TestChest® is a real-time teaching and training tool for mechanical ventilation management. It supports any kind of artificial respiration in anesthesia, intensive care, emergency medicine and home care. This booklet describes the physical representation of the physiological models built into TestChest®. The information provided herein is intended for clinicians who wish to exploit the full capabilities of TestChest®.

1. 1
TestChest® Physiological Model
presented by the neosim Academy

2. 2
neosim academy
c/o neosim AG
Susenbühlstrasse 12
CH-7000 Chur
Switzerland
www.neosim.ch
Written by Josef X. Brunner, PhD, Chur, c/o neosim AG, Susenbühlstrasse 12, CH-
7000 Chur, Switzerland
Reviewed by A. Timothy Chen, PhD, Hong Kong c/o Trinity Trading Company Ltd,
Unit A, 13/F, Goodwill Industrial Bldg. No. 36-44, Pak Tin Par Street, Tsuen Wan,
New Territories Hong Kong
This work is subject to copyright. All rights are reserved, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction and storage in data banks.
Product liability: The publisher can give no guarantee for information about drug
dosage and application thereof contained in this book. In every individual case, the
respective user must check accuracy.
TestChest® is patented technology (EP 2 715 706 B1) and a Registered Trademark of
Organis GmbH, Landquart, Switzerland.
ISBN 978-3-9524884-0-9
Year of publication: 2017, Rev. 1.0
Printed in PRC

3. 3
“TestChest is very impressive in terms of physiological reality,
especially spontaneous breathing”.
Dr. Lise Piquilloud, PD & MER, Médecin associée CHUV Lausanne,
Switzerland, moderator at the 3 day simulation training session held with
TestChest® during the ESICM congress 2017 in Vienna, Austria.

4. 4
Contents
INTRODUCTION............................................................................................................5
OVERVIEW .....................................................................................................................7
LUNG MECHANICS......................................................................................................9
SPONTANEOUS ACTIVITY......................................................................................13
GAS EXCHANGE........................................................................................................15
METABOLISM .............................................................................................................18
HAEMODYNAMICS ....................................................................................................19
LIST OF PARAMETERS............................................................................................21
LIST OF VARIABLES .................................................................................................24
GLOSSARY...................................................................................................................25
LITERATURE................................................................................................................27

5. 5
INTRODUCTION
TestChest® is a real-time teaching and training tool for mechanical
ventilation management. It supports any kind of artificial respiration in
anesthesia, intensive care, emergency medicine and home care.
This booklet describes the physical representation of the physiological
models built into TestChest®. The information provided herein is intended for
clinicians who wish to exploit the full capabilities of TestChest® and is not
intended to be a textbook of physiology. In order to make the physiological
models of TestChest® feasible, some simplifications were necessary. These
are explained in the text.
As a unit of pressure, mbar is used. Note: mbar = hPa.
TestChest® simulates the human cardio-respiratory system for teaching and
training purposes. It can be used either as stand-alone skills training station
or integrated in a complete human body simulator. For more information
please consult www.neosim.ch
TestChest® implements the respiratory mechanics, spontaneous breathing
plus the following features:
• remote controllable lung mechanics (resistance, compliance,
spontaneous activity level, leakage)
• programmable FRC and non-linear (sigmoid) compliance curve

6. 6
• spontaneous breathing by providing pre-determined changes of
respiratory rate and respiratory activity
• interaction with haemodynamics and thus allows to test closed-loop
controlled ventilators by providing SpO2, and Pulse Pressure Variation
POPv in response to the ventilator setting

7. 7
OVERVIEW
TestChest® is a fully interactive, physical lung model with two access
points: airways and peripheral circulation (artificial finger). The airways
provide the opportunity for both, therapy and diagnosis while the artificial
finger provides the result of the therapy: oxygen saturation and
hemodynamic stability. TestChest® is loaded with a set of parameters to
define a certain patient and then acts completely independent and in
interaction with the environment such as a ventilator, an anesthesia machine
or even an ambu-bag. This principle is illustrated in Figure 1.
Figure 1: TestChest® is set-up by the operator/trainer with a set of parameters to
simulate a certain patient case and then reacts completely autonomous to respiratory
interventions at the airways, for example mechanical ventilation, CPAP, etc.

8. 8
Patient parameters and output variables of the physiological model
An overview of the basic physiological model is given in Figure 2, lung
mechanics are provided in Figure 3, and 4 and the relationship between lung
collapse and venous admixture is given in Figure 7.
Figure 2: Lung/heart model. Details of lung mechanics are given in Figure 3,
description of each parameter and output variable is given in text.
Parameters are, for example, compliance and resistance – variables are, for
example, airway flow and pressures. A list of parameters and variables are
provided further down below.

9. 9
LUNG MECHANICS
Lung mechanics are usually described as multi-compartment models with
mechanical elements like springs and dash-pots (friction) or with electrical
elements like resistors and capacitors. Independent of these descriptive
elements, lung mechanics is always described in lumped parameter models
and never in its anatomical complexity. The equation of motion describes the
interdependence of the variables (pressure, flow, volume) and the impact of
the parameters compliance and resistance as shown in Figure 3.
Figure 3: Elements constituting the equation of motion; “const” is an arbitrary value

10. 10
Compliance is measured in volume per pressure and can be constant or
sigmoid. Lung compliance CL and chest wall compliance CW are arranged in
series and together form the respiratory compliance Crs.
1/Crs = 1/ CW + 1/ CL
Resistance Raw is pressure drop per unit of flow, is never constant but often
assumed to be constant. Pleural pressure is pressure in the pleural cavity.
Although varibale along the gravitational axis, only one pressure is usually
taken to represent a “mean” pleural pressure.
Figure 4: Pressure-volume curve for static conditions; explanations see text
The lungs can have pressure-equilibrium at different volumes, depending on
the muscle tension, lung elasticity, fluid status, etc. Figure 4 shows the

11. 11
pressure-volume curve with the equilibrium position at 2000ml (zero PEEP
i.e. FRC@0PEEP, open airways, no muscle tension, zero airway pressure).
This FRC@0PEEP, also called minimal FRC (FRCmin) is a parameter in
TestChest® . Lung collapse is modelled by setting FRCmin lower than FRC
predicted (FRCpred).
Figure 4 shows the ideal-typical sigmoid pressure-volume curve starting with
VLee equal to FRC at zero PEEP. Compliance is the slope at each point of the
pressure-volume curve and as follows:
Crs : compliance of the respiratory system, between lower and upper
inflection point
C1: compliance below the lower inflection point
C3: compliance above the upper inflection point
LIP: lower inflection point, first point of maximal curvature on the pressure
volume curve
UIP: upper inflection point, second point of maximal curvature on the
pressure volume curve
Pthreshold: recruitment threshold
Pcollapse: collapse threshold
RClh: time constant of lung-heart interaction
RCrecol: time constant of lung recruitment and collapse

12. 12
FRC@0 PEEP: The volume at zero pressure (meaning at atmospheric
pressure) is called Functional Residual Capacity FRC. Since mechanically
ventilated patients may have an elevated lung volume by virtue of ventilator
pressures, the end-expiratory Lung Volume (VLee) is also used. Calculation of
VLee is done as follows in TestChest® : The end-expiratory lung volume VLee
follows a decrease of measured VL immediately (simulation of immediate
collapse), yet takes some time to follow an increase in lung volume with the
time constant of about 3 seconds.
Lung collapse: in supine position, a small part of the lungs will temporarily
collapse. Consequently, lung volume will be reduced. Usually, an inherent
vascular reflex will close those collapsed areas and re-distribute blood to
well perfused areas (hypoxic vasoconstriction). In absence of this reflex, the
collapse lung areas will still be perfused but that blood will not be
oxygenated.
Lung collapse and recruitment: collapsed lung can sometimes be recruited
by increasing the pressure above a certain threshold. In Figure 4, this
threshold is called Pthreshold. If the pressure in the TestChest® bellows
(alveolar pressure) rises above that threshold, the apparent compliance of
the lung increases to Cr (Compliance of recruitment) and the lung volume
expands. If alveolar pressure is lower than Pcollapse, then lung volume is
reduced at the rate determined by the RCcollapse.

13. 13
SPONTANEOUS
ACTIVITY
Intercostal and diaphragmatic muscle tissue contribute to effective
ventilation. The movement is quite complex and can depend on many
factors, including exercise, stress, disease, filling level of the bladder, etc. To
simplify matters, however, usually one single representative muscle is used
as depicted in Figure 3.
Respiratory muscle activity is sometimes measured in patients by the
occlusion pressure P0.1. For this reason, TestChest® allows to enter P0.1. The
user can adjust spontaneous activity by entering the respiratory activity P0.1
and the respiratory rate f. The TestChest® then applies a muscular pressure
Pmusc during a brief inspiratory effort of about 0.5 seconds and then is passive
again.
Respiratory activity can also be described over the entire respiratory cycle as
a waveform, not just as the onset of inspiration as described above with the
P0.1 approach. TestChest® takes such waveforms and allows thus to control
both, inspiratory and expiratory activity. The files containing the muscular
pressures is a text file with two columns and exactly 599 lines with two
values per line separated by semicolons. The first line contains the keyword
<ID> and the name of the breath. The following lines contain the amplitude
of pressure in micro bar (mbar*1000). Examples are given in Figure 5.

14. 14
Figure 5: Three sets of muscular presure Pmusc as delivered by TestChest® .
NOTE: appart from inspiratory effort, other parameters also need to be set in
order to realistically simulate spontaneous breathing. Table 1 shows
examples.
Table 1: Breathing activity examples.
Parameters Passive Weak
activity
Normal
activity
Strong
activity
CW [ml/mbar] 120 120 120 100
V’CO2 [mlSTPD] 150 200 250 350
P0.1 [mbar/100ms] 0 2 4 8
f [/min] 0 5 12 15

15. 15
GAS EXCHANGE
Respiratory gas exchange takes place by diffusion at the alveolo-capillary
boundary (see Figure 6). Before such exchange can occur, however, fresh
gas needs to be transported down the tracheo-bronchial tree, passing the
anatomical dead space Vd. This dead space can be set on the TestChest®
and defines alveolar ventilation V’A together with the tidal volume Vt and the
rate f as applied to the TestChest® . The formulas are given in Figure 6.
The concepts of the Riley three compartment model and “ideal alveolar gas
composition” are modified as follows to TestChest® : one part of the lung
(the “ideal” part) consist of the bellows and exchanges gas with the blood.
The ideal alveolar oxygen partial pressure is actually measured with a sensor
(PAO2). TestChest® allows to introduce a diffusion barrier Pdiff in the ideal
compartment. The measured PO2 is modified by this diffusion limitation Pdiff
as shown in Figure 6. For example, if Pdiff is 100 then there is no diffusion
impairment. If Pdiff is larger than 100, then diffusion is limited and ideal
alveolar oxygen partial pressure (PO2eff) is reduced. Finally, PO2eff is converted
to oxygen saturation in the blood by the standard formula of Severinghaus
Sc = 1/(23400/(PO2eff
3
+ 150 * PO2eff) + 1))*100
*Severinghaus, J. W. Simple, accurate equations for human blood O2
dissociation computations. J Appl Physiol. 46(3): 599-602. 1979.

16. 16
Figure 6: Alveolar gas exchange, explanations see text.
The second part of the lung, the one that does not exchange gas, is virtual
and calculated as the difference between the measured end-expiratory lung
volume (VLee)and the predicted lung volume (FRCpred). The former is the
result of the therapy, the latter is an the entry to TestChest® . The quotient
of the two values is assumed to be venous admixture. This way, TestChest®
models the effect of lung collapse (and missing hypoxic vasoconstriction) on
venous admixture (Qs/Qt) by a linear relationship (see Figure below). For
example, TestChest® will increase Qs/Qt if the current lung volume (VLee,
see Figure 7) falls below this predicted FRC. This allows to control the level
at which lung collapse is associated with an increase in venous admixture.

17. 17
Figure 7: relationship between lung collapse (assumed to be proportional to actual
lung volume at end of expiration, VLee , divided by predicted FRC, FRCpred) and venous
admixture.

18. 18
METABOLISM
Metabolism is modeled by introducing pure CO2 into the bellows of
TestChest® . The rate at which CO2 is introduced (V’CO2)can be controlled by
the user.
NOTE: due to the fact that the mass-flow of CO2 is controlled, end-tidal CO2
can rise above physiological values if alveolar ventilation is not adquate.
Eventhough oxygen uptake is not modelled, the influx of CO2 dilutes the
fraction of oxygen and so simulates oxygen uptake.
Consequently, expiratory volume is larger than inspiratory volume, albeit only
marginally, still measurable.
NOTE: respiratory quotient is assumed to be 1, thus
V’O2 = V’CO2

19. 19
HAEMODYNAMICS
In patients, haemodynamic stability can be affected by many factors.
TestChest® implements some heart-lung interaction as they might occur, for
example, in hypovolemia.
NOTE: the simulation of haemodynamic instability is done on a simple
lumped parameter model and only for the purpose of simulating the
phenomenon.
The basic principle is taken from the observation that intrathoracic
pressurevariations can have an influence on pulse pressure. If pulse
pressure (amplitude of the arterial blood pressure waveform) changes in the
rhythm of respiration, it may indicate hemodynamic instability. In the case of
TestChest® , the pulse-oximeter plethysmogram amplitude variation (POPv)
is used in-lieu of pulse pressure variation to show heart-lung interaction and
is calculated as follows:
Intrathoracic pressure effecting the heart and venous return is taken to be
the pleural pressure Ppl which is calculated in real-time as follows, where k is
an arbitrary constant:
Ppl(t) = VL(t)/CW +Pmusc(t) + k
This pressure is further low-pass filtered by RClh yielding Pcardio and Pcardio is
finally used to modulate the amplitude of the pulse-oximeter plethysmogram.

20. 20
The degree of POPv is not constant but made dependent on the actual Pcardio
at three different levels of Pcardio. The levels allow for a masking of the effect
at lower pressures.
Table 2 illustrates possible modeling of levels of hemodynamic stability: no
instability, Moderate instability , Severe instability . Each level of
hemodynamic instability is modeled by a specific relationship between Pcardio
and POPv .
Table 2 : Link between and POPv and Pcardio at 3 levels of hemodynamic instability.
No instability Moderate instability Severe instability
Pcardio POPv Pcardio POPv Pcardio POPv
10mbar 0% 10mbar 10% 10mbar 10%
20mbar 0% 20mbar 60% 20mbar 90%
30mbar 0% 30mbar 80% 30mbar 90%
IMPORTANT: Please note that hemodynamic instability will occur only, if the
pleural pressure is actually high. For this to occur, high airway pressures, low
respiratory efforts and a low chest wall compliance are prerequisites.

21. 21
LIST OF
PARAMETERS
TestChest® is governed by the parameters described above which can be
selected by the operator. The output (flow, volume, etc.) is dependent on
these parameters and the therapy applied by the trainee.
Table 3: Set of parameters that govern TestChest® . Upload of the parameters to
TestChest® can be done by any terminal program.
Abbreviation Unit Range Category
CW ml/mbar 1 ... 200 Lung mechanics
V’CO2 mlSTPD 0 ... 500 Circulation
P0.1 mbar/100ms 0 ... 15 Respiratory muscle
Crs ml/mbar 8 ... 120 Lung mechanics
Raw mbar/(L/s) Rp5,Rp20,Rp50,Rp200 Lung mechanics
f spont /min 0 ... 100 Respiratory muscle
FRCmin ml 100 ... 4000 Lung mechanics
LowerInflection UIP mbar 0 ... 95 Lung mechanics
UpperInflection LIP mbar 5 ... 100 Lung mechanics
C1 ml/mbar 1 ... 150 Lung mechanics
C3 ml/mbar 1 ... 150 Lung mechanics
Pthreshold mbar -30 ... +120 Recruitment
Pcollapse mbar -30 ... +120 Recruitment
RClh s 0.1 … 10.0 Heart-lung interact.

22. 22
Abbreviation (cont) Unit Range Category
RCrecol s 0.1 … 100.0 Recruitment
FRCpred ml 100 ... 4000 Recruitment
Tdelay s 0.1 … 10.0 Heart-Lung interact.
Vdaw ml 175,190,205 Gas exchange
Cr ml/mbar 1 ... 150 Recruitment
RCcollapse s 0.1 ... 100.0 Recruitment
Pdiff -- 1 ... 1000 Gas exchange
QT ml/min 500 ... 10000 Circulation
POPv@Pcardio=10mbar % 0 … 100 Heart-Lung interact.
POPv@Pcardio=20mbar % 0 … 100 Heart-Lung interact.
POPv@Pcardio=30mbar % 0 … 100 Heart-Lung interact.
Leak level arbitrary none, small, medium,
large
Technical
HeartRate /min 20 … 300 Circulation
Note: Pcardio is a TestChest® variable that represents pressure affecting the heart.
Pcardio is proportional to Ppl but filtered by the time constant RClh .
Any given combination of the parameters in Table 3 defines a patient, and
consequently the results of appropriate or inappropriate therapy, particularly
ventilator settings. No operator interaction is needed once the parameters
are set. The results are automatic. Of course, all parameters can be changed
to effect a sudden event, for example bronchoconstriction, with the software
provided. Examples of patient cases are given in the following Table 4.

23. 23
Table 4 : Patient examples provided by Organis.
ParameterunitsID
Normal
stable
Normal
unstable
Obese
stable
Obese
unstableARDSstable
ARDS
unstable
COPD
stable
CWml/hPa0120608060806080
V’CO2mlSTPD1150150200200280280200
P0.1hPa/100ms20000008
Crsml/hPa360604040303030
RawhPa/(L/s)@1L/s4Rp5Rp5Rp5Rp5Rp5Rp5Rp50
f(spont)/min512121212353523
FRCminml62100210012001200100010002700
LowerInflectionhPa788151515156
UpperInflectionhPa840404040303040
C1ml/hPa942422121101060
C3ml/hPa1042422121101010
PthresholdhPa1125253535353550
PcollapsehPa12003535202050
RClhs130.510.50.51.50.51
Rcrecols1410101010606010
FRCpredml152500250025002500250025002500
Tdelays16110.80.80.80.81
Vdawarbitrary17mediummediummediummediummediumlargelarge
Crml/hPa1820204343303010
RCcollapses1910101010606010
PdiffmmHg20200200200200300300100
QTml/min214000300035003500600030004000
POPv@Pcardio=10hPa%225505505505
POPv@Pcardio=20hPa%231050105010505
POPv@Pcardio=30hPa%241550155015505
Leaklevelarbitrary25nonenonenonenonenonenonenone
HeartRate/min2670807885809577

24. 24
LIST OF
VARIABLES
TestChest® provides all internally used variables for data collection and
display. Table 5 shows those variables.
Table 5: Curves available for download at 50 samples per second
Index Variable Range
Arg0 Flow[ml/s] 0 ... 3000
Arg1 VL[ml] 0 ... 2500
Arg2 Palv[mbar] -30 ... 120
Arg3 Paw[mbar] -30 ... 120
Arg4 x[cm] -100 ... 100
Arg5 Ppl[mbar] -30 ... 120
Arg6 Pcardio[mbar] -30 ... 120
Arg 7 FO2[fraction] 0 ... 1
Arg 8 PB[mbar] 800 ... 1100
Arg 9 Temp[C] 0 … 50
Arg 10 VLee [ml] 0 ... 2500
Arg 11 Qs/Qt 0 ... .99
Arg 12 PO2ee[Torr] 0 ... 1100
Arg 13 PO2eff[Torr] 0 ... 1100
Arg 14 Sc[%] 0 ... 99.9
Pulse oximeter saturation and pulse-oximeter plethysmogram are further
output variables of the model, available at the serial output.

25. 25
GLOSSARY
ARDS acute respiratory distress syndrome
C1 compliance below LIP, ml/mbar
C3 compliance above UIP, ml/mbar
Ca the oxygen content of the arterial blood
Cc the oxygen content of the capillary blood
CL lung part of Crs, ml/mbar
COPD Chronic Obstructive Pulmonary Disease
Cr determines how much recruitment can be done, ml/mbar
Crs total respiratory compliance, ml/mbar
CPAP Continuous Positive Airway Pressure, mbar
Cv the oxygen content of mixed venous blood
Cw chest wall part of Crs, ml/mbar
FRC functional residual capacity, ml
FRCpred predicted FRC for a healthy lung of a certain patient size, ml
LIP lower inflection point, mbar
Paw pressure at the airway opening, mbar
PB barometric pressure in mbar
Pcardio low-pass filtered pleural pressure, mbar
Pcollapse collapse threshold pressure, mbar
Pdiff diffusion limitation factor
PEEP Positive End-Expiratory Pressure, mbar
PL Transpulmonary pressure, mbar
PR Pressure drop across airway resistance, mbar
Pmusc muscular activity, mbar
PO2 partial pressure of O2 inside the bellows, kPa
PO2eff effective partial pressure of oxygen, kPa
POPv Pulse-Oximeter Plethysmogram variation
Ppl pleural pressure, mbar
Pthreshold recruitment threshold pressure, mbar

26. 26
PW Pressure drop across chest wall, mbar
QS the ml/min of blood not exchanging gas with the lung
Qt the total blood flow in ml/min
Raw airways resistance, mbar/(L/s)
RCrecol the time constant of recruitment
RCcollapse the time constant of lung collapse
RClh the time constant of the lung-heart transfer function or the time
constant with which the pleural pressure impacts the blood pressure
SaO2 oxygen saturation in the arterial blood
ScO2 oxygen saturation in the alveolar capillaries
SvO2 oxygen saturation in the venous blood
UIP upper inflection point, mbar
V’CO2 CO2 production, ml/min STPD
VdS, Vdaw dead space, ml
VL lung volume, ml
VLee End-expiratory lung volume,ml

27. 27
LITERATURE
Yee J, Fuenning C, George R, Hejal R, Haines N, Dunn D, Gothard MD, Ahmed RA: Mechanical
Ventilation Boot Camp: A Simulation-Based Pilot Study. Critical Care Research and Practice,
2016, Article ID 4670672, http://dx.doi.org/10.1155/2016/4670672
Hare A, Simonds A: Simulation-based education for non-invasive ventilation. Breathe 2013, 9/5
367-371 DOI: 10.1183/20734735.006413
Tuttle RP, Cohen MH, Augustine AJ, Novotny DF, Delgado E, Dongilli TA, Lutz JW, DeVita MA:
Utilizing Simulation Technology for Competency Skills Assessment and a Comparison of
Traditional Methods of Training to Simulation-Based Training. Respir Care 2007;52(3):263–270
P.Dieckmann: Using Simulations for Education, Training and Research. Papst Science
Publishers, 2009, Lengerich, Germany, ISBN 978-3-89967-539-9
West JB: Bioengineering Aspects of the Lung: Lung Biology in Health and Disease Volume 3.
Executive Editor: Claude Lenfant 1977 Marcel Dekker Inc, New York ISBN-0-8247-6378-5
Dickinson CJ: A Computer Model of Human Respiration. MTP Lancaster 1977. ISBN 0-85200-
173-8
Winkler T: Ventilationsmechanik und Gasaustausch. Dresden: w.e.b.-Univ.-Verl.2000. ISBN 3-
033592-85-2

28. 28
neosim is authorized TestChest® distributor in Europe
neosim AG Susenbühlstrasse 12 CH-7000 Chur Switzerland
www.neosim.ch