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484
actions, a closed-loop
cardiovascular
vascular
system
circulations.
better
understanding
of the behavior
of the global hemodynamic interlumped parametercomputational model was developedforthe human
detailedcompartmental
Construction of the model
with
was
logical
characterization of hemodynamicsusing an electrical analog method and solution of
the goveming ditTerential
equatiens of the model was carried out by use of a fourth-order
Runge-Kutta
either
Most
with
of
the
the
hemodynamic
clinical
measurements
forcomputer-aided
posttreatment
prediction,
serve
as
method.
consonant
as
a usefu1
diagnosis
and
tool
assistant
treatment,
surgical
as well
1. Introduction
The human
of a series
of
cardiovascular
subsystems
functionally
interact
with
significance
cardiovascular
is a
system
thatstructurally
each
other.
combination
connect
to
and
Therefore,
itisof
always
contrast,
a series of
Lu,
man
et al.
(2) developed
cardiopulmonary
diopuLmonary
arranged
in series
was
and
constructed
closed-loop
open-loop
ones
to complex
multi-compartmental
closed-
study
on
reasonable
'
"
"'
closed
the
seven-compartment
forthehuman
cardiovascular
cardiovascular
response
simple
in parallel
to form a
cir-
dependingon
from very
culatory
tionalmodel
purpose,ranging
model
system.
system
a mathematical
to
computa-
in their
system
orthostatic
stress.
be efi
hemodynamic parameters within
of predicphysiologicalranges by good fits
models
were
eyinced
to
simplified,
vessel
system
or concentrated
specific compartments
none
of
with
the models
on
hemodynamics insome
the remainder
simultaneously
neglected
or
embodied
JSMEIntemationalJoumal
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of Mechanical
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of
4S5
a
cardiac-pulmonary
thehuman
cardiovascular
system
isan integrated
closed-
main
tional
are
compartments
cardiovascular
model.
through
where
other
order
to
modeled
tonomic
nervous
system
also contributes
predictinghemodynamic
regultttiens
against
various
perturbations,The right-]eft
heart interactionmodel
proposedby Sun, et al.(i) was
adopted
as the basisfor developing the presentmode],
The
peripheralcirculation was partitionedintofourparallelregionalcirculations branchingfrornthe aorta at fourspecific sites, In modeling each regional circulation, distinctions were made
among
arteries,
arteriolar
and
capillary
beds and yeins to account forthe time-dependent transferof hemodynamic parametersthrough different
vascularsystems.
In addition, several modifications
were
made
computational
model
capable
arteries,
arterioles
capillaries
nutrient
of
and
circuare
associated
with
an
ethcacious
mathematically
computational
well
eters
method
system
where
an
is
electri-
isfrequently
employed
since hemodynamic paflow
can
as blood pressure,
and resistance
cal analog
rameters
effective
thiscomplex
represent
the
be
hemodynamic
concurrent
The
quantitatively.
to
way
via
construct
such
mimicked
by the
including
voltage,
Figure 2(b) shows
corresponding
current
and
electrical
param-
resistor.
three-dimensional computer
based on anatomical
data,which includes266 arteries with diameters ranging
from 2.4cm to lessthan 1.5mm.Such
a model
may
favor
a direct
unstanding of the structure of the cardiovascular
model
system
of
the
and
mentalizing
tree
arterial
providean
constructed
anatomical
the cardiovascular
forcompart-
evidence
system
in the
model
devel-
waurpvee
forthe yenous elastance model and the time-variant elastance heartmodel to reflect the volume
related
change
in
yenous
compliance
and the variation in systolic duration
with
and
interactions.In
model
for
the system,
a lot of simplifications
have to be made because the details
of the system are too complicated to be
each
interactions.
The presentmodel
to each other
lation
where
not functionally
independent
but closely
vascularsubsystems.
is a
beds, and
circulations
capillary
Between the
above
interactionsinrigorously
terms due to
quantitative
the lack of a comprehensive
inclusionof the main cardio-
above
and
in ene computa-
namic
namic
the
of
arteriolar
mentioned
synthesizing
likelyfitforinvestigating
thedynamic hemody-
not
of arteries,
bloodisdistributed
to organs, tissuesand skeletal muscles,
then final]y
isreturned back to the rightheartby veins.
requires simultaneously
perturbations
namic
illustrated
in Fig. 1, Each
combination
llmtls
e..
mullry
pwas1!
c:va8me
7emusws:
$massc
pt gKidnevs
data or the general physiologicalknowledge. Varying dehaye been made forsome parameters
grees ofadjustments
to achieve reasonable
fits
of predictionsto clinical
mea-
leen
surements.
'
2. Methods
The
whole
cardiovascular
system
can
be
approxi-
Geenadictg.mmwwmpww
mately
and
toww
Hrmios
the
as
Fig.1 A
sketch
of
the human
vascular
system(b)
The Japan
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486
k.'.ts'i
CcrebratandLl'pperI.imbCirculatiens
.v
-L+
ethtldit
t.-
s.-,
Right}-IeEvt
L.
tt
a.t.M
t.A
.t t..
la
lt.
PulmonarvCircutation
Lev
re"
t"
X-
fl-
n..L-
I""It'va.'1''j[..t'
-.
L-
tttthEwhAorta
t'-
t
VenaCaya
s-
;ttttt
1.cft Heart
m.
L.,
".
ts.
R.
/.
ttttt.tttt...)t.tt..t
'l/t/.Ilt
rtttltttttt'.tx''"S,'.y'1
s.
L.
R.
H,tttAr
Lpt
s.li-Skliul
za,t-
g.
kttrw
lp
smuM SNEt,,tintttreEpmemh'r,
5.,ercs.t.
--"--t.t.tt.x---S--/t
.or.}./'-/1.:.1--' tt/
'..../1//...ll.
..g/,X"L/Ft
sttt
slatt
s.E.s.
n.pL
E.
F-
'ttttt/t'tttttt]tt;x.'"'fi="t'ttt'
Pge
se'-tt.
---v
Pb
RcnaiCireulatien
LuSeEL,
t.he
vetuatfu,snen-
S-
th-is.
Rw
./3a
l..
'x,'/,.1'tttt
L,-st.l'w
.t//
thk
'1,.'t'
SplanchnicCirculutiun
Hpt
t.ptsptHpt
L-L-t-RT
t.th,s,.asRpt
{.z3
ctt
LiitiL
ttt-/Edi
'
/
LowerLirnbCircuiation
Rft, t.-shaA-thi,.t-/H,v
/t.
'
j
/
t't
Lhas-re-
-.tt{
'/l''
SbE-
tLiLtL
Fig,2
An
electrical analog
arterial
LH
E!astance
Viscoelastence
the human
J
cardiovascular
'r'/1ll
l,
system
and
a computer
model
of
the
treeTlable
RH
ela, el.Sm,
of
1I111
1Parameters intheelectrical
analog
AADA
SPLLLBULBvvcPU
KID
circuit
EpSpLpRp
E,,S.L.R.
Ed,sdaLdsda
EkidSkidLkidKid
EsplSop1LspdRsp1
EllbSllbLdlbRllb
EthSlllbLulbK,b
kS.LRvEvtSvcL'cR'c
era,ens,,,
S-L",
Si-Lmvt
opment.
Based
seven-compartment
on
by a
closed-loop
cardiovascular
system
are
and
characrepre-
illustrated
in Fig,2 (a),
by the time-variant elas-
circuit as
represented
the
scending
ney,
aortas,
the
splanchnic
organs,
limbs,respectively,
vena
cava, and
scripts
attached
PU
the
indicatethe kid-
lowerlimbsand theupper
M VC denotethe systemic
means
to them
the
pulmonary
veins
circulation.
and
Sub-
e.g, a, a4
and
the
peripheralcirculations
are each
mimicked
c, v
JSMEIntemationatJourual
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487
- vo]ume
in vascular pressure
Thble2
(P-V)relationship.
uv
systems,
vascular
to have
assumed
ls wrltten
an
inthispaper,vascular
P-V
exponential
nv
en
is
compliance
relationship{i),
LA
EaEhTcTr6,eO.07O.4O.02
O.07o,ege.4O.05
1.2O.05O.4O.02
O,04O,06O.4O.05
countfbrthenonlinearvascularelasticpropertiesofdifferent
Parametersinthe heartmodelCi)
which
as:
(1)
p=Eee"/ZZ
Where Eo [mmHgmL-i]denotesthe
zero-volume
elas-
Thbie3 Parametersintheassistant
equations
heartmodel
ofthe
tance,
vascular
elastance
curves
by Dahn, et
reported
al.
2.1 Representationoftheheart
In the presentmodel, the four chambers
of the heaTt
are each represented
by the use of a time-variant elastance,
which
varies
over
cardiac
charge-discharge
ponential
baseline
and an amplitude
heart model
according
cycle
wavefbrm
characterized
componept.
initially
constructed
was
to an ex-
by
[mmHgmL-i]and
elastance)
mathematica]
are
basically
ina
similar
duration,etc. The
systolic
representations
the
of
fourcardiac
chambers
form.
Ei,.F,
+El,blF.,
elv=
(eiv
lr,, )
Ogtst,
ela
sistingof
`[talk
threeelastic compartments,
namely,
Piv E,,
E.t+
eltt
Vlv+
Es+elv
et,
erL,,etu and
pressures in
as:
'Prv
(5)
'piv
(6)
and
erv
Prv=Es'
Es+erv
erv
Vrv+
Es+erv
where
E, refers to the elastic compartment
representing
the shift of the septum,
ln addition, systolic durationmust be redefined when
the heart works at a yariable heartrate. With thisinmind,
a sigrnoidal
functionisproposed to relate the moment
of
systolic
to
a
cardiac
cycle
in
the
elastance
peak
present
model;
the functionis shown
below:
(Tsmax-Tsmin)
lt ls wrltten
as,
T, [sec]
isthe moment
where
Ts,min[sec]
and
(3)
mum
values
of
denotethemoment
[sec]
tar<t<(tr+tac)
of
thepeak
of
controlling
shape
the
of
systolic
peak systolic
elastance,
T,,min[sec]
are the minimum
and
maxiT,, respectively, 6 and e [sec]
are the con-
(ela1t..-Etab)'e-(t-tt:t)tTyar
the
+Eiab
(7)
(;iltl+e4
ts<t<tr
Elaa(1-e-(t-tac)/nt:c)
+Elah
tacStStar
t,t,t,
independently
but interact
E,[mmHgmL-i],
the leftand right
stants
Where
1.0e.2259O.4299
other
Ts=Tsmm+
+EtvbfFs
atrium),
(left
lkmaxLmm
through a so-called
pressure"across
the interventricular
septum.
In addressing
thisproblem,
Maughan, et al. (8} proposed a mathematical
model con-
TEiubfF,e-(t-ts)kvr
Ll
1--e,-;,i[l';lii'
(2)
(i-e
t"la)
380
each
The mathematical
by Sun, et al.(i)and
fi
heartsdo
with
C7)
Vmax
of
sigmoidal
curve.
the coeMcients
Listed
used in
heart modet.
2.2 Vbnouscompliance
Other than the arteries,
the
refers
and a cardiac cycle, respectively
tac[Secl
the moment
when
the atrium begins to contract, tar [sec]
the systemic
veins
and the
indicatesthe moment
when
the atrium begins to relax, and
vena cava often operate in low-pressure
condition. They
F, is a scaling factorintroducedto refiect the loaddepento
may even co]lapse when transmural pressureisreduced
dence of myocardial contractility and nolinearity of the
a negative
value.
In fact,the compliance
of vein shows
an
starling curve of the leftventricle.
A simple first
erder
approximately
constant
value
under low transmural preslinearfunctionof F, isdefined as:
sures ranging from O up to 10mmHg(ii). However, if
elastance
to
Fs=1-Vlvdell'1llux
Where vi,d,[mL]indicatesthe end diastolicvolume
(4)
the
Moreof
JSMEInterncitionctlJoitrnal
is forced to increaseto
the venous transmural pressure
higher level,for example,
during the Valsalva maneuver,
vein
will
congestion
essary
stiffen
significantly
caused
blood
return
by venous
to the
to
prevent excessive
venous
b]oodpoolingsuch thatnec-
heartcan be
maintained.
There-
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488
Thble4
Pararneters
inthe
venous
elastance
qin
rnodel
Evdmin EvdmExVvn
kvEveomio
EveomfixVvcn
kve
O,OOOI
400
O,06260
200
O.OOOS5
2900
O,O15
9eut
L
smp
Sdeu,n
fore,the ro]e
regulation
isof great
of venous
compliance
importance in determining cardiac output and thatmaintaining arterial blood pressure, In the present study, several empirical
formulas relating venous
elastance
to venous volume are developedto account forthe nonlinear
venous P-V relationship. In the formulas,
the change of
venous
elastance
is characterized
as a series of arrange-
Eup
IE l
Edovn
(a)
Fig.3
(b)
electrical analog
model
linear
firstorder dynamic blockin time domain such thatbothvolnodes of elastance (E)
and inertance
(L),respectively. In
in elastance can be acumetric and temporal variations
total,62 differential
equations are derived
at the 62 correment
of a sigmoidal
for.Furthermore, we distinguishbetween the systemic veins and the yena cava regarding
theirdifferences
counted
invascular
elastic
properties.two groups
of equations
are
constructed.
they are
veins,
written
as:
(exp(
(exp(
V(t)k-,Vhn
1+
Vb"
V(t)i,
Evumin+ Eve...
Evo(v,t)
))
(8)
=qin
And at node
EvtD(v,t)
i+
V(t)i,.Vbcn
1/(Eui)zup+s.p
=
(11)
slopes
in[fable
4.
2.3 Governingequationsandnumericalmethod
marized
on
the
electrical
the presentmode]
of
enforcing
mass
-qR
'
(13)volum
dt
))
))
TeL/c
Based
L:
dvdoritn
-EdotmZlfJu)n-Sdoti)n'
(10)
dEvc(V,t) -Evc(v,t)+Evco(v,t)
equations
(12)
(exp(V(t)k-,l[l
(exp(
cn
Evcomm+Evcomax
lingthe
the
d:"tp
(9)
dt
of
the
-q..t
Tt
cava,
Because
nodes.
))
dE,(v,t) mE,(v,t)+E,o(v,t)
dt
Tev
And fbrthe vena
sponding
conservation
SeriesC, Nla1.
48, No.4, 2005
analog
can
and
circuit,
the
governing
be derived
by means of
forceequilibrium
at the
Where
v[mL]
the)IL vascular
represents
forother nonlinear
heart,
the cardiac
in intervals
of 5 time
tions
of
the
is proved
numerically
elements
and
such
venous
steps.
stable.
the
as
Such a
The
elastances
valves,
numerical
simulation
scheme
software
is
completelywritteninaC++languageandrunsonaDELL
werkstation.
3. ResultsandDiscussion
3.1 Hemodynamicsoftheheart
Figure 4 illustratesthe
computed
atrioventricular
inthe left
and right hearts
over a carby the use of thepresent
computational
model.
pressurewaveforms
diaccycle
The shapes
the pressurewaveforms
of
general in vivo
dictedvalues
match
well
with the
and
in addition, the preboththe systolic and the diasreasonable
ranges.
physiological
measurements,
in terms
tolicpressuresare
within
of
JSuaInternationalJourn(
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-a=EEvB8di8-em
30252015"o5o.Et..
-orrEEif:to9trvo-oan
140120"ooBO604020
----RightAtrium
Right Ventricle
le
a
Vy
o
o.o
o.2
o.4
o.6
e,o
o.s
o,2
e.4
Time(s)
(a) Rightheart
7ol
ri30
+t+
ix.
,,"1
'
1/
'lxy',
1
O.4
Time(s)
O.6
change
0.0
O.8
ation)
(simul
(b) Leftheartvolumetric
'
O.6
O.8
' '
(simulation)
change
AsoEv-oLvo-om
'
txttt.tx''tt'
tt
tt.
ttl
ttt'''''
50
'''
-50-100
O.4
Time{s)
400
---Putmonstyvenousflovt
-vsnousretufnficrw
350300250200150100
TransmitFelfiow
---Trenstrle-spldfiow
.t
:.EYeqvo!co
s..
O.2
400
350300250200ri501OOE
50
the left
hearts
i::
'i"xl1"'
60tuO t1Xx,,t1
50
40
O.O
O.2
(a)
right and
i'l,.Rdg.htvih;giefi
g,
'tNtl
goJo
so8
blood pressuresforthe
'R/ghtAtrlum/
4
,i
O.8
(b) Leftheart
Fig.4 Simulatedatrioventricular
130
/t
120."oEbldOOg
o.6
Time(s}
O.2
O.4
O.6
o '
-50-100
''''''''st
.
..6.s
Time(s)
and venous
(c) Thristricupid
return
fiows(simulation)
o.2
o.4
'
q.s
o.6,
'
Time(s)
'"
(d) Transmitralandpulmonary
venous
flow(simulation)
130
?120
g11o
-]e100
>
o
90
so
70
.g
ca
60
50
O.2
D.4
O.6
O.8
Time(s>
(e) Leftventricular
Fig.5
volumetric
Modei-basedsimulations
reproduced.
The computed
righthearts over
and
of
volume
a cardiac
cycle
are
forventricles,
(b),Specifically,
the
volumetric
the left
and
in Fig.5(a)
the basic property
yarying curyes of
shown
JSMEhitemationalJournal
(measurement)
change
hemodynarnics
of cardiac
nation
ric
as
the predictions,measurement
1,
of
variation
of
the leftventricle
over
on
the
a cardiac
in Fig.5(e)OO).
The ventricular
presented
yolume
yolumetcycle
is
iscom-
The Japan
TheJapanSociety
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490
30282624222et816141210
ooo
400
g.gg[voom
g.g)9Lvooas
300
200
100
.100
O.2
(a) Aorta
O.4
O.6
O.8
Time(s)
160ri40.-.
Brains
throughthe
Fig.7 Predictedblood flowwaveforms
ancl capillary
beds of the upper limb and
arteriolar
cerebral
circulations
120gg
lool9
oo
soL8
1co
6oodi
4020e.20
48ig
>o#ovas8=rst
t05
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so
an
(b)
Fig.6
Large
:.ge
arteries
Predictedblood flowwaveforms
largearteries
through
the
aorta
op
O.O
Figure 5(c)
simulations
of
and
(d)also
75
and
the model-based
transmitralflowsand
right atriums.
The typi-
O.2
O,4
ec
O.8
O.6
firne(s)
inthe aorta
Fig.8 Predicted blood pressures
and
theupper limb
arteriolarbed
shows
waveforrns
through the
arteriolar
and
capillary
beds of
the
flow waveforrns
through these vascular
systems
are pletted in Fig,9, where
blood flows are observed
to again be-
come
upper
more
and
more
system
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491
due to the infiuence
of the pulsating right
heartdown-
values
of
the two
parameters and
making
correspondingly
fbrother parameters
inthe heartmodel,
hemodynamic in various grades of diastolicdys-
slight adjustments
stream.
3.3 Model
representation
of
blood volume
distri-
system
cardiac
functioncan be
The cardiac
simulated
the presentmodel.
with
hemodynamics in threegrades of diIn Fig.10, the pretion in the cardiovascular system issummarized
in [fable astolic dysfunction
was simulated.
with the in vivo Doppler ve5. Good agreement betweenthe model-based predictions dictedresults are compared
The
model
representation
of
blood
distribu-
voLume
locityrecordings
andthedatareportedinRefs.(13)and(14)impliesthatthe
values
assigned
compliances
are
wjthin
ranges.
physiological
3.4 Heartabnormality
reasonable
Diastolicdysfunetionisa
found in the elderly, which
transmitral
common
diseaseof-
cardiac
the transmitral
of
flows(S),
Grade I ischaracterized
ation, a decreased
E wave and
companied
pulmonary
and
venous
by theprolonged relax-
of the
an increasedA wave
fiow and the strengthening
of the S waye
acby a impaired D wave of the pulmonary venous
forapproximate
floware observed. Grade IIischaracterized
by the stiffen30% of heartfailure.
In patientswith isolated
diastolic ingof the leftventricle, namely, pseudo-norrnalization.
In
dysfunction,
there isoften a preserved
systolic function, thiscase, increased
flowreversal intothe pulmonary vein ,
ten
accounts
fractioncomparable
ejection
isobserved
due to the increased diastolicfi11ingpressure.
one in the normal
case; however, uncontrolled
Grade IIIdysfunction isspecified by a severe deterioration
progression
of diastolic
dysfunction may still be an important
causaof the left
ventricle compliance. Under thiscondition, the
in dunionof the onset and progression
of systolic dysfunction. A wave of the transmitralflow isgreatlyshortened
isassociated with the proration
and reduced
in magnitude,
correspondingly,
the S
Generally,
diastolic
dysfunction
longed relaxation and the stiffening of myocardiumC9}
of
wave
isdecreased,
reflecting
the presence of a highpresshow
realeftventricle. From the pointof view of model simulasure in the left
atrium. Overal],
the predictions
and
sonable
agreements
with
the measurements.
tion,the durationof relaxation
the stifftiess of myocardium(9)
of leftventricle
can be represented
by the left
3.5 Limitations
ventricular
baseline
elastance
Et,b,and the time constant
Limitations
of the present model
mainly
arise from
namely,
Ti,,
a maintained
in the heartmodel,
to the
Via changing
respeetively.
the
ThroughSystemieVeins
Towards Vena Cava
200
ThreughVenaCava
TewardsRightAtrium
150
Ath>Evl-eLpooas
t
1OO
h"
--nv-----.fmu
t/
50
the model.
hemodynamic
system,
the
propertiesofthe cardiovascular
representation of
presentmodel contains a comprehensive
the main vascular circulations. Data on the comp]iances
and resistances of
]argeveins
tal
the
we
O.8
-50
Fig. 9
resistances
estimated
veins
the vena
and
through
waveforms
miin
the
and
vascu]ar
aorta,
the to-
and
circulations
be
can
the systemic
the
arteriolar
and
based
to pre-
resistances
capi]lary
adjusted
of
o
O.4Time(s).O.6
assignment
suMcient
x.
tt
O.2
va]ue
N".
""
the
the
arteriolar
and
bed
capillary
bloodflowand pressurewaveforms
are
beds. Although these estimations
and
cava
to
compliances
realistic predictions
ofblood
yield physiologically
volume
in these vascular
likelyto pose
not
serious
of the globalhemodynamproblems to simulation
ics,theymay 1argely
lirpit
the achievement
of highfidelity
BteodllolumeDisnibutien
MedelRepresentation
local
in
arteriolail
of
hemodynamics
and capilprediction
HeartMlmenarycirculation
3SO4SO11S6S.270650160.35032oe
3S2438'7S148215608I50360
Tlable5
Model
representation
of
blood
volume
distribution
Pulmona-''arteries
tions.
Pulmonary[apillaries
and
there
'
of
arterial
Pulmonarvveins
compliances
to
basedon the,anatomical-data-based
Systemic
of
Systemiccapillaries
,Systemicveins
rsME Ineernatiotiat
JourtLal
.32S2
regional
resistances
were
ar-
circula-
firstly
Systemicarteries
arterieles
the
3D
computer
modgl
arterial
tree.
Seriesg,1'ol.48,
No.4, 2005
The Japan
TheJapanSociety
Society ofMechanicalEngineers
of Mechanical Engineers
492
t5egtoel
iso:t
400loc70C,oo
sD
50
gii
100
inRef.(12).
The computable arterialblood
volumes
model
of the arterial
basedon the 3D computer
tree also provided valuable
evidences
forthe estimation of
arterial complian6es
in consideration of thefactthatarterial compliance
deterrnines
thebloodyolume contained
Although
most
of the paramein arterial compartment.
ters estimated
dataor the
partiallybased on the anatomical
general physiologicalknowledgehavebeenproved able to
ments reported
Axv
!o-
o-Aeo.200-]oo
07e.e
UETIme/E/
to
o
n.oO.7O'4T/me{e)06o.s1.0
reasonable
experimental
(a) Normal
1aoot3ee200leo
)
Kiii
A
i:
400]omooe/om
LNx.?K''''(
iI,:
o.:p{Tme/t/pm:c
m./oo!oo.ibG
e'
O,1D'dT/mece}O'ees/o
hemodynamics seems
sr::i/
l!l]i
Df.4
"iii
gl,I
,,,,
boundaryconditions
and
the active change in hemodynamictiwith phytiiologicalstate, thehigh accuracy of
highdimensional
simulation may be greatlycompromised
on
Gradeldysfunction
ISO100tEnlb)/EO,.eo50
Xil
1
n.? odTrmE/srGnsto
i(N
;.Eg[1s
//
D4...-
!
-teo-aeel-soot'
tffo/tl
O.7
to
D.
t.o
/'''A
ifsimulation
isperfbrmed with fixedboundary condit{ons,
At this point,low dimensional computational approaches
likethe presentmodel, though only able to providelow
low accuracy
dimensional,
or to say the least,
predictions
of hemodynamics,
may
favor an integrativecomprehenof the global hemodynamic behaviors
under
various
conditions.
physiological
Moreover,inconsideration of the factthat the present
sion
model
was
(c) Gradelldysfunction
tions
EAA11
of
ological
4504DO]soseo150lno/'se/oo50
leD2fiD700/so/DOso
;.gE:
Di""i'
state
x,,xin
case
Eis s,Ki/--
XAY
o.?o.t
the
on
baseline hemody-
islimited
to predichemodynamics in normal or seminormal physistates becausemarked
changes in physiological
will activate
present model
regulatory
in the
mechanisms,
short
term
to
hemodynamics at a specific levelthroughregulations
of vascular tone, cardiac function
and totalblood
model
fitfor predictions
volume, etc. A mathematica]
of hemodynamics
in various physiologicalstates must include
both a model of the cardiovascular system and other
mainly
the
autonomic
nerveus
reflex,
that
work
maintain
.)-so./DO
11
based
constructed
parameters,the
namic
o.sTlh/e/sl
'c
e
o.204T/me[n}e6o.s/.n
models
a model
describing
various regulatory mechanisms,
Such
development
in
our
ongoing
is current]y under
study.
(d) Gradellldysfunction
Fig. 10
Predictions
and
measurements
flowsunder
pulmonary venous
conditions
4.
Conclusions
cardiovascular
system
is a
hemodynamics
in
any
separate
segclosed-loop
ment
isdetermined by hernodynamic interactions
throughsystem,
JSME InternationalJbumal
NII-Electronic
NII-Electronic
Library Service
of Mechanical
Mechanical Engineers
Engineers
of
493
Althoughtherehave been many
experimental studies on hemodynamics of
the whole
out
numerical
system.
and
differentdimensions
until
now,
most
with
them
of
degrees of
have been focused
various
accuracies,
understanding
the
of
the
significance
of
the
closed-loop
concep-
within
them
satisfactorily
ranges
physiological
reasonable
agreed
with
the
avai]able
and
some
in vivo
of
ComputationalModeling of Cardjovascular
Response
to Orthostatic
Stress,
J.Appl. Physiol.,
Vbl.92(2002),
pp.1239-1254.
(5) Roelandt,J.R.T.C.and Pozzoli,M., Non-InvasiveAssessment
of LeftVentricular
Diastolic
(Dys)Function
and
may
serve
as a usefu1
assistant
regulations
nia.Dahn,
(7)
(9)
(2005),pp.1203-l208.
(10) Iwase, H. and Liu, H., Computational
S.R
(1997),pp.H1499-H1515.
J.W., Jr.,Ghorbel, F.H.,Ware, D.L.
and Bidani,A., A Human CardiopuLmonary System
Model Applied to the Analysis of the Vblsalva ManLu, K., Clark,
JSneInternationatJournat
at a
Am. J.Physiol.,
Nlo1,272
Circ.Physiol.,
Vbl.41)
(Heart
A.C.,
(1) Sun, Y/,Mazen, B.,Rechard,J.L.and Salvatore,
tionundertheInfluenceofPericardiumandBarorefiex,
and
Glance,
References
(2)
of
pp.1321-1329.
by grant-in-Aidfor
ScientificResearchNo.(B)17300141,JSPS.
Modeling
LeftVentricle
Dynamics and Flow Based on U]trasonoData,
JSME
Int.J.,Ser.C, Nbl.46,No.4 (2003),
graphic
Acknowledgments
is,in part,supported
Model in Isolated
Canine Hearts.Am. J.Physio].,Nbl.253 (Heart
Circ. Physiol.,Vbl.22) (1987),
pp,1381-1389.
Han, H.,Jonathan,R.,Paul,E, Daniel,B. and Mathew,
S,M.,Role of ImpairedMyocardialRelaxationinthe
Production of ElevatedLeft Ventricular
FillingPressure, Am, J,Physiol,,
Circ,Physiol.,va]1,288)
(Heart
tance
form an integrated
computational
model
eapable
of predicting
hemodynamicsin various physiologicalsthtes.
work
I.B.J,
and Nilson,R.,Plethysmographic
in Vivo
Determination of Elastic Propenies of Arteries in Man,
J.Appt, Physio],,Nbl.28 (1970),
pp.328-332,
to
This
tool
ogy,
mea-
surements. In addition,
the successful
application
of the
presentmodel to sirnulate the cardiac hemodynamic characteristics
in patients
with
heart abnormalities
suggests
latorymechanisms
(1998),pp.H1733-H1747.
(4) Heldt,T., Eun, B.S.,Roger,D,K. and Roger, G.M.,
presentmodel
itunderscores
some
isolated
cardiovascular
segments,
little
attention
has been givento the globalhemodynamic interactions
that naturally exist in the system. The present
computationalmodel provides a quantitative
insightintothe global
Am. J.Physiol.,
Circ.Physiol.,
Nbl,281)
(Heart
(2001),pp.H2661-H2679.
between CarotidBaroregula(3) Ursino,M,, Interaction
exclusively
on
hemodynamics,
erver,
1299.Engelberg,
(13)
monary
PhysioL,Vol.196C1959),pp.401-414.