Empirical Investigations

Validating Lung Models Using the ASL 5000 Breathing Simulator

Amanda Dexter, MS, RRT, CHSE; Objective: This study sought to validate pediatric models with normal and altered pulmonary
mechanics.
Neil McNinch, MS, RN; Methods: PubMed and CINAHL databases were searched for studies directly measuring
pulmonary mechanics of healthy infants and children, infants with severe bronchopulmonary
dysplasia and neuromuscular disease. The ASL 5000 was used to construct models using
Destiny Kaznoch;
tidal volume (VT), inspiratory time (TI), respiratory rate, resistance, compliance, and esoph-
ageal pressure gleaned from literature. Data were collected for a 1-minute period and re-
Teresa A. Volsko, MBA, MHHS, RRT, peated three times for each model. t tests compared modeled data with data abstracted
CMTE, FAARC from the literature. Repeated measures analyses evaluated model performance over mul-
tiple iterations. Statistical significance was established at a P value of less than 0.05.
Results: Maximum differences of means (experimental iteration mean clinical standard
mean) for TI and VT are the following: term infant without lung disease (TI = 0.09 s,
VT = 0.29 mL), severe bronchopulmonary dysplasia (TI = 0.08 s, VT = 0.17 mL), child with-
out lung disease (TI = 0.10 s, VT = 0.17 mL), and child with neuromuscular disease
(TI = 0.09 s, VT = 0.57 mL). One-sample testing demonstrated statistically significant differ-
ences between clinical controls and VT and TI values produced by the ASL 5000 for each
iteration and model (P < 0.01). The greatest magnitude of differences was negligible (VT <
1.6%, TI = 18%) and not clinically relevant.
Conclusions: Inconsistencies occurred with the models constructed on the ASL 5000. It
was deemed accurate for the study purposes. It is therefore essential to test models and
evaluate magnitude of differences before use.
(Sim Healthcare 13:117–123, 2018)

Key Words: Pediatric, infant, pulmonary mechanics, bronchopulmonary dysplasia, neuromus-

cular disease, simulation, physiologic modeling.

L aboratory evaluations are often used to examine ventilator

performance because simulated models of the respiratory system
carry no risk of harm and are less cumbersome to work with than
using humans or animals to evaluate medical devices.1–3 Unlike
human subjects, whose disease condition may worsen or im-
prove over short or long periods, the pulmonary characteristics
of models do not vary. Therefore, during ventilator performance
evaluations, any differences in the observed measurements are
presumed to be related only to ventilator performance and not
secondary to changes in the load imposed on the mechanical
ventilator during its interaction with the patient.
From the Respiratory Care Program (A.D.), Rush University, Chicago, IL; Department of
Kinesiology (A.D.), University of North Carolina at Charlotte, Charlotte, NC; Rebecca D
Considine Research Institute (N.M.), Akron Children's Hospital, Akron; Kent State
University (D.K.), Kent; and Nursing Administration (T.A.V.), Akron Children's Hospital,
Akron, OH.
Reprints: Teresa A. Volsko, MBA, MHHS, RRT, CMTE, FAARC, Department of
Nursing Administration, Akron Children's Hospital, Akron, OH 44308 (e‐mail:
tvolsko@akronchildrens.org).
A.D. was formerly employed as a clinical educator for Ingmar Medical, the manufacturer
of the ASL. This work was a component of her graduate thesis work at Rush University
and completed in May of 2013, before her employment at Ingmar. The manuscript, based
on this work, commenced after A.D. left Ingmar Medical for a position in academia. Ingmar
Medical did not have a role in this study or in her graduate work. The work was completed at
Akron Children's Hospital under the mentorship of T.A.V., who does not have a relationship
with Ingmar Medical. D.K.'s involvement was sponsored by the Summer Pediatric Research
Student Program (SPRS), at Akron Children's Hospital. T.A.V. served as the SPRS mentor
but received no compensation for the role. N.M. discloses no conflicts of interest.
Presented at the American Association for Respiratory Care (AARC) International
Congress, November 17, 2013, Anaheim, CA.
Copyright © 2018 Society for Simulation in Healthcare
DOI: 10.1097/SIH.0000000000000277
The ASL 5000 lung simulator (IngMar Medical, Pittsburgh,
PA) has been used to evaluate ventilator performance and
demonstrate differences in operational characteristics.4 This
simulator uses a computer-driven piston to displace vol-
ume. The piston is controlled by the equation of motion,
which enables the user to input values for airways resistance
and pulmonary compliance to construct either a single- or
double-compartment lung model (Fig. 1). The ASL 5000 can
simulate passive, or no respiratory effort, and active breathing.
The latter is accomplished by modeling the muscle pressure
(PMUS) waveform in addition to setting the resistance and com-
pliance for the model.
A dearth of information exists in the literature using
simulation to construct and validate pediatric models based
on actual pulmonary mechanics in health and with pulmonary
pathophysiology. Different disease states impose varying con-
ditions of load, which can affect the manner in which respiratory
equipment operates or interacts with the patient. Conditions that
increase load include (1) increased airways resistance, (2) de-
creased compliance, (3) increased respiratory rate (RR), and
(4) abnormalities in chest wall compliance. There is a need
to construct and validate infant and pediatric normal and dis-
ease state models to identify whether changes in ventilator per-
formance and/or patient-ventilator interaction will occur under
varying pulmonary conditions.
The purpose of this study was to construct and validate
four neonatal and pediatric models. We hypothesized that
the ASL 5000 will validate a simulated model for a term infant
without lung disease, infant with severe bronchopulmonary

Vol. 13, Number 2, April 2018 117

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FIGURE 1. Equation of motion. PTR(t) is the change in transrespiratory pressure, or difference between the airway opening pressure
and body surface pressure as a function of time (t).This pressure is measured relative to end-expiratory airway pressure and is the pres-
sure generated by a ventilator during an assisted breath. PMUS(t) is ventilatory muscle pressure, or the difference as a function of time (t);
the theoretical chest wall transmural pressure difference that would produce movements identical to those produced by the ventilatory
muscles during breathing maneuvers (positive during inspiratory effort, negative during expiratory effort. R and C are the resistance
and compliance of the respiratory system.

dysplasia (BPD), child without lung disease and child with
neuromuscular disease.
METHODS
The ASL 5000 was used to construct and validate the pulmo-
nary mechanics and spontaneous effort models for a term in-
fant and child with normal lung function (healthy controls)
and two disease states: infant with severe BPD and child with
neuromuscular disease (Table 1). This study was independently
conducted, without affiliations with the manufacturer of the
ASL 5000. Although there are models available on the Ingmar
Medical Web site for use with their lung simulator, the models
created and validated in this study predated those currently
available with the manufacturer.
PubMed and CINAHL databases were used to perform a
literature search of human trials in which pulmonary mechan-
ics were measured in infants and children without lung pathol-
ogy, infants with severe bronchopulmonary dysplasia, and
pediatric patients with neuromuscular disease and respiratory
compromise. Key words used in the search included the
following: human, English language, age of neonate to
18 years, simulation, biological models, respiratory mechanics,
bronchopulmonary dysplasia, neuromuscular, mechanical
ventilation, medical education, respiratory insufficiency, and
airways resistance. The search returned a total of 186 results,
of which 15 were relevant to the populations of interest and
purposes of this study. There were two references specifically
for the controls (term infant and child without lung disease),
two directly related to bronchopulmonary dysplasia, and one

TABLE 1. A Description of the 4 Lung Models Tested, and the Type of Load Each Respective Model Would Impose During a Respiratory Device Evaluation
Model Description Load

Term infant without lung disease
Infant with severe BPD
Child without lung disease
Child with neuromuscular disease
A baby born anytime between weeks 39 and 40 with
no health-related risks.
Chronic lung disease in infants, which is a common
cause of respiratory insufficiency and ventilator
dependence in children born prematurely.
An infant 12 mo old with no health-related risks.
Impairment of the central or the peripheral nervous system,
which may require mechanical ventilatory assistance.
No load
Decreased compliance and increased pulmonary resistance
increase the infant's work of breathing.
No load
A highly compliant chest wall is unable to endure the
negative pressures generated during inspiration and
may collapse inward causing inconsistent or asynchronous
motion of the rib cage and abdomen, causing an increased
work of breathing.

118 Validating Lung Models Simulation in Healthcare

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TABLE 2. The Physical Characteristics of Normal and Disease State Models Based on
Demographic and Anthropometric Measures Reported in the Literature
Model Model Description Age Weigh, kg
Term infant without lung disease 5–7
Normal Newborn 3.8
Infant with severe BPD7–9 Disease state 2 wk 3.8
Child without lung disease5–7 Normal 12 mo 10.0
Child with neuromuscular disease7,10 Disease state 12 mo 9.0
for neuromuscular disease. The remainder supported all models
and/or study concepts. Characteristics of the respiratory system
were gleaned from the literature and used to create each of the
simulated models. These published reports provided a direct
measurement of lung compliance and pulmonary conduc-
tance, inspiratory and expiratory flows, esophageal pressure,
and functional residual capacity, which were used to construct
the models. The age and weight characteristics of each simu-
lated lung model were obtained from the Centers for Disease
Control (CDC). For the term infant and child without lung
disease models, weights for males and females were obtained
using the CDC growth chart at 50% of the growth curve.
The CDC growth chart was also used for the infant with severe
BPD and child with neuromuscular disease models; however,
weights for the disease state models were obtained at 25% of
the growth curve, which correlated with anthropometric mea-
sures reported in the literature. Table 2 specifies the age and
weight characteristics of each model. Table 3 outlines the tidal
volume (VT), inspiratory time (TI), RR, airways resistance, and
pulmonary compliance gleaned from patient characteristics
reported in published clinical trials and used to construct each
model. Muscle pressure is not typically measured in humans
but was a necessary component to the script, because it was
used to produce the desired VT for each of the models. Esoph-
ageal pressure provided the initial starting point for PMUS, after
which adjustments to PMUS were made as needed to produce
active breathing at the target VT for each model. The charac-
teristics for each model were entered into the ASL 5000 simu-
lation editor using a single-compartment lung model. Figure 2
illustrates the compartment settings used for the child with
neuromuscular disease model. The breath configurations for
each of the models of interest were manually scripted or indi-
vidually programmed. Active breathing was simulated by
adjusting PMUS on the ASL 5000 to produce the target VT of
7 mL/kg. The term infant and child without lung disease
served as the healthy control models, which did not impose
extra load during ventilatory assistance.5–7,11,12 Infant with se-
vere BPD7–9,12–16 and child with neuromuscular disease7,10,12,17,18
were the two experimental (disease state) models that imposed
a load on respiratory equipment. The control and experimen-
tal models were individually scripted and tested (Table 4). The
increase % and release % settings were adjusted to sculpt the
breath with the intention of achieving a sinusoidal breath pattern
and an TI, which met the specifications of the desired targets
for each of the models. Before initiating the study protocol,
the calibration procedure for the simulator was performed in
accordance with manufacture recommendations.
Before collecting data, each model ran for a 2-minute pe-
riod to allow for piston stabilization. Data were then collected
for a 1-minute period. This procedure was repeated three
times for each model. Although the ASL 5000 provided several
data output values, the variables of interest for this validation
study were VT and TI. Data from the ASL 5000 were reviewed
in the postrun analysis section of the software. Using the util-
ities option, data were exported to Excel (Microsoft, Red-
mond, CA) for management and SAS (Version 9.3; SAS
Institute Inc, Cary, NC) for analysis.
Statistical Analysis
The primary outcomes of interest (VT, TI) obtained from
the ASL 5000 were compared with data abstracted from the lit-
erature by a one-sample t test. Follow-up testing was performed
using Wilcoxon signed rank test to account for departures from
normality, with similar findings noted. For repeated measures
of primary variables of interest, the Friedman test with post
hoc multiple pairwise comparisons was used to assess for dif-
ferences between each of the experimental iterations, for each
model. Statistical significance was established at a P value of
less than 0.05, unless otherwise noted.
Post hoc assessment of clinical relevance, as it relates to sta-
tistical significance, was completed once all results were available.
RESULTS
One-sample testing revealed evidence of statistically significant
differences between published characteristics or the clinical
standard used in this study and values produced by the ASL
5000 (VT and TI) for each iteration and model (P < 0.01 for
all). The maximum differences of means (experimental itera-
tion mean − clinical standard mean) are the following: term
infant without lung disease (TI = 0.09 s, VT = 0.29 mL), infant
with severe BPD (TI = 0.08 s, VT = 0.17 mL), child without
lung disease (TI = 0.10 s, VT = 0.17 mL), and child with neu-
romuscular disease (TI = 0.09 s, VT = 0.57 mL). The maxi-
mum difference of means in VT noted for all models was less
than 1.6% of the scripted values. The maximum difference

TABLE 3. Characteristics of the Respiratory System Gleaned From the Literature and Used to Create Each of the Simulated Models for the Validation Study
RR Mean (Range) Inspiratory Resistance, Expiratory Resistance, Compliance, Mean Esophageal Pressure,
Model (Patient Weight in kg) VT, mL Breaths per Minute TI, s Mean (Range), cmH2O/L/s Mean (Range), cmH2O/L/s (Range), mL/cmH2O Mean (Range), cmH2O

Term infant without lung 26.6 50 (40–60) 0.5 52 (44–94) 70 (45–149) 7.5 (4–11) 7 (6–9)
disease (3.8 kg)5–7,11,12
Infant with severe 23.4 60 (60–80) 0.4 69 (44–94) 87 (80–140) 1.8 (0.88–3) 11.5 (10–12)
BPD (3.8 kg)7–9,12–16
Child without lung 70.0 25 (22–28) 0.8 46 (29–63) 46 (29–63) 15.0 (12–17) 7 (6–9)
disease (10 kg)5–7,11,12
Child with neuromuscular 37.8 25 (22–28) 0.8 46 (29–63) 46 (29–63) 14.5 (12–17) 7 (6–9)
disease (9 kg)7,10,12,17,18

Vol. 13, Number 2, April 2018 © 2018 Society for Simulation in Healthcare 119
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FIGURE 2. An illustration of setting the resistance and compliance for the single-compartment lung model representing a child with neu-
romuscular disease. Rin and Rout represent airways resistance during inspiration and expiration, respectively. C represents pulmonary
compliance.

of means in TI ranges was 18% for all models. Table 5 provides
the summary statistics by model and iteration.
The Friedman test results provided strong evidence of an
overall difference in VT and TI for the infant with severe BPD
model (P < 0.01 for both) and evidence of an overall difference
in TI for the child with neuromuscular disease model (P = 0.03).
There were no statistically significant differences in the term
infant without lung disease or child without lung disease
models for TI and VT (P = 0.3, 0.1, 0.9, and 0.7, respectively).
Table 6 provides results of Friedman test along with Tukey
multiple pairwise comparisons for each of the models. Post
hoc analysis of Friedman test with multiple pairwise compar-
isons using Tukey adjusted α demonstrated statistically signif-
icant differences for VT between the first and second iterations
(difference of medians = 0.01 mL), as well as the first and third
iterations (difference of medians = 0.02 mL) in the infant with
severe BPD model. Inspiratory time was significantly different,
in the infant with severe BPD model, between the first and
third iterations (difference of medians = 0.01 s) as well as between
the second and third iterations (difference in medians < 0.01 s).
In the child with neuromuscular disease model, TI was signif-
icantly different between the first and third iterations as well as
between the second and third iterations (difference in me-
dians < 0.01 s for both).
DISCUSSION
Simulation studies are often used to examine device perfor-
mance using models of the respiratory system19 because they
carry no risk of harm and, compared with using humans or
animals, are less cumbersome to work with. However, if the
simulated model is unable to consistently replicate the model
characteristics, it is difficult to distinguish whether the differ-
ences in the variables of interest were due to inconsistencies
in the model or differences in the operational characteristics
of the devices evaluated. This study used the ASL 5000 lung
simulator. The precision with which this simulator can pro-
duce consistent results is dependent on the lack of variation
with which the piston moves within the casing. This variation
is most likely to occur between experimental iterations.20 There-
fore, time or the number of repeated iterations of each model was
an important factor to consider when validating a simulated
model. Repeating each script more than once enabled the re-
searchers to determine whether the ASL 5000 was able to pro-
duce consistent breath characteristics over repeated iterations.
Once the model was scripted, simulator calibration and a
stabilization period were the essential steps performed before
collecting our data. Although the ASL 5000 was calibrated be-
fore use and a stabilization period was provided, there exists
the potential for variation in piston movement, which can af-
fect results. A 2-minute stabilization period was used to pre-
vent any initial disruption in piston motion, which may
occur as the script was initializing, from contaminating data
collection. The 2-minute period was chosen from our previous
experience modeling disease states and using pediatric models
to evaluate respiratory equipment.19–22
The ASL 500 has a 500-Hz sampling rate. Based on this
sampling rate and our previous experience with device evalua-
tion using simulated models, a 1-minute data collection period
was considered sufficient to obtain respiratory breath data.19–22
With respect to this study, the inconsistencies or variation in VT

TABLE 4. A Script of the Pulmonary Characteristics of Each Model Used in the Validation Study
Inspiratory Expiratory
Pmax, Resistance, Mean, Resistance, Mean, Compliance, Mean, Spontaneous Rate, Uncompensated
Model (Weight in kg) Increase %* Release %* cmH2O cmH2O/L/s cmH2O/L/s mL/cmH2O Breaths per Minute Residual Capacity, mL

Term infant without lung 42 42 9.8 52 70 7.5 50 50

disease (3.8 kg)
Infant with severe BPD (3.8 kg) 41 41 16.5 69 87 1.8 60 50
Child without lung 25 25 9.0 46 46 15.0 25 177
disease (10 kg)
Child with neuromuscular 25 25 5.0 46 46 14.5 25 207
disease (9 kg)
*“Increase %” and “release %” settings were adjusted to sculpt the breath and obtain a sinusoidal breath pattern. The settings reported were those used to produce an TI that most closely
resembled the TI reported in the literature, for each of the models.

120 Validating Lung Models Simulation in Healthcare

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TABLE 5. Summary Statistics by Model and Iteration, With One-Sample t Test Results
Iteration Variable n Mean SD Median Min Max Test Location One-Sample t Test, P

Term infant without lung disease

1 I time, s 53 0.59 0.02 0.59 0.58 0.72 0.50 <0.01
Insp VT, mL 53 26.88 2.81 26.48 26.42 46.88 26.60 <0.01
2 I time, s 55 0.59 0.02 0.59 0.58 0.72 0.50 <0.01
Insp VT, mL 55 26.86 2.75 26.46 26.43 46.88 26.60 <0.01
3 I time, s 51 0.59 0.02 0.59 0.58 0.72 0.50 <0.01
Insp VT, mL 51 26.89 2.87 26.46 26.41 46.93 26.60 <0.01
Infant with severe BPD
1 I time, s 60 0.48 0.01 0.48 0.47 0.49 0.40 <0.01
Insp VT, mL 60 23.23 0.02 23.22 23.21 23.28 23.40 <0.01
2 I time, s 60 0.48 0.01 0.48 0.47 0.49 0.40 <0.01
Insp VT, mL 60 23.24 0.02 23.23 23.21 23.28 23.40 <0.01
3 I time, s 60 0.48 0.01 0.48 0.47 0.50 0.40 <0.01
Insp VT, mL 60 23.25 0.01 23.24 23.22 23.28 23.40 <0.01
Child without lung disease
1 I time, s 25 0.90 0.01 0.90 0.89 0.91 0.80 <0.01
Insp VT, mL 25 69.83 0.07 69.81 69.77 70.14 70.00 <0.01
2 I time, s 25 0.90 0.01 0.90 0.89 0.92 0.80 <0.01
Insp VT, mL 25 69.83 0.06 69.82 69.77 70.11 70.00 <0.01
3 I time, s 25 0.90 0.01 0.90 0.89 0.92 0.80 <0.01
Insp VT, mL 25 69.83 0.07 69.83 69.75 70.14 70.00 <0.01
Child with neuromuscular disease
1 I time, s 25 0.89 0.01 0.89 0.88 0.90 0.80 <0.01
Insp VT, mL 25 38.37 0.04 38.36 38.31 38.51 37.80 <0.01
2 I time, s 25 0.89 0.01 0.88 0.88 0.90 0.80 <0.01
Insp VT, mL 25 38.38 0.04 38.37 38.34 38.52 37.80 <0.01
3 I time, s 25 0.89 0.01 0.88 0.88 0.90 0.80 <0.01
Insp VT, mL 25 38.37 0.04 38.36 38.32 38.53 37.80 <0.01

and TI between iterations were manifested in small changes analysis by traditional repeated measures analysis of variance,
(10ths–100ths of mL and seconds, respectively). Variation was necessitating the Friedman test approach. This minimal varia-
minimal enough between experimental iterations to prevent tion provides evidence of simulator precision over time.

TABLE 6. Results of Friedman Test With Tukey Multiple Pairwise Comparisons

Term infant without lung disease
Insp VT, mL P = 0.0839 I time, s P = 0.343
Iteration compared Difference 95% CI Iteration compared Difference 95% CI
3–2 0.010 −1.293 to 1.313 3–2 0.000 −0.009 to 0.009
3–1 0.032 −1.259 to 1.324 3–1 0.002 −0.007 to 0.011
2–1 0.022 −1.257 to 1.301 2–1 0.001 −0.008 to 0.010
Infant with severe BPD
Insp VT, mL P = 0.0001 I time, s P = 0.0011
Iteration compared Difference 95% CI Iteration compared Difference 95% CI
3–2 0.006 −0.002 to 0.014 3–2 0.003 0.000 to 0.006 *
3–1 0.014 0.007 to 0.022 * 3–1 0.005 0.002 to 0.008 *
2–1 0.008 0.001 to 0.016 * 2–1 0.002 −0.001 to 0.005
Child without lung disease
Insp VT, mL P = 0.6882 I time, s P = 0.8739
Iteration compared Difference 95% CI Iteration compared Difference 95% CI
3–2 0.000 −4.981 to 4.981 3–2 0.000 −4.981 to 4.981
3–1 0.000 −4.981 to 4.981 3–1 0.000 −4.981 to 4.981
2–1 0.000 −4.981 to 4.981 2–1 0.000 −4.981 to 4.981
Child with neuromuscular disease
Insp VT, mL P = 0.5273 I time, s P = 0.0227
Iteration compared Difference 95% CI Iteration compared Difference 95% CI
3–2 0.001 −0.027 0.028 3–2 0.005 0.000 to 0.010 *
3–1 0.007 −0.020 0.034 3–1 0.006 0.001 to 0.011 *
2–1 0.007 −0.020 0.034 2–1 0.001 −0.004 to 0.005
*Significant.

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 Statistically significant differences were found between ASL
5000 values and published or target values for VT and TI. In
evaluating those differences, it was essential to consider their
relevance to the outcome of our work. The greatest magnitude
of differences between published values and the values obtained
from the ASL 5000 were negligible. Maximum difference in VT
was less than 1.6%, which equates to 0.6 mL. Similarly, the
maximum difference in TI was 18% or less than 0.1 second.
During normal breathing, variations in VT and TI do occur,
and because the variations we observed between published
values were so small, the researchers assessed these differences
as not clinically relevant.
Although statistically significant, the magnitude of dif-
ferences and standard deviations found in VT and TI between
the iterations for each model were very small, relative to the
scripted values obtained from the literature. Our post hoc de-
termination of clinically irrelevant differences was supported
in the literature reviews used to construct the models we
sought to validate.
These differences or inconsistencies were smaller than those
that naturally occur with breathing in human subjects. Small
variations between iterations were less than variations in VT
breaths that occur in human subjects without lung disease.6
Limitations of the Simulated Models
The propensity for great variations in VT in infants and
children with lung disease and respiratory muscle weakness
depends on the severity of lung disease and the amount of
muscle wasting and respiratory muscle dysfunction, respec-
tively.23 We did not account for this variability in our child
with neuromuscular disease model because of the specific in-
tent with which we will use the model. This is, however, a lim-
itation of our model and perhaps its use. There are situations
where it would be essential to account for and script the previ-
ously mentioned variations in a simulated model. Those vari-
ations in respiratory muscle function would be important to
incorporate in a model if the model were used to evaluate a
specific interaction between a simulated subject and a device.
An example of this would be constructing a simulated model
(n of 1) to determine ventilator settings, which would enhance
synchrony for a neuromuscular patient transitioning from a
ventilator in the intensive care unit to a portable ventilator
for home use. A simulated model of the patient, used to
determine the settings for ventilator parameters to enhance
patient-ventilator synchrony, would replace the need for a
“trial-and-error” method of adjusting these settings while the
patient is receiving mechanical ventilation. In an n of 1 study,
where the clinician may want to model the characteristics of a
patient to determine ventilator settings that would improve
synchrony or evaluate the effect certain ventilator changes
will have on lung distension, it is crucial to use a double-
compartment lung model. In our clinical practice, we routinely
use the ASL at the bedside to evaluate sensitivity and positive
end expiratory pressure (PEEP) settings before transitioning
a technology dependent patient a ventilator used in an inten-
sive care unit to a portable home ventilator. For this use, it is
standard to use a double-compartment lung model.
Because a single-lung compartment was used for each of our
models, their utility may be limited. A single-compartment lung
122 Validating Lung Models
Copyright © 2018 by the Society for Simulation in Healthcare. Unauthorized reproduction of this article is prohibited.
model does not account for differences in heterogeneity in re-
spiratory mechanics, which occurs with disease states. There-
fore, our models may not accurately reflect the heterogeneity
in respiratory mechanics, which may be an important consider-
ation, such as in the previously mentioned n of 1 construct.
CONCLUSIONS
Because inconsistencies can occur with simulated models, it is
essential to evaluate magnitude of differences between the de-
sired and measured variable(s) of interest before use. In our
study, the magnitude of variation within and between itera-
tions for each model was minimal with clinically irrelevant sig-
nificant effects noted in the disease state models. The ASL 5000
lung simulator was demonstrated to be an effective way of val-
idating these neonatal and pediatric respiratory models.
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