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The JapanSociety

The
Japan Society

of Mechanical Engineers

ofMechanicalEngineers

484

A CIosed-LoopLumped Parameter ComputationalModel for


Human Cardiovascular System"
Fuyou LIANG"
For purposeof

actions, a closed-loop
cardiovascular
vascular

system

circulations.

and Hao LIU'"'

better
understanding
of the behavior
of the global hemodynamic interlumped parametercomputational model was developedforthe human
detailedcompartmental
Construction of the model
with

descriptionof the heart and the main


implemented based on a phenomeno-

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

parameters predictedby the present model


or within
reasonable
physiological
ranges. Furthermore,
the present
model was applied to predict
the clinical cardiac hemodynamic
characteristics
observed
in patients
with
heart abnormalities.
Reasonable agreements
between predictions
and
measurements
indicatethat the presentcomputational
model
can
were

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

key 1-?)nts:Human CardievascularSystem,Regulatory Behavior, Closed-Loep, Lumped


ParameterComputational
Model,Hemodynamic lnteraction

loopones. Sun, et al.(i) proposed a computationa]


model
forright-left heartinteraction
and
agreements
begood
tween predictions
and clinical observations were obtained.

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

to take into account the effect of the global


system
in studies focused on hernodyamics

in some specific cardiovascular


segments.
Due to the highlycomplicated
stmcture
of thecardiovascular system, highdimensional
numerical approaches
]imited to studies on local hemodynamics, in
lumped parameter models,
which
mathematically represents the characteristics of hemodynamicswith
are

always

contrast,

a series of

may providea quantitative


insight
parameters,

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

Al] of their computational


fectivein representing

simple

in parallel
to form a

cir-

]oop. A mathematical mode] forthe cardiovascular system


and
itsinteractionwith carotid baroregulation was proposed by Ursino(3),who,
in his study, separated the peripheral
circutation intosplanchnic and extrasplanchnic circulations
in consideration
of the difference
in their responses
to nervous
control.
Heldt,et al. (4}

dependingon

from very

In their work, the cardivided intoseveral subsystems

culatory

tionalmodel

purpose,ranging

for the hu-

model

system.

system

intothe behavior ofthe globalhemodynamics, There have


been various such models varying in complexity
and form
study

a mathematical

to

computa-

in their

system
orthostatic

stress.

be efi
hemodynamic parameters within
of predicphysiologicalranges by good fits
models

were

eyinced

to

Received26thMay, 2005 (No.05-4044)


Graduate
Schootof Scienceand Tlechnology,
Chiba University,
1-33 Yayoi-cho, Inage-ku, Chiba 263-8522,
Japan.E-mail:fuyouliang@graduate.chiba-ujp
Departmentof Electronics
and MechanicalEngineering,
Chiba University,
1-33 Yayoi-cho,Inage-ku,Chiba 263-

tionsto clinical measurements. Nevertheless,


most of their
on left-right
heart
studies were either focused exclusively
interactionsby assuming
a simplified
representation
of

8522, Japan, E-mail: hliu@faculty.chiba-u.jp

simplified,

SeriesC, Vbl.48, No.4, 2005

vessel

system

or concentrated

specific compartments
none

of

with

the models

on

hemodynamics insome

the remainder
simultaneously

neglected

or

embodied

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of

4S5
a

detaileddescriptionof both peripheralcirculation and


circulation.
Inasmuch as the factthat

cardiac-pulmonary

thehuman

cardiovascular

system

isan integrated
closed-

loop system, a better


understanding
of the nature of the
hemodynamic interactions
and the mechanisms
by which
the system operates and regulates inresponse to hemodythe

main

tional
are

compartments

cardiovascular

In thissense, these models

model.

in series, The pulsating


heartprovidespower forthe whole circulatory system by
rhythmically
pumping bloodto the peripheralcirculation
veins that connect

through

where

other

order

to

The purpose of the presentstudy isto develop a comcomputational


model thatprovides
reasonable
prehensive
of hemodynamics in the main cardiovascular
predictions
circulations
and
tool fbr quantitayieldsa mathematical
tiyelyinvestigating
the behavior of the global hemody-

modeled

tonomic

nervous

system

also contributes

in which the functiQn of the auis involvedto form an integrated

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

lefthearts isthe pulmonary


bloodisoxygenated,
These circulations
right

and

heartrate. Moreover, considering


the influence
of intrathoracic
pressureon venous transmural pressure, the vena
cava was
separated
into two portions,one
insideand another outside the thoracic chamber. Where
available, values of the parameters
involvedinthe present
model
are mainly
detemined on the basis of previous rea variable

circuare

associated

with

an

ethcacious

mathematically

computational

simplest and most

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

lumped parameter modeling

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.

basis for furtherwork

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

whereas values parameters


not derivable
from literports,
ature have been estimated basedon either the anatomical

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

dividedintoseven subsystems includingthe left


right hearts,
the upper limb and the cerebral circula-

mately
and

tions,the renal circulation, the splanchnic


circulation,
lower ]imb circulation and the pulmonary circulation
JSMEInternationulJo{trnal

toww

Hrmios

the
as

Fig.1 A

sketch

of

the human

vascular

system(b)

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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

InertanceResistance LdaRrm,Rav Lp,'R.,,Rps

opment.

Based

seven-compartment

on

the arterial tree computer


model
concept(4),
the hemodynamic

teristicsof the human


sented

by a

closed-loop

Herein the heartsare

cardiovascular

system

are

and

characrepre-

illustrated
in Fig,2 (a),
by the time-variant elas-

circuit as

represented

the

scending
ney,

KID, SPL, LLB, ULB

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.

have genera] meanings,

and

Sub-

e.g, a, a4

indicateartery, arteriole, capillary and vein, respecby an assembly


of e]ectric
elements
thatcharacterize
the
tively. Value identification
of these parameters
isin two
hemodynamics in arteries, arteriolar and capillary beds, ways: thefirst
way isto refer to previous
literature
where
roughly
values
and veins, respectively. Other than some previous
available,
and
the
second
to
estimate
the
pure
mathematical
models,
each
element
in the present model
based on the anatomical
data or the general physiological
has a specific physical meaning,
which
may
facilitate
a
knowledge at the first
step and subsequently
repeatedly ador anatomical databased parametervalue
them until reasonable agreements betweenpredictions
physiological
just
identification
and adjustment. Considering
thatthe numan in vivo clinical dataare obtained.
ber of the parameters and variables involvedin the present
The presentmodel encompasses
a number
of descripmodel
isover 153, fbrthe sake of simplification,
a glostions of not on]y arteries and veins but also arteriolar and
sary isoutlined
in [fable
1 instead
of a detailed
statement
capillary
beds.These vessel systems operate at transmulevelsand with different
fOreach of the parameters.
LH, RH refer to the leftheart ral bloodpressures
of different
and
righthearts,AA, DA refer to the ascending
and deblood volume
baselines,exhibiting remarkable
differences
tances,

and

the

peripheralcirculations

Series C, M]1.48, No. 4, 2005

are each

mimicked

c, v

JSMEIntemationatJourual

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487
- vo]ume
in vascular pressure

Thble2

(P-V)relationship.

Moreover, itis also not true that vascular


compliance
is fixed
because of the nonlinear hemodynamic properties,Tb ac-

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-

Z[mL] refers to the volume


constant,
and
vLmL]
indicatesthe blood volume
contained
in vessel, Accordingto Eq. (1),
the different
vascular elastic characteristics
of
of different
vascular systems
can be reflected by means
definingdifferentvaLues for Eo and Z. Such a mathematical description
of P-V relationship
isfoundto well fitthe

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.

Two examples are givenbelow:


For the LV (left
ventricle),
itis givenby,

Ei,.F,

+El,blF.,

elv=

(eiv
lr,, )

Ogtst,

ela

sistingof

`[talk

threeelastic compartments,

namely,

According to this model,


ventricles
can be expressed
etv

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

inTables2 and 3 are the values

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

not actually work

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

And for the LA

Ll

1--e,-;,i[l';lii'
(2)

(i-e
t"la)

380

each

The mathematical
by Sun, et al.(i)and

is adopted in thispaperwith several modifications made


to facilitate
the adjustment of E... (maximum systolic

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

leftventricie and Vin,.[mL]is a volume


constant,
over, the interrelationship
betweenthe leftand rightventriclesis noteworthy
inasmuchas that the leftand right

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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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)

Schematicsofthe basicunits inthe

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

static characteristic and a

for.Furthermore, we distinguishbetween the systemic veins and the yena cava regarding
theirdifferences
counted

invascular

elastic

properties.two groups

of equations

are

constructed.

For the systemic

they are

veins,

written

as:

(exp(
(exp(
V(t)k-,Vhn

1+

Vb"

V(t)i,

Evumin+ Eve...
Evo(v,t)

))

(8)

this paper,herein only

=qin

And at node

EvtD(v,t)
i+

V(t)i,.Vbcn

1/(Eui)zup+s.p
=

(11)

Where subscripts v and vc denotethesystemic veins and


thevena cava, respectively. Vl.,Vl..[mL]are the vo]ume
K,, and KL. [mL]are two parameters controlof the static functions
at the central
point,
Tev, Teue [sec]
are the time constants
indicating
the timevariant
rate.
E,omin,E,,,o.i.LmmHgmL-i1are the minimum eiastances,
and
E,o..., E,dl... [mmHgmL-i]the
maximum
elastances.
E,o(v,t),E,.o(v,t)[mmHgmL-i]
are the static elastances
determined by venous
volume,
and E,(v,t),
E,.(v,t)
[mmHgmL-i]are the time-variant
elastances. Valuesof theparameters
in the equations are
determined by rnatching the computed
volume-elastance
curve
with
the reported
dataCii).
The parameters are sumconstants.

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

limitationof the length

the

d:"tp

(9)

dt

of

the

-q..t

Tt

they are givenby:

cava,

Because

nodes.

general fbrmsof these equationsare elucidated.


Tlypically,
the general forms can be
described
by two equations, ene isthe mass preservation
equation
and another
isthe fbrce equilibrium
equation,
according
to Fig.3 (a)
and (b),
they are written as fo11ows:
At node E:
dv
of

))

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

]represents the bloodflowthrough a vascular


q [mLsec-i
of the other
compartment,
Definitions
parameters can be
found in [fable1.
Allowing forthe nonlinear
coupling
of the 62 differential equations, the solution of these equations is perforrned by the use of a fourth-orderRunge-Kutta method
with
acljustable
step ranging
from O.5 ms to 2 ms. Equa-

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

etc. are so]ved

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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Library Service

The Japan Society


TheJapan
Society

of Mechanical Engineers

ofMechanicalEngineers

489
-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)

Rigbt heart volumetric

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

Moreover,the well known a wave, x descent,v wave and


y descenton the atrial pressurecurves are also accurately
'

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

variation over a cardiac cycle charac-

JSMEhitemationalJournal

(measurement)

change

hemodynarnics

of cardiac

quick reduction in systole and a two-stage


expansion
in diastole
has been truly reproduced
by the
ventricular volumetric variation curve plotted
in
predicted
Fig.5. For the purposeof a clinical databased examiterized

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-

SeriesC, Vbl.48, No,4, 2005

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Society ofMechanical
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Engineers

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

46g$8-

so

an

(b)
Fig.6

Large

:.ge

arteries

Predictedblood flowwaveforms
largearteries

through

the

aorta

op
O.O

putedfrom the three-dimensionalleftventricle model constmcted


basedon a set ofultrasonic medical imagestaken
the simina healthyman. Accordingto Fig.5 (b)and (e),
with the measureulated result issatisfactorily consistent
ment,

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

the transtricupid and

waveforrns

through the

arteriolar

and

capillary

beds of

limband cerebral circulation are illustrated


in
fbund
Fig.7. The pulsatile
features
of the bloodfiowsare
to be greatly
dissipated
at the arteriolar leveland be further damped to a nearly constant
fiow pattern
in the cappredicted,
3.2 [hransferofbloodflowandpressurewaveforms illarybed. This phenomenon can be mainly ascribed to
in the peripheral
circulation
the presence
of largevascular resistances to blood flows
Shown in Fig,6(a) and (b)are the computed
blood in the arteriolar and capillary beds. Evidence can also be
flow waveforrns
through the aorta and the big arteries
foundinterms of the change in blood pressurewaveform
along
the vascu]ar
systems
as shown
inFig.8,where
the
branchingto the upper limbsand brain,
the splanchnic oris
reduced
from
100
to
lower
limbs.
The
commean
value
of
the
arterial
the
kidneys,
as
well
as
the
pressure
gans,
upper
limb
arterioles
accompanied
results
are
approximately
in
with
the
about
45
mmHg
in
the
phase
general
puted
of pulsatile
in vivo measurements(i2)
in terms Df the shapes of fiow
by a reduction in the amplitude
pressurefrom
about
40 mmHg
to approximate
1.5mmHg.
waveforms,
the phasedifference
among bloodflowstodifin early
Leading from thecapillary bedsto therightheartare
ferent
circuiations and the reverse flows occurring
thesystemic veins and the vena cava. Simulatedblood
diastole.
thevenous flowsto the leftand
cal E, A waves of the ventricular
perfUsionflowand the S,
D waves of the atrial perfUsion flowhavebeen reasonably

the

In order to gain a betterunderstanding


of the transfer
and the change inwavefOrm
shape of bloodflowthrough
the vascular systems, the model
generatedblood flow

flow waveforrns
through these vascular
systems
are pletted in Fig,9, where
blood flows are observed
to again be-

SeriesC, Vbl.48, No.4, 2005

come

upper

more

and

more

along the venous


pulsatile

system

JSME lhtemational
Journal

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Society

of Mechanical
Mechanical Engineers
Engineers

of

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

bution in the cardiovascular

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

for the vascular

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

the known total resistance of each circulation


dictreasonable pressurefa]1in these vascular levelsand
on

adjusted

Predicted blood flow

of

information on the arteriolar and capillary comIn the presentstudy,


partments is available in literature.

o
O.4Time(s).O.6

fbra hostof parameters


involvedin
For purposeof reproducing the closed-loop

assignment

suMcient

x.

tt

O.2

va]ue

fbund in Refs.(2) and (4). Valuesof parameters in the


heartmodel havebeenderived
from Ref, (1),However, in-

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

lary beds. In addition,


terial resistances

Pulmona-''arteries

tions.

Pulmonary[apillaries

and

there

In the present study,

'

of

arterial

roughly calculated according

Pulmonarvveins

is a]so lack of data on the

compliances

to

basedon the,anatomical-data-based

Systemic

of

Systemiccapillaries

,Systemicveins
rsME Ineernatiotiat
JourtLal

.32S2

regional

resistances

were

ar-

circula-

firstly

the law of fluid


mechanics

Systemicarteries
arterieles

the

3D

computer

modgl

Subsequently the arterial resistances


were
adjusted
carefully
so as to obtain arterial bloodflow
waveform
comparable
to theinvivo measurepredictions
the

arterial

tree.

Seriesg,1'ol.48,
No.4, 2005

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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

predictionsof hemodynamics, direct


data is still imperativeif a more deliberate
model
were
to be deyeloped,
As to the application
of the present model, we have
to proclaim that the presentlumped parametermodel is
able to predict
hemodynamic parameters within reasonIn
able physiologicalranges but not with high accuracy.
fact,we have sought to construct a computational model of
the cardiovascular system capable of providing
rational inhemodynamic behaviors as well
vestigations of the global
hemodynamic interactionsamong
the reas the reciprocal
circulations.
High
dimensional
simulation
of
local
gional
provide

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

Neverpossess high accuracy.


high
dimensional
simulation
are
theless,applications of
always
limitedto some specific cardiovascular
segments.
Moreover, al]owing for the high dependence of prediction
(b)
Et"//vlVl11

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

SeriesC, V}I.48, No.4, 2005

for transmitral and


diastolic
dysfunction

4.

Conclusions

Inasmuch as the hurnan

cardiovascular
system
is a
hemodynamics
in
any
separate
segclosed-loop
ment
isdetermined by hernodynamic interactions
throughsystem,

JSME InternationalJbumal

NII-Electronic
NII-Electronic

Library Service

The Japan Society


TheJapan
Society

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

dynamic hemodynamic interactions


among
different
recardiovascular
circulations.
Despite
the
fact
that
gional
the

the

significance

of

the

closed-loop

concep-

tion in studies concerning hemodynalnics.Most of the


hemodynarnic parameters
by the present
model
predicted
were

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

thatthe present model

may

serve

as a usefu1

assistant

regulations

nia.Dahn,

(7)

(8) Maughan, W,L., Sunagawa, K, and Sagawa, K,,


NkentricularSystolic
Interdependence:VOIume Ela-

(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

Science Ltd., Oxford.

E,M., Nadim, A. and Larsen,J.,Numerical Simulation and Experimental


Validation
of Blood Flow inArteries with Structed-Tree
Outfiow Conditions,Annals
of BiomedicalEngineering,
Nlo].28 (2000),
pp.l281-

Comprehensive Model forRight-Left Heart Interac-

Am. J.Physiol.,
Nlo1,272
Circ.Physiol.,
Vbl.41)
(Heart

GM, J.S., The Cardiovascular


System
Blackwell
(l999),

02) Olufsen,M.S., Peskin,C,S,, Kim, W,Y., Pedersen,

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

(il) Aaronson,RI,,Ward, J,RT.,Wiener,C.M., Schulman,

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

FillingPressure, 2nd Virtual Congress of CardiolArgentine Federatien


ofCardiology,
(2001).

R.L.,BasicTransportPhenomena inBiomed(6) Fournier,


icalEngincering,
Tlaylor& Francis,Pennsy]va(1998),

tool

forcomputer-aided diagnosis and treatment of cardiovascular diseases.


Moreover,considering thathemodynamics may change significantly dependingon the physiologicalstate, the present computational
model
may
provide
a basisfor further
incorporation
of mode]s
of the autonomic
nervous
system
and other models describing
reguinvolved in hemodynamic

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.,

islimitedto low dimensional prediction,

presentmodel

itunderscores

PulsatingHeart:A Mathematical Medet,


Am. J.Physiol.,
Nbl.275(Heart
Circ.Physiol.,
Vbl.44)
tion and the

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

helps deepen the

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

J. and DuBois, A.B., Mechanics of PulCirculation


in IsolatedRabbit Lungs, Am. J.

PhysioL,Vol.196C1959),pp.401-414.

(14) Guyton, A,C,, Tlextbookof Medical Physiology,8th


Ed.,(1992),pp.150-254,Saunders,Philadelphia,RA.

SeriesC, Vol.48, rvo.4, 2005

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