Blood Vessels
Blood
vessels are the 'tubes' that transport blood from the heart to the body and
back again. All blood vessels contain an innermost lining called endothelium, a type of epithelial
tissue. It plays an important role in regulating blood pressure, vessel growth
and movement of substances into and out of vessels.
All
blood vessels except capillaries also contain vascular smooth muscle (VSM) in their walls. They can be
arranged in circular or spiral layers. When they contract they cause vasoconstriction of the vessel, and
when they relax they cause vasodilation
of the vessel. These changes in blood vessel diameter have a significant impact
on blood flow and blood pressure.
Current
research indicates that the various components of the wall of blood vessels
play an active role in how the blood vessel behaves. The muscle cells of VSM
are not electrically coupled (as in cardiac cells), so each muscle cell must be
stimulated individually to contract. Graded contractions in VSM are achieved by
gradual changes in membrane potential and their contraction depends on Ca2+
entry. There are both voltage-gated and chemically-gated Ca2+
channels in smooth muscle. VSM maintains a constant state of partial
contraction, this is termed muscle tone.
Many things, like neurotransmitters, hormones, paracrines, etc., affect muscle
tone. Also, the endothelial cells of blood vessels can secrete vasoactive
paracrines, factors that can alter vessel diameter and thus flow of blood.
Briefly
listed here are descriptions of the important blood vessels in the systemic
circuit, going from arterial to venous systems:
1.
Arteries: Thick walled (3 layers), elastic vessels for high pressure
blood.
2.
Arterioles: Resistance vessels, less elastic, more muscular, large
changes in diameter.
3.
Capillaries: Thinnest walled, smallest diameter vessels for exchange.
4.
Venules: Drains capillaries, has endothelium and some VSM, participates
in exchange.
5.
Veins: Thinner walled (3 layers), large diameter vessels for returning
low pressure blood back to heart.
1. Arteries Carry Blood away from the Heart
Large
arteries, like the aorta and other
major arteries, are thick walled (3 layers), stiff and springy. They contain
VSM with fibrous tissue and elastic tissue, so that they exhibit elasticity.
They
have 2 important roles: 1) they transport high pressure blood to the
body; and 2) they help to maintain arterial pressure. The
high-pressure blood in these vessels stretches the elastic fibers, and when
pressure is reduced (as ventricles relax), they recoil to their original shape,
thus not allowing the arterial pressure to fall too low before the next
ventricular contraction begins.
2. Arterioles
Arterioles
are the Resistance vessels in the
body. Their wall has only 2 layers (endothelium and VSM) and they can exhibit large changes in diameter due to the
VSM. As we will see, even small changes in blood vessel diameter can cause significant
changes in resistance to blood flow - which will impact blood pressure.
Peripheral resistance is often defined as the resistance in arterioles (Rarterioles).
As Rarterioles increases, the pressure gradient must also increase,
in order to overcome this resistance.
3. Capillaries are the Vessels of
Exchange
Capillaries
(and post-capillary venules) are where exchange
of contents between blood and the tissues occur. The capillary walls are the
thinnest of all vessels, made of flat endothelium that is only one-cell thick
and supported on a basement membrane. There are leaky junctions between cells
(except at the blood-brain barrier) to facilitate exchange. As we shall see
later, there are different types of capillary beds in the body. Each has a slightly
different arrangement to best suit its function.
Blood
flow through the capillaries is determined by a combination of the driving
force mean arterial pressure (MAP) and the amount of resistance in the
arterioles. The rate of blood flow within a single capillary bed is
proportional to the MAP and inversely proportional to the resistance of the
arteriole regulating flow into that capillary bed. See previous Cardiovascular
notes regarding Flow = DP/R.
4. Venules
Blood
flows from capillaries to venules. Small venules are distinguished from
capillaries by convergent flow pattern, that is, they collect the blood exiting
the capillary beds and become larger vessels. Venules have very thin walls and
can participate in some exchange but some also have a little smooth muscle and
are larger than capillaries in diameter. Venules drain into veins.
5. Veins
Veins
are similar to arteries in that their walls have 3 layers, but the walls of
veins are thinner than arteries. Veins are more numerous than arteries and have
larger diameter (despite having
thinner walls). They hold more than 1/2 of the circulating blood and as such
veins act as a volume reservoir, often termed the Venous Reservoir. Veins are where the pressure of blood is the
lowest. Blood flows down a pressure gradient, so if blood is to flow from
arteries > arterioles > capillaries > venules > veins, then each
next vessel must have lower pressure then the previous, thus veins must be the
lowest. By definition, veins transport blood back to the heart. Due to the low
pressure in these vessels, there are some strategies that the venous system
uses to help get blood back to the heart.
Mechanisms
to Increase Venous
Return
1)
Venous Valves: Veins have venous
valves. As in the heart, vales in veins are to prevent retrograde flow of
blood. The segmentation of veins with valves means that once the blood in the
next compartment, it cannot drop back to the one before it. In this way, blood
in veins "inches" back to the heart at low pressure (but because the
diameters are large, the flow is relatively high).
2)
Skeletal Muscle Pump: Many veins are
situated next to skeletal muscle. When this muscle contracts, it compresses the
veins nearby, and because of the valves in veins, the blood can only move 'up',
toward the heart when these vessels are compressed. Therefore, muscle
contraction helps augment venous return of blood to the heart.
3)
Respiratory Pump: Breathing in and
out requires contraction of the diaphragm (a skeletal muscle). When we breath
in (diaphragm contracts) the pressure in the thoracic cavity decreases. This
small decrease helps blood flow from the venae cavae (this term means both the
inferior and superior vena cava) into the right atrium. When we breath out
(diaphragm relaxes) the pressure in the thoracic cavity increases, so flow is
slowed a little, but each breath in helps flow more than the out breath hinders
flow.
BLOOD PRESSURE
Ventricular
contraction creates the driving force of blood pressure (BP). The elastic
recoil of arteries helps to sustain the high pressure in these vessels
(arteries) that push blood forward. Because they are located close to the
ventricle and they are elastic, arteries are high-pressure vessels in which
blood moves with a pulsatile flow. If a person has been cut and is bleeding,
you can distinguish a cut artery from a cut vein by looking for uneven flow
that reflects the pulse. The major arteries of the body are located deep inside
the tissues, where they are protected from superficial trauma. In contrast, the
many veins are closer to the surface of the body. Although you cannot see the
major arteries, you can feel them wherever you can find a pulse. Major pulse
points of the body include the carotid arteries, which are found in the neck on
either side of the trachea, the femoral arteries, which are found in the groin
area, the brachial arteries, which are found on the inside of the arms just
above the elbow, and the radial arteries, which are found on the lateral side
of the wrists. In these locations the arteries emerge closer to the body
surface in order to cross bones.
Blood Pressure in the Systemic
Circulation is Highest in the Arteries and Lowest in the Veins
Pressure
decreases moving from arteries to veins due to blood pressure resistance. Veins
have no pulse. Systemic pressure is maximum in the aorta.
Blood
Pressure (BP) is expressed as Systolic pressure (the higher value) over
Diastolic pressure (the lower value). Typical normal values for a 70 Kg man are 120/80 (where systolic pressure =
120 mm Hg and diastolic pressure = 80 mm Hg). Pulse occurs from rapid pressure
increase that occurs when ventricles push blood into aorta. Pulse amplitude
decreases over distance due to friction. Pulse pressure can be defined as the
measure of the change in amplitude of the pulse pressure wave - and can be
calculated with this formula: Pulse Pressure
= Systolic - Diastolic (in e.g., 120 - 80 = 40 mmHg).
Arterial Blood Pressure Reflects
the Driving Pressure for Blood Flow
Arterial
blood pressure is estimated by using sphygmomanometer. Briefly, the process is
as follows: Inflating the cuff cuts off blood flow as it exceeds the pressure
in the vessel. Gradually deflating the cuff allows pressure to begin to fall.
When blood pressure in the vessel is greater than the cuff, blood flows past.
Turbulent flow makes the Korotkoff sound. Systolic pressure is detected as
the pressure at which blood flow is first heard, i.e., highest pressure.
Diastolic pressure is detected as the pressure at which all sound disappears
(lowest pressure). We may test for these sounds in lab.
If
we assume that arterial blood pressure reflects ventricular pressure and that arterial
pressure is pulsatile, then measure of mean arterial pressure (MAP) gives a
single value that represents the driving pressure.
The
formula for MAP is: MAP = Diastolic P + 1/3 (Systolic P -
Diastolic P)
For
a person with BP of 120/80, MAP = 93 mm Hg. Use the above formula to calculate
this value. This formula applies for people with a resting heart rate range of
60-80 beats per minute (bpm). The heart actually spends more time in diastole
(relaxation) than in systole (contraction) and this formula for MAP reflects
that. If it were a straight mean, it would be calculated as: (120 + 80) divided
by 2 = 100 mmHg. Abnormally high or low arterial blood pressure can indicate
problems. Low pressure may indicate impaired blood flow and oxygen delivery.
High pressure (hypertension) may increase the risk of hemorrhage.
WHAT ARE THE MAIN FACTORS
INFLUENCING MEAN ARTERIAL PRESSURE (MAP)?
1) Cardiac Output (C.O.)
2) Peripheral Resistance (Rarterioles)
3) Total Blood Volume
4) Distribution of Blood in Body
1) Cardiac Output
Mean
Arterial Pressure (MAP) is the major determinant of blood flow. Then what
determines MAP? It is a balance between
blood flow into and out of arteries. If the flow into arteries is greater than
the flow out, then there is an increased MAP. If the flow out of arteries is
greater than the flow in, then there is a decreased MAP. Most simply put, MAP
is a function of cardiac output (CO) and resistance of arterioles (or
peripheral resistance). Cardiac Output (CO) determines blood flow into arteries
and peripheral resistance determines blood flow out (e.g., greater R, less flow
out).
2) Peripheral Resistance
(Resistance in the Arterioles)
More
than any other type of vessel, the arterioles are the main site of varying systemic
resistance. The Vascular Smooth Muscle (VSM) in their walls allows for large
changes in diameter. VSM contraction leads to vasoconstriction and VSM relaxation leads to vasodilation. Remember, R ยต
1/r4. As the result of tonic sympathetic stimulation, all arterioles
except those of the brain and lungs maintain a tonic state of contraction, in
other words, they are always a little constricted. The ANS has control of blood
vessel diameter through sympathetic stimulation that maintains vascular tone.
To constrict vessels further, sympathetic stimulation is increased; to get
dilation, there is a reduction in sympathetic stimulation.
Arteriole
resistance is also influenced by local control. These factors usually act to
match tissue blood flow to tissue's metabolic needs. For example, if some
tissues have low O2 content, then blood flow to that region will
increase (vessels dilate) to supply the tissues using up their O2.
Conversely, if tissues have adequate O2 levels, then blood flow may
decrease (vessels constrict) to that region. Reflex (long distance)
vasoconstriction and vasodilation by the ANS and hormones is superimposed on
the tonic control to ensure that arterial blood pressure remains adequate. Clinical
note: Most cases of hypertension are associated with increased peripheral
resistance.
3) Total Blood Volume
Changes
in blood volume affect blood pressure. As blood volume increases, blood
pressure increases. The converse is also true; As blood volume decreases, blood
pressure decreases. Therefore, blood volume and blood pressure (BP) are directly proportional, if volume
increases (and all else remains constant) then BP will also increase.
How
is blood volume controlled? Blood volume adjustments are primarily the
responsibility of kidneys. For example, if you drink large amounts of water,
this will increase blood volume. In response, the kidneys will act to excrete
more water. This way, the volume is decreased and BP is reduced, the response
from the kidneys is integrated with the cardiovascular system. Kidneys can only
conserve water, they cannot create more water when you are dehydrated.
Therefore if you have low blood volume, this lost fluid must be replaced by
drinking or IV infusions. The cardiovascular system compensates if you are
experiencing decrease blood volume: As you will see, increased sympathetic
activity causes vasoconstriction.
4) Distribution of Blood in the
Body
Blood
distribution to the tissue depends on metabolic needs and this is governed by a
combination of local and reflex control. For example, at rest skeletal muscle gets
20% of cardiac output (CO); when exercising it gets 85%. The blood distribution
depends partly on number and size of arteries feeding an organ. The kidneys,
digestive tract, liver, and muscles together receive over 2/3 of the CO. Blood
flow variations are possible because arterioles are arranged in parallel. Remember
that total blood flow through all arterioles = CO. Flow through individual
arterioles depends on their resistance. As resistance increases, blood flow
decreases. Blood diverted from high-resistance arterioles flows through
low-resistance arterioles -blood flow takes the path of least resistance. In
other words, blood flows into dilated blood vessels more easily than
constricted ones. Within a tissue, capillary blood flow can be regulated by
pre-capillary sphincters.
At
rest, the relative distribution of blood in the vasculature of the body is as
follows: Arteries about 11 % total blood; Veins at least 60%, they are the blood
reservoir of the body. If arterial pressure falls, the sympathetic division of
the ANS causes venous constriction, literally squeezing blood from the veins
back into the heart (increases venous return) and this results in an increase
in arterial blood volume.
Myogenic Autoregulation
Automatically adjusts Blood Flow
Myogenic
autoregulation means that vascular smooth muscle can regulate its own state of
contraction. For example, if there is an increase in blood pressure, this leads
to an increase arteriolar blood flow. However, the arteriole walls are
stretched due to the increase in pressure and this triggers constriction of the
arteriole wall, leading to a decrease in blood flow. The exact mechanism is
unclear, but it is hypothesized that there are stretch sensitive Ca2+
channels on VSM. The signal may also consist of vasoconstrictive paracrines
(endothelins) from endothelial cells themselves.
Paracrines alter Vascular Smooth
Muscle Contraction
Tissue
and endothelial paracrines locally control arteriole resistance. In the body, nitric
oxide (NO), previously known as endothelial-derived relaxing factor
(EDRF) causes relaxation of VSN and hence vasodilation of blood vessels in the
body. The heart drug used for angina (pain from cardiac ischemia) nitroglycerin is metabolized in the body
to NO and causes systemic vasodilation and a large drop in blood pressure. The
amino acid arginine is a precursor to NO, and is converted into NO by the
enzyme NO synthase. In the body, NO is
broken down in seconds.
There
is a family of signal molecules called Prostaglandins which have been known
to have an effect on blood vessels. The vasoactive substance
histamine is often released by defense cells in times of an
inflammatory response. Like NO, histamine can cause local or systemic
vasodilation and decrease BP.
Adenosine
acts as a vasodilator in myocardial tissue. Myocardial hypoxia causes the
release of adenosine which causes vasodilation. Not all vasoactive paracrines
reflect changes in metabolism: Kinins and histamine are potent vasodilators
that play a role in inflammation.
Serotonin
can act as a vasoconstrictive paracrine released by activated platelet cells to
slow blood loss. Sumatriptan is a vasoconstrictive serontonin agonist used to
treat migraines.
The Sympathetic Division is
Responsible for Most Reflex Control of Vascular Smooth Muscle
Neural
and hormonal signals affect smooth muscle contraction. As we have seen, most systemic
arterioles are innervated by sympathetic neurons. The exceptions include: the brain
arterioles and erectile arterioles of penis and clitoris. Sympathetic neuron
activity: Tonic norepinephrine (NE) helps maintain myogenic tone. NE acts on a-receptors
on smooth muscle causing vasoconstriction. An increase in NE release means
increases in constriction. A decrease NE release causes a decrease in
constriction (i.e., causes vasodilation). Epinephrine (E) from adrenal medulla
also binds to a-receptors,
these a-receptors
respond to NE more greatly than they respond to E, but both NE and E cause
vasoconstriction.
The
b-receptors
respond primarily to circulating E, when they are bound by E they cause
vasodilation in this tissue being supplied by blood vessels with b-receptors.
These b-receptors
are found in vascular smooth muscle of heart,
liver, skeletal muscle, so this means that blood supply to these organs
increases when b-receptors
are stimulated. Remember the fight-or-flight response? Generally speaking, NE
has a greater affinity (binding power) for a-receptors
and E has a greater affinity (binding power) for b-receptors.
Exchange at
the Capillaries
Exchange
between the plasma of blood and the cells occur at capillaries. Capillaries
have thin walls and pores to allow passage of gases, water, dissolved solutes.
Proteins and blood cells are too large to pass through the capillary wall.
Molecules move from the blood to the interstitial space by diffusion and are aided
by hydrostatic pressure. Most cells are within 0.1 mm of nearest capillary,
this means that rapid diffusion is possible. Capillary density is directly
related to metabolic needs of tissue, the higher the metabolism – the more
capillaries. The total adult capillary exchange surface area is about 6300 m2
(nearly 2 football fields). Remember, the greater the surface area, the greater
the rate of diffusion?!?
There
are three types of capillaries (or capillary beds):
1. Continuous capillaries:
these are closely joined cells with tight junctions holding together adjacent
endothelial cells. Small molecules cross through pores and larger molecules
cross in vesicles via transcytosis.
2. Fenestrated capillaries:
Have fenestrations, which mean “pores”. Molecules can pass rapidly. These are found
in the kidney and intestine, associated with absorptive epithelia. The bone
marrow has fenestrated capillaries with the ability to temporarily open gaps
wide enough for proteins and blood cells to squeeze through to enter the blood.
3. Sinusoidal capillaries:
The most permeable of all capillary beds. They have large gaps in the
endothelial lining and are highly convoluted (twisted) capillaries. Found in
the liver and the spllen
The Velocity of Blood Flow is
Lowest in the Capillaries
Low
velocity allows diffusion to go to equilibrium. The total cross-sectional
surface area of all capillaries determines the velocity of blood. A large total
capillary cross-sectional area gives a low velocity of blood flow. The fastest
flow of blood is seen in the arterial system, where no exchange (diffusion)
occurs.
Most Capillary Exchange Takes
Place by Diffusion and Transcytosis
Diffusion
rate for permeable solutes is determined by concentration gradient between
plasma and interstitial fluid (ISF). O2 and CO2 diffuse out freely.
Concentrations reach equilibrium by the venous end of the capillary system.
Blood cells and most plasma proteins are too large to leave. Lymphatic system
returns those proteins that do escape. Protein hormones and cytokines enter ISF
by: Large pores in certain capillaries. Transcytosis in others
Capillary Filtration and
Reabsorption take Place by Bulk Flow
Bulk
flow is the mass movement of water and dissolved solutes between blood and the interstitium
as the result of two forces: Hydrostatic Pressure (HP) and Colloid osmotic
pressure (COP). Remember from the beginning of semester, HP is the force of a
fluid on the walls of its container. HP is the driving force for filtration,
which is the net movement of fluid from the capillary into the interstitium.
Colloid
osmotic pressure is a force generated by protein in solution. COP is the
driving force for reabsorption, which is the net movement of fluid back into
the capillary from the interstitium.
In
most capillaries, net filtration occurs at the arterial end and net
reabsorption occurs at the venous end.
HP
forces water and solutes out of capillary through pores but it decreases along
length of capillary (from arterial to venous) as energy is lost to friction. Colloid
osmotic pressure remains constant along capillary length. The overall flow is determined
by the difference between hydrostatic and colloid osmotic pressures. The bulk
flow filters out a volume of about 3 L/day (entire plasma volume) into the
interstistium. This represents about 10% of the total fluid that is not
reabsorbed, the lymphatic system returns this lost fluid to the cardiovascular
system.
THE LYMPHATIC SYSTEM
Lymphatics
interact with 3 systems:
1) Cardiovascular
system – where it returns filtered fluid and proteins from the tissue spaces
(interstitium) back to the circulatory system.
2) Digestive
system – where it transfers (absorbs) fat from the small intestine to
circulatory system.
3) Immune
system – where it traps pathogens for the immune system to deal with.
In
terms of interaction with the circulatory system, the most important function
of the lymphatic system is its role as a one-way pump, moving ECF from the tissues
and returning it to the circulatory system. The closed-ended lymph capillaries are
closely associated with blood capillaries, in fact they are found almost
everywhere that blood vessels are found. Lymph vessels have thinner walls than
capillaries and are anchored to surrounding connective tissues and fibers so
the vessels are held open. The large gaps allow bulk flow of fluid, proteins
and bacteria into the lymph capillary, thus they are considered highly permeable vessels. The fluid
inside the lymphatic system is called lymph
(Gk, meaning ‘milk’). Lymph capillaries join to form larger lymph vessels and
pass through lymph nodes. Lymph nodes are nodules containing immunologically
active cells. They act to filter lymph along its route to return to the heart. The
largest lymph vessels (thoracic and right lymph duct) empty into large veins
just under collarbones.
Lymph
flow depends on several things. For one, there are contractile fibers in their endothelial
cells and the smooth muscle in the walls of larger vessels also contract
rhythmically, creating a sort of automated lymph pump. Larger vessels also have
one-way valves, as do vein, to ensure unidirectional flow. Just as in veins, external
compression by skeletal muscle also assists the return of lymph to the
cardiovascular system. Inhibition of the muscle pump results in edema (see
below).
The
lymphatic system is pivotal in recycling plasma proteins and keeping the low
interstitial protein concentration that is critical in maintaining homeostasis.
The force of colloid osmotic pressure opposes capillary hydrostatic pressure. If
hydrostatic pressure were unopposed, it would result in excess fluid movement
into interstitial space (edema). For example, during an inflammatory response,
histamine makes capillary walls leakier, more fluid and proteins move into the
interstitium and causes edema.
What is Edema?
Edema
is an increase in interstitial fluid volume. It usually has one of two causes.
It’s either due to inadequate drainage of lymph or capillary filtration greatly
exceeds capillary reabsorption
Let’s
examine both causes. Inadequate lymph drainage can be due to obstruction of
lymph flow. Parasites, cancer, fibrotic tissue growth can block lymph movement.
In some surgeries for breast cancer, the lymph nodes along the arm are removed
in order to assess the spread of the disease. Removal of the lymph drainage in
the arm may then result in edema of the arm.
Edema
can also be the result of alterations in capillary exchange. Here are some of
the factors that disrupt normal capillary filtration-absorption balance:
Increase in capillary hydrostatic pressure. Usually from increased venous
pressure, e.g. Heart failure. Decrease in plasma protein concentration from
liver failure or severe malnutrition. Also, if there is an increase in
interstitial proteins, perhaps due to excessive leakage of proteins into
interstitial fluid. Patients are instructed to keep immobilized injured limbs
elevated (above the heart) so that gravity will aid lymph flow. Physical and
massage therapists will use gentle massage toward the heart to help force lymph
past the one-way valves. This can decrease edema in an arm or leg. Imbalances
can cause your body to attempt to compensate. For example, hemorrhage or severe
dehydration can lead to a drop in arterial pressure. This causes a drop in
capillary hydrostatic pressure which in turn will cause increases in
reabsorption.
REGULATION OF BLOOD PRESSURE
Located
in medulla oblongata, the medullary cardiovascular control center integrates
neural control of blood pressure.
The Baroreceptor Reflex is the
Primary Homeostatic Control for Blood Pressure
Baroreceptors
are stretch-sensitive mechanoreceptors that are located in the walls of the carotid
artery and aorta. As you may recall, these are tonic receptors, so they do not
adapt even if the signal being sent remains the same (they are slow to adapt).
The Baroreceptor reflex is illustrated below:
If
we use the standard blood pressure of 120/80 as “normal”, then the baroreceptors
in the aorta and carotid arteries will constantly fire AP’s to the integration
center, which is the cardiovascular control center in the medulla oblongata.
1)
If there is an increase in blood pressure, then the rate of signaling of the
barorecptors to the MO will increase. Then there may be a change in the body
directed by the MO to alleviate or oppose the increase in BP, e.g.,
vasodilation and reduction of heart rate.
2)
If there is a decrease in blood pressure, then the rate of signaling of the barorecptors
to the MO will decrease. Then there may be a change in the body directed by the
MO to oppose the decrease in BP, e.g., vasoconstriction and increase heart rate
and stroke volume.
What is Shock in Terms of the
Cardiovascular System?
Shock
is the failure of the cardiovascular system to adequately perfuse the body. In
class we’ll discuss four major ways that shock can arise in the body.
1. Cardiogenic Shock
This
type of shock is characterized by a failure of the heart to provide the driving
force for blood flow, in other words, this is when the central pump fails. An
example of this is cardiac arrest (when the heart has stopped beating). If the
heart is no longer beating, then the blood pressure will quickly fall and fail
to adequately perfuse the tissue. Another example of this is congestive heart
failure, when one side of the heart cannot maintain the pumping ability of the
other side of the heart. Again, the heart cannot generate adequate pressure to
perfuse tissues. The act of cardiovascular pulmonary resuscitation (CPR) is
done in emergencies when you believe that someone’s heart is no longer pumping.
Compression of the chest above the heart is an attempt to continue the pumping
role of the heart until medical assistance arrives.
2. Volumetric Shock
The
normal blood volume of a 70 Kg man is about 5 L. As we have seen earlier (page
4 above), the total blood volume will have an impact on MAP. Volumetric shock
will occur if you loose a significant volume of blood (decrease in blood volume
=> decrease in MAP). For example, if a person is injured and hemorrhaging
occurs (blood loss), there is a chance of going into shock due to the reduction
in vascular volume. Even if a person is bleeding internally, this is still a
loss of blood from the vascular system and shock will ensue if blood loss is
substantial. This is why inhibiting further blood loss (by compression and
elevation of affected area) is so important. Another part of restoring vascular
volume is to give fluids to a person suffering from volumetric shock.
3. Septic Shock
If
a person has a specific bacterial infection, this may lead to septic shock.
When certain bacterial gain access to the blood stream (for example from an
open cut or through the G.I. tract) they illicit an appropriate immune
response, and defense cells like masts cells and basophils release histamine. Histamine
is a potent vasodilator. If histamine is released systemically, then systemic
vasodilation will occur and this will lead to a rapid and dramatic drop in MAP.
The body naturally counters this response with the release of vasoconstrictors,
namely NE and E (a
receptors stimulation = vasoconstriction). HOWEVER, the bacterial releases a
blockers and these inhibit the body from being able to cause vasoconstriction.
The result is a continued drop in MAP that may lead to septic shock. Often treatment
will involve the administration of several vasoconstrictors in order to remedy
the drop in MAP.
4. Anaphylactic Shock
An
allergy is an inappropriate immune response, in that the immune system responds
aggressively to a substance in your body that is not a real danger. Anaphylactic shock involves an allergic
inflammatory response that results in the systemic release of histamine (the
potent vasodilator). A common example is if someone were allergic to bee
stings. The bee venom, which is harmless, elicits a major inflammatory
response, histamine is released systemically and MAP drops significantly.
Typically, the bodies attempt to counteract this with vasoconstrictors is
overwhelmed by the massive vasodilation. This is why those who know they are
allergic to bees or peanuts carry an “epi-pen” with them. This is a supply of
epinephrine which is injected intramuscularly (IM) to commence systemic vasoconstriction
in an attempt to restore MAP.
CARDIOVASCULAR DISEASE
Diseases
of the heart and blood vessels account for nearly 1/2 of all deaths in the US
Risk Factors for Cardiovascular
Disease Include Gender, Age, and Inheritable Factors
It
is possible to predict a person's likelihood of developing cardiovascular
disease by examining controllable and uncontrollable risk factors. The uncontrollable
risk factors include: Gender: Men are 3-4x more likely than women to develop
coronary artery disease. Age: After 55, deaths from coronary heart disease in
men and women (not on hormone replacement) are nearly equal. In general, risk
increases with age. Heredity: Close relatives with coronary artery disease
increase risk. Diabetes mellitus: Diabetes mellitus increases risk because it
contributes to fatty deposits in the blood vessels. Controllable risk factors
include: Cigarette smoking; obesity; sedentary lifestyle; elevated serum
cholesterol and triglycerides; untreated high blood pressure; and diabetes
mellitus (to some extent).
Smoking:
Nicotine is a poison. Organic gardeners soak cigarette tobacco in water overnight
and spray the resultant nicotine solution on bugs to kill them. Nicotinic
receptors stimulate sympathetic neurons at pre- ganglionic synapses – remember
that ACh is the NT released in the ganglion by the pre-ganglionic neurons. As a
result of activation of sympathetic pathways, there is vasoconstriction that
increases blood pressure. Smoking also increases the risk of atherosclerosis
(hardening or arteries). Finally, cigarette smoke contains significant amounts
of carbon monoxide, which binds to hemoglobin and decrease the oxygen carrying
capacity of blood. If decreased blood flow due to narrowing of the coronary
vessels is compounded by less oxygen being carried in the blood, the heart
muscle is likely to be damaged even if flow is not totally occluded.
The
role of elevated cholesterol in development of coronary artery disease is
critical. Cholesterol isn't soluble in plasma (lipids are hydrophobic), so they
need carriers in the blood. The two types of cholesterol carriers High-Density Lipoprotein,
HDL the "Healthy" type of cholesterol carrier and the Low-Density Lipoprotein,
LDL, the "Lethal" type of cholesterol carrier. The HDL transports
cholesterol from the body to the liver. This is more desirable because it's
associated with lower risk of heart attacks.
Normal
LDL levels are necessary for cells to uptake cholesterol. In the cells,
cholesterol is used to make cell membranes and steroid hormones. However,
excess cholesterol gets carried around the body by LDL’s and deposited into
arterial walls. The macrophages then ingest LDL-cholesterol and this
contributes to the formation of fatty streaks just under the endothelial lining
of larger arteries. Macrophage paracrines attract smooth muscle cell migration
and reproduction. The streaks grow into bulging plaques (containing Ca2+)
that narrow the lumen of the vessels. These plaques harden into calcified
regions and fibrous collagen caps. Plaques can be divided into two groups:
stable plaques and vulnerable (unstable) plaques. Stable plaques have thick
collagen caps that separate the core from the blood. Vulnerable plaques have
thin caps that are likely to rupture and trigger formation of blood clots
(thrombi). One theory suggests that macrophages release enzymes that dissolve
collagen and convert stable plaques to vulnerable plaques. If a thrombus blocks blood flow to the heart
muscle, a heart attack (myocardial infarction) results. Blocked blood flow
decreases heart muscle's O2 supply which can cause heart damage.
This can lead to electrical conduction disruption and irregular heartbeats
(arrhythmia), cardiac arrest and death.
Hypertension Represents a Failure
of Homeostasis
Hypertension
is chronically elevated blood pressure (BP), with systolic greater than 140
mmHg and diastolic greater than 90 mmHg (140/90). It is the single most common
reason for a visit to a physician and use of prescription drugs in the USA
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