Blood-Hammer

Phenomenon

in Cerebral

Hemodynamics

TRAIAN
DAMSA
Centre of Mathematical Statistics,
21 Calea Grivijei I Bucharest 12, Romania
ESTERA APPEL
The Insritute of Neurology and Psychiatry,
42 Povernei, Bucharest, Romania
AND

VASILE CRISTIDIS
The Institute of Hydrotechnical Studies and Researches,
29 Republicii Street, Bucharesi, Romania
Communicated

by J. Jacquez

ABSTRACT
In this paper

we have studies

the hemodynamic

mechanism

of cerebral

hemorrhage,

using the mathematical

methods of the mechanics
of fluids. The work analyzes the
consequences
of the phenomenon
of deviation from the normal of the morphologic
and
rheologic
parameters
of the cerebral circulation.
The paper tries to demonstrate
the
analogy between yielding of the blood vessels and that of pressure pipes due to rapid
pressure changes as studied in engineering. This phenomenon
is described in hydraulics as
water hammer
(and, by analogy, we have used the term blood hammer),
i.e., the
occurence of an appreciable
rise in pressure inside a pipe containing a flowing fluid, when
the flow is sharply

1.

interrupted.

INTRODUCTION

The phenomenon
we are considered is the following [lo, 131: Let a pipe
be assumed in which a fluid flows under steady conditions. A sharp change
in the rate of flow, caused, for instance, by an obstruction,
initially produces an overpressure, then a decompression,
followed by several oscillations, which are gradually damped with time. Overpressures are produced
locally next to the obstruction and propagated along the pipe at the speed
of sound. The longer the pipe and the more abrupt the closure, the more
violent these phenomena
are. The overpressure is added to that of the
MA THEMA TICAL BIOSCIENCES

29, 193-202 ( 1976)

0 American Elsevier Publishing Company, Inc., 1976

193

194

TRAIAN

DAMsA

ET AL.

steady state; it does not, however, depend on the latter, but only on the flow
velocity, the density and compressibility
of the fluid and the elastic characteristics of the material from which the pipe is made. The essential factors
damping overpressure are the elasticity of the conduit and the compressibility of the fluid; shunting systems (surge tanks) may also contribute to the
damping effect. If the fluid and pipe material were not compressible, then,
the kinetic energy of the suddenly stopped mass would be transformed into
mechanical
work with no displacement,
and the force developed would
accordingly produce an infinite pressure. Actually, owing to the elasticity of
the vessel-fluid system, a part of the quantity of motion is transformed into
elastic deformation energy.
To describe the relationships between the rheologic parameters used in
the calculation [8], let V, be the flow velocity at a given moment throughout
a cylindrical vessel, pO the pressure of the fluid and t, the moment at which
the vessel is obstructed. At the site of the obstruction, the velocity of the
fluid will be zero. Assuming, at first, that the walls of the vessel are rigid, we
deduce that from moment t,, in an interval of time dt, the fluid, owing to its
compressibility,
will continue to enter the volume L?ds adjacent to the
obstruction
(52= area of the vessel cross-section;
ds =length
of the vessel
segment adjacent to the obstruction), resulting in an increase in pressure, Ap
(Fig. 1).
Applying
the Newtons second law to the mass pflds of the fluid
(p= density of the fluid), whose velocity changes from V, to zero, the

FIG. 1.

Overpressure

Ap in the obstructed

pipe.

BLOOD-HAMMER

PHENOMENON

change in the momentum

195

will be equal to the impulse of force in interval dt:

(pOds).V,,=[-f2p,+O(p,+Ap)]dt.

Let ds/dt = a be the velocity at which the overpressure Ap is propagated,

designated as celerity, and equal to the speed of sound in the fluid-pipe
system considered; then
Ap = pa V,,.

(I)

The over-pressure is transmitted backwards from the site of obstruction

during an interval L/a (L=length
of vessel from the obstruction,
in a
direction opposite to the initial flow up to the larger vessel supplying the
obstructed pipe). At this moment, the movement of the fluid ceases for a
short interval and the entire column is compressed. The equilibrium being
unstable, a decompression
occurs, and after several oscillations, a resting
state is reached. Now, on taking into considerations
the elasticity of the
pipe, the qualitative relationships are maintained, but the celerity is smaller,
and hence the overpressure will be lower. The celerity is calculated according to formula:
1
I+ (EIE)(D/e)

where p = density of the fluid; E= bulk modulus of elasticity (compressibility) of the fluid; E =modulus
of elasticity of the vascular wall; D =inner
diameter of the vessel; e = thickness of the vascular wall. The overpressure
Ap, added to the preexisting pressurep,, gives rise in the vessel to a pressure
P=PO+AP.

The pressure created acts uniformly on the walls of the circular pipe
(Fig. 2.), subjecting them to a distension stress of (I= a,+Aa (a,= initial
distension stress due to po; Au = overload due to Ap):
POD
u=2e+2e.

FIG. 2.

Distension

APD

stress (I in the vascular

(11)

wall.

196

TRAIAN

DAMsA

ET AL.

The essential problem in the present study is whether the vascular wall
can resist a distension stress exceeding normal conditions.
In order to solve this problem, several arguments will be brought forward
in favor of the applicability
of these relationships
to the cerebral blood
circulation, after which the values of the parameters will be calculated.
2.

ARGUMENTS
LENDING
SUPPORT TO THE APPLICABILITY
OF THE QUALITATIVE
RELATIONSHIPS
TO BLOOD CIRCULATION

2. I

The blood vessels are cylindrical pipes with distensible walls responding
to the interior pressure of the circulating blood; hence, the distensions stress
in the wall may be characterized by the general laws of the strength of
materials. In this connection it has been demonstrated
[14] that at different
loads on the blood vessel, the longitudinal
and circumferential
stresses
increase with the inner pressure and longitudinal
loading; collagen fibers
are assumed to behave in the same way with regard to longitudinal loading.
In contrast, the radial stress is small compared to the others and does not
substantially
depend upon pressure and longitudinal loading.
This shows that the blood vessels respond to mechanical stress in the
same way as ordinary pipe.

The compressibility
of the blood [12] is almost equal to that of water
and, physiologically,
may be neglected in comparison with the elasticity of
the vascular wall. The density of the blood is p= 1.055 g/cm3.
These properties of the blood circulation
are comparable
to those in
hydraulic phenomena.
2.3

Although in the aorta and large vessels the blood flow takes place under
conditions
of relatively high Reynolds number (1000-l 100) in the small
vessels and capillaries, this constant, which characterizes the turbulence of
flow (Re=( vD/v)p,
where V= flow velocity, D =diameter
of the vessel,
v = coefficient of kinematic viscosity (31) is smaller [ 111; the phenomenon
is
more accentuated in the small vessels, where an abnormal viscosity of the
blood is found (the Fahreus-Lindquist
phenomenon
of decrease in the
viscosity of the blood, explicable by the sigma effect). Hence, the flow is
markedly laminar; therefore, the loss of internal energy is much smaller
than in the large arteries.
The immediate implication
of interest to us, is that the flow is more
economic from the viewpoint of the fluid energy. A measure of the

BLOOD-HAMMER

PHENOMENON

197

economy of flow in the capillaries is V/D, the ratio of flow velocity to the
diameter (a relative velocity), which in the case of the aorta is of the order
of magnitude 10 and in the capillaries l@ diameters per second.
2.4

For the vascular bed, the order of magnitude of D/e, which is involved
in the calculation of celerity, is D/e= 10. The order of magnitude of the
celerities of certain rubber tubes, having D/e= 10, and therefore comparable to normal blood vessels, is a = 2. lo3 cm/set [8].
2.5

There are many possibilities of sudden temporary arrest of the blood

flow in a cerebral vascular segment, phenomena described in physiology,
and which represent the primum moved triggering the blood hammer.
2.6

Finally, the intensity and the requirements of a quasistationary

flow and
the morphologic
particularities
of the vascular network distribution
are
further
arguments
for comparing
the cerebral
circulation
with a
hydrodynamic
network.
These similarities allow us to apply the general results obtained in
hydraulics to the particular case of the cerebral blood circulation.
3.

THE BLOOD-HAMMER
PHENOMENON
OBSTRUCTING
MECHANISM

IN TERMS

OF THE

Taking into account the physiological

and pathological
situations in
which the circulation is arrested in the cerebral vascular bed, the quantitative characteristics
of the blood-hammer
phenomenon
can be calculated.
Several situations (Fig. 3) in which this phenomenon may occur will now be
analyzed, using the classical description of the microcirculation
provided by
Chambers and Zweifach [ 111.
3.1.

SUDDEN

CONSTRICTION

OF THE PRECAPILLA

R Y SPHINCTERS

The capillaries, which represent the surge tanks for the arterioles, are
no longer part of the circuit; the metarterioles,
which likewise have a
vasoconstriction
potential, become an insufficient
reserve device, or are
suppressed by their own constriction.
Arrest of the circulation
may be
important even following moderate constriction of the blood vessel: a 16%
decrease in the radius of the vessel lowers the blood output by 50% [ 111,
which is equivalent to a suppression of the surge tank. Hence, the site of
obstruction
being the precapillary
sphincters, the arteriole will bear the
brunt of the blood hammer.

198

TRAIAN

FIG. 3.

Vascular

DAMsA

ET AL.

bed scheme.

In this case, introducing

in (I) the specific parameters of the normal
arteriolar circulation, the hemodynamic
parameters of the blood hammer
may be calculated. Considering
V,= 2 cm/set
[2, 111, the overpressure
developing in the vessel will be
A~=pay,=l.055~.2.103~.2~=4.22.103~,
cm3
and from (II) the overload

cm2

(III)

on the wall will be

3-.dyn
cm2

3o=A~+e=4.22~10+~5=21.1~10
cm2

(IV)

In order to have a standard of comparison

for this additional
load,
let us be the working load for an arteriolar pressure at p,=50mmHg=
66.64. 103dyn/cm2:
POD
2e

3 dyn

a,=-=66.64.10

-.5=333.2.10
cm2

3 -.
dyn

cm2

(V

Therefore,
o=u

+A0=354.3*

cm2

Hence, it may be seen that, under normal conditions, a blood-hammer

phenomenon
does not significantly affect the load on the vascular wall (Fig.
4).

BLOOD-HAMMER
3.2.

SUDDEN

199

PHENOMENON
INCREASE

IN THE

VENOUS

PRESSURE

(1) If the blood can flow back from the venule into the capillary bed,
which is not used to its maximum capacity, then the site of obstruction will
likewise be the precapillary sphincters, but the blood-hammer
blow will be
borne by the capillary.
(2) If the blood cannot flow back from the venule to the capillary bed,
because the capillary is full to its utmost capacity, then the obstruction will
occur at the capillary-venule junction, and the blood hammer will be borne
by the venule wall.
(3) Finally, blocking of the return circulation corresponds to obstruction
of the capillary-venule
junction, with the occurrence of the blood-hammer
phenomenon
at the capillary level.
Apart from these situations, other physiologically possible ones may be
imagined, whose occurrence still remains to be established experimentally.
Normal compensation
of the blood-hammer
overpressure
is accomplished in the first place by the marked elasticity of the vascular wall; this
lowers the celerity, and hence the induced overpressure is negligible. Secondly, the capillary vascular density is sufficient to bear the excess overpressure, the capillary bed representing its own surge tank.
4.

YIELDING
OF THE VASCULAR
TO THE BLOOD HAMMER

WALL

It has been shown that, physiologically, the blood-hammer

phenomenon
cannot be avoided. We are now concerned with the situations in which the
amplitude of the phenomenon
is so great that the overload Au results in
yielding of the vascular wall. To this end we shall study the situations in
which there is a change in the parameters of the relations (I) and (II), so
that the values of Ap and Aa exceed the adaptation
capabilities of the
vascular bed.
Thus, although an increase in the density of the blood, p, may occur
under certain physiological and pathological conditions, and the increase in
the velocity of the circulation, VO,may be very important, the celerity is the
factor whose order of magnitude shows a lo- to 30-fold increase, brought
about by a decrease in the elasticity of the vascular wall, involving an
equivalent
multiplication
of the overpressure values Ap. A decrease in
elasticity may be produced by sclerosis of the arteries, arterioles and
capillaries, and by a powerful initial distension of the vascular wall, which
deprives the vessel of the capability for elastic reaction; significant distension, influencing the diameter and the wall thickness, may also intervene as
a multiplier of the stretching force.

200

TRAIAN DAMsA ET AL.

t0

FIG. 4.

Normal

tc +At

compensation

of the blood-hammer

overpressure

It is worth noting for the sake of comparison that the celerity of ligneous
vegetable fibers [S] may reach values 40 times those of rubber.
Let us substitute for the physiological parameters in (III), (IV) and (V)
values of an order of magnitude appropriate for cerebral vascular disease:
V,=4cm/sec;
D/e=(1.25/0.75).10=
16.9;p,=75mmHg=99.96~10adyn/
cm2; a=30.10scm/
sec. (These might be accepted as maximum values in
pathology;
similar results are obtainable
even for lesser values.) Then
(Fig. 5)
A~=1.055~~30~103~~4~=126.6~10
cm3

3-.dyn
cm*

Hence
Au=126.6~103~~16.9~0.5=1069103~
cm*
The working load in the pathological

00=99.96.103*

The hoop
magnitude

cm*

stress in the vascular

u=ua+Au=

case considered

cm*
is

+X45=844.103*

cm*

wall will therefore

1913-,dyn
cm*

be of the order

of

BLOOD-HAMMER

201

PHENOMENON

P
(dyn/cm2)
t

FIG. 5.

t0

to +At

Blood-hammer

overpressure

in pathological conditions.

a value 5 times that of the usual stress, allowing for violent rupture of the
vascular wall with subsequent hemmorrhage. A particular instance is that of
repeated blood-hammer
shock, of moderate intensity, in the same area,
which damages parietal resistence to erythrocyte diapedesis, without rupture
of the wall.
Even if evaluation of the quantitative values includes certain variations,
it is difficult to accept that the vascular wall, in itself pathological, can resist
even to a two- or threefold increase in the mechanical stress to which it is
submitted by the blood-hammer
phenomenon.
On the other hand, in pathology, vascular yieldings are caused by the
association of several factors determining the blood-hammer
phenomena:
vascular sclerosis, arterial hypertension,
constriction
of the precapillary
sphincters, increase in venous pressure, increase in the velocity of the
circulation, weakening of the vascular wall due to an aneurysm or angioma,
and diminished function of the surge tank due to a decrease [l] in the
density of the vascular network of the cerebral capillaries. The compression
of the bulbar vessels, likewise due to edema, with consequent anoxia of the
vasopressor centers, resulting in an increase in arterial pressure [2, 41, is
another factor favoring the blood-hammer
phenomenon.
Certain cerebral vascular areas, being more affected appear worthy of
additional attention: the Sylvian area and the brain stem.
Within the area of the Sylvian artery the capillary network derives
almost directly from the trunk of a large artery, with comblike ramifications
[7]; hence the blood-hammer
effect is transmitted
directly; similarly the
upstream distribution of the network with respect to the main artery of the

202

TRAIAN

DAMSA

ET AL.

collaterals leads to the formation of secondary waves [lo], which are added
to the primary wave.
The brain stem may be affected by several factors:
(1) the basillary artery, with a relatively large diameter, divides rapidly
into several branches;
(2) the venous system of Galen is susceptible to blockage, raising the
venous pressure through clamping
[9], between the pituitary, corpora
quadrigemina
and corpus callosum, its anastomoses
being but slightly
efficient, especially for the affluent vessels from the pons;
(3) to these factors, in the case of edema or primary supratentorial
hemmorrhage
[S, 61, may be added traction on the vascular wall by
downward slipping of the brain stem with regard to the basillary artery,
which is relatively immobile.

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