Vascular resistance depends on blood flow

which is divided into 2 adjacent parts : a plug flow,

Vascular
resistance
refers
to flow,
the
highly concentrated
in
RBCs, and
a sheath
resistance
that
must
be
overcome Both
to
more
fluid plasma
release-cell
layering.
push blood
the circulatory
and
coexist
andthrough
have different
viscosities, system
sizes and
create flow.
Thein
resistance
offered
by the peripheral
velocity
profiles
the vascular
system.
circulation is known as the systemic vascular
resistance
(SVR)
may sometimes
referred to
Effects
of or
systemic
vascularberesistance
the the antiquated
term in
total
peripheral
on
body A decrease
SVR (e.g.,
during
resistancewill
(TPR),
resistance
by
exercising)
resultwhile
in anthe
increased
flow offered
to tissues
the anvasculature
of the
as
and
increased venous
flowlungs
back toistheknown
heart. An
the pulmonary
resistance
(PVR).
increased
SVR will vascular
decrease flow
to tissues
and
Systemic venous
vascular
resistance
is used
in calculations
decrease
flow
back to the
heart.
of blood vascular
pressure,
blood flow, and cardiac
Pulmonary
resistance
function. Vasoconstriction (i.e., decrease in blood
vessel The diameter)
increases
SVR,
major
determinant
of
vascular
whereas vasodilation
diameter)
resistance
is small(increase
arteriolarin(known
as
decreases arterioles)
SVR.
resistance
tone. These vessels are from
450 m down to 100 m in diameter. (As a
Calculation
of vascular
resistance
The 5
comparison,
the diameter
of a capillary
is about
basic
tenet of calculating resistance is that flow is
to
10 m.)
equal to driving pressure divided by resistance.
Another determinant of vascular resistance
is
the pre-capillary arterioles. These arterioles are
where
less
100 m in diameter. They are sometimes
*R isthan
Resistance
known
as change
autoregulatory
vessels
they can
*P is the
in pressure
acrosssince
the circulation
dynamically
change
in diameter
increase or
loop (systemic
/ pulmonary)
from itsto
beginning
reduce
blood flow.
(immediately
after exiting the left ventricle / right
Any
change
viscosity
of the
blood
(such
as due
to
ventricle)
toin
itsthe
end
(entering
right
atrium
/ left
aatrium)
change in hematocrit) would also affect the
measured
vascular
resistance.
*Q is the flow
through
the vasculature (when
discussing SVR this is equal to cardiac output)
Coronary vascular resistance
Systemic vascular resistance
The regulation
of vascular
tone in resistance
the coronary
calculations
The systemic
can
arteries
is be
a complex
are a 5
number
therefore
calculatedsubject.
in unitsThere
of dynscm
as
of mechanisms for regulating coronary vascular
tone, including metabolic demands (i.e. hypoxia),
neurologic control, and endothelial factors (i.e.
POnis, endothelin).
where mean arterial pressure is 2/3 of diastolic
blood pressure
plus 1/3 control
of systolic
blood
Local metabolic
(based
onpressure
metabolic
[or Diastolic
1/3(Systolic-Diastolic)].
demand)
is +the
most important mechanism of
In otherofwords:
control
coronary flow. Decreased tissue oxygen
Systemic
Vascular
Resistance
=2content
80x(Mean
content
and
increased
tissue CO
act as
Arterial Pressure
- Mean
Pressure
or
vasodilators.
Acidosis
acts Venous
as a direct
coronary
CVP) / Cardiac
vasodilator
andOutput
also potentiates the actions
of adenosine on the coronary vasculature.
Mean arterial pressure is most commonly measured
using factors
a sphygmomanometer, and calculating a
Other
specialized
systolic and
diastolic
Manyaverage
of thebetween
platelet-derived
substances,
blood pressures.
also known
including
serotonin, Venous
are pressure,
vasodilatory
when
as central
venous
is measured
at the right
the
endothelium
is pressure,
intact and
are vasoconstrictive
atrium
is usuallyisvery
low (normally around
when
theand
endothelium
damaged.
4 mm Hg). As a result, it is sometimes disregarded.

Cholinergic stimulation causes release

of endothelium-derived relaxing factor (EDRF) (later
it was discovered that EDRF was nitric oxide) from
intact endothelium,
causingare
vasodilation.
the
where the pressures
measured inIf units
endothelium
is
damaged,
cholinergic
stimulation
of millimetres of mercury (mmHg) and the cardiac
causes
output vasoconstriction.
is
measured
in
units
Adenosine
likely
does The
notpulmonary
play a role
in
of litres permost
minute
(L/min).
artery
maintaining
the vascular
resistance
in the resting
wedged pressure
(also called
pulmonary
artery
state.
However,
causesis avasodilation
and
occlusion
pressure it
or PAOP)
measurement
in
decreased
vascular
resistance
during
hypoxia.
which one of
the pulmonary
arteries
is occluded,
Adenosine
is formed
in the myocardial
during
and the pressure
downstream
from the cells
occlusion
is
hypoxia,
vigorous work,
due the
to the
measuredischemia,
in order toorapproximately
sample
left
[4]
breakdown
of high-energy
compounds
atrial pressure.
Therefore, phosphate
the numerator
of the
(e.g.,
AMP). Most
of the
aboveadenosine
equation monophosphate,
is the pressure difference
between
adenosine
that
produced leaves
the cell
and acts
the input to
theispulmonary
blood circuit
(where
the
as
a right
directventricle
vasodilator
the pulmonary
vascular
heart's
connectsonto the
wall.
Because
a direct
trunk)
and the adenosine
output of theacts
circuitas(which
is the
vasodilator,
not dependent
on The
an above
intact
input to the itleftis atrium
of the heart).
endothelium
to cause vasodilation.
equation contains
a numerical constant to
compensate for the units used, but is conceptually
Adenosine
causes vasodilation in the small
equivalent
to the following:
and medium-sized resistance arterioles (less than
100 m in diameter). When adenosine is
where Rit is can
the pulmonary
vascular
administered
cause
a coronary
[8]
resistance
(fluid
resistance),
P
is
the
pressure
stealphenomenon, where the vessels in healthy
difference
across
the pulmonary
circuit,tissue
and Q
is
tissue
dilate
as much
as the ischemic
and
the
rate
of
blood
flow
through
it.
more blood is shunted away from the ischemic
As
anthatexample:
If Systolic
120
tissue
needs it most.
This ispressure:
the principle
mmHg, Diastolic
pressure:
80 mmHg,
Right atrial
behind
adenosine
stress testing.
Adenosine
is
mean pressure:
mmHg,
output:
5 l/min,
quickly
broken 3down
byCardiac
adenosine
deaminase,
Then Mean
Arterial
Pressure
would
be: (2 wall.
Diastolic
which
is present
in red
cells and
the vessel
pressure
+
Systolic
pressure)/3
=
93.3
mmHg,
and
Systemic vascular resistance
Systemic vascular resistance: (93 - 3) / 5 = 18
Wood Units. Or Systemic vascular resistance: 18 x
80 = 1440 dyns/cm5. These values are in the
normal limits.

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Regulation of vascular resistance

There are many factors that alter the vascular
resistance. Factors that influence vascular
resistance are represented in an adapted form of
the HagenPoiseuille equation:
where
R = resistance to blood flow
L = length of the vessel
= viscosity of blood
r = radius of the blood vessel
Vessel length is generally not subject to change in
the body.
In HagenPoiseuille equation, the flow layers start
from the wall and, by viscosity, reach each other in
the central line of the vessel. But according to
Thurston,[5] there is a plasma release-cell layering
at the walls surrounding a plugged flow. It is a fluid
layer in which at a distance , viscosity is a

Front page
[5]

where
R = resistance to blood flow
c = constant coefficient of flow
L = length of the vessel
() = viscosity of blood in the wall plasma releasecell layering
r = radius of the blood vessel
= distance in the plasma release-cell layer
Blood resistance varies depending on blood
viscosity and its plugged flow size as well, and on
the size of the vessels.
Blood viscosity increases as blood is more
hemoconcentrated, and decreases as blood is more
dilute. The greater the viscosity of blood, the larger
the resistance will be. In the body, blood viscosity
increases as red blood cell concentration increases,
thus more hemodilute blood will flow more readily,
while more hemoconcentrated blood will flow more
slowly.
The major regulator of vascular resistance
in the body is regulation of vessel radius. In
humans, there is very little pressure change as
blood flows from the aorta to the large arteries, but
the small arteries and arterioles are the site of
about 70% of the pressure drop, and are the main
regulators of SVR. When environmental changes
occur (e.g. exercise, immersion in water), neuronal
and hormonal signals, including binding of
norepinephrine and epinephrine to the 1 receptor
on vascular smooth muscles, cause either
vasoconstriction or vasodilation. Because resistance
is inversely proportional to the fourth power of
vessel radius, changes to arteriole diameter can
result in large increases or decreases in vascular
resistance
The blood flow resistance in a vessel is
mainly regulated by the vessel radius and viscosity
when blood viscosity too varies with the vessel
radius. According to very recent results showing the
sheath flow surrounding the plug flow in a vessel,
[7]
the sheath flow size is not neglictible in the real
blood flow velocity profile in a vessel. The velocity
profile is directly linked to flow resistance in a
vessel. The viscosity variations, according to
Thurston,[5] are also balanced by the sheath flow
size around the plug flow. The secondary regulators
of vascular resistance, after vessel radius, is the
sheath flow size and its viscosity.