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Output
and
Blood
Pressure
Cardiac Output
Cardiac output is the volume of
blood pumped by the heart per
minute (mL blood/min). Cardiac
output is a function of heart
rate and stroke volume.
Theheart rate is simply the
number of heart beats per
minute. The stroke volume is
the volume of blood, in
milliliters (mL), pumped out of
the heart with each beat.
Increasing either heart rate or
stroke volume increases cardiac
output.
Control
of Heart
Rate
The SA node of
the heart is
enervated by
both
sympathetic and
parasympathetic
nerve fibers.
Under
conditions of
rest the
parasympathetic
fibers release
acetylcholine,
which acts to
slow the
pacemaker
potential of the
SA node and
thus reduce
heart rate.
Under
conditions of
physical or
emotional
activity
sympathetic
nerve fibers
release
norepinephrine,
which acts to
speed up the
pacemaker
potential of the
SA node thus
increasing heart
rate.
Sympathetic
nervous system
activity also
causes the
release of
epinephrine
from the
adrenal
medulla.
Epinephrine
enters the blood
stream, and is
delivered to the
heart where it
binds with SA
node receptors.
Binding of
epinephrine
leads to further
increase in heart
rate.
Control of Stroke
Volume
Under conditions of rest, the heart
does not fill to its maximum
capacity. If the heart were to fill
more per beat then it could pump
out more blood per beat, thus
increasing stroke volume. Also, the
ventricles of the heart empty only
about 50% of their volume during
systole. If the heart were to contract
more strongly then the heart could
pump out more blood per beat. In
other words, a stronger contraction
would lead to a larger stroke
volume. During periods of exercise,
the stroke volume increases because
of both these mechanisms; the heart
fills up with more blood and the
heart contracts more strongly.
1. increase in end-diastolic
volume
2. increase in sympathetic
system activity
End-diastolic Volume
An increase in venous return of
blood to the heart will result in
greater filling of the ventricles
during diastole. Consequently the
volume of blood in the ventricles at
the end of diastole, called end-
diastolic volume, will be increased.
A larger end-diastolic volume will
stretch the heart. Stretching the
muscles of the heart optimizes the
length-strength relationship of the
cardiac muscle fibers, resulting in
stronger contractility and greater
stroke volume.
Starling's
Law
Starling's
Law
describes
the
relationship
between
end-
diastolic
volume and
stroke
volume. It
states that
the heart
will pump
out
whatever
volume is
delivered
to it. If the
end-
diastolic
volume
doubles
then stroke
volume
will
double.
An Increase in Sympathetic
Activity Increases Stroke
Volume
If excess
fluid cannot
be returned to
the blood
stream then
interstitial
fluid builds
up, leading to
swelling of
the tissues
with fluid,
this is
callededema.
Causes of Edema
1. Reduced concentration of
plasma proteins. When the
concentration of plasma proteins
drops, the osmotic potential of
plasma drops, thus less interstitial
fluid is absorbed into the capillaries.
The rate of filtration, however,
remain unchanged. Therefore, the
ratio of filtration to absorption
increases, leading to a build up of
interstitial fluid. Any condition that
would lead to a reduction in plasma
proteins could potentially cause
edema. Examples of conditions that
reduce plasma proteins include:
2. Increased capillary
permeability. During an
inflammatory response, tissue
damage leads to the release of
histamine from immune cells.
Histamine causes an increase in the
size of capillary pores. As
capillaries become more permeable,
the rate of filtration increases.
Regulation of
Blood Flow
Blood Flow through Vessels is effected by
Pressure and Resistance
The flow of blood through the vessels of the circulatory system is a
function of the pressure in the system and the resistance to flow
caused by the blood vessels. Blood flow is directly proportional to
pressure and inversely proportional to resistance.
If the pressure in a vessel increases then the blood flow will increase.
However, if the resistance in a vessel increases then the blood flow
will decrease.
1. Length of the vessel. The longer the vessel the greater the
resistance.
2. Viscosity of the blood. The greater the viscosity the greater
the resistance.
3. Radius of the vessel. The smaller the radius the greater the
resistance.
The relationships between factors that effect blood flow are described
by Poiseuille's Law, which states:
Of all of the
factors that effect
blood flow, the
radius of the
blood vessel is
the most potent.
Blood flow is
proportional to
the 4th power of
vessel radius.
This means that
if the radius of a
blood vessel
doubles (by
vasodilation)
then the flow will
increase 16 fold
(2 to the 4th
power is 16). On
the other hand, if
the radius of a
vessel is reduce
in half (by
vasoconstriction),
then the blood
flow will be
reduced 16 fold.
Because small
changes in vessel
radius make very
large changes in
blood flow, it is
no surprise that
the body controls
blood flow to
specific areas of
the body by
controlling the
radius of
arterioles
servicing those
areas.
Extrinsic Regulation
of Blood Flow
Extrinsic regulation refers to a form
of control that comes from an
outside source. The extrinsic
regulation of blood flow refers to
the control of arteriolar radius by
both the autonomic nervous system
and the endocrine system.
Sympathetic Control of
Arteriolar Radius
Arterioles are
enervated by the
sympathetic
nervous system
only.
(Parasympathetic
enervation of
arterioles only
occurs in the
male penis,
where it results
in erection.)
Sympathetic
nerve fibers
secrete
norepinephrine.
Binding of
norepinephrine
to receptors on
the smooth
muscles of
arterioles causes
contraction and
thus leads to
vasoconstriction.
Arterioles
servicing tissues
at rest receive a
baseline amount
of sympathetic
stimulation and
thus are slightly
constricted
(vessel b in the
figure). This
baseline level of
constriction is
called Vascular
Tone.
Vasodilation is
accomplished by
decreasing
sympathetic
stimulation
below baseline
(vessel a).
Vasoconstriction
is accomplished
by increasing
sympathetic
stimulation
above baseline
(vessel c).
Endocrine Control of
Arteriolar Radius.
Intrinsic Regulation of
Blood Flow
Intrinsic regulation refers to local
control of arteriolar radius. Intrinsic
regulation allows some organs to
regulate their own blood flow
regardless of what may be
happening elsewhere in the body.
Intrinsic regulation take the form of
metabolic control or myogenic
control.
Metabolic
Control
As a result of
metabolic
activity, cells
produce by-
products called
metabolites.
When a tissue
increases its
activity the
production of
metabolites will
also increase. If
blood flow to
the area
remains
constant in the
face of this
change, then
the metabolites
will build up in
the tissues. The
major
metabolites that
build up
include CO2,
ADP,
extracellular
K+ and organic
acids. These
metabolites
directly
stimulate the
vasodilation of
local arterioles,
thus increasing
blood flow.
This
mechanism, in
which an
increase in the
activity of a
tissue induces
an increase in
blood flow to
the area, is
called active
hyperemia.
This increase in
blood flow
eventually
lowers the
levels of
metabolites
thus removing
the original
stimulus for
vasodilation. In
the absence of
excess
metabolites the
arteriole returns
to its original
diameter.
Myogenic Control
The smooth muscles in blood
vessels are directly affected by
pressure. If blood pressure and flow
of blood to an organ are low then
the smooth muscles of adjacent
arterioles relax. The resulting
vasodilation restores adequate blood
flow. Conversely, if blood flow to
an organ is excessive then smooth
muscles of the arterioles will
vasoconstrict, thus reducing flow to
appropriate levels. Through
myogenic control, arterioles are
somewhat self-regulating.
1. An increase in cardiac
output. Exercise activates
the sympathetic nervous
system. Increased
sympathetic output to the
heart causes an increase in
heart rate and stroke volume.
Heavy exercise increases
venous return of blood to the
heart via the skeletal muscle
pump and the respiratory
pump. An increase in venous
return leads to an increase in
end-diastolic volume (EDV),
which in turn, causes an
increase in stroke volume.
2. Vasodilation of skeletal
muscle arterioles. The most
important factor governing
flow of blood to exercising
muscles is local metabolic
control (active hyperemia).
As muscular activity
increases, metabolites build
up and directly induce the
vasodilation of local
arterioles. Additionally,
beta-adrenergic stimulation
by epinephrine causes
vasodilation of arterioles in
skeletal muscle.
3. Vasoconstriction of
arterioles in the viscera
and skin. As a result of
alpha-adrenergic
sympathetic stimulation,
arterioles in the viscera and
skin vasoconstrict during
exercise. However, as
exercise progresses and body
temperature rises, cutaneous
arterioles dilate in order to
radiate heat and reduce body
temperature.
Regulation of
Blood Pressure
Constant and adequate pressure in
the arterial system is required to
drive blood into all of the organs.
Abnormally low blood pressure
results in inadequate perfusion of
organs, while abnormally high blood
pressure can cause heart disease,
vascular disease and stroke.
Therefore, it is essential that blood
pressure be maintained within a
narrow range of values that is
consistent with the needs of the
tissues.
Cardiac Output
Blood Volume
Baroreceptor Reflexes
in Short-term
Regulation of MAP
Blood pressure is contolled on a
minute-to-minute basis by
baroreceptor reflexes. Baroreceptors
are specialized stretch receptors that
detect changes in blood pressure.
Baroreceptors are located in the
walls of arteries, veins and the heart.
The most important baroreceptors
being those found in the carotid
sinus and the aorta. Baroreceptors,
which constantly monitor blood
pressure, communicate with the
Cardiovascular Control Center
(CCC) found in the brain stem.
Changes in blood pressure effect the
frequency of action potentials sent
to the CCC from the baroreceptors.
The CCC responds to changes in
baroreceptor input by initiating
compensatory mechanisms that
restore blood pressure back to
normal.
The diagram
to the right
illustrates the
efffect of
blood
pressure on
the
production of
action
potentials by
the
baroreceptors.
80 mmHg is a
baseline
MAP for a
typical person
(given a
measured
blood
pressure of
120/60). At a
baseline of 80
mmHg a
baroreceptor
will produce
a constant
baseline
frequency of
action
potentials
(seen as
small,
vertical, blue
lines in the
diagram). If
blood
pressure rises
above
baseline, the
baroreceptor
increases its
frequency of
action
potential
output. On
the other
hand, if blood
pressure
drops below
baseline, then
the
baroreceptor
decreases its
frequency of
action
potential
output.
Conversely, a decrease in blood pressure causes a decrease in action potentials sent to the
cardiovascular control center, which causes an increase in sympathetic input, which
causes vasoconstriction and increased cardiac output, which causes a rise in blood
pressure, thus restoring blood pressure back to normal.
Plasma, the liquid portion of blood, is part of the extracellular fluid (ECF). If the kidneys
retain water, then the volume of the ECF rises and blood volume rises. If the kidneys
retain salt (NaCl), then the ECF becomes saltier and thus capable of retaining more water
(water follows solute). Higher ECF volume leads to higher blood volume and thus higher
blood pressure.
Summary of Factors that Effect Mean
Arterial Pressure
Table of
Quiz
(Revised September 17 1999) Contents
The art on this page is reproduced by
permission from McGraw-Hill Companies,
Inc.
Bibliographic information
Title Exercise Physiology for Health Fitness and Performance
M - Medicine Series
Edition illustrated
Subjects Medical
General
==================================================================================
2. CARDIAC CYCLE
The normal electrical and mechanical events of a single cardiac
cycle of the left heart are correlated in Fig. 1. The mechanical
events of the left ventricular pressurevolume curve are
displayed in Fig. 2. During a single cardiac cycle, the atria and
ventricles do not beat simultaneously; the atrial contraction
Blood pressure is measured in units called millimeters of mercury (mmHg). A normal systolic blood
pressure is less than 140 mmHg; a normal diastolic blood pressure is less than 90 mmHg. Blood
pressure higher than normal is called hypertension,and one lower than normal is called hypotension.
Hence, normal mean arterial pressure is between 60 and 90mmHg. Mean arterial pressure is
normally considered a good indicator of tissue perfusion and can be measured directly using
automated blood pressure cuffs or calculated using the following formulas:
MAP = DBP + PP/3 or MAP = [SBP + (2 DBP)]/3
where PP = SBP DBP; MAP is mean arterial pressure, DBP is diastolic blood pressure, PP is pulse
pressure, and SBP is systolic blood pressure.
Blood flow throughout the circulatory system is directed by pressure gradients. By the time blood
reaches the right atrium,which represents the end point of the venous system, pressure has
decreased to approx 0 mmHg. The two major determinants of blood pressure are: (1) cardiac output,
which is the volume of blood pumped by the heart per minute; and (2) systemic vascular resistance,
which is the impediment offered by the vascular bed to flow. Systemic vascular resistance is
controlled by many factors, including vasomotor tone in arterioles, terminal arterioles, or precapillary
sphincters. Blood pressure can be calculated using the formula
BP = CO SVR
where BP is blood pressure, CO is cardiac output, and SVR is systemic vascular resistance.
Blood pressure decreases by 35 mmHg in arteries that are 3 mm in diameter. It is approx 85 mmHg
in arterioles, which accounts for approx 50% of the resistance of the entire systemic circulation. Blood
pressure is further reduced to around 30 mmHg at the point of entry into capillaries and then becomes
approx 10 mmHg at the venous end of the capillaries.
The speed of the advancing pressure wave during each cardiac cycle far exceeds the actual blood
flow velocity. In the aorta, the pressure wave speed may be 15 times faster than the flow of blood. In
an end artery, the pressure wave velocity may be as much as 100 times the speed of the forward
blood flow.
As the pressure wave moves peripherally through the arterial system, wave reflection
distorts(menggalakkan) the pressure waveform, causing an exaggeration of systolic and pulse
pressures. This enhancement of the pulse pressure in the periphery causes the systolic blood
pressure in the radial artery to be 2030% higher than the aortic systolic blood pressure and the
diastolic blood pressure to be approx 1015% lower than the aortic diastolic blood pressure.
Nevertheless, the mean blood pressure in the
radial artery will closely correspond to the aortic mean blood pressure.
Noninvasive Arterial
Blood Pressure Monitoring
Noninvasive blood pressure assessment is the most utilized and simplest technique to monitor arterial
blood pressure. This technique utilizes a blood pressure cuff and the principle of pulsatile flow. A
blood pressure cuff is applied to a limb such
as forearm or leg and is inflated to a pressure greater than
systolic blood pressure, which stops blood flow distal to the
inflated cuff. As the pressure in the cuff is gradually decreased,
BP = CO SVR
CO = HR SV
MAP = 1/3 SBP + 2/3 DBP
where BP is blood pressure, CO is cardiac output, SVR is systemic vascular resistance, HR is heart
rate, SV is stroke volume,MAP is mean arterial pressure, SBP is systolic blood pressure, and DBP is
diastolic blood pressure. Stroke volume is dependent on preload, afterload, and contractility (Fig. 8).
In general, arterial blood pressure monitoring involves two techniques: noninvasive (indirect) and
invasive (direct) methods. The decision to utilize either blood pressure monitoring method depends on
multiple factors such as cardiovascular stability or instability, need for frequent arterial blood samples,
frequency of blood pressure recordings, or major surgery and trauma. One of the advantages of an
invasive blood pressure monitor is that it provides continuous, beat-to-beat blood pressures (see
JPEG 1 on the Companion CD). Direct arterial blood pressure monitoring is considered a requirement
during cardiopulmonary bypass surgery. Because there is no pulsatile flow during such surgery, the
noninvasive methods to monitor blood pressure cannot be employed.
Typical clinical sites for intraarterial cannulation for arterial pressure monitoring are the radial,
brachial, axillary, or femoral arteries. Although the ascending aorta is the ideal place to monitor
arterial pressure waveforms, this is not practical in most clinical settings. However, it should be noted
that pressure measurements in the more peripheral arteries become distorted when compared to
central aortic pressure waveform (Fig. 10) Fig. 10. Arterial blood pressure wave. A typical optimally
damped arterial blood pressure waveform. The peak portion of the waveform corresponds to the systolic blood
pressure and the trough corresponds with the diastolic blood pressure. The dicrotic notch is associated with
closing of the aortic valve. Information about cardiovascular function can be estimated from the waveform. The
upstroke correlates with myocardial contractility. The downstroke and position of the dicrotic
notch give information about systemic vascular resistance. The stroke volume is estimated by integrating the
area under the curve..
Peripherally, the systolic blood pressure may be higher and diastolic blood pressure lower, and the
MAP is usually similar to central aortic pressure. The pressure waveform becomes more distorted as
pressure is measured farther away from the aorta. This distortion is caused by a decrease in arterial
compliance and reflection and oscillation of the blood pressure waves. For example, an arterial
pressure wave monitored from the dorsalis pedis will be significantly different from a central aortic
wave when it is graphically displayed (Fig. 11). There is also a loss in amplitude or absence of the
dicrotic notch, an increase in systolic blood pressure, and a decrease in diastolic blood pressure. One
should also be aware of the possible appearance of a reflection wave as the blood pressure is
monitored from a peripheral site. Importantly, risks associated with an indwelling intraarterial
pressure catheter include thrombosis, emboli, infection, nerve injury, and hematoma.