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Article1379235922 - Verma Et Al
Article1379235922 - Verma Et Al
A theoretical study of respiratory stability, based on a simple CO2 and O2 model of the respiratory
system has been investigated. A model of the human respiratory system is proposed which has a
satisfactory performance under different physiological conditions. It is shown that the central
component is not involved in respiratory instability phenomena such as periodic breathing whereas the
peripheral component plays a major role.
Key words: Respiratory, CO2 and O2 model, instability.
INTRODUCTION
Mathematical modeling of the respiratory system started
with the work of Gray (Gray, 1949) which was published
in 1945. He formulated pulmonary ventilation in relation
to hydrogen ion concentration, carbon dioxide and oxygen tensions of arterial blood in the steady-state and in
doing so becomes the first person to provide a mathematical description of the chemical control of ventilation.
Periodic breathing, characterized by rhythmic waxing and
waning of the ventilation of the lungs, occurs in respiretory disease. The phenomenon is accompanied by cyclical changes in arterial carbon dioxide partial pressure,
which rises with increased ventilation and falls with
Verma et al.
331
d(vTCT ( t ))
v dpACO2
= QCAT( t ) QCvT( t ) + M +
.
dt
pb 47 dt
p ACO2 p ICO2 dv
+
.
pb 47
dt
Where;
QC AT
(1)
QC vT
sues with the venous blood, M the rate at which CO2 is produced
inside the tissue, v is the volume and (pb 47) is barometric pressure less water vapour pressure at body temperature.
Now, the rate change in the amount of CO2 in the lungs is
expressed as:
Equations (1) and (2) can be written in terms of related CO2 partial
pressures by assuming a single straight line:
C AL ( t ) = p AL ( t ) + , C AT ( t ) = p AT ( t ) +
C vL ( t ) = p vL ( t ) + , C vT ( t ) = p vT ( t ) +
(4)
C T ( t ) = pT ( t ) +
(5)
p AL ( t ) = p L ( t )
(6)
The CO2 partial pressure in the arterial blood entering the tissues is
equal to the CO2 partial pressure in arterial blood leaving the lungs
that is, equation (6) becomes:
dp ACO2
d (v L C L ( t ))
v
= QC vL ( t ) QC AL ( t ) + vC I vC L ( t ) +
.
dt
pb 47 dt p AT ( t ) = p AL ( t rA ) = p L ( t rA )
p ACO2 PICO2 dv
+
.
pb 47
dt
(2)
(C
aO2
p IO2 p AO2 dv
+
.
pb 47 dt
dp AO2
v
.
p b 47 dt
(7)
pvT ( t ) = pT ( t )
(8)
p vL ( t ) = p vT ( t rv ) = pT ( t rv )
(9)
S T .dCTCO2
dt
(10)
332
S T .dCTO2
(11)
dt
1
C vBO2 .QB = C aO
.QB MRBO2
2
S B .dC BCO2
(12)
dt
S B .dC BO2
(13)
dt
From equations (3) to (8) into equation (1) and (2), we get:
dp ACO2
dpT ( t )
QpT ( t ) Q
M
v
=
+
p L ( t rA ) +
+
.
dt
vT
vT
vT p b 47
dt
p ACO2 p ICO2 dv
.
dt
pb 47
(14)
dp ACO2
Q + vp L ( t ) vp I
dp L ( t )
Q
v
=
pT ( r rv )
+
+
.
dt
vL
vL
vL
p b 47
dt
p ACO2 p ICO2 dv
.
pb 47
dt
(15)
v( t ) = C pT ( t ) + C
Where the constant parameters
(16)
C ( C > 0 )
and
are
dp ACO2
dpT ( t )
Q
Q
M
v
= pT ( t ) +
pL ( t ) +
+
.
dt
vT
vT
vT pb 47 dt
p ACO2 pICO2 dv
.
pb 47
dt
(17)
dpL ( t )
p + Q
Q + C
= C 1
pT ( t )
pL ( t ) C pT ( t ) pL ( t )
dt
vL
vL
vL
C pI
vL
(18)
Verma et al.
( pT ( t ), pL ( t )) ( pT , pL )
dp
p
pICO2 dv
Q
M
v
pT ( t ) +
+
. ACO2 + ACO2
. =0
vT
pb 47
dt
vT pb 47 dt
(19)
C p1 + Q
vL
pT
Q + C
vL
pL
C
vL
pT pL +
p ACO2 pICO2 dv
.
pb 47
dt
C p1
vL
dpACO2
v
.
pb 47 dt
(20)
pT = pL
pL2 =
dp
p
pICO2 dv
M
v
. ACO2 + ACO2
.
+
Q pb 47 dt
dt
pb 47
dp ACO2
M C
p + MB MpI
v
+
PI pL C I
+
.
Q C
C
Q pb 47 dt
p
pICO2 dv
+ ACO2
. =0
pb 47
dt
RESULTS AND DISCUSSION
In this chapter, a simple model of the CO2 plant was
derived from physiological considerations taking into
account the fundamental parameters of respiration the
CO2 metabolic production rate in tissues, the CO2 partial
pressure in the inspired air, the blood flow, the arterial
and venous circulation time lags, the volume of tissues
and lungs and slope of the CO2 dissociation curve (Figure
2). The description of the plant is based on a classical
two compartment representation (the tissues and the
333