Models and Simple Controllers

Journal of The Institution of Engineers, Singapore
Vol. 45 Issue 6 2005
MODELS AND SIMPLE CONTROLLERS FOR BLOOD

PRESSURE REGULATION
IN POST CARDIAC SURGERY PATIENTS
H.W. Lee1, S. Lakshminarayanan1, G.P. Rangaiah1*
ABSTRACT
Automatic control of blood pressure in post cardiac surgery patients is desirable for
better patient care, reducing the workload of healthcare staff and costs. Many studies
have been reported on modeling and/or control of blood pressure in patients. Motivated
by the need for simple and effective controllers for clinical applications, this study
focuses on the ubiquitous and proven PID controllers for blood pressure control. First, a
detailed and realistic model of a hypertensive patient is successfully developed and
implemented; it consists of the drug response model of Slate et al. (1980), models for two
internal reflexes of the body and random disturbances. Next, proportional-integralderivative (PID) controller is tuned by several methods and the resulting controllers are
tested on sensitive, nominal and insensitive patient models, for a pressure drop of 30
mmHg. Performance of these PID controllers is compared among them and with that of
internal model control (IMC) and enhanced internal model control (EIMC). All
controllers are tried with and without adaptation. Results indicate that EIMC and PID
controller with Smith predictor have better performance for blood pressure control of the
three patient models.
INTRODUCTION
The human body involves many complex feedback control systems that are collectively
called as homeostasis, some of which may be disrupted during surgery. Hence, postsurgery patients require intravenous administration of suitable drugs to maintain key
physiological variables such as blood pressure within desired limits. These allowable
limits are rather narrow and small excursions beyond them may lead to undesirable
outcomes. Hence, introducing automatic control of key physiological variables is
beneficial for better patient care and reducing workload of healthcare staff. The simplest
and potent type of automatic controllers is based on the feedback concept. Automatic
feedback control systems are designed to control crucial variables by adjusting
manipulated variables such as drug infusion rate based on the measured feedback signal.
The regulation of mean arterial pressure (MAP) in post cardiac surgery patients is an
example where automation is particularly attractive. In such patients, patient's blood
pressure is measured and the infusion of the fast-acting vasodilator - sodium nitroprusside
(SNP) is adjusted as necessary.
Department of Chemical and Biomolecular Engineering, National University of Singapore,

Singapore 117576.
Author for correspondence; Email: chegpr@nus.edu.sg. Fax: (65) 6779 1936; Phone: (65) 6874 2187
14

SNP became commercially available for blood pressure control only in 1974. Isaka and
Sebald (1993) reported that Jackson et al. and Sheppard et al. worked on blood pressure
regulation using a proportional-integral (PI) controller for administering SNP to patients
in intensive care unit (ICU). Asla and others (Isaka and Sebald, 1993) had shown that
automatic controller was able to maintain blood pressure within 5 mm Hg in almost
94% of the 110 hours of testing as compared to the 52% achieved by an experienced
clinician. Isaka and Sebald (1993) reviewed the works on blood pressure control to
consolidate the past contributions and to find a clearer direction for further research.
Gopinath et al. (1995) and Rao et al. (1999) worked on multiple drug delivery which
includes SNP for controlling vascular resistance and dopamine for regulating cardiac
output of patients. A review of these and other works on modeling and control of blood
pressure in patients is available in Lee (2004).
Many different controllers were designed and studied for blood pressure regulation.
Noting that the controllers should be as simple as possible for clinical applications, Hahn
et al. (2002) employed internal model control (IMC) coupled with adaptation for blood
pressure regulation in models of sensitive, nominal and insensitive patients. The
controller worked well for nominal and sensitive patients but was unable to fulfill one of
the performance criteria for the insensitive patient. Subsequently, Ng (2003) tested
enhanced IMC (EIMC) of Zhu et al. (1995) for these patients but there was not much
improvement in control performance. In both these studies, model for the patient's
internal reflex (renin-angiotensin system, RAS) was not implemented properly and
baroreceptor reflex system (BRS), which is another relevant internal reflex in human
body, was not included at all. The two main objectives of the current study are (1) to
develop and employ a realistic patient model for blood pressure regulation and (2) to
evaluate several simple controllers including the ubiquitous proportional-integralderivative (PID) for a range of patient dynamics.
PATIENT MODEL FOR BLOOD PRESSURE
A comprehensive model of patient for studies on blood pressure regulation should have at
least four components: a drug response model, models for internal reflexes, measurement
dynamics and random noise due to respiration, patient movements etc. (Fig. 1). Similar to
industrial processes, patient dynamics will generally vary from one individual to another
as well as with time. Slate et al. (1980) performed extensive clinical studies on patients to
find a model that relates the change in MAP to the infusion rate of SNP. Based on graybox analysis of experimental results to programmed SNP infusion rate as pseudo-random
binary signals, Slate et al. (1980) derived a simple linear first-order transfer function with
two time delays for drug response of patients. Although the drug response model should
consider both multivariable and nonlinear characteristics, it was found that the blood
pressure response to SNP is reasonably linear over a certain operating point and hence
can be analyzed by assuming piece-wise linearity. Like many earlier studies (e.g., Hahn
et al., 2002), this work too employs the model of Slate et al. (1980) for drug response:
15

Pd ( s) Ke Ti s (1 + e Tc s )
=
I ( s)
s + 1
(1)
where Pd(s) is the change in MAP (mmHg) and I(s) is the infusion rate of SNP (ml h-1).
Figure 1: Schematic of blood pressure model showing drug response model (Gp),
internal reflex (RAS) model (Gr) and random disturbances (Slate et al., 1980)
Table 1: Parameters for the different patients (Hahn et al., 2002)

Parameter
Units
-1
Sensitive
Nominal
Insensitive
Steady-state gain, K(1+)

Recirculation,
mmHg/(ml h )
-
-9
0
-1.0
0.4
-0.25
0.4
Initial transport delay, Ti
20
30
60
Recirculation time, Tc
Time constant,
s
s
30
45
40
75
60
In eq. 1, K (mmHg/(ml h-1)) is a measure of the sensitivity of a patient in responding to

the uptake of SNP, and a higher absolute value of K reflects higher sensitivity. The
dimensionless parameter, gives the fraction of SNP available for recirculation after
initial absorption. According to the unpublished study of Sheppard (Slate et al., 1980),
the steady state gain given by K(1+), varies between -0.29 and -9.0 mmHg/(ml-h-1).
Obviously, the higher the patients sensitivity to SNP, the lower the value of will be as
most of the drug is absorbed before recirculation. The other three parameters in eq. 1 (all
in seconds) are: initial transport delay (Ti) which is the amount of time required to
transport the drug from the injection site to the effectors site, recirculation transport
delay (Tc) which is the time delay for recirculation, and the system time constant, is the
effective time for site uptake of SNP, drug-cells reactions and other biotransformations
leading to changes in the total peripheral vasculature resistance. As clearly stated by Slate
et al. (1980), the model in eq. 1 is only valid for small changes in SNP infusion rate and
does not take into account changes due to circumstances other than SNP infusion such as
delivery of other drugs. The nominal values of parameters in eq. 1 are: K = - 0.72, = 0.4,
Ti = 30, Tc = 45 and = 40 (Slate et al., 1980). Table 1 summarizes parameter values for
16

three patients - sensitive, nominal and insensitive, reported in Hahn et al. (2002), which
include the above nominal values.
There are several short- and long-term internal reflexes in human body to regulate blood
pressure (Guyton, 1980). Only the short-term mechanisms are relevant in post-surgery
patients since desired settling time of a controller is less than 20 minutes. After reviewing
these, Lee (2004) identified that RAS and BRS should be included in the complete model
of a patient for studies on blood pressure control. The former is an internal blood pressure
buffering system that is activated when MAP drops below a threshold value. Through a
series of chemical reactions from renin to angiotensin II, RAS can alter the total
peripheral resistance of arterioles and hence increase blood pressure. Kaneko et al. (1967)
noted that the typical range of threshold for activation of RAS is between 70 to 75 mmHg
for the general population. In this work, the average value of 72 mmHg will be used.
Also, RAS has a range of MAP (50 to 110 mmHg) where it remains effective. Although
Hahn et al. (2002) noted the existence of threshold and range for RAS, the simulation
system was based on deviation variable (and not on actual MAP). Consequently, the
threshold value was not representative enough and the RAS system will always be
activated even though the patients MAP does not fall below 72 mmHg. Hence, an
improved model is developed and employed in this study.
15
-1.6
deviation variable
Threshold
Pin
-1.4
1
P_input
G_r
Saturation
Threshold
Gr
Transport
Delay1
Pout
240.0s+1
Effective range
240.0s+1
Tr
P_output
2
P_ref
Figure 2: Model of Hahn et al. (2002) on the left and the improved model on the
right for RAS
In order to have a better representation of patient's internal reflexes, the RAS model
developed here in Simulink will receive the actual MAP as the input. However, the
measurement system dynamics shown in Figure 1 was ignored for simplicity. Fig. 2
shows the model of Hahn et al. (2002) and the improved model. In the latter, the switch
simulates the RAS threshold of 72 mmHg whereas the saturation block represents the
range of MAP (50 110 mmHg) where RAS remains effective. Another minor change is
the gain of the RAS system from -1.4 to -1.6 that is based on the value reported in
Cowley et al. (1971). The responses of the two models are compared for a drop of blood
pressure from 130 to 100 mmHg (Fig. 3a) and from 100 to 70 mm Hg (Fig. 3b). For the
sake of comparison, the 30 mmHg pressure drop was fed into both models as standalone
units without the influence of the other transfer functions in the closed-loop system. Since
the MAP does not become lower than the threshold value of 72 mmHg for the case of Fig.
3a, RAS was not activated and this was clearly simulated by the new model, which does
not produce an output due to the drop of blood pressure from 130 to 100 mm Hg.
However, model of Hahn et al. (2002) produces a response which is not realistic for
17

simulating the patients internal response due to RAS. If a change of pressure from 100
mmHg to 70 mmHg was effected (assuming 70 mmHg as the final desired pressure is
realistic), both models produce the output indicating the activation of RAS (Fig. 3b). The
final output according to the model of Hahn et al. (2002) in Fig. 2a is (-30+15)(-1.4) =
21 mmHg while that by the modified model in Fig. 2b is (-30)(-1.6) = 48 mmHg.
25
50
45
20
35
P (mmHg)
15
P (mmHg)
Hahn's RAS model

New RAS model
40
Hahn's RAS model

New RAS model
10
30
25
20
5
15
10
-5
500
1000
Time (s)
1500
200
400
600
800
1000 1200
Time (s)
1400
1600
1800
2000
Figure 3: Comparison of response of RAS model of Hahn et al. (2002) with that
of the improved model for a 30 mm Hg step change from 130 to 100 mm Hg (on the
left) and from 100 to 70 mm Hg (on the right)
Figure 4: Theoretical response curve of baroreceptor reflex following an increase

in MAP when other pressure regulating mechanisms are removed (Guyton, 1980)
The BRS was incorporated together with the drug response model of Slate et al. (1980)
and the improved model for RAS. Although Slate et al. (1980) mentioned that BRS
response is not significant in the patients that were under our consideration, this might
not be always true. Several other researchers working on patient modeling for blood
pressure control often incorporated BRS into their simulation models (e.g., Gopinath et
al., 1995 and Rao et al., 1999). Being a nervous response, it might be true that the BRS
does not play an important role as post open-heart surgery patient may have some nerves
being destroyed. However, BRS pressure sensors are not only located at the aorta, they
are also located at the carotid artery at the neck. Chances of damaging these sensors at the
carotid artery during open-heart surgery are very minimal. Furthermore, the blood
pressure regulation under consideration uses SNP and RAS that act directly on blood
vessels of the entire human body. Blood pressure regulation via cardiac output is not
18

considered at the moment since the model of Slate et al. (1980) does not support a multivariable system. So, even though the nerves around the heart might be destroyed, the
entire BRS will not come to a halt due to surgery. The basic structure for BRS will still
be intact, from sensors to effectors, which are the nerve endings located at various blood
vessels in the body.
In this study, BRS was modeled as a black box based on the theoretical response curve
of MAP due to BRS alone following an increase of MAP (Fig. 4 taken from Guyton,
1980). In this figure, a sudden rise of MAP caused the baroreceptor reflex to respond so
that it approaches the value before the disturbance. (Similar response from the
baroreceptor reflex but in opposite direction is expected for a sudden drop of MAP.) The
"feedback" correction when the BRS is functional but all other pressure control systems
are removed can be seen to have an offset but the onset of the system is immediate or
within seconds (Fig. 4). Based on the typical response in Fig. 4, the transfer function of
the BRS is estimated as:
G clb = 1
(40 / 60) 8s + 0.333

=
8s + 1
8s + 1
(2a)
which is for a closed loop system similar to that in the right hand side of Fig. 1. The
corresponding open-loop transfer function is
Gb =
2
24s + 1
(2b)
deviation variable
1
-2
Pin (baro)
24s+1
70
Switch
Saturation
1
Pout (Baro)
Baroreflex
Constant
2
P_ref
Figure 5: SIMULINK model for baroreceptor reflex
Using this transfer function, the simulation model in Fig. 5 was created for BRS. Again,
the signal which was initially in terms of deviation variable is changed to the actual value
by adding the reference MAP value (P_ref). Similar to RAS, BRS is active in the range of
70 to 160 mmHg, which is simulated via the switch and saturation block (Fig. 5).
Baroreceptors are well known for their ability to adapt or reset; i.e., if they were
exposed to an elevated pressure for a period of time (varies from 6 to 48 hours), their
activity slowly decreases until they return to normal even though the blood pressure
remains elevated. Similar reset mechanism also holds true for the baroreceptors that are
exposed to a lowered MAP. This adaptation makes BRS suitable for only short term
19

MAP regulation. For the purpose of this study, since the adaptation mechanism takes
hours to complete whereas the desired settling is within 20 minutes, the adaptation was
neglected. Even though the adaptation has not been completed, BRS gain reduces in
magnitude; hence, an average gain of -2 for the first 20 minutes was used.
DESIGN AND EVALUATION OF CONTROLLERS
Fig. 6 shows the closed-loop system for blood pressure control with the PID controller,
drug response model (Gp), disturbance block incorporating RAS and BRS in the feedback,
random disturbances and an adaptation block for estimating (process) gain and
consequently updating controller gain. Random disturbances, following Hahn et al.
(2002), are simulated as white noise passing through a first order filter with gain of 12
and time constant of 30 seconds. Many simulations with various controllers on the
sensitive, nominal and insensitive patients (Table 1) showed that the same controller
(with settings based on the nominal patient) results in instability in the case of sensitive
patient. This is because of large variation in steady-stage gain among the three patient
types (see the parameter values in Table 1). Hence, the adaptation scheme of Hahn et al.
(2002) was modified for PID controllers and included in Fig. 6. The adaptation
mechanism estimates the patients gain from the controller output and MAP data, and
controller gain was then calculated using the tuning formulae. Simulation results showed
that the adaptive controllers are more sluggish than non-adaptive controllers due to the
extra time needed for estimating the correct gain of the patient. But, with adaptation, all
the three patient models can be regulated without instability (Lee, 2003). An a is
appended to each of the controllers/tunings given later to indicate the inclusion of
adaptation in the control system.
Dev
PID controller
Pi
Pd
P_nom
Controller
Gp
Set-point
P_d
Out1
P_a
P_ref
Adaption
pressure profile
Disturbance
Kc
Random Disturbances
Figure 6: Schematic of the closed-loop system with the PID controller, drug
response model, RAS and BRA in the disturbance block in the feedback path,
random disturbances (simulating stochastic activities in Fig. 1) and adaptation for
estimating process/controller gain
20

The PID controller was tuned by several techniques: classical Cohen and Coon (CC);
integral of absolute error minimization to set point change (IAE-servo) and to load
disturbance (IAE-load); settings determined from optimization using a genetic algorithm
(PID-GA) (Shen, 2002); and settings to mimic dynamic matrix control (PID-DMC)
(Haeri, 2002). To reduce the overshoot with IAE-load settings, set-point weighting (SPW)
was also implemented. Note that the patient model in the blood pressure regulation
experiences both a set-point change and disturbances from internal reflexes and random
noise. Since time delay in the patient models (Table 1) is significant, time delay
compensation by classical Smith Predictor (SP) and by modified Smith Predictor (MSP)
was also tried. PID controller with either SP or MSP was tuned by IAE-servo method
because of its superiority for blood pressure regulation. Vrecko et al. (2001) developed
MSP with two PI controllers - one for set-point tracking and another for disturbance
rejection. Details of all these tuning methods and the resulting controller settings are
available in Lee (2004). For the purpose of controller tuning, the drug response model (eq.
1) with parameter values corresponding to the nominal patient (Table 1) and neglecting
the recirculation dynamics (which will then be a first-order-plus-time-delay, FOPTD
model) was used. Details on the settings of EIMC can be found in Ng (2003) and Lee
(2004).
Based on several methods, the PID controller was tuned using the nominal patient model
(without recirculation dynamics) and then implemented for all the three patient models
(Table 1). RAS threshold, as discussed earlier was set at 72 mmHg. Some patients may
have a threshold of more than 100 mmHg, the nominal value of MAP that may also vary
among the population (Kaneko et al., 1967). Since the infusion of SNP is to lower the
patients blood pressure from a high MAP to the nominal value of between 80 to 100
mmHg, RAS is unlikely to be activated if the threshold is 72 mm Hg. Hence, this work
considered two cases for RAS threshold: a value of 72 mm Hg for normotensive patients
and a value of 110 mmHg for the hypertensive patient (assuming the patient has a history
of hypertension even before surgery); note that this value of 110 mmHg was an educated
guess. For testing each controller, a step input of 30 mmHg drop in MAP from 130 to 100
mmHg was introduced. The following performance criteria put forward by Slate et al.
(1980) for a step decrease of 30 mm Hg in the blood pressure: (1) settling time of
between 5 and 20 minutes; (2) overshoot of no more than 10 mm Hg; and (3) no steady
state offset with an error tolerance of 5 mm Hg, are used for evaluating the
performance of PID controllers in this work.
21

Table 2: Closed-loop performance of various adaptive controllers influenced by new

disturbances: RAS threshold at 110 mmHg
IAE for
Patient
Type
Controller/
Tuning
3
aCC
aIAE
1, 3
aIAE
2
aE-IMC
2
aIMC
2
aPID-GA
2
aPID-DMC
2
aIAE-SP
aMSP
aCC
aIAE (servo)
2
aIAE (load2
aE-IMC
2
aIMC
aPID-GA
aPID-DMC
2
aIAE-SP
aMSP
3
aCC
3
aIAE
3
aIAE (loadaE-IMC
aIMC
3
aPID-GA
aPID-DMC
1, 3
aIAE-SP
aMSP
Sensitive
Insensitive
Nominal
72 mm
Hg
110 mm
Hg
17230
18150
14770
13770
13810
19620
19070
16480
13630
30360
35020
27160
24040
34900
33960
32030
25330
29760
5743
5647
8492
6390
6400
7434
14460
17960
13970
14990
15040
20470
18240
14480
13630
28960
32260
26200
27780
37830
31750
29960
27340
32690
6635
5459
6593
7539
7533
5428
5624
4035
6884
5067
Settling Time (s) for Overshoot (mmHg) for

72 mm
Hg
110 mm
Hg
1750
1032
1170
1438
1500
1522
590
770
570
770
1790
1970
1750
1960
1230
1170
660
660
1500
1640
1780
1880
1340
1370
1070
1540
1540
>2000
1730
1850
1630
1750
1030
1510
1420
1810
136
1481
620
882
132
1168
300
450
300
450
165
878
Large oscillations
780
1010
190
280
72 mm
Hg
110 mm
Hg
17
18
16
<1
<1
19
17
10
<1
30
30
32
<1
<1
29
28
5
<1
7
6
12
<1
<1
9
14
16
13
<1
<1
15
14
6
<1
23
21
24
<1
<1
22
20
<1
<1
12
5
8
<1
<1
4
5
<1
6
<1
22

140
aIAE (servo)
aIAE (load) with SPW
aE-IMC
aPID-GA
aPID-DMC
aIAE-SP
aMSP
130
M A P (m m H g )
120
110
100
90
80
200
400
600
Time (s)
800
1000
1200
Figure 7: Performances of various controllers with adaptation on the nominal

patient model with RAS threshold at 110 mmHg. Note that responses of aPID-GA,
aPID-DMC and aIAE (servo) are almost same
140
aIAE (servo)
aE-IMC
aPID-GA
aPID-DMC
aIAE-SP
aMSP
130
M A P (m m H g )
120
110
100
90
80
70
200
400
600
800
1000 1200 1400 1600 1800 2000

Time (s)
Figure 8: Performances of various controllers with adaptation on the insensitive

patient model with RAS threshold at 110 mmHg. Note that responses of aIAE
(servo), aPID-GA and aPID-DMC are overlapping
23

135
aIAE (servo)
aE-IMC
aPID-GA
aIAE-SP
aMSP
130
125
M A P (m m H g )
120
115
110
105
100
95
90
50
100
150
200
250 300
Time (s)
350
400
450
500
Figure 9: Performances of various controllers with adaptation on the sensitive

patient model with RAS threshold at 110 mmHg
The performance results of controllers/tuning methods tested on the three patient models
and two threshold values for RAS, are presented in Table 2. In general, performance of a
controller is better in terms of lower IAE and settling time when the RAS threshold is 72
mmHg compared to that when the RAS threshold is 110 mmHg. This is reasonable since
only BRS was activated in the former case. Figs. 7 to 9 show the closed-loop servo
responses by the controllers for the three patient models when the RAS threshold is 110
mm Hg. For comparison, results by IMC (Hahn et al., 2002) and EIMC (Ng, 2002) are
included in Table 2 and Figs. 7 to 9; since EIMC has better performance than IMC, only
the response for the former are shown in the figures. Many of the controllers/tunings
tested have no steady-state offset or have oscillations within the tolerance of 5 mmHg;
in the few exceptions too, oscillations are within 10 mmHg; details on these are
available in Lee (2004).
In assessing the performance of the controller, it is important to compare and contrast its
performance for all three patient models as well as settling time and overshoot. Results in
Table 2 show that aEIMC is the best among the controllers/tunings studied although it
registered a settling time of 1540 seconds, 28% higher than the desired 1200 seconds for
set-point tracking of insensitive patient. The aIAE-SP controller is able to track the set
point with a settling time of only 1510 seconds for the insensitive patient, surpassing the
aEIMC, but it was off the mark by 26% longer settling time than desired. It also gives
slower response for the nominal patient compared to the aEIMC although still within the
acceptable limit. For the drug sensitive patient, an unexpectedly longer settling time is
required for aIAE-SP probably due to the model mismatch resulting in initial large
fluctuations that took some time to settle. Between aEIMC and aIAE-SP, the former
requires the determination of optimal gain in the additional path appended to the aIMC
structure.
24

On the whole, adaptive model-based controllers (such as aEIMC and aIAE-SP) tend to
give better performance than the adaptive PID controllers for blood pressure regulation.
The former are based on simple techniques of time delay and process model
compensation. This is in line with the objective of designing simple controllers for the
purpose of administering SNP to patients. Although aMSP uses 2 decoupled PI
controllers, its performance varies depending on the disturbances and patient type. The
entire scheme is complex compared to the SP for time delay compensation and has many
parameters; all these defeat the purpose of designing a simple and manageable controller.
CONCLUSIONS
Modeling and control of blood pressure regulation in post cardiac surgery patients are
studied. A detailed and realistic model for blood pressure regulation is developed by
including the drug response model of Slate et al. (1980) and models for two internal
reflexes (namely, RAS and BRS) of body in addition to the random disturbance. The
model is then implemented in Simulink for control studies. Several PID controllers are
designed using different tuning methods and/or time delay compensation and then tested
on three patient types - sensitive, nominal and insensitive, for a set-point change of -30
mmHg in blood pressure. The controller designed/tuned for the nominal patient model is
tried on all three patient models with two different thresholds values for RAS. Results
show that adaptation of controller gain is necessary in order to regulate satisfactorily the
blood pressure of all three patient models. Among the PID controllers, aIAE-SP (i.e., the
controller tuned for IAE minimization and with Smith predictor for time delay
compensation) seems to be the best choice. EIMC controller is somewhat better than the
aIAE-SP controller. Further studies on modeling and control of blood pressure regulation
are needed for the common practice of multiple drug infusion to post-surgery patients.
The multiple drugs include those to regulate cardiac output and total peripheral resistance,
and hence appropriate models will have to be included and suitable controllers will have
to be studied.
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Vol. 45 Issue 6 2005