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The Mathematical Relationship between Heart Rate,

Cardiac Output and Pulse Pressure in the Human Systemic


Vasculature
by

E R Lowe

Cardiac Output
(litres/min)

Total Systemic
Arterial Loop
Resistance
(mmHg per
ml/min)

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Introduction
It is a matter of observation, not conjecture, that any and all heart rate readings (HR)
taken at random from an individual, regardless of the time of day or prevailing stress
level, exhibit a simple mathematical relationship to each other, expressible in the form
of an elementary algebraic equation involving two other parameters - the
simultaneous indicated pulse pressure (Pp) and cardiac output (CO) at the time the
pulse rate is taken. The equation states simply that pulse rate is proportional to the
quotient of cardiac output divided by indicated pulse pressure.
As a consequence of this relationship, the behaviour of these three parameters, heart
rate, the indicated pulse pressure and cardiac output, as well as several other variables
of the systemic vasculature, can be shown to be precisely ordered, conforming to the
basic laws of physics and natural science and neither as independent nor random in
behaviour as at first appears. This paper shows that, based upon their mutual
relationship, their instantaneous values may be calculated from observed values of the
others and thereby their behaviour may be monitored non-invasively at all times.

Background
Superficially there appears to be no clear correlation between the rate at which the
human heart beats and indicated systolic and diastolic pressures, as measured
conventionally by auscultation or even more sophisticated and accurate methods
including applanation tonometry at points over the brachial or radial arteries. High
pressures are often associated with low pulse rates but just as often with high or
‘normal’ ones, and low pressures with high pulse rates or low ones, with any
combination in between. Historically this has led to the assumption that no
mathematical relationship exists between what is called ‘blood pressure’ and the heart
rate, but this is not the case and the assumption is wholly incorrect.

Thesis
The relationship between true stroke volume and indicated pulse pressure is almost
directly linear. For the present purpose of calculating the values of the parameters
involved, any deviation from linearity is so small as to allow it to be ignored1 without
significant loss of accuracy. From their mutual proportionality, therefore, the standard
definition of arterial compliance2 at the proximal aorta is expressible as:
SV = C × Pp (equation 1)
where SV is stroke volume, C is the compliance of the walls of the ascending aorta,
and Pp is the indicated pulse pressure. The product identity {C × Pp} can therefore be
substituted for SV in the cardiac output equation (CO = HR × SV) and, by designating
pulse rate as HR, cardiac output (CO) may be expressed as:
CO = HR × {C × Pp} (equation 2).
From this, it is possible to compute the pulse rate as:
1
Levick R.J. An Introduction to Cardiovascular Physiology, 2nd Edition, Chapter 6.4, pp 73, Figure 6.4(c)

2
Morhrmann & Heller, Cardiovascular Physiology, 5th Edition, Chapter 6, pp. 112, para. 2
2
CO
HR = (equation 3)
{C ×Pp }

The ratio of any heart rate HR1 to any other, HR2, then clearly is:
CO 1 CO 2
HR1 : HR2 = Pp 1 : Pp 2

where CO1, Pp1, CO2 and Pp2 are respectively the corresponding cardiac outputs and
pulse pressures. The compliance coefficient C effectively cancels out, allowing the
heart rate at any time to be calculated from any previous reading:
CO 2 Pp 1
HR2 = HR1 × × Pp 2 (equation 4)
CO 1

Stroke volume is measured nowadays routinely on a clinical basis using Doppler or


other methods as a means of determining cardiac output (HR × SV), so if pulse rate
and pulse pressure are both recorded simultaneously with CO, then C, the compliance
modulus of the ascending aorta, may be obtained by dividing stroke volume by the
indicated pulse pressure.
Under relaxed bodily conditions, the compliance of the walls of the aorta remains
essentially unchanged over a wide range of internal arterial pressures even though
other factors influence its value, so for working purposes C may be assumed to be a
constant whose value is specific to that individual. Inserting the values for measured
cardiac output (CO) and pulse pressure (Pp) into equation 3 shows that only one pulse
rate satisfies it. All the elements of equation 3 being known, and the value of each
term being determinable, allows the heart rate to be calculated and what follows is an
actual clinical example of it in practice.

Calculation of Heart Rate (HR)


The stroke volume of a patient was measured using Doppler methods and recorded as
95mls and the simultaneous indicated measurements of radial arterial systolic and
diastolic pressures were 180/98 mms.Hg. The simultaneous heart rate was monitored
as 66 bpm.
Pulse pressure was therefore 82 mms.Hg, and by dividing the measured stroke volume
by this value the aortal wall compliance C can be calculated as 1.1585 mls/mm.Hg.
Using equation 2, cardiac output can now be calculated as:
66 × {1.1585 × 82} = 6270
and by applying these values to equation 3, the pulse rate can be computed as:

6270
= 66 bpm
{1.1585 ×82 }

It can be seen that the pulse rate calculated using equation 3 is exactly equal to the
measured rate.

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The Common Relationship between all Random Heart Rate
Measurements
In practice, HR is rarely constant and varies continuously but equation 3 makes clear
that it is impossible for it to vary independently. All such HR variations must be offset
by compensating changes in either (or, more usually, both) cardiac output or pulse
pressure. This is because, rearranging equation 4, the generalized mathematical
relationship between all HR, Pp, and CO readings is:
HR 1 CO 2 Pp 1
× × Pp 2 = 1
HR 2 CO 1

This is a permanent and universal mutual relationship and therefore none of the three
parameters, HR, Pp, or CO can ever be independently variable, enabling the
instantaneous pulse rate at any subsequent time to be calculated simply by using
equation 4 and inserting the appropriate (simultaneous) pulse pressure and cardiac
output values.

Calculation of Pulse Pressure


The ability to calculate and even predict pulse rate in this way may well appear
superficially to be little more than an entertaining party-piece which can be verified
by counting beats over any interval. However, many (and more significant) corollaries
follow from it in relation to the other variables as shown below.
Using equation 3 as a basis, the instantaneous (indicated) value of Pp can also be
calculated for any given values of cardiac output and pulse rate:
CO
Pp =
(C ×HR )

So using the same values obtained from the patient above, the pulse pressure can be
calculated as:
6270
= 82 mms.Hg
(1.1585 ×66 )

This again demonstrates that the calculated value of a parameter (in this case pulse
pressure) is exactly equal to the measured value.

Calculation of Cardiac Output


In precisely the same way as for pulse rate and pulse pressure, for any configuration
of these parameters there can be only one value for cardiac output and because no
further involvement of Doppler techniques is required its calculation is simpler still.
From equation 2, and denoting the original measured cardiac output, heart rate, and
pulse pressure as before as CO1 HR1, and Pp1 respectively and any subsequent cardiac
output, pulse rate and pulse pressure as CO2, HR2 and Pp2, it is possible to calculate
the value of the subsequent cardiac output as:
{HR 2 × Pp 2}
CO2 = CO1 × (equation 5)
{HR 1 × Pp 1}

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As an example of this in practice, and again using the same original parameter values
as before, let us assume that on a subsequent occasion the same patient’s heart rate
HR was (say) 78 instead of 66 bpm, whilst the indicated pulse pressure Pp had
dropped from 82 to (say) 50mms.Hg. Using equation 5, the patient’s cardiac output
can be calculated as:
(6270 ×{78 × 50})
CO2 = = 4158 mls/min
{66 ×82}

The combined slight rise in pulse rate and fall in pulse pressure (and stroke volume)
results from a reduction of roughly one-third of cardiac output.

Relationship between Stroke Volume and Pulse Rate


With regard to the mathematical relationship between pulse pressure and pulse rate
however, this is not the end of the story. Whilst there is but one pulse pressure
consistent with any pair of simultaneous cardiac output and pulse rate readings, its
value is critically dependent upon yet another parameter, the ratio of stroke volume to
SV
pulse rate, . This is explicit in equation 1 and manifests itself implicitly in
HR
Pp
equation 2 as the indicated ratio . This makes clear that any one of an infinite
HR
number of combinations of different but complementary pulse rates and stroke
volumes can generate the same cardiac output.
For example, a cardiac output of 5000mls/minute can be achieved by the heart
ejecting 50mls of blood one hundred times a minute, or 100mls fifty times a minute,
or 72mls just over 69 times a minute, or any number of similar combinations. The
range is limitless, as shown in the curve resulting from plotting stroke volume against
pulse rate (see Figure 1).

Figure 1
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The significance of this ratio cannot be overstated, because ipso facto the
proportionality existing between pulse pressure and stroke volume also causes pulse
pressure to increase not linearly but parabolically with decreasing pulse rate. This
means that, although in practice the ability to deliver the required cardiac output to
meet the demands of the organs it serves at the prevailing heart rate is limited by the
heart’s efficiency as a pump, the stroke volume necessary to achieve the cardiac
output is theoretically unlimited. The lower HR is, the greater SV must be to generate
the required cardiac output and, by extension, so must the pulse pressure rise to quite
disproportionate levels.
As an example of this, and using the same original parameters as before, if the
patient’s pulse rate for the 6270 mls/min cardiac output were not 66 but 60 bpm, then
the pulse pressure would need to rise by 10%, from 82 to 90.2 mm/Hg, and if it were
still lower, say 55 bpm, then the rise required would be from 82 to 98.4 bpm. (see
Figure 2).

Figure 2

Somewhat fortuitously, entirely due to the range scales involved, it is possible to


combine (as shown in Figure 3) the two curves in Figures 1 and 2 to illustrate how the
three Pp readings, when superimposed, almost precisely overlay the SV curve when
plotted against pulse rate. The small discrepancy, of course, arises because in one
curve cardiac output is 5 L/min and in the other it is 6.270 L/min.

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Figure 3

The considerable rise in pulse pressure induced by artificially lowering the heart rate
must by extension be reflected in excessive systolic pressure Ps, even at rest, but
when the body is placed under stress and additional systemic arterial flow is
demanded, then if the pulse rate is inhibited (typically by beta blocking) from rising
properly to fulfil its natural role in delivering extra output, gross and disproportionally
high systolic pressures clearly will result, posing a risk to the structural integrity of
blood vessels at all levels on the arterial tree.
Mathematically, the processes above show that the three parameters CO, Pp and PR at
all times have mutually interdependent values whose loci inhabit a 3-dimensional
shell-surface, the shape of which is shown in Figure 4. All possible configurations of
a patient’s CO, Pp, and PR lie on this curved plane surface and each triple
configuration constitutes a single point on the surface shell. This graphically
illustrates why, as pointed out in earlier paragraphs, there can be only one pulse rate
for any specific value of CO and Pp, but more significantly, there is only one single
value of CO for any specific combination of Pp and PR, and only one value of Pp
corresponding to any pair of CO and PR values.

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Figure 4 3

From a medical (as distinct from a mathematical) standpoint however, it is clear that
the values of any two variables uniquely determine that of the third. Therefore, if the
indicated level of any is perceived to be ‘too low’ or ‘too high’ (typical examples of
which would be, for example, so-called ‘isolated hypertension’ indicated by an
excessive pulse pressure, or tachycardia evinced by a pulse rate deemed excessive or
through impaired cardiac output), then consideration of the area of the 3-D shell upon
which the cardiovascular system is operating would appear to merit being the primary
focus of investigation rather than artificial intervention simply to ‘correct’ the
apparent abnormality.
An ‘abnormality’ in any of the three parameters cannot exist in isolation. An
‘abnormally high’ pulse rate, for instance, might well be the brain’s natural, optimum
and perhaps only mechanism of achieving the correct cardiac output. Artificially
lowering it (if the cause is an impaired stroke volume) can have only one outcome -
exacerbating the condition. Artificially lowering the pulse rate and thereby raising
pulse pressure must, if cardiac output is maintained, inevitably raise systolic pressure
unless diastolic pressure is reduced by a corresponding amount, simply because Ps is
the sum of Pd and Pp.
The only circumstance under which artificially lowering pulse rate can result in a
reduction in systolic pressure is where cardiac pump-action is impaired and the heart
is incapable, because of its characteristic curve, of delivering the required flow of
blood at the appropriate pressure. Cardiac output therefore falls, diastolic pressure
(the product of the reduced cardiac output and total systemic loop resistance) falls as
well, and if the fall is greater than the artificially induced rise in pulse pressure then
systolic pressure will also fall. Lowering of systolic pressure has therefore been
achieved under these conditions but at the expense of optimum flow.

Diastolic Pressure
Unlike pulse pressure, no simple mathematical relationship exists between heart rate
and diastolic pressure. Nor is it possible to compute its behaviour over time in relation
to other systemic parameters, because irrespective of wherever it is measured, its
instantaneous value (whether indicated or true) at that point simply reflects the
volume of blood at pressure at that instant in that section of the vascular loop. Thus
the extent to which it is dilating and expanding the arterial walls, and thereby being
pressurized by their reactive forces, determines the internal pressure.
In turn, because blood neither collects at any point within nor escapes from the elastic
plenum comprising the systemic vasculature, the total pressurised contained volume
at any moment depends firstly upon run-off, tending to deplete it, and secondly by the
efficacy of its replenishment i.e., cardiac output, tending always to restore it. Thus, if
run-off exceeds cardiac output, both true and indicated diastolic pressure fall. If

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The topography of the surface of the 3-D shell is the same, irrespective of whether stroke volume or pulse pressure is used for
the third axis, due to their proportionality. As it is more relevant to the haemodynamics of the system, the former has been used
in this instance.
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cardiac output exceeds run-off, both true and indicated diastolic pressures rise, and if
cardiac output equals run-off then equilibrium is established and diastolic pressures
(both indicated and true) remain roughly constant.4

Systolic Pressure
The value of both true and indicated systolic pressure therefore is the sum of (a) the
pulsatile component Pp whose value is highly sensitive to heart rate and quantifiable
non-invasively and (b) a relatively steady non-pulsatile component upon which it is
superimposed whose level is determined by a completely different mechanism wholly
unrelated to the heart rate. This being the case, systolic pressure is not susceptible to
mathematical analysis. In reality, it is little more than a by-product reflecting the
behaviour of two widely differing physiological mechanisms.
Because the indicated pulse pressure of a young healthy adult at rest is much less than
the diastolic pressure, systolic pressure, the sum of the two, by and large simply
follows variations in diastolic pressure. Observed differences between peak systolic
and diastolic values are due to the continuous but relatively minor ‘hunting’ of pulse
pressure levels caused by heart rate variations as shown in Figure 2.
However, in the dynamic (as opposed to static) mode of operation, when the body is
stressed (as opposed to static mode, when it is relaxed), indicated pulse pressure can
easily equal and even surpass the diastolic pressure and the behaviour of systolic
pressure becomes quite different. It rises, reflecting increased pulse pressure, while
diastolic pressure frequently does not, being held steady (as far as possible) by
vasodilatation and may be observed even to drop initially when run-off exceeds
cardiac output.
The limits are set by (a) the heart’s performance as a pump and (b) the parabolic
nature of the vasodilatation curve, which approaches maximum asymptotically when
dilation of the blood vessels reaches its practical limit and the resistance to flow is the
minimum attainable.

Mean Arterial Pressure


The so-called ‘Mean Arterial Pressure’ or MAP, commonly held to be the pressure
impelling blood round the systemic vascular loop and computed by adding roughly
one third of pulse pressure, or Pp/3, to the diastolic pressure, is considered to be the
‘weighted mean’ of the pulse pressure waveform and their sum is supposedly the
equivalent of the analogous RMS value of a complex electrical waveform. This is
used usually in relation to the Law of Flow, (sometimes called the Mean Pressure
Equation) or Darcy’s Law, in which flow, pressure, and the resistance to flow
conform to the equation:
MAP = CO × TPR
TPR being the effective resistance to flow presented by the systemic loop and taken to
be mostly that of the peripheral arteries.
The concept of ‘Mean Arterial Pressure’ and all its derivatives such as ‘Central Aortic
Mean Arterial Pressure’ are however entirely spurious, because the pulse pressure

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The qualification arises due to the transit time required for blood to traverse the loop. Pressures and flows in phase cause non-
linear localised gradients to develop, leading to minor non-linear gradients of diastolic pressure.
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wave is a travelling longitudinal wave of pressure only, not flow, and in common with
all such waves performs no work upon the medium through which it passes. Its
velocity through the blood is roughly an order of magnitude greater than that of blood
flow itself and, apart from losses, none of its energy is dissipated in the process.
Impelling blood requires the expenditure of energy and none being dissipated by the
pulse pressure wave in its transit means that the pulse pressure wave plays no part in
its translation down the vascular loop, leaving diastolic pressure as the only source of
the forces driving blood round the systemic vascular loop.

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