Proceedings of the 7th IFAC Symposium on

Modelling and Control in Biomedical Systems

Aalborg, Denmark, August 12-14, 2009

A Mathematical Physiological Model of the

Pulmonary Capillary Perfusion
Mads Lause Mogensen, Kristoffer Lindegaard Steimle,
Dan Stieper Karbing and Steen Andreassen

Department of Health Science and Technology, Aalborg University,

Denmark

Abstract: This study presents a stratified model that simulates the pulmonary capillary blood
flow under influence of different lung volumes. The model includes capillary geometry, capillary
wall elasticity, pressure exerted by the heart, blood viscosity, the effect of the chest wall and
hydrostatic effects of the lung tissue and of the blood. The model simulates highly pulsatile
blood flow with a heterogenous flow distribution down the lungs, in agreement with previous
experimental studies. Moreover the model is in agreement with experimentally measured total
capillary flow, total capillary volume, total capillary surface area and transition time of red
blood cells passing through the pulmonary capillary network. The presented model is the first
to describe the link between lung volume and perfusion.

Keywords: physiological models, pulmonary perfusion, pulmonary capillaries, lung mechanics

1. INTRODUCTION 2. METHODS

2.1 Model introduction

The model has been implemented in MatLab (Mathworks,

Appropriate ventilator settings for intensive care patients
with respiratory disorders are crucial for reducing recov-
ery time and minimizing the probability of ventilator in-
duced lung injury (VILI) (Fenstermacher and Hong, 2004)
(Lumb, 2003). Finding the settings is difficult and requires
a tradeoff between adequate gas exchange without stress-
ing the lungs and damaging the alveoli. Positive end expi-
ratory pressure (PEEP) and tidal volume affect both the
lung mechanics and the gas exchange. It has been indicated
that low tidal volumes reduce lung damage (ARDSNet,
2000). Furthermore high pressures by means of PEEP
have proven to prevent alveolar collapse and improve gas
exchange in the diseased lungs (Fenstermacher and Hong,
2004). It is still not clear how to improve gas exchange
while reducing lung damage (Fenstermacher and Hong,
2004). In order to understand gas exchange, pulmonary
ventilation and perfusion need to be understood. The per-
fusion has not been studied as intensely as the ventilation
even though it is indicated that the lung volume has great
effect upon the perfusion (Baile et al., 1982). No previous
models of the pulmonary capillary perfusion has described
how the perfusion is affected by the lung volume.
This paper presents a physiological model that describes
the pulmonary microcirculation, enabling simulation of
capillary blood flow around the alveoli in the entire lung.
The model describes the geometry, hemodynamics and
blood rheology of a capillary. The model includes the extra
alveolar pressure which is dependent on the lung height
and the total lung volume. This enables a simulation of the
flow distribution in the entire pulmonary microcirculation
during mechanical ventilation of a simulated subject.
Natick, MA). The model simulates a healthy human sub-
ject at rest in the supine posture during mechanical ven-
tilation. Fig. 1 illustrates the model representation of the
pulmonary system. The lungs are modelled by 20 layers
each reflecting a vertical height. A constant lung height
of 16 cm is assumed (anterior to posterior). The height
must be included in the model because the lung tissue
weighs down on the layers below causing a hydrostatic
gradient Phydro,tissue . The blood in the capillary network
also imposes a hydrostatic gradient that increases the
blood pressure down the lungs Phydro,blood . The hydro-
static pressure is calculated by (1).
Phydro,i = ρ · g · hi (1)
where ρ is the density of lung tissue (300 kg/m3 ) or blood
(1060 kg/m3 ), g is the gravitational acceleration (9.81
m/s2 ) and hi is the height measured from the top of the
lungs.
The chest wall pressure and the hydrostatic pressure for
tissue compose the extra alveolar pressure Pea as stated
in (2). The chest wall can either exert a recoil pressure at
high lung volumes or an opposite directed pressure at low
lung volumes. This has been measured experimentally by
(Konno and Mead, 1968). Fig. 2 shows the measured data
points and a fitted curve. The curve fit is stated in (3).
Pea,i = Pcw + Phydro,tissue,i (2)
95%
Pcw = 0.71kP a − ln( − 1) · 0.58kP a (3)
%T LC − 22%
The capillary transmural pressure is defined by (4).
Pcap,tm = Pcap − Pea (4)

978-3-902661-49-4/09/$20.00 © 2009 IFAC 157 10.3182/20090812-3-DK-2006.0020

7th IFAC MCBMS (MCBMS'09)
Aalborg, Denmark, August 12-14, 2009

ea
cap1,tm cap2,tm cap3,tm

ea
cap,1 art cap,2 cap,3 cap,4 ven

a a,tm

cap,tm Fig. 3. Schematic representation of the capillaries divided

cap
into three pieces each having a pressure drop. Pea
extra alveolar pressure. Part and Pven arterial and
ven venous blood pressure. Q̇ blood flow. Pcap,tm capillary
transmural pressure. Pcap capillary pressure.


heart
where Part,i is the arterial capillary blood pressure, Pven,i
is the venous capillary blood pressure and Rcap,i is the
resistance to flow in the capillary. The venous blood
hydro, hydro, art pressure is assumed to be constant during systole and
blood
tissue cw diastole, only changing with the hydrostatic pressure down
the lungs. The venous pressure is 1.066 kPa measured
Fig. 1. Illustration of the total lung model. Pea extra at the level of the pulmonary valve (Despopoulos and
alveolar pressure. Pa the airway pressure. Pcap cap- Silbernagl, 2003). Part,i can be calculated by (6).
illary pressure. Pcap,tm and Pa,tm capillary and alve-
olar transmural pressures. Part and Pven arterial and Part,i = Pheart + Phydro,blood,i (6)
venous blood pressure. Pheart pressure exerted by
the heart. Pcw pressure exerted by the chest wall. where Pheart is the pressure exerted by the heart measured
Phydro,tissue and Phydro,blood hydrostatic pressure due at the level of the pulmonary valve which is assumed to
to lung tissue and blood. i index controlling layer be 5 cm down the lungs.
height measured from the top. Assuming that the blood flow is laminar and that the
blood is a Newtonian fluid, the resistance Rcap,i in (5)
can be determined by Poiseuille’s law stated in (7).
[Konno and Mead, 1968]
8 · Lcap + ηblood (rcap,i )
1 TLC Rcap,i = 4 (7)
π · rcap,i
0 FRC where Lcap is the length of a capillary, ηblood is the blood
[kPa]

viscosity and rcap,i is the capillary radius.

cw

−1 The radius of a capillary is dependent on the capillary

P

Tidal
breathing
−2
−3
30 40 50 60 70
Percent of TLC [%]
80
Fig. 2. The graph shows a curve fitted to data (Konno
and Mead, 1968) (RMS=4.092 r2 = 0.9915). The
chest wall pressure is identified for functional residual
capacity (FRC) and total lung capacity (TLC). The
pressure range during a normal tidal breathing of
approximately 500 ml is also indicated. Assuming a
TLC of 6.5 l, the lung volume at FRC and after tidal
inflation of 500 ml comprise 34.3 and 42% of TLC in
supine posture (Ibanez and Raurich, 1982).
As indicated in Fig. 1, Pea affects both the capillary and
alveolar transmural pressures. In this way the blood flow
is coupled to the total lung volume.
The lungs are assumed to contain 300 mio. alveoli (De-
spopoulos and Silbernagl, 2003). Each layer is modelled
as containing an equal number of alveoli and an equal
number of capillaries surrounding an alveolus regardless
of layer number. However just one capillary per alveolus
is depicted in Fig. 1 for the sake of simplicity. The blood
flow through a capillary can be determined by (5).
Part,i − Pven,i
Q̇cap,i = (5)
Rcap,i
transmural pressure, see (4).
The capillary transmural pressure has so far been assumed
to be uniform along the entire length of a capillary.
However the capillary pressure should decrease along the
90 100 capillary before finally reaching the venous pressure. This
is approximated by modelling the capillaries as three
segments (N=3) of equal lengths each accounting for
a pressure drop as shown in Fig. 3. This causes the
radius to decrease and the resistance to increase along the
capillary length. This approach introduces the problem of
identifying the pressure drops caused by each segment,
however it is known that the flow in each of the three
segments must be equal as stated in (8). This leaves three
equations with three unknowns being Q̇, Pcap,2 and Pcap,3 .
Part − Pven Pcap,n − Pcap,n+1
Q̇cap = = ,n=[1:N ] (8)
Rcap Rcap,n
Summarizing in order to identify the pulmonary capillary
perfusion the following needs to be identified: Capillary
shape and radius, pressure exerted by the heart, blood
viscosity and the geometry of the pulmonary capillaries
being length and number.
2.2 Capillary shape and radius
Scanning electron micrographs of the alveolar wall reveals
a circular capillary cross section under zone III conditions
(Part > Pa > Pven ), but that the capillaries flatten under

158
7th IFAC MCBMS (MCBMS'09)
Aalborg, Denmark, August 12-14, 2009
7
[Sobin, 1972]
[Glazier, 1969]
6
Capillary radius [µm]
5
4 2
3 1.8
2
1
0 1
−2 −1 0 1
Capillary transmural pressure [kPa]
Fig. 4. The relation between capillary transmural pressure
and capillary radius. Data from two studies are rep-
resented according to the legend. A sigmoidal curve
has been fitted to the data points (RMS=0.3296 r2 =
0.9823). The shape of the capillaries is indicated at
different transmural pressures.
zone II conditions (Pa > Part > Pven ) (Weibel, 1986).
However this way of dividing the lungs into zones, assumes
that the airway pressure directly affects the capillaries,
neglecting the effect of Pea . The capillary transmural
pressure should be calculated as stated in (4) and not as
Pa − Pcap . Since no measurements of the extra alveolar
pressure have been performed the observations under dif-
ferent zones cannot be directly translated into transmural
pressures. However it seems reasonable that the capillaries
begin to flatten at negative transmural pressures. This mo-
tivates a model of the capillary cross section as being circu-
lar at positive transmural pressures and that they become
elliptic at negative transmural pressures. It is assumed that
the capillaries stretch at positive transmural pressures,
but merely deform at negative transmural pressures. The
deformation is modelled as the capillary circumference
being constant at negative transmural pressures.
The relationship between the capillary transmural pressure
and the radius of a capillary has been described (Sobin
et al., 1972) (Glazier et al., 1969). However the capillary
transmural pressure was defined as Pa − Pcap in those
two studies again neglecting the effect of Pea . Since these
studies are performed on excised lungs the effect of the
chest wall is removed and only the hydrostatic gradient
due to the lung tissue changes the extra alveolar pressure.
This implies that Pea can be calculated simply by (1).
From the data on the transmural pressure provided in the
studies the capillary pressure can be obtained if the airway
or capillary pressure are provided along with the height of
measurement. This is the case for Sobin et al. (1972) and
some of the data points from Glazier et al. (1969). The
points are plotted in Fig. 4 along with a fitted curve. The
curve fit is stated in (9).
rcap = 2µm +
1+e
2.3 Pressure exerted by the heart
A pressure profile during a heart beat is not measurable in
the capillaries, however such a profile has been measured in
the pulmonary artery (Takala, 2003). The mean pressure
from the pulmonary artery to the capillaries declines
Mean = 1.6839
2.6
2.4
2.2
Pheart [kPa]
1.6
1.4
1.2
2 3 4 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Time [s]
Fig. 5. The pressure exerted by the heart (Pheart ) pro-
file during one heartbeat. Note that the duration
is around one second since the subject is at rest.
The profile is measured in the pulmonary artery
(Takala, 2003), and scaled into the pressure range for
pulmonary capillaries (Despopoulos and Silbernagl,
2003).
approximately 20%, resulting in a pressure range of 1-
2.7 kPa at rest at the level of the pulmonary valve
(Despopoulos and Silbernagl, 2003). Fig. 5 shows the
pressure profile by Takala (2003) scaled into the pressure
range for the capillaries.
2.4 Blood viscosity
The blood viscosity is a function of the tube radius mainly
due to the behavior of erythrocytes at different radii
according to the Fahraeus-Lindqvist effect. Data from
several studies of this phenomenon in glass tubes have
led to a model of the capillary viscosity as a function
of the diameter of the glass tubes and hematocrit (Pries
and Secomb, 2003). This model has been adapted with the
hematocrit set to a normal value of 0.45 (Despopoulos and
Silbernagl, 2003). When the capillaries become elliptic,
the smallest radius in the ellipse is used to determine the
viscosity of blood in the model.
2.5 Model calibration
The capillary length and the total number of capillaries
are indeed decisive for the pulmonary perfusion. The
total number of capillaries is described as a number
of capillaries per alveolus, assuming that all alveoli are
surrounded by capillaries in the same manner. However
the capillary length and number of capillaries per alveolus
is not well described in the literature. The capillary length
has been reported to be approximately 600 µm for cat
lungs and 800 µm for dog lungs (Staub and Schultz,
1968). The number of capillaries per alveolus has not
11µm been quantified. The model has therefore some degree of
P (9)
−( cap,tm−2.11kP
0.8401kP a
a
) freedom regarding these two parameters, which have been
adjusted in order to obtain the best possible description of
a series of known output parameters. These parameters are
total capillary flow, total capillary volume, total capillary
surface area and transition time. This adjustment resulted
in a capillary length of 1000 µm and 5 capillaries per
alveolus. Since each capillary has been estimated to cross
5-12 alveolar walls (Staub and Schultz, 1968), this implies
that a cross section of an alveolus should show 25-60
159
7th IFAC MCBMS (MCBMS'09)
Aalborg, Denmark, August 12-14, 2009
capillaries. This seems reasonable by inspection of electron
microscopic pictures of the alveolar wall (Weibel, 1986).
3. RESULTS
Three model simulations have been performed for model
validation. The three simulations have been performed at
following lung volumes: 1) FRC 2) TLC 3) during a tidal
breathing of 500 ml. The breath starts from a lung volume
of 500 ml above FRC, then an expiration brings the lung
volume to FRC followed by an inspiration back to 500
ml above FRC. These three scenarios cover two extremes
supplying the total range of the output parameters and a
normal breathing enabling a comparison with data found
in the literature. The breath frequency is 17 breaths/min
and the heart rate is 60 beats/min.
The simulated extra alveolar pressure, capillary pressure,
transmural pressure, capillary radius and capillary flow
during a tidal breathing of 500 ml are shown as a func-
tion of time in Fig. 6. The simulation result of Fig. 6-D
indicates that the radius varies 2 µm (systole-diastole) and
approximately 2 µm (top-bottom). Fig. 6-E illustrates that
the flow is highly pulsatile. It can further be identified that
the flow is different from top-bottom. These results are
in agreement with data from experimental studies (Lee,
1971), (Hughes et al., 1968).
The simulation results describing flow distribution, cap-
illary perfusion, capillary blood volume, capillary surface
area and transition time in Figs. 7 - 11 can all be compared
with data described in the literature. The mean values
for the different simulations are listed in Table 1. The
transition time is listed as a range with the lowest value
being the mean value from the most dependent layer and
the highest being the mean value from the most non-
dependent layer.
Flow distribution The distribution of capillary flow at
different lung heights during the tidal breathing is plotted
in Fig. 7 against measured data from Kosuda et al. (2000).
It is well known that the blood flow is heterogenously
distributed according to lung height (Hughes et al., 1968).
The flow increases from the non-dependent lung and down-
wards, except for the very bottom of the lungs, where flow
decays again (Hughes et al., 1968). According to Fig. 7 the
simulated flow does increase from the non-dependent lung
and downwards, however the decrease in blood flow in the
most dependent lung is not seen.
Pulmonary capillary perfusion The total pulmonary
perfusion in Fig. 8 is simulated with a mean of 6.24
l/min. The pulmonary capillary perfusion should equal the
cardiac output which at rest is 5-6 l/min for a healthy
human (Despopoulos and Silbernagl, 2003).
The simulated mean pulmonary perfusion is 0.19 l/min at
TLC almost completely diminishing blood flow.
Pulmonary capillary blood volume The simulation result
for the pulmonary capillary blood volume in Fig. 9 shows
a mean value of 63.1 ml during normal tidal breathing.
This value is low compared to experimentally measured
values of 86 ml for men (Zanen et al., 2001). Even higher
values have been estimated in the range 100-200 ml in the
postmortem lungs (Glazier et al., 1969).
160
Pulmonary capillary surface area The result of the
simulation in Fig. 10 gives a total capillary surface area
of 40.6 m2 . The pulmonary capillary surface area has
been stated to be around 90 m2 (Lumb, 2003) (Hlastala
and Robertson, 1998), which is a factor of two higher
than the simulation. It has also been stated that the
capillary surface area is 10 % less than the alveolar
surface area. This ensures an almost maximal surface area
for gas exchange. Assuming that the alveolar radius is
150 µm at FRC and that the lungs contains 300 mio.
alveoli (Despopoulos and Silbernagl, 2003), this leads to an
alveolar surface area of 84 m2 implying spherically alveoli.
Transition time The pulmonary capillary transition time
for layer number 1, 5, 10, 15 and 20 is shown for the tidal
breathing simulation in Fig. 11-A and plotted against the
lung height in Fig. 11-B.
Model simulation resulted in transition times from 2.9-14.9
sec (bottom-top), see Table 1. This is slightly higher than
the values estimated by Wagner et al. (1986) of 1.6-12.3
sec (bottom-top) in anesthetized dogs.
Table 1. Mean simulation results
FRC Tidal breathing TLC
Surface area (m2 ): 37.9 35.4 17.4
Blood volume (ml): 72.4 63.1 13.2
Blood flow (l/min): 7.75 6.24 0.19
Transition time (s): 1.9 - 7.4 2.9 - 14.9 47.7 - 157.0
4. DISCUSSION
The model simulates the four presented output measures
well, however the total capillary surface area and total
capillary blood volume are lower than the presented data.
Zone IV As shown in Fig. 7, the model does not sim-
ulate a decrease in flow at the bottom of the lungs. The
decrease in flow at the bottom of the lungs has partly been
explained by the effect of vascular tone (Nemery et al.,
1983). This makes sense in the way that vascular tone
would constrict blood flow during hypoxia at the bottom of
the lung distributing the blood to better ventilated parts of
the lungs. Another explanation for the flow decrease at the
bottom of the lungs is due to extra capillary vessels being
more compressed at the bottom of the lungs, increasing
the flow resistance in this area (Hughes et al., 1968). These
effects could be a topic for future development since the
total pulmonary blood flow would become lower if vasocon-
striction was included in the model and hence the number
of capillaries per alveolus could be increased in order to
maintain a total flow of around 6 l/min. The increase
in number of capillaries per alveolus would increase the
total capillary blood volume and total capillary surface
area without affecting the transition time.
Since the flow decreases at the very bottom of the lungs
the transition time might also increase in this area. This
increase in transition time has not been measured by Wag-
ner et al. (1986). This disagreement could be a result of
the transition time not being measured at the very bottom
where the flow decreases, or that the capillary density is
lower at the bottom, reducing the flow measured in this
7th IFAC MCBMS (MCBMS'09)
Aalborg, Denmark, August 12-14, 2009

0.5 40
A FRC

Blood flow (Total) [l/min]

Tidal breathing
TLC
Pea [kPa]

30
0

20
−0.5
0 0.5 1 1.5 2 2.5 3 3.5
Time [s] 10
4
B
3
0
0 0.5 1 1.5 2 2.5 3 3.5
[kPa]

Time [s]
2
cap
P

1
Fig. 8. Simulation of the total capillary blood flow at
0
0 0.5 1 1.5 2 2.5 3 3.5 functional residual volume (FRC), total lung capacity
(TLC) and tidal breathing.
3
C
0.2
[kPa]

FRC

Blood volume (Total) [l]

2 Tidal breathing
cap,tm

TLC
0.15
P

0 0.5 1 1.5 2 2.5 3 3.5 0.1

6 0.05
D
5
Radius [µm]

4 0
0 0.5 1 1.5 2 2.5 3 3.5
3 Time [s]
2
0 0.5 1 1.5 2 2.5 3 3.5 Fig. 9. Simulation of the total capillary blood volume at
x 10
−13 functional residual volume (FRC), total lung capacity
E (TLC) and tidal breathing.
4
Flow [l/min]

3
60
2 FRC
Surface area (Total) [m2]

Tidal breathing
1 50 TLC
0
0 0.5 1 1.5 2 2.5 3 3.5
Time [s]
40

30
Fig. 6. Simulation results during a tidal breath for layers
20
1, 5, 10, 15 and 20 (most dependent, dashed line).
A: extra alveolar pressure (Pea ). B: capillary pressure 10
0 0.5 1 1.5 2 2.5 3 3.5
(Pcap ). C: capillary transmural pressure (Pcap,tm ). Time [s]
D: capillary radius. E: capillary flow. Pea decreases
during expiration and that Pea is higher at dependent Fig. 10. Simulation of the total capillary surface area at
part of the lungs. The capillary pressure is also functional residual volume (FRC), total lung capacity
highest at the dependent part of the lungs, due (TLC) and tidal breathing.
to the hydrostatic pressure. This results in varying
transmural pressures and capillary radii down the area without affecting the transition time.
lungs. Furthermore this leads to a highly pulsatile flow
indicated.
Supine posture The model assumes supine posture. It
140
Simulation: Tidal breathing has been indicated that the flow distribution in the lungs
Relative capillary perfusion [%]

[Kosuda, 2000]
is not only dependent on gravitational forces, and it is
120 indicated that an anatomical difference from the anterior
100 to posterior exists (Glenny et al., 1991). If a subject were
to be simulated in other postures than supine, the model
80
should include parameters reflecting the effects of posture.
60
Constant lung height The lung height is assumed con-
40
stant at 0.16 m. However during breathing the lungs ex-
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 pand. It has been reported that the height (anterior to
Dependent Relative lung height non−Dependent
posterior) of the human lungs varies from 10-16 cm with
lung volumes at residual volume and total lung capacity,
Fig. 7. Comparison of simulated pulmonary capillary per- respectively (Millar and Denison, 1989). This effect would
fusion with data from Kosuda et al. (2000). The data imply a smaller hydrostatic gradient and hence a smaller
is normalized to the maximal perfusion, contrary to difference in extra alveolar pressure down the lungs.
the simulation, which is plotted in respect to the mean
start of zone IV from the data (7 cm above the most Blood viscosity In vivo measurements of the blood vis-
dependent layer). cosity are poorly described and remains to be fully under-

161
7th IFAC MCBMS (MCBMS'09)
Aalborg, Denmark, August 12-14, 2009
150 A
Transition time [s]
100
50
0
0 0.5 1 1.5
Time [s]
2 2.5
15 B
Transition time [s]
10
5
0 2 4 6 8 10
Dependent Lung height below top [cm]
Fig. 11. Simulation of A: transition time during a tidal
breath in layer number 1, 5, 10, 15 and 20 (most
dependent, dotted line) and B: mean transition time
as a function of the lung height.
stood. However a few measurements of the blood viscosity
have been performed in vivo indicating much higher values
for viscosity at similar radii.
When the capillaries become elliptic, the smallest radius
in the ellipse is used to determine the viscosity. This could
cause an overestimation of viscosity since the erythrocytes
might be able to squeeze into a more elliptic shape.
PEEP The recoil pressure exerted by the chest wall is
determined by the volume of air in the lungs. PEEP results
in a higher amount of air in the lungs and will increase the
pressure from the chest wall and hence the extra alveolar
pressure resulting in a reduced radius of the capillaries
and decreased blood flow. Since the lung volume is input
to the model, an exact value of PEEP can not directly be
included. Steimle et al. (2009) have proposed a model of
the mechanical properties describing the pressure volume
relationship in the lungs. Combining these two models
would enable the link between PEEP and blood flow.
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