy specimens from the upper right lung and upper left lung in the
GV-treated group are shown in Figure 2
. The right lung specimen shows mild interstitial pneumonitis with
neutrophils, and the left lung specimen shows much more severe injury
with focal parenchymal necrosis, interstitial and alveolar
infiltration, fibrin deposition, and focal hemorrhage.
Physiologic Data
Physiologic data are shown in Table 1
. Injured lung peak inspiratory pressure significantly increased after
oleic acid administration in both the GV-treated and PLV-treated
animals (p = 0.030 and p = 0.004, respectively). Mean pulmonary
pressure increased after oleic acid administration in both the GV group
and the PLV group, but not in a statistically significant fashion
(p = 0.111 and p = 0.294, respectively). Initiation of PLV did not
change heart rate, mean arterial pressure, or mean pulmonary arterial
pressure in the PLV group when compared to the GV group at the post-1
and post-2 data points.
Gas Exchange
PaCO2,
PaO2 and Qs/Qt data are demonstrated
in Figure 3
. After oleic acid administration, impaired gas exchange was reflected
as hypoxia and hypercarbia at the injury data point, while Qs/Qt was
not statistically significantly changed. Although the GV-treated
animals remained hypercarbic for the period of the experiment, their
oxygenation gradually improved. In contrast, over the same time period,
the oxygenation and Qs/Qt worsened in the PLV-treated group.
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Figure 3. Graphs of PaO2,
PaCO2, and Qs/Qt. *, p < 0.05 when the
baseline and injury data points are compared within the groups.
 , p < 0.05 when the post-1 and post-2 data points are compared
between the groups. Data are presented as mean ± SEM.
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Q
Qt, Q-uninjured, Q-injured, and proportion of left lung flow to
total flow (Q-injured/Qt) are demonstrated in Figure 4
. Qt significantly decreased after administration of oleic acid
(p = 0.003, GV group; p = 0.001, PLV group). After initiation of
PLV, Q-injured in the PLV group increased significantly when compared
to that in the GV group without any change in Q-uninjured
(p = 0.002). This was associated with an increase in Q-injured/Qt in
the PLV group when compared to the GV group (p = 0.002).
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Figure 4. Graphs of Qt, individual pulmonary artery flows,
and Q-injured/Qt. *, p < 0.05 when baseline and injury data
points are compared within the groups. , p < 0.05 when the post-1
and post-2 data points are compared between the groups. Data are
presented as mean ± SEM.
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O2 and
CO2
Gas exchange was also compared by evaluating changes in individual
lung gas exchange as demonstrated in Figure 5
. In both groups, O2 in the
injured left lung (O2-injured)
decreased and O2 in the
uninjured right lung
(O2-uninjured) increased
significantly after induction of lung injury. Subsequently,
O2-injured of the PLV group
significantly increased when compared to that of the GV group at the
post-1 and post-2 data points (p = 0.006). The proportion of
O2-injured to total
O2
(O2T) of both groups decreased
significantly after oleic acid administration (GV, p = 0.008; PLV,
p = 0.010). Following initiation of PLV,
O2-injured/O2T
of the PLV group significantly increased when compared to that of the
GV group at the post-1 and post-2 data points (p = 0.004).
Similar results were observed for
CO2 (Fig 6 ). CO2 in the injured left lung
(CO2-injured) and the
proportion of VCO2-injured to total
CO2
(CO2T) in both groups
decreased significantly after induction of lung injury (GV
VCO2-injured: GV, p = 0.014;
PLV, p = 0.050;
CO2-injured/CO2T:
GV, p = 0.008; PLV, p = 0.010). However
CO2-injured and
CO2-injured/CO2T
of the PLV-treated group significantly increased when compared to the
GV at the post-1 and post-2 data points
(CO2-injured, p = 0.026;
CO2-injured/CO2T,
p = 0.009).
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Discussion
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A number of studies1
2
3
4
5
have evaluated the ability of
PLV to provide gas exchange in normal animals and in the setting of
lung injury. Such studies have, however, evaluated the efficacy of PLV
in the setting of bilateral lung injury. A number of
studies6
7
8
9
10
have suggested that the ventilation/perfusion
matching during PLV is such that oxygenation is limited in the normal
lung. Thus, liquid ventilation might adversely affect gas exchange if
it were to be performed in the setting of unilateral lung injury. There
are no studies, of which we are aware, that have undertaken to evaluate
the physiologic effects of PLV in the setting of unilateral lung
injury. In this present study, unilateral lung injury was induced by
left pulmonary arterial injection of oleic acid, which has been
documented to increase pulmonary vascular permeability, and mimics the
effects of fat embolism.11
12
Gross lung autopsy and
biopsy data suggest that a severe unilateral lung injury was indeed
achieved. A dose of 0.08 mL/kg of oleic acid was administered to induce
left unilateral lung injury. This dose is approximately 0.4 that of the
normal oleic acid dose that is used in many lung injury
models, since the volume of the left lung is approximately 40% of the
total lung volume.13
14
Oleic acid induces an acute lung injury associated with an increase in
pulmonary vascular permeability and thrombosis with resulting acute
lung edema and elevated pulmonary vascular resistance
(PVR).12
14
We speculate that the increase in PVR
may have been the cause of the decrease in Q-injured/Qt. However, it is
also important to note that Qt also decreased, which may be due to an
effect of oleic acid on cardiac function.13
The decrease
in blood flow to the injured left lung may also have been secondary to
the development of hypoxic pulmonary vasoconstriction associated with
atelectasis or lung injury.16
It is likely that one or
both of these phenomena increased PVR and decreased Q-injured. After
initiation of PLV, both
O2-injured and
VCO2-injured increased in the
PLV-treated group, which confirmed our hypothesis. However, we were
surprised to note that the systemic
PaO2 decreased and the Qs/Qt
increased following initiation of PLV. During the period of PLV, Q was
redistributed from the uninjured lung to the injured lung. It appears
that either performance of PLV resulted in a reduction in gas exchange
in the right (uninjured) lung or that the redistribution of Q toward
the left (injured) lung resulted in a greater proportion of blood flow
through a lung with inefficient gas exchange. Either way, the overall
effect was a decrease in PaO2 and an
increase in Qs/Qt.
It is interesting to speculate on the etiology of the redistribution of
Q toward the injured left lung during PLV. One possible mechanism is
resolution of local hypoxia in the injured left lung during PLV with
reopening of vessels constricted due to regional hypoxia. Aly et
al15
measured PVR in oleic acid-injured piglets and
demonstrated a decrease in PVR presumably due to resolution of hypoxic
pulmonary vasoconstriction during PLV in an oleic acid lung injury
model. In contrast, PVR may increase in the normal lung since gas
transfer may deteriorate during PLV. In addition, an increase in PVR
may be affected due to a hydrodynamic effect of the heavy
perfluorocarbon in the lungs, since the volume of perfluorocarbon may
be increased in the well-inflated, healthy lung when compared to
the atelectatic, injured lung, resulting in a greater effect on PVR in
one lung vs the other.
Although the PaO2 decreased and the
Qs/Qt increased during the period of PLV in our model, PLV did not have
a substantial detrimental effect on oxygen delivery in the setting of
unilateral lung injury. In addition, it should be realized that there
may be advantages to performing PLV in the setting of unilateral lung
injury, especially with the potential ability of the liquid to lavage
and to evacuate exudate out of the airways and to recruit lung regions.
In addition, there is mounting evidence that perfluorocarbon may reduce
lung injury, decrease neutrophil infiltration, and modulate the
neutrophil and macrophage inflammatory response.17
18
19
20
It is possible that a reperfusion injury may have occurred in the right
lung due to clamping of the right pulmonary artery. However, the period
of pulmonary artery clamp application was short (10 min) and was not
accompanied by discontinuation of bronchial artery flow. In any event,
histology of the right lung only demonstrated mild pneumonitis that
could also have been associated with other factors, such as mechanical
ventilation for > 3.5 h.
We conclude from these data that in our model of acute unilateral lung
injury that PLV is associated with an increase in
O2 and
CO2 in the injured lung and a
redistribution of pulmonary arterial blood flow toward the injured
lung. This is associated with an overall decrease in
PaO2 and increase in Qs/Qt. PLV
should be applied cautiously, therefore, in the setting of unilateral
lung injury, although the advantages of its lung lavage and recruiting
capabilities may make its use in this setting worthwhile.
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Footnotes
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Abbreviations:
FIO2 = fraction of inspired oxygen;
PLV = partial liquid ventilation; GV = gas ventilation;
O2 = oxygen consumption;
o2-injured = O2
of the injured left lung; O2T = total
oxygen consumption; CO2 = carbon
dioxide production;
CO2-injured = CO2
of the injured left lung; CO2T = total
carbon dioxide production; PVR = pulmonary vascular resistance;
Q = pulmonary blood flow; Q-injured = pulmonary blood low of the
injured left lung; Q-uninjured = Q of the uninjured right lung;
Qt = cardiac output; Qs/Qt = intrapulmonary shunt
Supported by National Institutes of Health grant No. R29-HL57224 and
the Alliance Pharmaceutical Corporation.
Received for publication December 20, 2000.
Accepted for publication July 15, 2001.
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Abstract
Introduction
