17

A Comparative
Approach to Analysis
and Modeling of
Cardiovascular
Function
John K-J. Li
Rutgers University
Ying Zhu
Adow Innovation
Abraham Noordergraaf
University of Pennsylvania
17.1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-1
17.2 Dimensional Analysis of Physiological Function . . . . . . 17-2
17.3 Invariant Numbers and Their Physiological
Applications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-4
17.4 Comparative Analysis of the Mammalian Circulatory
System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-4
17.5 Metabolic Turn-Over Rate and Cardiac Work . . . . . . . . . 17-7
17.6 Comparative Pulse Transmission Characteristics . . . . . 17-7
17.7 Optimal Design Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-10
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-10
17.1 Introduction
Although the cardiovascular system and its parts do not always work as simple linear systems, they fre-
quently work, similarly, and in some cases, optimally. One can only marvel at the amazing similarities that
exist, structurally and dynamically, across a large number of mammalian species. These similarities occur
in spite of grossly different body weights and socialecological environments of the many different species.
The constant biological transformations that occurred did not seemto alter these similarities signicantly.
Using physical principles andapplying engineering techniques, we canmodel the cardiovascular systems
of different mammals. However, the complexity of the beat-to-beat dynamic performance of the heart and
its interaction with the vascular systems makes this a major challenge. This complexity can be substantially
reduced when we rst impose appropriate biological scaling laws and identify relevant invariant features
that appear across species in the mammalian class.
In terms of structure and function, there are a number of characteristics that must vary with size, and
they are consequently scaled with respect to body weight. Examples include: size of the heart, volume of
17-1
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17-2 Biomedical Engineering Fundamentals
blood, length of the aorta, and cardiac output. Other characteristics however, are invariant. Examples are:
blood pressure, ejection fraction, heart beats per life time, capillary, and red blood cell sizes.
It was not until the 17th century that Harvey [1628], in his now famous De Motu Cordis, rejected
Gaelenus theory, and proposed the closed circulation. This allowed him to explain the intermittent
pumping function of the heart as a consequence of systolic ejection and diastolic lling. He also made
comparisons of circulatory function from his many Anatomical Exercises Concerning the Motion of the
Heart and Blood in Living Creatures, performed on several mammalian species, avians, and amphibians.
The quantication of blood pressure amplitudes and cardiac output in mammalian species, however, was
rst introduced by Hales [1733] a century later. Until this day, blood pressure and cardiac output are still
regarded as the most pertinent clinical variables that govern the function of the cardiovascular system.
DArcy Thompsons [1917] On Growth and Form paved yet another path to modern comparative
biological studies. This is followed by Huxleys [1932] work on the Problems of Relative Growth in
which he based many of his biological interpretations on allometric relations.
Allometry is dened as the change of proportions with increase of size both within a single species and
between adults of related groups. The allometric formula relates any measured physical quantity Y to
body mass M, with a and b as derived or measured empirical constants. This resulted in the now familiar
power law,
Y = aM
b
(17.1)
This formula expresses simple allometry. In the special case when the exponent is 0, Y is independent of
body mass M: the physical variable is said to be invariant with body mass. When b is 1/3, the variable is
said to be dependent on body length; when b is 2/3, Y is dependent on body surface area, and when b = 1,
Y is simply proportional to body mass. This provided what is known as the basis of the one-third power
law or geometric scaling [Lambert and Teissier, 1927]. It has recently been challenged by the one-fourth
power law as the basis of biological allometric formulation [West et al., 1997].
The allometric equation has proven to be powerful for characterization of similarities among species.
It is effective in relating a physiological phenomenon, either structural or functional, among mammals
of grossly different body mass. A similarity criterion is established when Y, formulated in terms of either
product(s) or ratio(s) of physically measurable variables, remains constant despite changes in body mass,
and is dimensionless. Thus, the exponent b must necessarily be zero. In other words, similarity is present
whenever any two, dimensionally identical, measurements occur in a constant ratio to each other. If such
a ratio exists among different species, then a similarity criterion is established as the scaling law. This
approach of establishing biological similarity criteria has been very useful [Stahl, 1963a, b, 1965; Gunther
and DeLa Barra, 1966a, b; Gunther, 1975; Li, 1987, 1996, 2000].
17.2 Dimensional Analysis of Physiological Function
The theorem of dimensional analysis was introduced by Buckingham in 1915. It states that if a physical
system can be properly described by a certain set of dimensional variables, it may also be described by a
lesser number of dimensionless parameters which incorporate all the variables.
We shall now illustrate the use of dimensional analysis with the application of Laplaces law to
mammalian hearts. The beat-to-beat pumping ability of the mammalian heart is determined by its
force-generating capability and the lengths of its constituent muscle bers, as governed by the Starlings
experimental observations on the heart. The formula for calculating force or tension, however, has been
based on the law of Laplace
T = pr (17.2)
which states that the pressure difference, p, across a curved membrane in a state of tension is equal to the
tension in the membrane, T, divided by its radius of curvature, r [Woods, 1892]. This lawhas been applied
2006 by Taylor & Francis Group, LLC
Comparative Approach to Analysis and Modeling 17-3
to both blood vessels [Burton, 1954] and the heart [Li, 1986a]. To apply this formula, a certain geometric
shape of the heart has to be assumed in order to arrive at the radius or radii of curvature. The ventricle
has therefore been described geometrically as either a thin-walled or thick-walled sphere or ellipsoid. The
myocardium, which encloses the ventricular chamber, actually, has nite wall thickness. Also, the long-axis
diameter that is, the base-to-apex distance is greater than the short-axis diameter. When the left ventricle
is considered as thin-walled ellipsoid, there are two principle radii of curvature, r
1
and r
2
. Laplaces law
dictates:
p = T(1/r
1
+1/r
2
) (17.3)
For the ventricle as a sphere, r
1
= r
2
so that
p = 2T/r (17.4)
In a cylinder such as the blood vessel, one radius is innite, so that
p = T/r (17.5)
which indicates that a greater tension in the wall is needed to balance the same distending pressure.
Both arterial pressure and ventricular pressure have been found to be similar in many mammalian
species.
The larger the size of the mammalian heart, the greater the tension exerted on the myocardium. To
sustain this greater amount of tension, the wall of the larger mammal must thicken proportionally with
increasing radius of curvature. This results in a larger heart weight. The Lame relation that accounts for
wall thickness, h, therefore substitutes Laplaces law:
T = pr/h (17.6)
A dimensional matrix can be readily formed by rst expressing T, r, p, and h in the mass (M), length (L),
and time (T) system, that is, 4T = M
1
T
2
, r = L
1
, p = M
1
L
1
T
2
, and h = L
1
:
T r p h
M 1 0 1 0
L 0 1 1 1
T 2 0 2 0
(17.7)
To derive dimensionless parameters (
i
), Buckinghams pi-theorem needs to be utilized. To reiterate, the
number of pi-numbers (j) is equal to the number of physical quantity considered (n = 4) minus the rank
(r = 2) of the matrix (Li, 1983, 1986a). Thus, there will be two pi-numbers, denoted
1
and
2
.

1
= T/ph and
2
= h/r (17.8)
They provide a description of the geometric and mechanical relations of the mammalian hearts and
Laplaces Law is implicit in the ratio of the two,
I =
1
/
2
= T/pr (17.9)
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17-4 Biomedical Engineering Fundamentals
17.3 Invariant Numbers and Their Physiological Applications
In general, both
1
and
2
and their ratio, I , are not only dimensionless, they are also independent of
mammalian body mass. That is,
2
indicates that ratio of ventricular wall thickness to its radius, h/r,
is invariant among mammals. This also establishes a scaling factor. They are thus considered invariant
numbers, that is, of the form [M]
0
[L]
0
[T]
0
= a dimensionless constant. This invariance implies that
Laplaces law applies to all mammalian hearts [Martin and Haines, 1970; Li, 1986a].
Clinical implications of some of this nding can be easily appreciated. For instance, in the case of
pathological cardiac hypertrophy, the h/r ratio is signicantly altered as a consequence of increased wall
thickness [Li et al., 1997]. This latter increase has been suggested as the result of an adaptation process
by which the wall tension is normalized Equation 17.6. While in an enlarged and failing heart, the greater
tension due to a larger radius of curvature results in excess myocardial oxygen demand.
Another example of scaling invariance can be found in blood ow in arteries. A dimensional matrix is
rst formed by incorporating parameters that are thought of as pertinent. These are the density () and
viscosity () of the uid, diameter (D) of the blood vessel, and velocities of the owing blood (v) and of
the pulse wave (c).
c D v
(g/cm
3
) (cm/sec) (cm) (poise) (cm/sec)
M 1 0 0 1 0
L 3 1 1 1 1
T 0 1 0 1 1
k
1
k
2
k
3
k
4
k
5
(17.10)
where k
n
s are Rayleigh indices referring to the exponents of the parameters. The pi-numbers can readily
be obtained. Two of these are the well-known Reynolds number (Re), essential for identifying viscous
similitude and laminar to turbulent ow transitions [Li, 1988], Re = vD/, and the Mach number,
Ma = v/c, or the ratio of blood velocity to pulse wave velocity. Allometric relation gives
Ma = 0.04 M
0.0
(17.11)
which is nondimensional and invariant with respect to mammalian body mass. Although the Reynolds
number is also dimensionless, it is not an invariant function of mammalian body mass,
Re = 260.76 M
0.42
(17.12)
Thus, dimensionless pi-numbers do not necessarily expose similarity principles, that is, scaling factors are
not necessarily invariant numbers.
17.4 Comparative Analysis of the Mammalian Circulatory
System
Allometric relations of anatomic structures and physiological functions are useful for identifying simil-
arities of the circulatory function of different mammalian species [Li, 1996, 1998]. Obvious factors that
are important in determining function are heart rate and size, cardiac efciency and contractility, stroke
found in other sources [Stahl, 1963a, b, 1965; Juznic and Klensch, 1964; Holt et al., 1968, 1981; Calder III,
1981, 1996; Dawson, 1991; Li, 1987, 1996, 1998].
2006 by Taylor & Francis Group, LLC
volume, and blood pressure. Some examples of circulatory allometry are given in Table 17.1, and can be
Comparative Approach to Analysis and Modeling 17-5
TABLE 17.1 Allometric Relations of Some Hemodynamic Parameters, Y = aM
b
(M in kg)
Parameter Y a b Reference
Heart rate (sec
1
) f
h
3.60 0.27 Adolph [1949]
Stroke volume (ml) V
s
0.66 1.05 Holt et al. [1968]
Pulse velocity (cm/sec) c 446.0 0.0 Li [1987, 1996]
Arterial pressure (dyn/cm
2
) p 1.17 10
5
0.033 Gunther and Guerra [1955]
Radius of aorta (cm) r 0.205 0.36 Holt et al. [1981]
Length of aorta (cm) L 17.5 0.31 Li [1987, 1996]
Metabolic rate (ergs/sec) MR 3.41 10
7
0.734 Kleiber [1947]
Heart weight (kg) M
h
0.0066 0.98 Adolph [1949]
In mammals, the ratio of heart weight to body mass is an invariant with the heart accounting for about
0.6% of body mass. In allometric form [Adolph, 1949; Gunther and DeLa Barra, 1966a], this is
M
h
= 6.6 10
3
M
0.98
(17.13)
where the heart weight M
h
and body weight M are both in grams. With M
h
in g and M in kg, this has
been given [Holt et al., 1968] as
M
h
= 2.61 M
1.10
(17.14)
It should be readily apparent that experimental conditions and ecological factors can inuence the empir-
ical constants a and b. The above exponents for the heart weight (M
h
), however, do not differ signicantly
from the theoretical exponent of 1.0 (M
1.0
). The deviations arise from statistical ts of regressions to
experimental data. It is also readily apparent that if a variable scales as M
1.0
, then the allometric equation
can be made invariant by taking a ratio with M in denominator, that is, normalizing with body mass.
The stroke volume (V
s
) is also an invariant when normalized to heart weight or to body mass,
V
s
= 0.66 M
1.05
ml or 0.74 M
1.03
ml (17.15)
Stroke volume has long beenconsidered a critical hemodynamic quantity inassessing ventricular function.
Its product with mean blood pressure, bears a direct relation to the energy expenditure of the heart, or
the external work, EW,
EW= pV
s
(17.16)
This is the work performed by the heart in order to perfuse the vasculature during each contraction, or in
other words, the work necessary to overcome the arterial load during each ejection. Blood pressures are
generally invariant with respect to body mass in mammals. Of course, there are exceptions due to unusual
body size and shape [McMahon, 1973, 1983], such as the giraffe [Goetz et al., 1960] for identiable
reasons. This also indicates that the heart is basically a pressure source; maintaining an average constant
blood pressure is of utmost importance. The process of blood pressure control is complex, and important
roles are played by baroreceptors, the reninangiotensin system and the autonomic nervous system, just
to name a few subsystems. Allometrically, the mean arterial pressure is expressed as
p = 1.17 10
5
M
0.033
dynes/cm
2
= 87.8 M
0.033
mm Hg (17.17)
The exponent is slightly, though statistically it is not signicantly different from 0 (p = aM
0
). Thus, the
external work is given by
EW= 0.87 10
5
M
0.063
ergs = 0.0087M
1.06
J (17.18)
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17-6 Biomedical Engineering Fundamentals
A larger ventricle generates a greater amount of external work. The quantity of blood that is ejected per
beat (stroke volume), however, is a constant fraction of the amount contained in the heart as end-diastolic
volume. Thus, ejection fraction, as it is termed, is thus an invariant among mammals,
F
ej
= V
s
/V
ed
= 0.60.7 (17.19)
In a failing heart, the ejection fraction can decrease substantially (to 0.2 say), as a result of a reduced stroke
volume and an enlarged heart size.
The smaller the mammal, the smaller is its heart weight, but the faster its heart rate (f
h
;7):
tf
h
= 4.02 M
0.25
sec
1
(17.20)
Smaller mammals have shorter life spans, since the total number of heart beats in a mammals lifetime is
invariant. Within an individual mammal, rapid (and random) heart rhythms beyond normal often result
in cardiac arrhythmias, such as ventricular tachycardia. On the other hand, it is interesting to note here
that cardiac slowing, which reduces heart rate, can actually have the benecial consequence of increasing
longitivity.
Cardiac output, deemed by Hales [1733] as a valuable quantity describing ventricular function is given
as the product of stroke volume and heart rate, or the amount of blood pumped out of the ventricle per
minute,
CO = V
s
f
h
= (0.74 M
1.03
)(4.02 M
0.25
)60/1000 = 0.178 M
0.78
l/min (17.21)
Cardiac output is closely related to metabolic rate, since the heart supplies oxygen and nutrients for
metabolism. Table 17.2 gives a comparison of cardiac output in several species. Deviations from this
equation have been found in very small mammals [White et al., 1968]. Since blood pressure is invariant,
cardiac output is limited by the total peripheral resistance to blood ow of the mammalian systemic
arterial tree, which is obtained as
R
s
= p/CO = 2.8 10
6
M
0.747
dyn sec cm
5
(17.22)
Thus, the peripheral resistance follows the 3/4 power of mass [West et al., 1997], and is inversely
proportional to the metabolic rate (+3/4). This relation can be strongly altered under local conditions,
such as vasoconstriction or vasodilation. This derived allometric equation can be compared to that
reported by Gunther and Guerra [1955] who gave an equation conforming more closely to the 2/3 power:
R
s
= 3.35 10
6
M
0.68
dyn sec cm
5
(17.23)
TABLE 17.2 Cardiac Output of Some
Mammalian Hearts Based on the Allometric
Equation CO = 0.178 M
0.78
l/min
Species
Body weight
(kg)
Cardiac output
(l/min)
Elephant 2000 67
Horse 400 19
Man 70 5
Dog 20 1.8
Rabbit 3.5 0.5
Mouse 0.25 0.06
Tree Shrew 0.005 0.003
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Comparative Approach to Analysis and Modeling 17-7
17.5 Metabolic Turn-Over Rate and Cardiac Work
The energy requirement of cardiac muscle bers and the useful work they can generate are of considerable
interest [Starling andVisscher, 1926; Robard et al., 1959; Li, 1983; Liao et al., 2003]. They dene the mech-
anical efciency of the cardiac pump. In hemodynamic terms, the efciency of the heart is dened as the
ratio of external mechanical work (EW) to myocardial oxygen consumption (MVO
2
):
e = EW/MVO
2
(17.24)
The efciency of the heart is an invariant among mammalian species [Li, 1983a, b].
EW is also termed stroke work and is represented as the area encircled by the left ventricular pressure
volume (PV) diagram during each heart beat. The external mechanical work generated by the heart per
unit body or heart weight is constant for mammalian species [Li, 1983a, b], that is,
EW/M = constant = (pV
s
)/M (17.25)
This result is also of considerable physiological importance, since it states that the cardiac external work
intensity, is invariant among mammals. Species differences in cardiac energetics, however, have been
reported [Loiselle and Gibbs, 1979]. For man, taking V = 75 ml, p = 100 mm Hg, M = 70 kg, and
M
h
= 370 g, the external work is about 1 J and the coefcient is about 2.7 J/kg. In terms of heart weight,
this is
EW= 2.7 J/kg or EW= 1/70 J/kg (17.26)
in terms of body mass. For a 2100-kg elephant, its left ventricle is estimated to generate about 30 J for each
heart beat. Examination of the dimensions gives:
EW/M = [M]
0
[L]
2
[T]
2
(17.27)
Although this ratio is constant among mammalian species, it is not dimensionless. Therefore, it is not an
invariant number.
17.6 Comparative Pulse Transmission Characteristics
Mammalian arterial system exhibits geometric and elastic nonuniformities. Geometric taper of the aorta
alone is associated with an increased elastic modulus away from the heart. Vascular branching occurs
where target organ perfusion is necessary, increasing the total vascular cross-sectional area. Arterial wall-
thickness-to-lumen-radius ratios are invariant at corresponding anatomic sites in mammalian species.
The ratio of aortic length to its diameter is also an invariant [Holt et al., 1981; Li, 1987]. In addition,
the sizes of terminal arterioles and capillaries, as well as of red blood cells are also virtually invariant
among mammalian species regardless of their body size. These represent structural invariants, giving rise
to global vascular perfusion characteristics that are amazingly similar.
Similar pressure and ow waveforms are recorded in aortas of different mammalian species [Kenner,
transmission characteristics may also be similar. Nonuniformities in geometry and elasticity, as well as
viscous damping, could give rise to varying impedances to blood ow along the arterial tree. Pressure and
ow pulses could therefore be modied as they travel away from the heart as they encounter mismatches
of these impedances. Impedance to pulsatile ow is like resistance to steady ow and can be viewed as
complex resistances that vary with frequency. Impedance is calculated as the complex ratio of pressure to
ow for each harmonic, or multiples of heart rate. When the impedance is determined at the ascending
aorta, or the entrance to the arterial tree, it is termed input impedance. Vascular input impedance (Z
in
)
can be used to characterize the global properties of the arterial system.
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1972; Noordergraaf et al., 1979; Li, 1987, 2000; Figure 17.1]. This suggests that corresponding pulse
17-8 Biomedical Engineering Fundamentals
FIGURE 17.1 Simultaneously measured ascending aortic pressure and ow waveforms in three mammalian species,
namely the horse, man, and dog, with grossly different body weights. Similarities in waveforms are obvious. Blood
pressure magnitudes are similar.
TABLE 17.3 Data for Different Mammals for Analysis of Arterial Pulse Transmission Characteristics
Reection coefcient
Body mass Heart rate Phase velocity System length Propagation
M f
h
c l constant l
(kg ) (beats/min) (cm/sec) (cm) (experimental) (non-dimensional) l
Horse 400 36 400 110 0.36 0.42 1.13
Man 70 70 500 65 0.38 0.45 1.06
Dog 20 90 400 45 0.39 0.42 1.01
Rabbit 3 210 450 25 0.41 0.48 0.93
Z
o
/R
s
= 0.1 is used in the calculation of and .
When the characteristic impedance of the proximal aorta (Z
o
) is matched to the input impedance of the
arterial tree, that is, Z
in
= Z
o
, maximum transmission is present and reection of the propagating pulse
does not occur. Under this matched impedances condition, the pulsatile energy is totally transmitted
to organ vascular beds. In normal physiological conditions, however, there is some mismatching of the
impedances close to the peripheral organs. This causes the reection of the propagating pressure and ow
pulses. The fraction of the propagating pulse that is reected is given by the reection coefcient [Li, 1986,
2004], related to the impedances as
= (Z
in
Z
o
)/(Z
in
+Z
o
) (17.28)
The magnitude of the reection coefcient at normal resting heart rate is about 0.4, similar for many
mammalian species (Table 17.3). The resolution of pressure and ow waveforms into their respective
Pulse propagation characteristics [Li et al., 1981] can be quantied with a propagation constant,
= +j (17.29)
where is the attenuation coefcient, describing pulse damping due to viscous losses and , the phase
constant, denoting the relative amount of phase shift or pulse transmission time delay due to nite
pulse propagation velocity, c. In the mammalian aorta, the pulse wave velocity is invariant, as seen from
the allometric relation
c = / = 446 M
0
cm sec
1
(17.30)
where = 2f
h
, f
h
= heart rate (sec
1
).
2006 by Taylor & Francis Group, LLC
forward and reected components [Li, 2000, 2004] are shown in Figure 17.2.
150
100 mm Hg
100 cm
3
sec
1
1000 cm
3
sec
1
0
0
200
Horse Man
2000
0
1 sec
Dog
Comparative Approach to Analysis and Modeling 17-9
FIGURE 17.2 Simultaneously measured canine aortic pressure and ow in the aorta when resolved into its forward
(P
f
, Q
f
) and reected (P
r
, Q
r
) components.
Left ventricle Arterial system
C
v
(t )
Q(t )
Z
o
P
a
(t)
P(t) R
s
R
v
Aortic
valve
+

Q
c
(t )
C(P)
FIGURE 17.3 The coupled model of the left ventricle (LV) and the arterial system (AS). The LV is represented
here by a time-varying compliance and a resistance. The AS is represented by the modied windkessel model with
characteristic impedance, Z
o
, peripheral resistance, R
s
, and compliance of the arterial system, C. C(P) denotes the
case when compliance is allowed to change with blood pressure levels.
To compare gross features of the arterial trees of different mammals, modeling approach can be
particularly useful. The modied windkessel model of the systemic arterial system that is coupled to the
heart (Figure 17.3) has been shown to represent well the features of the input impedance of the systemic
arterial tree. For this representation, the input impedance is
Z
in
= Z
o
+R
s
/(1 +jCR
s
) (17.31)
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115
110
105
100
95
90
85
0.1 0.0 0.1 0.2 0.3 0.4 0.5 0.6
P
r
P
r
P
A
o
r
t
i
c

p
r
e
s
s
u
r
e

(
m
m

H
g
)
Control-pressure
Time (sec)
100
80
60
40
20
0
20
40
0.2 0.1 0.0 0.1 0.2 0.3 0.4 0.5 0.6
Q
r
Q
Q
r
A
o
r
t
i
c

f
l
o
w

(
m
l
/
s
e
c
)
Control-flow
Time (sec)
17-10 Biomedical Engineering Fundamentals
dominated by Z
o
, R
s
, the systemic peripheral resistance as shown before, and C, the total systemic arterial
compliance, representing the elastic storage properties of the arteries:
C = 0.18 10
4
M
0.95
g cm
4
sec
2
(17.32)
It is clear that the peripheral resistance decreases, while compliance increases with mammalian body size.
Thus, the dynamic features of blood pressure and ow pulse transmission can be scaled through this kind
of modeling. The ratio of Z
o
/R
s
corresponds to the ratio of pulsatile energy loss due to oscillatory ow
to the energy dissipated due to steady ow (to overcome R
s
) and has been reported to be between 5 and
10% and is an invariant for the mammalian arterial circulation [Li, 1996, 2004].
Some of the pulse transmission characteristics for horse, man, dog and rabbit are summarized in
the aorta, l , equals about 6, independent of the body mass of the mammal. The product of l is about
1, again independent of the mammalian body mass and conrming that the propagation characteristics
along mammalian aortas are similar. The global reection coefcient is also practically invariant. This
occurs in spite of vast differences in heart rate, systemic peripheral resistance, total systemic arterial
compliance, and aortic characteristic impedance that are associated with different body sizes.
17.7 Optimal Design Features
These observed phenomena concerning pulse transmission, pulse wave velocity, and input impedance
as discussed above must all be attributed to a common mechanism [Li and Noordergraaf, 1991]. The
architecture of the branching arterial junctions is such that only a portion of the pulse wave generated by
the ventricle reaches the capillaries. Another part is reected in the periphery, principally in the arteriolar
beds. Reected waves encounter mismatched branching sites on their return trip to the ventricle. As a
result, a negligible fraction of the reected pulse wave actually reaches the heart, with the exception of
the lowest frequency component for which the wavelength is comparable to the effective length of the
vascular system.
Another important feature of the optimal design of the mammalian arterial tree network is that there
is minimal loss of pulsatile energy due to vascular branching [Li et al., 1984]. The vascular junctions
are practically impedance matched. In other words, the characteristic impedance of the mother vessel
is closely matched to the branching daughter vessels. This implies that the geometric and elastic properties
of the daughter vessels match that of the mother vessel. As such, pulse transmission at a vascular branching
junction is met with minimal local reection. This results in the facilitation of vascular perfusion with
minimal energy loss en route to organ vascular beds.
References
Adolph, E.F. Quantitative relations in the physiological constitutions of mammals. Science 109: 579, 1949.
Buckingham, E. On physically similar systems; illustrations of the use of dimensional equations. Phys.
Rev. 4: 345, 1915.
Burton, A.C. Relation of structure to function of the tissues of walls of blood vessels. Physiol. Rev. 34:
619642, 1954.
Calder, W.A., III. Scaling of physiological processes in homeothermic animals. Ann. Rev. Physiol. 43: 301,
1981.
Calder, W.A. III. Size, Function and Life History. Dover, New York, 1996.
Dawson, T.H. Engineering Design of the Cardiovascular System of Mammals. Prentice-Hall, Englewood
Cliffs, NJ, 1991.
Goetz, R.H., J.V. Warren, O.H. Gauer, J.L. Patterson Jr., J.T. Doyle, E.N. Keen, and M. McGregor.
Circulation of the giraffe. Circ. Res. 8: 10491058, 1960.
2006 by Taylor & Francis Group, LLC
Table 17.3. The ratio of pulse propagation wavelength, , for the fundamental harmonic, to the length of
Comparative Approach to Analysis and Modeling 17-11
Gunther, B. Allometric ratios, invariant numbers and the theory of biological similarity. Physiol. Rev. 55:
659, 1975.
Gunther, B. and L. DeLa Barra. Physiometry of the mammalian circulatory system. Acta Physiol. Lat.-Am.
16: 32, 1966a.
Gunther, B. and L. DeLaBarra. Theories of biological similarities, non-dimensional parameters and
invariant numbers. Bull. Math. Biophys. 28: 9102, 1966b.
Gunther, B. and B. Guerra. Biological similarities. Acta Physiol. Lat.-Am. 5: 169, 1955.
Hales, S. Statical Essays Containing Haemostaticks. London, 1733.
Harvey, W. De Motu Cordis. London, 1628. Dover edition, New York, 1995.
Holt, J.P., E.A Rhode, and H. Kines. Ventricular volumes and body weights in mammals. Am. J. Physiol.
215: 704, 1968.
Holt, J.P., E.A. Rhode, W.W. Holt, and H. Kines. Geometric similarity of aorta, venae cavae, and certain
of their branches in mammals. Am. J. Physiol. 241: R100, 1981.
Huxley, J.S. Problems of Relative Growth. Methuen, London, 1932.
Juznic, G. and H. Klensch. Vergleichende physiologische untersuchunger uber das verhalten der indices
fur energieaufwand und leistung des herzens. Arch. ges Physiol. 280: 3845, 1964.
Kenner, T. Flow and pressure in arteries. In Biomechanics, Y.C. Fung, N. Perroue, and M. Anliker (Eds.).
Prentice-Hall, NJ, 1972.
Kleiber, M. Body size and metabolic rate. Physiol. Rev. 27: 511541, 1947.
Lambert, R. and G. Teissier. Theorie de la similitude biologique. Ann. Physiol. Physiocochem. Biol. 3: 212,
1927.
Li, J.K.-J. A new similarity principle for cardiac energetics. Bull. Math. Biol. 45: 10051011, 1983a.
Li, J.K.-J. Hemodynamic signicance of metabolic turnover rate. J. Theor. Biol. 103: 333338, 1983b.
Li, J.K.-J. Comparative cardiac mechanics: Laplaces law, J. Theor. Biol. 118: 339343, 1986a.
Li, J.K.-J. Time domain resolution of forward and reected waves in the aorta. IEEE Trans. Biomed. Eng.
BME-33: 783785, 1986b.
Li, J.K.-J. Arterial System Dynamics. New York University Press, New York, 1987.
Li, J.K.-J. Laminar and turbulent ow in the mammalian aorta: Reynolds number. J. Theor. Biol. 135:
409414, 1988.
Li, J.K.-J. Comparative Cardiovascular Dynamics of Mammals. CRC Press, Boca Raton, FL, 1996.
Li, J.K.-J. A new approach to the analysis of cardiovascular function: allometry. In Analysis and Assessment
of Cardiovascular Function, G. Drzewiecki and J.K.-J. Li (Eds.). Springer-Verlag, New York, 1998,
pp. 1329.
Li, J.K.-J. The Arterial Circulation: Physical Principles and Clinical Application. Humana Press, Totowa, NJ,
2000.
Li, J.K.-J. Dynamics of the Vascular System. World Scientic, Singapore, New York, 2004.
Li, J.K.-J., J. Melbin, R.A. Rife, and A. Noordergraaf. Pulse wave propagation. Circulation Res. 49:
442452, 1981.
Li, J.K.-J., J. Melbin, and A. Noordergraaf. Directional disparity of pulse wave reections in dog arteries.
Am. J. Physiol. 247: H95H99, 1984.
Li, J.K.-J. and A. Noordergraaf. Similar pressure pulse propagation and reection characteristics in aortas
of mammals. Am. J. Physiol. 261: R519R521, 1991.
Li, J.K.-J., Y. Zhu, and M. Nanna. Computer modeling of the effects of aortic valve stenosis and arterial
system afterload on left ventricular hypertrophy. Comput. Biol. Med. 27: 477485, 1997.
Liao, J., J.K.-J. Li, and D. Metaxas. Characterization of time-varying properties and regional strains in
myocardial ischemia. Cardiovasc. Eng. Int. J. 3: 109116, 2003.
Loiselle, D.S. and C.L. Gibbs. Species differences in cardiac energies. Am. J. Physiol. 490498, 1979.
Martin, R.R. and H. Haines. Application of Laplaces law to mammalian hearts. Comp. Biochem. Physiol.
34: 959, 1970.
McMahon, T.A. Size and shape in biology. Science 179: 12011204, 1973.
McMahon, T.A. and J.T. Bonner. On Size and Life. Scientic American Library, New York, 1983.
2006 by Taylor & Francis Group, LLC
17-12 Biomedical Engineering Fundamentals
Noordergraaf, A., J.K.-J. Li, and K.B. Campbell. Mammalian hemodynamics: a new similarity principle.
J. Theor. Biol. 79: 485, 1979.
Robard, S., F. Williams, and C. Williams. The spherical dynamics of the heart. Am. Heart J. 57: 348360,
1959.
Stahl, W.R. Similarity analysis of biological systems. Persp. Biol. Med. 6: 291, 1963a.
Stahl, W.R. The analysis of biological similarity. Adv. Biol. Med. Phys. 9: 356, 1963b.
Stahl, W.R. Organ weights in primates and other mammals. Science 150: 10391042, 1965.
Starling, E.H. and M.B. Visscher. The regulation of the energy output of the heart. J. Physiol. 62: 243261,
1926.
Thompson, D.W. On Growth and Form. Cambridge University Press, 1917.
West, G.B., J.H. Brown, and B.J. Enquist. A general model for the origin of allometric scaling laws in
biology. Science 276: 122126, 1997.
White, L., H. Haines, and T. Adams. Cardiac output related to body weights in small mammals. Comp.
Biochem. Physiol. 27: 559565, 1968.
Woods, R.H. A few applications of a physical theorem to membranes in the human body in a state of
tension. J. Anat. Physiol. 26: 362370, 1892.
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