Chapter 14

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Transcript Chapter 14

Chapter 12:
Cardiovascular Physiology
Chapter 12:
Cardiovascular Physiology
CO = HR x SV, as follows.
The heart is the pump that moves the blood. Its
activity can be expressed as “cardiac output (CO)”
in reference to the amount of blood moved per unit
of time.
Chapter 12:
Cardiovascular Physiology (cont.)
A small fraction of cardiac muscle cells, called the
autorhythmic cells, determine the heart rate (HR).
A much larger group, making up 99% of the total cells in
the heart, constitutes the contractile cells. Their
activity determines the stroke volume (SV).
Chapter 12:
Cardiovascular Physiology (cont.)
Mean arterial pressure, which drives the blood, is the sum of
the diastolic pressure plus one-third of the difference
between the systolic and diastolic pressures.
The autonomic system dynamically adjusts CO and MAP.
Blood composition and hemostasis are described.
Section :A: Overview
Plasma includes
water, ions, proteins,
nutrients, hormones,
wastes, etc.
The hematocrit is a
rapid assessment
of blood composition.
It is the percent of the
blood volume that is
composed of RBCs
(red blood cells).
Figure 12-1
Figure 12-2
The heart is the pump
that propels the
blood through
the systemic and
pulmonary circuits.
Red color indicates
blood that is
fully oxygenated.
Blue color represents
blood that is only
partially oxygenated.
Figure 12-3
The distribution of blood
in a comfortable, resting
person is shown here.
Dynamic adjustments in
blood delivery allow a
person to respond to
widely varying
including emergencies.
Figure 12-4
Though pressure is higher in the lower “tube,” the flow rates
in the pair of tubes is identical because they both have the
same pressure difference (90 mm Hg) between points P1 and P2.
Section :B:
The major
external and
internal parts
of the heart are
shown in this
The black arrows
indicate the route
taken by the
blood as it is
pumped along.
Figure 12-6
Figure 12-7
Figure 12-8
The general route of the blood
through the body is shown,
including passage through the
heart (colored box).
Figure 12-9
Figure 12-10
Conducting system of the heart
Figure 12-11
Sequence of cardiac excitation
The sinoatrial node is
the heart’s pacemaker
because it initiates
each wave of excitation
with atrial contraction.
The Bundle of His and other parts
of the conducting system deliver
the excitation to the apex of the
heart so that ventricular contraction
occurs in an upward sweep.
The action potential of a
myocardial pumping cell.
The rapid opening of voltagegated sodium channels is
responsible for the rapid
depolarization phase.
Figure 12-13
The action potential of a
myocardial pumping cell.
The prolonged “plateau” of
depolarization is due to the slow
but prolonged opening of
voltage-gated calcium channels
closure of potassium channels.
Figure 12-12
The action potential of a
myocardial pumping cell.
Opening of potassium
channels results in the
repolarization phase.
Figure 12-12
The action potential of a
myocardial pumping cell.
The rapid opening of voltage-gated
sodium channels is responsible for
the rapid depolarization phase.
The prolonged “plateau” of
depolarization is due to the slow
but prolonged opening of
voltage-gated calcium channels
closure of potassium channels.
Opening of potassium
channels results in the
repolarization phase.
Figure 12-12
The action potential of an
autorhythmic cardiac cell.
Sodium ions “leaking” in through
the F-type [funny] channels
calcium ions moving in through
the T [calcium]channels cause a
threshold graded depolarization.
The rapid opening of voltage-gated
calcium channels is responsible
for the rapid depolarization phase.
Reopening of potassium channels
closing of calcium channels
are responsible for the
repolarization phase.
Figure 12-13
Figure 12-14
The relationship between
the electrocardiogram
(ECG), recorded as the
difference between currents
at the left and right wrists,
an action potential typical
of ventricular myocardial
Einthoven’s triangle
Figure 12-15a
Figure 12-15b
Figure 12-16
Excitation contraction coupling in cardiac muscle
Calcium ions regulate the
contraction of cardiac muscle:
the entry of extracellular
calcium ions causes the
release of calcium from the
sarcoplasmic reticulum, the
source of about 95% of the
calcium in the cytosol.
Figure 12-17
Refractory period of cardiac muscle
The prolonged refractory period of cardiac muscle
prevents tetanus, and allows time for ventricles to
fill with blood prior to pumping.
Figure 12-18
Mechanical events of the cardiac cycle
Systole: ventricles contracting and ejection
Figure 12-19a
Diastole: ventricles relaxed and filling
Figure 12-19b
Figure 12-20
Pressure and volume changes
in the left heart during a
contraction cycle.
Pulmonary circulation pressures
Pressure changes in the right heart during a contraction cycle.
Figure 12-21
Heart Sounds
Figure 12-22
The cardiac output: control of heart rate
Figure 12-23
Figure 12-24
To speed up the heart rate:
• deliver the sympathetic hormone, epinephrine, and/or
• release more sympathetic neurotransmitter (norepinephrine), and/or
• reduce release of parasympathetic neurotransmitter (acetylcholine).
Frank-Starling mechanism
To increase the heart’s stroke volume:
fill it more fully with blood. The increased stretch of the ventricle will
align its actin and myosin in a more optimal pattern of overlap.
Figure 12-25
Stroke volume and sympathetic nerves
To further increase the stroke volume:
fill it more fully with blood
AND deliver sympathetic signals (norepinephrine and epinephrine);
it will also relax more rapidly, allowing more time to refill.
Figure 12-26
Figure 12-27
Effects of sympathetic stimulation on ventricular contraction and relaxation
Sympathetic signals (norepinephrine and epinephrine) cause a
stronger and more rapid contraction and a more rapid relaxation.
Factors determining the cardiac output
To increase SV, increase:
end-diastolic volume,
norepinephrine delivery from
neurons, and
from the
To increase HR, increase:
norepinephrine delivery from
sympathetic neurons, and
delivery from
adrenal medulla
Figure 12-28
It is not possible, under normal circumstances, to increase one
but not the other of these determinants of cardiac output.
Section C:
The vascular system
Pressures in the systemic vessels
Figure 12-29
The blood moved in a
single heart contraction
stretches out the arteries,
so that their recoil
continues to push
on the blood, keeping it
moving during diastole.
Figure 12-30
Figure 12-31a
Figure 12-31b
Figure 12-32
To estimate systolic and diastolic pressures, pressure is released
from an inflatable cuff on the upper arm while listening as blood flow
returns to the lower arm.
Dynamic adjustments in the blood distribution to the
organs is accomplished by relaxation and contraction
of circular smooth muscle in the arterioles.
Figure 12-33
Local control of organ blood flow
Active hyperemia and flow autoregulation differ in their
cause but both result in the production of the same
local signals that provoke vasodilation.
Figure 12-34
Figure 12-35
Sympathetic stimulation of alpha-adrenergic receptors cause
vasoconstriction to decrease blood flow to that location.
Sympathetic stimulation of beta-adrenergic receptors lead to
vasodilation to cause an increase in blood flow to that location.
Figure 12-36
Major factors affecting arteriolar radius
Diversity among signals that influence contraction/relaxation
in vascular circular smooth muscle implies a diversity of
receptors and transduction mechanisms.
The capillary is
the primary
point exchange
between the
blood and the
interstitial fluid
clefts assist the
Figure 12-37
a single
Figure 12-38
Capillaries lack smooth muscle, but contraction/relaxation of circular
smooth muscle in upstream metarterioles and precapillary sphincters
determine the volume of blood each capillary receives.
Six balls in per minute
Figure 12-39
mandates six balls out per minute.
Therefore, the velocity of the balls in the smaller tubes is slower.
Figure 12-39
There are many, many capillaries, each with slow-moving
blood in it, resulting in adequate time and surface area
for exchange between the capillary blood and the ISF.
Distribution of the total blood volume
in different parts of the CVS
At rest, approx. 60% of the
total blood volume is in the
veins. Sympathetically
mediated venoconstriction
can substantially increase
venous return to the heart.
Figure 12-44
Skeletal muscle pump
Figure 12-45
Venous flow is assisted by the skeletal muscle pump
mechanism working in combination with one-way valves.
Major factors determining
the peripheral venous return
Figure 12-46
Alterations in “venous return” alter end-diastolic volume (EDV);
increased EDV directly increases stroke volume and cardiac output.
The lymphatic system
Figure 12-47
Lymphatic fluid, formed
by the slight mismatch
between filtration and
absorption in the
capillaries, returns to
the blood in the veins.
Section C:
Regulation of systemic arterial pressures
Dynamic changes in vasodilation/vasoconstriction due to changes
in the resistance of arterioles can alter the mean arterial
pressure (represented as P).
Figure 12-49
Figure 12-50
Compensatory changes in arteriolar resistance occur to protect
the maintenance of mean arterial pressure (represented as P).
Figure 12-51
A summary of dynamic changes in MAP and TPR.
Figure 12-52
Blood loss causes a
reduction in MAP, which, if
left unchecked, would
result in rapid and
irreversible damage to the
brain and the heart.
Figure 12-53
Baroreceptor neurons
function as sensors in
the homeostatic
maintenance of MAP
by constantly
monitoring pressure
in the aortic arch and
carotid sinuses.
Figure 12-54
The action potential frequency in baroreceptor neurons is
represented here as being directly proportional to MAP.
Figure 12-55
i.e., MAP is
set point
i.e., reduce cardiac output
Baroreceptor neurons deliver MAP information to the
medulla oblongata’s cardiovascular control center (CVCC);
the CVCC determines autonomic output to the heart.
Figure 12-56
The information reported by
baroreceptor neurons sets in
motion autonomic responses not
only to the heart, but also to
arterioles and veins.
MAP is more readily moved
back closer to the “set point” by
this combined approach.
Figure 12-57
Whatever the cause, an abnormal increase in MAP
“squeezes” more fluid out of the blood and into the urine,
leading to a reduction in blood volume, which then
reduces MAP back closer to the “set point” value.
Figure 12-58
Loss of blood causes immediate reductions in MAP, but
compensatory responses in cardiac output and total
peripheral resistance act quickly to restore MAP.
Figure 12-59
At capillaries, reduced MAP increases absorption and
reduces filtration to help “protect” blood volume.
Figure 12-61
Distribution of the systemic CO
Dynamic adjustments
in blood-flow distribution
during exercise result from
changes in cardiac output
and from changes in regional
Summary of CV changes during mild exercise
Figure 12-63
Control of the CVS during exercise
Using stored knowledge, along with information from the
periphery (afferent input), the CNS coordinates changes in
cardiac output and blood-flow distribution during exercise.
Changes in CO, HR, SV
with increasing workload
in untrained and trained
The benefits of
training include
capacity during
Figure 12-64
Figure 12-65
Heart failure leads to increased fluid retention, leading to
increased blood volume and greater stroke volume;
however, the failing heart is less able to handle a large EDV.
Coronary artery disease and its treatment
An example of
and treatment
of blocked
blood flow in an
impaired heart.
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