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Departments of 1 Medicine and of 2 Physiology and Biophysics, University of Washington, Seattle, Washington 98195-6522
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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To explore mechanisms of hypoxemia after acute pulmonary embolism, we measured regional pulmonary blood flow and alveolar ventilation before and after embolization with 780-µm beads in five anesthetized, mechanically ventilated pigs. Regional ventilation and perfusion were determined in ~2.0-cm3 lung volumes by using 1-µm-diameter aerosolized and 15-µm-diameter injected fluorescent microspheres. Hypoxemia after embolization resulted from increased perfusion to regions with low ventilation-to-perfusion ratios. Embolization caused an increase in perfusion heterogeneity and a fall in the correlation between ventilation and perfusion. Correlation between regional ventilation pre- and postembolization was greater than correlation between regional perfusion pre- and postembolization. The majority of regional ventilation-to-perfusion ratio heterogeneity was attributable to changes in regional perfusion. Regional perfusion redistribution without compensatory changes in regional ventilation is responsible for hypoxemia after pulmonary vascular embolization in pigs.
pulmonary embolism; ventilation-perfusion mismatch; pigs; gas exchange; aerosol; fluorescent microspheres
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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PULMONARY EMBOLISM occurs in an estimated 500,000 people per year in the US (24), and many of these patients develop
clinically significant hypoxemia. The exact mechanism by which this
hypoxemia occurs remains in dispute. Potential mechanisms of hypoxemia
in pulmonary embolism include regions of low ventilation-to-perfusion ratio
(
A/
)
(2, 20), right-to-left shunting of deoxygenated blood (1, 23),
diffusion limitation at the alveolar-capillary interface due to
regional decreases in capillary transit time (25), and decreased mixed
venous oxygen tension secondary to decreased cardiac output (14, 15).
Although studies of pulmonary embolism in humans with use of the
multiple inert-gas-elimination technique (MIGET) have
demonstrated the dominant role of
A/
heterogeneity in the genesis of arterial hypox-emia (10, 20), the
mechanisms by which this
A/
heterogeneity and, in particular,
low-A/
regions develop remain unknown. Regions of low
A/
may develop from redistribution of perfusion to areas of low
ventilation or from decreased regional ventilation in areas of
preserved perfusion. Redistribution of ventilation after vascular
embolization has been variably reported as nonexistent to significant
by using a variety of methods and models (2, 13, 17, 20).
Robertson and co-workers (18) recently introduced a method for
determining regional ventilation by using aerosolized 1-µm fluorescent microspheres. By combining this technique with
simultaneously injected 15-µm fluorescent microspheres (6),
measurements of regional
A/
matching can be obtained. To better understand the determinants of
hypoxemia after acute pulmonary vascular embolization, we
simultaneously administered aerosolized and intravenous microspheres before and after vascular embolization with 780-µm polystyrene beads.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Animal preparation. The experiments were approved by the Animal Care Committee at the University of Washington. Five juvenile pigs, of either gender and weighing 12-18 kg, were studied. Anesthesia was induced with ketamine (20 mg/kg) and xylazine (2 mg) injected intramuscularly. In the first animal, anesthesia was maintained with a continuous infusion of a 2:1 mixture of ketamine and valium. In all subsequent animals, anesthesia was maintained with a continuous infusion of thiopental sodium at 160-200 mg/h as needed to inhibit inspiratory efforts. The animals were mechanically ventilated via tracheostomy with a tidal volume of 10-15 ml/kg and a respiratory rate adequate to maintain an arterial carbon dioxide tension (PaCO2) of 30-35 Torr. Tidal volumes and respiratory rates, once set, were kept constant throughout the study. One carotid and one femoral artery and one external jugular and both femoral veins were cannulated. A pulmonary artery catheter was inserted through the remaining jugular vein, and the animal was placed in the prone posture. A 30-ml/kg bolus of 0.9% saline was given at the beginning of the study to maintain hemodynamic stability after vascular embolization. After a stable minute ventilation was achieved, an intravenous infusion of a standard solution of six inert gases (sulfur hexafluoride, ethane, cyclopropane, halothane, diethyl ether, and acetone) was allowed to equilibrate for a minimum of 30 min.
Study protocol. Figure 1 is the timeline for the experimental protocol. Before data collections or interventions, each animal was hyperinflated to twice the tidal volume to minimize atelectasis. Baseline values for temperature, mean arterial pressure, pulmonary artery pressure, and peak airway pressure were recorded, along with an average of three thermodilution cardiac output measurements. Tidal volume was measured with a Wright spirometer and averaged over 10 breaths. The respiratory exchange ratio was calculated with the inspired and expired fractions of O2 and CO2 measured by mass spectrometry (MGA1100, Perkin-Elmer, Norwalk, CT). Arterial and mixed venous blood and mixed expired gas were collected for MIGET analysis and blood-gas determination. Aerosolized 1-µm microspheres were delivered over a 10-min period as described by Robertson et al. (18). Simultaneously, 15-µm microspheres were intravenously injected in multiple, small, evenly spaced increments over the duration of aerosol delivery. Full data collection, including administration of a second pair of aerosolized and injected microspheres, was repeated after 30 min to assess temporal variation in ventilation and perfusion distributions.
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Lung preparation and data collection. A sternotomy was performed, the main pulmonary artery and left atrium were cannulated, and the aorta was ligated. The pulmonary vasculature was flushed with a dextran solution by gravity feed, and the lungs and trachea were dissected from the chest cavity and dried inflated at 25-cmH2O pressure.
The dried lungs were fixed in a rapid setting foam, sliced, mapped, and diced into cubes of 1.5-2.0-cm3 volume, yielding 551-851 pieces/animal (7). Each piece was weighed, visually scored for airway and blood content, and soaked for 2 days in 1.5 ml of 2-ethoxyethyl acetate to extract the fluorescent dyes. The fluorescent signals for the six colors were measured in each piece with a fluorimeter (LS50B, Perkin-Elmer). In three of five animals, one kidney was removed and ~20% (by weight) was dissolved with 4 M KOH. Each kidney sample was filtered through a 10-µm-pore filter, the filter paper was soaked in 2-ethoxyethyl acetate, and the fluorescent signal was measured to determine whether systemic shunting of fluorescent microspheres occurred. Inert gas concentrations in arterial and mixed venous blood and exhaled gas were measured on a gas chromatograph (model 3300, Varian, Palo Alto, CA) by using previously described techniques (8).Data analysis and statistics. All values are presented as means ± SD. Paired t-tests are used for statistical comparisons among hemodynamic and gas exchange, with P < 0.05 considered a significant difference.
Between 41 and 161 pieces per animal were excluded from analysis because of airway content
25%. Background fluorescence for the six
colors was subtracted from each piece, and remaining fluorescent signals were converted to millimeters per minute by using measured values for cardiac output and minute ventilation. Up to eight pieces
per animal were excluded from each data set because of an isolated
ventilation signal greater than three times any other ventilation or
blood flow signal. These rare, unexplained signals were confined almost
exclusively to the orange color and mirror the findings of Robertson et
al. (18).
Temporal variability was evaluated by calculating the Pearson
correlation coefficient (
) between time
1 and time 2 (preembolism) for regional perfusion
([1:2])
and for regional ventilation ([1:2]).
The effect of vascular embolization on regional perfusion and
ventilation distribution was evaluated by calculating between
pre- and postembolization times for perfusion
([2:3]) and for ventilation
([2:3]).
Confidence intervals were calculated for each correlation by using the
bootstrap technique (3). Briefly, a data set for one animal consists of
n number of pieces with measurements
of perfusion and ventilation at times
1, 2, and
3. Because regional perfusion is
spatially correlated and therefore dependent on neighboring regional
perfusion (5), each piece was grouped with the 30 closest pieces,
yielding n clusters. A new data set
was then generated by sampling the clustered set
n/30 times, with replacement allowing some clusters to be sampled more than once and some not to be sampled
at all. A new set of correlations for perfusion and ventilation between
times 1 and
2 and between times
2 and 3 were
calculated. This was repeated 2,000 times, generating distributions for
[1:2], [2:3],
[1:2],
and
[2:3]
from which 95% confidence intervals were calculated. If the 95%
confidence intervals for [1:2]
and
[2:3]
(or for
[1:2]
and
[2:3])
did not overlap, a significant effect of embolization was identified.
The effect of embolization on regional perfusion and ventilation
heterogeneity was quantified by ANOVA. The total variability of
regional perfusion and ventilation within each animal across the entire
experiment may be partitioned into components that are determined by
structure, effect of vascular embolization, and temporal and error
variation. By structure, we mean an average flow of inhaled gas or
blood for a piece (designated by i and ranging from 1 to the number of pieces in a given animal,
n) across all experimental
conditions and replications. Thus structure defines those influences
that remain constant over time and experimental condition. In the case
of blood flow, this is thought to be due to flow resistance in the
branching vascular structure (7). For ventilation, this would include
influences from airway resistance and local parenchymal compliance
differences. The embolization and time/error effects may be thought of
as adding or subtracting flow from the structural component. The
embolization effect is designated by
j, with values of 1 or 2 for pre- or
postembolization condition. The time/error effect is estimated with
repeated measurements designated by k
within an experimental condition.
The variance component due to changes in measured ventilation from time
and method error (
) is
estimated by
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(1) |
i,j,k
is the ventilation to piece i, with
condition j, during replication
k; and
is the mean ventilation to piece i
across replications within condition
j. Because repeat measurements were
not made after embolization, only data from condition
j = 1 are used in estimating
. The variance component
due to changes in ventilation with embolization 
is estimated by
|
(2) |
is
the mean ventilation to piece i across
all replications and experimental conditions. Because there are two
measurements preembolization and only one after embolization, the
numerator is weighted by Wj, which has a
value of two for the preemboli condition
(j = 1) and a value of one for
the postemboli condition (j = 2). The variance component due to changes in ventilation across
pulmonary structure (
) is
estimated by
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(3) |
is the mean ventilation
to all pieces across all replications and experimental conditions.
The contribution of each component to the total variance in ventilation
can be calculated as a percentage to aid in comparison across animals.
The same analysis is repeated for perfusion in each animal.
To evaluate whether regional
A/
is determined by changes in regional perfusion or ventilation after
vascular embolization, each piece was plotted with the log ratio of
perfusion or ventilation postembolization to preembolization on the
abscissa and
log A/ postembolization on the ordinate.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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In four of five animals, measurements were obtained twice before embolization and once after embolization. The first animal had only one successful measurement preembolization due to a malfunction of the aerosol generator that prevented adequate microsphere delivery.
No significant differences were seen in the measured physiological parameters between the two preembolization periods. After embolization, PaO2 decreased by an average of 44.1 ± 3.6 Torr, PaCO2 increased by 9.8 ± 0.3 Torr, A-aDO2 increased by 32.4 ± 3.7 Torr, and mean pulmonary pressure increased by 17.1 ± 6.2 (SE) mmHg. Cardiac output and mean arterial pressure were not significantly changed by embolization.
No regions of intrapulmonary shunt (ventilation = 0 with perfusion >0) were detected by the microsphere method. Extrapulmonary shunt, estimated from the presence of fluorescent microspheres in the kidneys, was not detected in the three animals examined. The average shunt measured by MIGET was 1.5% of the cardiac output and did not change significantly after embolization.
A/
heterogeneity increased and mean perfusion-weighted
A/
decreased after embolization as measured by both MIGET and microsphere
data. After embolization, the coefficient of variation for regional
perfusion increased from a mean of 0.57 to 0.84. In contrast, the
coefficient of variation for regional ventilation was not significantly
different. Correlation of regional ventilation and perfusion decreased
from a mean of 0.89 preembolization to 0.67 after embolization
(Table 1).
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Correlations for regional ventilation and perfusion (Fig.
2) are shown in Table
2. Both
[1:2]
and
[1:2]
were <1 due to temporal variability and method error. After
embolization, regional perfusion was redistributed as shown by
nonoverlapping confidence intervals between
[1:2]
and
[2:3]
for all animals. A consistently smaller difference existed between
[1:2] and
[2:3]
with 95% confidence intervals overlapping in three of four animals
(Fig. 3). This suggests possible
redistribution of regional ventilation after embolization, albeit to a
much lesser degree than regional perfusion redistribution.
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The percent variances from pulmonary structure, embolization, and error/time for regional perfusion and ventilation in each animal are shown in Table 3. Redistribution after embolization was responsible for an average of 30.6% of the total variance in perfusion over the entire experiment. In contrast, the average percent variance in ventilation from embolization was 11.0% of the total variance. The percent variances of both regional perfusion and ventilation measurements due to temporal variability and method error were similar at 5.0 and 4.9%, respectively. ANOVA could not be calculated in the first animal because only one preembolization measurement of regional ventilation and perfusion was obtained. However, the correlation between pre- and postembolization regional ventilation for all pieces was 0.95 compared with 0.78 for regional perfusion. This supports ANOVA results from the other four animals showing a much greater redistribution of regional perfusion than regional ventilation after embolization.
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To evaluate effects of perfusion redistribution on gas exchange
abnormalities, the postembolization log
A/
was plotted against the ratio of perfusion postembolization to
preembolization (Fig. 4). The average
coefficient of determination
(2) for the five experiments
was 0.77. The same analysis using ventilation post- and preembolization
gave an average 2 of 0.07 (Table 4).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The important finding from this study is that hypoxemia after acute
pulmonary embolism can be explained by new,
low-A/ regions resulting from redistribution of regional perfusion without adequate compensatory changes in regional ventilation.
Hypoxemia from pulmonary embolization must be due to
A/
heterogeneity, shunt, or diffusion limitation. Decreased mixed venous
O2 content due to reduced cardiac
output may also contribute to hypoxemia. In this study, inert bead
microembolization in anesthetized, mechanically ventilated pigs caused
significant gas-exchange abnormalities due to increased
A/
mismatch. Shunt did not increase after embolization; however, these
animals were mechanically ventilated with fixed tidal volumes and
hyperinflated before any measurements to minimize atelectasis. In a
spontaneously breathing animal, shunt may occur after embolization if
pulmonary perfusion redistributed to regions of atelectasis.
A/
heterogeneity after pulmonary embolization may result from
redistribution of regional perfusion alone or from poorly matched
regional ventilation and perfusion redistribution. Our high-spatial-resolution measurements show significant redistribution of
regional perfusion after embolization that correlates poorly with
baseline regional perfusion. In contrast, regional ventilation postembolization remains highly correlated with baseline values, indicating minimal redistribution. ANOVA analysis quantifies the contribution of regional perfusion redistribution to overall
postembolization perfusion heterogeneity to be ~31%. In contrast,
ANOVA analysis indicates that regional ventilation remains much more
dependent on innate structural determinants after embolization.
Wilson and Beck (26) described
A/
heterogeneity as a sum of the individual heterogeneities of perfusion
and ventilation minus a component due to their correlation. Our study
demonstrates that, in normal lungs,
A/
matching is preserved despite significant heterogeneity in both
regional perfusion and ventilation by the close correlation between
ventilation and perfusion. After vascular embolization, increased
A/
heterogeneity was associated with both an increase in regional
perfusion heterogeneity and a fall in correlation between ventilation
and perfusion.
We estimate that regional perfusion and ventilation redistribution
accounts for 77 and 7% of
A/
heterogeneity postembolization, respectively. This is derived from
logarithmic plots of
A/ as a function of perfusion or ventilation. This analysis can
potentially force a correlation between
log A/
and
log 3/2
because the independent and dependent variables are coupled by
the common presence of
3 (12, 16). The
same should be true of
log A/ and
log 3/2,
yet little correlation is present. Another way to
evaluate the dependence of postembolization
A/
heterogeneity is to examine a plot of ventilation vs. perfusion (Fig.
5), wherein a line drawn through any
given point and the origin has a slope equal to the
A/
at that point. Each point can by classified by its relative change in
ventilation or perfusion, and the relationship between this change and
the postembolization
A/
can be evaluated. Figure 5A
demonstrates that pieces with 20% increase in perfusion after
embolization have a low
A/,
pieces with 20% decrease in perfusion have a high
A/,
and pieces with <20% change in perfusion have a
A/
near one. In contrast, Figure
5B shows the majority of pieces to
have <20% change in ventilation after embolization, and those pieces
that changed by 20% appear not to predict
A/.
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Changes in regional ventilation after clinical pulmonary embolism may
exceed those seen in our experimental model. Redistribution of
ventilation after pulmonary artery occlusion has been attributed to
alveolar hypocapnia (11, 21, 22). In these studies, occlusion of a main
pulmonary artery and, in one study, flushing of the common dead space
with 100% O2 resulted in
significant alveolar hypocapnia. In our study, high dead space from the
ventilator circuit and small size of the regions embolized may have
prevented adequate alveolar hypocapnia from developing because of
reinspiration of dead space gas. In a spontaneously breathing person,
atelectasis due to splinting on the affected side or alteration in
surfactant production (4) would cause
low-A/
areas and/or shunt if any perfusion persisted. Biologically
active mediators released by a thrombus may cause bronchoconstriction
and a greater degree of regional ventilation redistribution than seen
with inert emboli. In a spontaneously breathing human, the normal
response to pulmonary embolism is hyperventilation, demonstrated by
decreased arterial CO2 tension.
This causes a rightward shift in the
A/
distribution minimizing
low-A/
areas and hypoxemia. However,
A/
heterogeneity, demonstrated by an increased
A-aDO2,
is still present, as a manifestation of mechanical redistribution of
regional perfusion.
The results of this study emphasize the importance of the determinants of regional ventilation and perfusion as well as the degree of correlation between the two in determining gas exchange. These findings also suggest that inadequate compensatory changes in regional ventilation after perfusion redistribution may play an important role in hypoxemia seen with clinical diseases such as pulmonary embolism. Determinants of basal regional ventilation may play a more significant role in determining gas exchange than local ventilatory regulation. Given the degree of regional ventilation heterogeneity observed recently (9, 18, 19), further research into the determinants of ventilation distribution along with mechanisms that match regional ventilation and perfusion is warranted.
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ACKNOWLEDGEMENTS |
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The authors thank Dowon An, Dr. Susan Bernard, and Pam Campbell for technical assistance.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: W. A. Altemeier, Div. of Pulmonary and Critical Care Medicine, BB-1253 Health Sciences Bldg., Box 356522, Seattle, WA 98195-6522 (E-mail: billa{at}u.washington.edu).
Received 17 March 1998; accepted in final form 26 August 1998.
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REFERENCES |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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A. J. Gerbino, S. McKinney, and R. W. Glenny Correlation between ventilation and perfusion determines VA/Q heterogeneity in endotoxemia J Appl Physiol, June 1, 2000; 88(6): 1933 - 1942. [Abstract] [Full Text] [PDF]
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W. A. Altemeier, S. McKinney, and R. W. Glenny Fractal nature of regional ventilation distribution J Appl Physiol, May 1, 2000; 88(5): 1551 - 1557. [Abstract] [Full Text] [PDF]
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J. Y. C. Tsang, D. Frazer, and M. P. Hlastala Ventilation heterogeneity does not change following pulmonary microembolism J Appl Physiol, February 1, 2000; 88(2): 705 - 712. [Abstract] [Full Text] [PDF]
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W. A. Altemeier, H. T. Robertson, and R. W. Glenny Pulmonary gas-exchange analysis by using simultaneous deposition of aerosolized and injected microspheres J Appl Physiol, December 1, 1998; 85(6): 2344 - 2351. [Abstract] [Full Text] [PDF]
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, pieces in which perfusion
increased 
, pieces in which perfusion
decreased 
, pieces in which perfusion
changed <20%. Note that pieces with increased perfusion have a low