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Chapter 4
The circulatory system
contains several very different components, including the heart,
a hollow muscular pump that stands at the operational center of the system that
pumps liquid blood throughout the body through three types of
flexible tubes, the blood vessels (Fig.
4.1). The arteries channel blood from the heart to
all parts of the body needing service. Once there, the blood passes through
narrow arteries and enters the capillaries, which are the
narrowest blood vessels. Many substances and some blood cells pass into and out
of the blood by moving through the thin porous capillary walls. The blood is
then carried through the veins, which return the blood to the
heart. The passage of blood through the vessels in a part of the body is called
perfusion of that part.
Some materials that are
carried away from a region of the body do not pass into the blood but are
collected by vessels called lymph capillaries (Fig. 4.2).
The materials in these vessels make up a liquid called lymph,
which is carried through the lymph vessels toward the heart.
Along the way, the lymph passes through lymph nodes where
harmful chemicals and microbes that might have entered it are removed. The
lymph is finally added to the blood in the veins shortly before the blood
enters the heart.
MAIN
FUNCTIONS FOR HOMEOSTASIS
One main function of the
circulatory system is transportation of materials within the body. Transportation
helps maintain homeostasis by ensuring that the concentrations of substances
surrounding body cells are kept at proper and fairly steady levels. Materials
consumed by the cells are immediately replenished, and materials produced by
the cells are swept away before their concentrations become too high.
The flowing blood also
transports useful materials from their point of entry into the body to the
organs that need them. For example, oxygen from the lungs and nutrients from
the digestive system are delivered to muscles. Furthermore, some cells
manufacture substances (e.g., hormones) needed by cells in other organs, and
the circulatory system provides the delivery service for them.
As a person's rate of activity
changes, the rate of activity of that person's body cells also changes. This
causes the rate of consumption of nutrients and the production of wastes and
hormones to fluctuate. The circulatory system helps the body adapt to these
changes by altering the rate of blood flow through each part of the body.
The circulatory system
also makes an important contribution to the defense of the body. Lymph nodes
trap and destroy dangerous chemicals and microbes before they can spread
throughout the body. For example, toxins and bacteria that enter the lymph from
an infected wound are inactivated as they pass through the lymph vessels. Blood
and lymph contain several types of white blood cells (WBCs).
Some WBCs eliminate dangerous materials contained in blood and lymph, while
others leave the blood in the capillaries and travel among the cells of the
body to seek out and destroy noxious materials and microbes. Other defense
cells, located on the inner walls of blood vessels, monitor the contents of the
flowing blood and remove undesirable materials.
Like transportation,
defense is increased or decreased to meet changing needs. The number and speed
of movement of WBCs and their rates of producing defensive chemicals increase
temporarily whenever harmful microbes or foreign materials are detected within
the body.
Another homeostatic
function of the circulatory system is temperature control. Temperature
regulation and the role of dermal blood vessels in this process were discussed
in Chap. 3.
Another way in which the
circulatory system contributes to thermal regulation is by distributing heat
from heat‑producing sites to areas that cannot keep themselves warm. For
example, muscles produce much heat, and blood carries some of it to smaller
structures such as the spinal cord, slower‑acting organs such as bones,
and cooler areas such as the skin. In this way heat distribution helps prevent
overheating in any single area of the body while sustaining activities in all
its regions.
Besides being sensitive
to heat, many substances in the body are altered by the balance between acidic
and basic (alkaline) materials in their
surroundings. The relative amounts of acids and bases are usually indicated by
a numerical value called pH. The normal
range for the body is about pH 7.35 to pH 7.45. An acid/base balance
resulting in a pH within this range preserves the proper shape and activities
of molecules in the body. Deviations from this range adversely alter these
molecules, leading to malfunction, damage, and even the death of cells.
Maintaining proper
acid/base balance requires the constant action of negative feedback systems
because the ongoing activities of most cells result in the formation of acids.
Foods and beverages can also add acids or bases to the body. Excess amounts of
acid or base must be neutralized or eliminated to maintain a proper pH. This is where the circulatory system makes a major
contribution. Certain minerals and protein molecules in blood plasma and red
blood cells – buffers – act as reservoirs for acids These buffers
absorb and store excess acids. When bases become too abundant, some stored acid
is released to balance them, preserving the acid/base balance. These buffers
have a limited capacity for balancing pH, and acid/base balance also depends on
the activities of the respiratory and urinary systems.
We will now examine
components of the circulatory system in greater detail, beginning with the
heart.
Chambers and the Cardiac Cycle
The heart consists of
four chambers (Fig. 4.3).
Blood from the veins enters the two upper chambers, called atria.
Blood from the lungs returns to the heart through several pulmonary veins,
which deliver it to the left atrium. This blood has a high
concentration of oxygen, which was added as the blood passed trough the lungs. The oxygen is needed by all the cells in
the body.
While blood from the
lungs is entering the left atrium, blood from the body is flowing into the right
atrium via two large veins. This blood has had most of its oxygen
removed by body cells and contains a high concentration of a waste product
called carbon dioxide, which was produced by body cells. It also
carries many useful substances (e.g., nutrients and hormones) added by various
organs.
The blood flows easily
from each atrium into the ventricle just below it because the
ventricles relax and tend to widen at this time ((Fig. 4.4).
The flow is aided by a relatively weak contraction of the atria. Once the ventricles
have been filled, they contract powerfully, squeezing the blood and pumping it
into the arteries. The ventricles contract for a fraction of a second and then
relax again.
The blood from the left
ventricle is pushed very forcefully into a large artery, the aorta.
Branches from the aorta deliver this oxygen‑rich and nutrient‑rich
blood to all parts of the body except the lungs. Special branches from the
aorta – coronary arteries – transport some blood to the walls of
the heart.
The right ventricle
pumps blood through the pulmonary arteries to the lungs. Most of
the carbon dioxide in this blood is removed while the blood is in the lungs. At
the same time, oxygen is added to the blood for delivery to the rest of the
body.
When the ventricles
contract and force blood into the arteries, the blood pressure rises quickly to
a peak value called systolic pressure (Fig. 4.4).
When the ventricles relax and blood in the arteries flows into the capillaries,
the arterial blood pressure drops to a low value called diastolic
pressure. Diastolic pressure does not reach zero because the ventricles
remain relaxed for only a fraction of a second before contracting again. Also,
as will be described later, the elasticity of large arteries helps prevent it
from falling too low.
While the ventricles are
contracting, the atria relax and then begin to fill with the next volume of
blood that will enter the ventricles and be pumped to the body.
This completes one
heartbeat or cardiac cycle. By repeating this process over and
over, the heart keeps the blood circulating. The blood must pass through the
heart twice to make one complete circuit around the body (Fig. 4.1).
The rate of flow depends on the amount pumped per minute: the cardiac
output (CO). Cardiac output equals the amount pumped by
each beat of either the left or the right ventricle [stroke volume (SV)]
times the number of beats per minute [heart rate (HR)].
Therefore, CO = SV x HR.
The highly coordinated
and well‑timed operation of the heart chambers is controlled by special
muscle cells. A patch of these cells in the right atrium signals when each beat
is to begin. For this reason, the patch of cells is called the pacemaker,
a name shared by the artificial electronic devices sometimes used to restore
the proper heart rate to a diseased heart. Other cells send the signal through
the atria and then the ventricles. As the signal spreads, causing other muscle
cells to contract, the contracting cells produce electrical impulses that can
be detected and recorded. The recording is called an electrocardiogram
(ECG or EKG).
Valves are located within
the openings leading from the atria to the ventricles and from the ventricles
to the arteries. The movement of blood from the atria into the ventricles and
from the ventricles into the arteries pushes the valves open. When the
ventricles begin to contract, some of the blood within them begins to move
backward toward the atria. Similarly, when the ventricles relax, blood in the
arteries starts to flow back into them. This causes the valves to swing shut,
stopping the backward flow of blood. Thus, the valves ensure that the blood
moves only in the correct direction (Fig. 4.4).
The heart wall is
composed of three layers: the endocardium, myocardium, and epicardium.
Endocardium The inner lining of the
heart is called the endocardium (Fig. 4.5).
This layer must be very smooth and must have no gaps that allow blood to
contact the underlying collagen. Blood that contacts rough spots or collagen
will clot, and clots formed in the heart can move into arteries and block blood
flow.
Myocardium The middle layer of the
heart - the myocardium - is a thick layer that constitutes most
of the wall of the heart. The myocardium consists mostly of heart muscle (cardiac
muscle), though it also contains fat tissue and collagen fibers.
Contraction of the cardiac muscle provides the force that pumps the blood.
The myocardium in the
atria is thin because the atria pump blood only into the neighboring
ventricles. The myocardium of the right ventricle is of moderate thickness
because it must pump blood somewhat farther through the lungs. The myocardium
of the left ventricle is much thicker because it pumps blood farther and
through many vessels in all other regions of the body.
Epicardium The outer layer of the heart – the epicardium – contains some connective tissue
coated with a smooth, slippery layer of epithelial cells. This coating allows
the beating heart to move easily within the pericardial cavity. At the top of
the heart, the epicardium tethers the heart to other structures in the chest so
that it does not shift out of position.
The heart muscle must
have a steady supply of energy to pump blood continuously. It gets this energy
through a complicated series of chemical reactions that combine oxygen with
nutrients such as blood sugar. These materials must be delivered to the
myocardial cells by the blood flowing through the coronary arteries
(Fig. 4.6).
The heart muscle cannot get materials directly from the blood inside the heart
chambers because molecules do not pass easily through the thick wall of the
heart.
In addition to producing
useful energy, the reactions in heart cells produce wastes such as water and
carbon dioxide, which are removed from the heart by blood in the coronary
capillaries and veins. These wastes are finally eliminated by the lungs and
kidneys.
If myocardial cells do
not get enough oxygen for their energy requirements, they malfunction and the
heart cannot pump blood adequately. People in this condition get out of breath
easily. They feel weak and lethargic, tire quickly, may become dizzy and faint,
and can suffer heart attacks. Therefore, the coronary arteries must deliver
plenty of oxygen‑rich blood to the myocardium.
Recall that as the rate
of activity of body cells changes, the amount of blood flow around the cells
must also change to provide for their varying needs. This is especially
important when levels of physical activity change because active muscles use
materials and produce wastes much faster than resting muscles do. One way in
which blood flow is adjusted is an alteration in cardiac output caused by
changes in stroke volume or heart rate. Since alterations in CO must be made to
maintain homeostasis, the heart is controlled by negative feedback systems. The
nervous system detects changes in internal body conditions when exercise begins
or ends. Cardiac output is then adjusted through changes in the nerve impulses
sent to control the heart. Levels of hormones that influence the heart are also
adjusted. Finally, the heart has intrinsic mechanisms to increase or decrease
its own stroke volume as needed. As a result, the parts of the body receive the
right amount of blood.
Though aging causes
several changes in the heart, these age changes do not result in an alteration
in cardiac output when a person is at rest. This is the case because the
changes are slight and because adjustments that compensate for detrimental
changes occur. These adjustments include changes in the atria and the
myocardium that increase heart strength and increases in blood levels of norepinephrine,
which stimulates the heart.
As aging occurs, changes
occur in the way the heart adjusts CO to meet the varying demands of the body.
However, as with resting conditions, the changes are not very great, and most
detrimental changes in the heart are overshadowed by compensatory changes. For
example, the heart compensates for an age-related decrease in maximum heart
rate by increasing the amount it pumps per beat. Therefore, the maximum cardiac
output which can be achieved when a person is exercising as vigorously as
possible (cardiac reserve capacity) remains essentially
unchanged. The compensatory change that seems most important involves
norepinephrine: As age increases, its blood level rises faster and reaches a
higher peak value after vigorous activity begins.
An adverse age change in
the heart for which there is no compensatory adjustment is an increase in the
amount of blood remaining in the left ventricle after contraction. This
residual blood causes a slight inhibition of blood flow from the lungs,
resulting in an accumulation of blood in the lungs - pulmonary congestion
- which raises the blood pressure in lung capillaries and forces extra
fluid out through the capillary walls. This fluid accumulation (pulmonary
edema) reduces respiratory functioning and causes people to feel out of
breath sooner and more intensely when they exercise strenuously.
Another important age
change involves the declining efficiency of the heart. A stiffer, dilated and
thickened older heart consumes more oxygen to pump the same amount of blood
pumped by a younger heart. This is not important as long as the coronary
arteries remain completely normal because these arteries widen and allow blood
to flow adequately when the heart needs more oxygen. However, most people do
not have completely normal coronary arteries. In these cases, the decreased
efficiency of the heart and the resultant increased demand for oxygen can
become serious. In fact, individuals who show even slightly low coronary blood
flow when exercising are very likely to have a heart attack.
In summary, because there are both positive and negative age changes in the normal heart, its ability to adjust the pumping of blood to supply the varying needs of the body remains essentially unchanged. However, the maximum rate of exercise people can perform normally declines with advancing age. This chapter and Chaps. 5, 6, 8, and 9 will show how this is due to a variety of factors outside the heart, including age changes in other parts of the circulatory system and in the respiratory, nervous, muscle, and skeletal systems. The maximum rate of physical activity decreases even more when diseases of the heart, blood vessels, or other body systems are present.
Though the effects of initiating exercise programs on the hearts of younger people have been well studied, only a few of the effects of training on the older heart have been elucidated. Results for elders are quite variable among studies and among individuals, and depend heavily on the nature of the exercise program (e.g., type, intensity, frequency of exercise, duration of each exercise session, duration of entire program). For the older heart, these effects include no change in the maximum heart rate attainable. Some exercise programs produce a decrease in the resting heart rate, decreases in the maximum heart rate required for maximum activity, and increases in stroke volume and cardiac efficiency. However, it is expected that other beneficial effects of regular exercise on the older heart will be discovered. We will see later in this chapter that regular exercise has beneficial effects on other parts of the circulatory system.
To affect an older heart,
an exercise program must involve fairly vigorous exercise performed for an
extended period during each session. The sessions must occur frequently, at
least once every few days. The degree of improvement is proportional to the
intensity, duration, and frequency of activity. Exercise at a low level,
performed for a short time, or conducted infrequently has no effect on the aged
heart. Beneficial changes in cardiac output can be observed within days to a
few weeks after beginning an exercise program, and regressive detrimental
changes in CO occur within the same time frame when a person ends the program.
Thus far we have seen
that aging of the heart does not significantly alter its ability to meet the
needs of the body. However, few adults have a completely normal heart, and in
most individuals some degree of disease adversely affects the heart. Both the
incidence and seriousness of such disease increases with age.
The reasons for these
increases are the same as the reasons for those which lead to an age‑related
rise in other diseases: declining resistance to adverse conditions and slower
repair; more time for the development of slowly progressing diseases; and
higher chances for exposure to disease‑producing factors plus increasing
occasions and durations of exposure to such factors.
Heart disease has been
the fourth leading chronic disease among people between the ages of 45 and 64
and ranks third among chronic disease in people over age 64 (#1 is high blood
pressure, #2 is arthritis). It is a leading cause for seeking medical care
among those over age 64 and a major cause of disability and altered lifestyle.
Though the incidence of death from heart disease among the elderly has been
declining for decades, it is still the leading cause of death for people 65 and
over.
Health,
United States, 2013, U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Centers for
Disease Control and Prevention National Center for Health, “During 2001–2002
through 2011–2012, heart disease prevalence remained stable among men and women
in all age groups except among women aged 65 and over, where the prevalence
declined.” https://www.cdc.gov/nchs/data/hus/hus12.pdf
Health,
United States, 2017, U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Centers for
Disease Control and Prevention National Center for Health, “During 2006–2016,
the prevalence of heart disease increased with age. The prevalence remained
stable among men and women aged 45–54, and declined among men and women aged
55–64 and 65 and over. In 2016, among those aged 45–54, the prevalence was
similar for men (10.5%) and women (9.9%). Among those aged 55–64, the
prevalence was higher among men (16.4%) than women (12.5%). Among those aged 65
and over, about one-third of men (33.9%) and one-quarter of women (23.6%)
reported a history of heart disease.” https://www.cdc.gov/nchs/data/hus/hus17.pdf
For the latest statistics and data, see:
“OlderAmericans 2016: Key Indicators of Well-Being”
FederalInteragency Forum on
Aging-Related Statistics
https://agingstats.gov/data.html
CDC (Centers for
Disease Control and Prevention)
National Center for Health Statistics
“Interactive
Summary Health Statistics for Adults”
https://www.cdc.gov/nchs/nhis/ADULTS/www/index.htm
U.S. Department of Health & Human Services National Center for
Health Statistics (https://www.cdc.gov/nchs/index.htm),
including
National
VitalStatistics ReportsVolume
68, Number 6 June 24, 2019U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Centers
for Disease Control and Prevention National Center for Health Statistics
National Vital Statistics System Deaths: Leading Causes for 2017 by Melonie
Heron, Ph.D.
(https://www.cdc.gov/nchs/data/nvsr/nvsr68/nvsr68_06-508.pdf)
and (https://www.cdc.gov/nchs/data/nvsr/nvsr68/nvsr68_06-508.pdf#tab01).
|
Causes of death for all ages |
|||
|
Rank |
Cause of death |
Number (thousands) |
Percent of total |
|
|
All
causes |
2,814 |
100.0 |
|
1 |
Diseases
of heart |
647 |
23.0 |
|
2 |
Malignant
neoplasms |
599 |
21.3 |
|
3 |
Chronic
lower respiratory diseases |
170 |
6.0 |
|
4 |
Cerebrovascular
diseases |
160 |
5.7 |
|
5 |
Alzheimer
disease |
146 |
5.2 |
|
6 |
Diabetes
mellitus |
121 |
4.3 |
|
7 |
Accidents
(unintentional injuries) |
84 |
3.0 |
|
8 |
Influenza
and pneumonia |
56 |
2.0 |
|
9 |
Nephritis,
nephrotic syndrome and nephrosis |
51 |
1.8 |
|
10 |
Parkinson
disease |
47 |
1.7 |
|
|
All
others (approx.) |
780 |
26.0 |
|
Causes of death for all ages 65
year and older |
|||
|
Rank |
Cause of death |
Number (thousands) |
Percent of total |
|
|
All
causes |
2,067 |
100.0 |
|
1 |
Diseases
of heart |
519 |
25.1 |
|
2 |
Malignant
neoplasms |
427 |
20.7 |
|
3 |
Chronic lower
respiratory diseases |
136 |
6.6 |
|
4 |
Cerebrovascular
diseases |
125 |
6.1 |
|
5 |
Alzheimer
disease |
120 |
5.8 |
|
6 |
Diabetes
mellitus |
59 |
2.9 |
|
7 |
Accidents
(unintentional injuries) |
55 |
2.7 |
|
8 |
Influenza
and pneumonia |
46 |
2.3 |
|
9 |
Nephritis,
nephrotic syndrome and nephrosis |
41 |
2.0 |
|
10 |
Parkinson
disease |
31 |
1.5 |
|
|
All
other causes |
503 |
24.4 |
Though several different heart
diseases become more common and more serious with age, disease of the coronary
arteries stands out as the most common of these disorders. (Suggestions:
Chap 04 - 76-2-2)
Functions of Coronary Arteries
When a person is at rest, the coronary
arteries are normally wide enough to allow ample blood to pass through to the
cardiac muscle cells. However, the demand of cardiac muscle for oxygen goes up
and down as the amount of work performed by the heart rises and falls.
Conditions requiring more work and higher amounts of oxygen include increases
in heart rate, stroke volume, width, and thickness and in blood pressure. Such
increases occur when a person becomes physically active and as part of aging.
The heart normally accommodates these increases by dilating its arteries to
allow more blood to flow through them.
Effects of Atherosclerosis
The coronary arteries are prevented from
supplying adequate blood flow to the heart by a disease called atherosclerosis.
Atherosclerosis, which is described in greater detail later in this chapter, involves
the formation and enlargement of a weak scar-like material called plaque
in the walls of arteries. Plaque causes coronary arteries to become narrower
and thus reduces blood flow (Fig. 4.7).
It also stiffens the arteries, reducing their ability to dilate when more
oxygen is needed by the heart muscle. Finally, plaque causes roughening of the
inner lining of the arteries and exposure of the underlying collagen. Roughness
and collagen cause the blood in arteries to form clots; clots clog arteries and
can stop blood flow quickly and completely.
Whenever the amount of
oxygen needed by the heart is lower than the amount supplied, the cardiac
muscle cells become weak and cannot pump enough blood to body organs. In
addition, the muscle cells begin to produce a waste product called lactic
acid, which upsets the normal acid/base balance. This imbalance injures
the muscle cells, which become even weaker, and blood flow to the body drops
further. All the organs begin to perform less well. The brain, kidneys, lungs,
and heart are especially in danger because these organs require high levels of
blood flow. A person in this condition often feels weak and out of breath and
frequently experiences chest pain as injury to the heart cells develops. In
mild cases the pain will subside if the person rests because the oxygen demand
of the heart drops back to the level being supplied. Such temporary pain is
called angina.
If oxygen demand is
brought back into balance with oxygen supply soon enough, the heart begins to
function normally again. Of course, the arteries are still diseased and the
problem will most likely recur. The incidents may become more severe as the
degree of coronary artery disease increases.
If the oxygen supply is
very low for just a few minutes, the cardiac muscle cells begin to die. This
condition is a true heart attack, also called a myocardial
infarction (MI) (Fig. 4.8).
The heart becomes much weaker, and the pumping of blood drops precipitously.
Cells in the brain and other organs deteriorate, and the person is in danger of
dying. In fact, first‑time heart attacks are fatal approximately 50
percent of the time. Individuals who survive the initial effects of a heart
attack still face many problems. The heart attack can cause damage to the heart
valves or may produce a hole between the left and right ventricles, in which
case the blood will flow in the wrong direction within the heart. Incorrect
blood flow tends to overwork the heart, causing more heart disease and often
preventing the lungs from functioning properly. An MI can also cause blood
clots to form inside the heart chambers and then be pumped to other organs. If
clots travel to the brain, they can cause a stroke. Finally, the heart can
become so weak that the person may require lengthy medical treatment and face
long‑term disability. The person's social contacts, sense of well‑being,
normal daily routines, and employment often undergo radical undesirable
changes.
All that has been said
thus far about coronary atherosclerosis may seem like bad news, but there is
also good news about this disease. Most of the factors contributing to the
development of atherosclerosis have been identified, and many of them can be
avoided or greatly reduced. This is the main reason for the dramatic decline
since 1950 in the incidence of deaths from heart disease. Furthermore, reducing
or eliminating one or more of the risk factors reduces the chances of being
affected by this disease regardless of the age at which the decrease in risk
factors occurs. Of course, the earlier the risk‑reducing steps are taken,
the greater is the benefit.
Another
important fact regarding risk factors is that certain risk factors alter the
effects of other risk factors in a given individual. Contrary to previously
held beliefs, the interactions are poorly understood, quite complex, and they
differ from person to person. Thus, a close approximation of an individual’s
total risk for coronary artery disease can be made by simply adding the effects
from each risk factor present. However, a more accurate approximation can be
obtained by taking into account the known interactions among the risk factors
present, which can lead to better interventions in risk management to reduce
the risk of coronary artery disease. In conclusion, for a
person with multiple risk factors, reducing or eliminating one risk factor may
have a greater-than-expected decrease in the total risk of developing coronary
artery disease.
When
determining a person’s total risk for coronary artery disease using only a risk
calculator, one must first decide for what specific problem the determination
is being made. Examples of specific problems include having dangerously reduced
heart function; having one’s first heart attack; dying from a heart attack; and
having one of these problems within a specific time (e.g., the next ten years). The same is true for determining the risk of
having a stroke from atherosclerosis (Chap. 6). Risk calculators used for
determining a person’s total risk may be based on one of these specific
problems or a combination of them, and may include stroke and other problems
from atherosclerosis. Moreover, different calculators use different risk
factors, assign different values to each risk factor, and use different
assumptions and statistical methods to determine total risk values. Thus, each
risk calculator may find different total risks for the same individual. More
accurate determination of a person’s total risk would include individual
consultation with a health professionals.
Thus,
“Cardiovascular risk calculators weigh the same risk factors differently. For
each risk factor, the relative risk increase from the calculator with the
highest increase was generally three to eight times greater than the relative
risk increase from the calculator with lowest increase. This likely contributes
to some of the inconsistency in risk calculator estimation. It also limits the
use of risk calculators in estimating the benefits of therapy.” (Quoted from
“Variation among cardiovascular risk calculators in relative risk increases
with identical risk factor increases”, G. Michael Allan,
Faeze Nouri,
Christina Korownyk,
Michael R. Kolber,
Ben Vandermeer,
and James McCormack,
BMC Res Notes. 2015; 8: 417. , PMCID:
PMC4561470,
PMID: 26346935,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561470/)
A person can find
their total risk of coronary artery disease using a risk calculator with any of
the following.
CardioRisk Calculator ™
https://www.circl.ubc.ca/cardiorisk-calculator.html
“FRAMINGHAM RISK SCORE (FRS)Estimation of 10-year Cardio
vascular Disease (CVD) Risk”
“ASCVD Risk Estimator Plus”
American College of Cardiology
http://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/
“Heart
Disease Risk Calculator”
Mayo Clinic Health System
“Heart Risk Calculator”
© Ahead
Research Inc 2013-2020
http://www.cvriskcalculator.com/
“Omnibus Risk Calculator”
http://static.heart.org/ahamah/risk/Omnibus_Risk_Estimator.xls
“Calculator:
Cardiovascular risk assessment (10-year, men: Patient education)”
UpToDdate
EBMcalc
is Copyright © 1998-2020 Foundation Internet Services, LLC
“Reynolds Risk Score”
http://www.reynoldsriskscore.org/
“Heart
Risk Calculator”
http://www.cvriskcalculator.com/
References
about problems from risk factor interactions and other issues in determining a
person’s total risk include the following.
“Variation
among cardiovascular risk calculators in relative risk increases with identical
risk factor increases”
G. Michael Allan, Faeze Nouri, Christina Korownyk, Michael R. Kolber, Ben Vandermeer, and James McCormack
BMC Res Notes.
2015; 8: 417.
PMCID:
PMC4561470
PMID: 26346935
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561470/
“Assessing Cardiovascular Risk:
Systematic Evidence Review From the Risk Assessment
Work Group, 2013”
U.S. Department of Health and human
Services
National Institutes of health
https://www.nhlbi.nih.gov/sites/default/files/media/docs/risk-assessment.pdf
“Variation
among cardiovascular risk calculators in relative risk increases with identical
risk factor increases”
G. Michael Allan,
Faeze Nouri, Christina Korownyk, Michael R. Kolber, Ben Vandermeer, and James McCormack
BMC Res Notes.
2015; 8: 417.
PMCID:
PMC4561470
PMID: 26346935
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561470/
“Significant
interactions between traditional risk factors affect cardiovascular risk
prediction in healthy general population”, Jussi A. Hernesniemi,
Juho Tynkkynen,
Aki S. Havulinna,
Niku Oksala,
Erkki Vartiainen,
Tiina Laatikainen
& show all
Pages 53-60 |
Received 31 May 2014, Accepted 24 Sep 2014, Published online: 18 Nov 2014
Annals of Medicine, Volume 47, 2015 - Issue 1
https://www.tandfonline.com/doi/full/10.3109/07853890.2014.970570#
Some risk factors create
more problems than others do. The following six factors provide the highest
levels of risk. The actual amount of increase in risk from each one depends on
when the risk factor first existed; its intensity, frequency, and duration; and
its interaction with other risk factors.
Smoking Inhaling
tobacco smoke increases blood pressure and adds substances to the blood that
seem to promote the formation of plaque. The effect of smoking on arteries is
greatly magnified in women who take birth control pills. Smoking and taking
birth control pills interact. Thus, having both risk factors increases
the risk of having a heart attack more than the simple sum of each individual
risk factor, perhaps as much as 18‑fold. The solution is not to smoke.
High Blood Pressure
High blood pressure seems to cause
repeated minor injuries to the arteries. As the arteries try to repair the
damage, they form scar tissue and plaque. High blood pressure also makes the
heart work harder, increasing the amount of oxygen it needs, and eventually
weakens the heart.
Having blood pressure
checked regularly and, if it is high, seeking professional advice on how to
reduce it are especially important as people get older. Blood pressure tends to
rise with age, and an abnormal increase has more of an effect on the arteries
as a person ages.
High Blood LDLs
Blood contains a variety of lipoprotein
molecules. The lipids in these lipoproteins are obtained from the diet and made
by the body. Most of the lipid in blood lipoproteins is cholesterol and
triglycerides (fats), and lipoproteins containing predominately cholesterol are
called low-density lipoproteins (LDLs). When LDLs are in high
concentrations, the cholesterol can accumulate in the walls of arteries and
contribute to the formation of plaque. The accumulation of cholesterol is
reduced by other lipoproteins called high‑density lipoproteins
(HDLs). As age increases, many individuals have an increase in
the concentrations of LDLs with a simultaneous decrease in HDLs.
To reduce the risk of
developing high blood LDLs, the amounts of cholesterol and saturated fats in
the diet should be kept low. Foods containing high amounts of these lipids
include egg yolks, dairy products containing milk fat or cream, red meats such
as beef and pork, solid shortening, and oils such as palm oil and coconut oil.
High alcohol consumption should be avoided since it promotes the formation of
LDLs. However, consuming low or moderate levels of alcohol, eating foods
containing certain dietary oils (e.g., safflower oil), and exercise can reduce
blood LDLs while increasing HDLs. Blood lipoprotein levels should be checked
and professional guidance should be followed if the ratio of LDLs to HDLs is
found to be too high.
Diabetes Mellitus
Diabetes
mellitus is a disease that alters many aspects of the body, including
blood glucose levels and the maintenance and repair of arterial walls. In so
doing, it promotes the formation of plaque.
Individuals should be
aware of the warning signs of diabetes mellitus, which include excessive hunger
and thirst, fatigue, unusual weight gain or loss, excessive formation and
elimination of urine, and slow healing of wounds. Suspected cases require
diagnosis and treatment by a qualified professional.
Family History
Several genes increase the
chances of developing coronary atherosclerosis. Progress has been made in
determining mechanisms by which these genes act.
“Genetic Markers for Coronary Artery Disease”
Nevena Veljkovic,1 Bozidarka Zaric,2 Ilona
Djuric,3
Milan
Obradovic,2
Emina Sudar-Milovanovic,2 Djordje Radak,4,5,6
and Esma R. Isenovic2,*
Medicina (Kaunas).
2018 Jul; 54(3): 36.
Published online
2018 May 28. doi: 10.3390/medicina54030036
PMCID: PMC6122104
PMID: 30344267
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122104/
“Network analysis of coronary artery disease risk genes
elucidates disease mechanisms and druggable targets”
Scientific Reports volume 8,
Article number: 3434 (2018)
https://www.nature.com/articles/s41598-018-20721-6
Individuals from families
with a history of atherosclerosis may have inherited the genes that predispose
them to this disease. Though these individuals cannot alter their genes, they
should try to reduce or eliminate as many other risk factors as possible. They
should also inform their health care providers of their family history so that
problems can be detected and necessary treatments can be initiated early.
Advancing Age
Advancing age increases the risk
of problems from coronary artery disease in several ways. First, aging causes
arterial stiffening. Second, there is an increase in the heart's oxygen demand
because the heart becomes less efficient. Third, aging is associated with
higher blood pressure, elevated blood cholesterol and LDLs, lowered blood HDLs,
an increased incidence of diabetes, and decreased physical activity. Fourth,
increasing age provides more time for other risk factors to take effect and for
the slow process of plaque formation to progress significantly.
Though nothing can be
done to alter the passage of time, people of advanced age should reduce other
risk factors as much as possible. Other risk factors are of moderate importance
compared with the six just discussed. They include the following.
High Blood Homocysteine Homocysteine
(Hcy) is produced and released into the
blood when the body breaks down an amino acid called methionine.
Having high blood levels of Hcy increases the risk of
developing atherosclerosis. Blood levels of Hcy rise
with increasing age and when women pass through menopause. High blood levels of
Hcy also develop in people with deficiencies in vitamin
B6 or the vitamin B12 (cobalamin). These vitamins
are essential for adequate disposal of Hcy. Finally,
some people are born with a metabolic abnormality that causes them to produce
excess Hcy.
Usually
blood levels of Hcy can be kept low by eating a diet
with adequate vitamin B6 and vitamin B12. Since there is little vitamin B12 in
plants, vegetarians are at risk for vitamin B12 deficiency. People with
abnormalities of the stomach may be unable to absorb adequate vitamin B12.
Vitamin supplements can help people who do not get adequate vitamin B6 or vitamin
B12 from foods.
Physical Inactivity The cells of people who are physically
inactive require less blood flow, and the heart therefore gets less exercise
because it does not have to work hard. Like every other muscle, heart muscle
that gets little exercise becomes weaker and less efficient and loses some of
its blood vessels. Such a heart is unprepared to increase the pumping of blood
when a person suddenly begins strenuous activity. When such activity begins, an
imbalance in the oxygen demand and supply of the heart occurs. In addition,
lack of exercise promotes increases in blood pressure and in the ratio of LDLs
to HDLs; both changes promote the development of atherosclerosis.
Engaging in a regular program
of vigorous physical activity or in an occupation or hobby that includes such
activity greatly reduces or eliminates this risk factor. This occurs because
the heart is strengthened and develops more blood vessels, blood pressure is
kept low, blood levels of HDLs are increased, body weight is less likely to
become excessive, and psychological stress is minimized. All these effects
reduce the risk of coronary artery disease. Planning involvement in physical
activity is especially important for persons of advanced age because of the
tendency toward age‑related reductions in physical activity.
Obesity Being
very overweight weakens the heart and makes it less efficient because the heart
is being overworked and tends to become invaded with fat. Obesity also promotes
high blood pressure, high levels of blood cholesterol and LDLs, diabetes
mellitus, and low levels of physical activity. Obesity can be prevented or
reduced by participation in a planned program of diet modification and regular
exercise.
Stress A
sustained high level of emotional tension or stress promotes atherosclerosis by
causing prolonged periods of high blood pressure.
Emotional stress can be
reduced in many ways. One way is to avoid stress‑inducing situations.
When this is not possible, taking breaks or vacations from such situations
helps. Exercise, hobbies, and other diversions can also provide relief. Talking
with a trusted confident can help, and some individuals can benefit from
professional counseling.
Menopause The
decline in estrogen and progesterone that occurs at menopause ends the
protective effect those hormones have on the arteries. Surgical removal of the
ovaries has the same effect.
Some women can benefit
from hormone replacement therapy. Such therapy should be conducted only on the
advice and under the continued direction of a physician knowledgeable in this
area.
Male Gender
Coronary artery disease occurs
more frequently in men than in women, probably because the lifestyle of men
generally includes more and higher levels of the risk factors associated with
this disease. The incidence rate for women has been approaching that for men as
women have become more involved in the same activities. Furthermore, the
incidence among women approaches that of men as the age of a population
increases because of losing the protective effects of female hormones after
menopause.
Personality Individuals
with certain personality characteristics seem to be at higher risk for
developing coronary atherosclerosis. These characteristics include being highly
competitive, striving for perfection, and feeling that there is never enough
time to accomplish one's goals. These characteristics indicate a high level of
stress. Recent evidence suggests that stress is the key feature and that
personality contributes little if any risk.
High Blood Iron Levels
Another possible risk factor,
which some scientists think provides a risk exceeded only by that from smoking,
is having higher than average levels of iron in the blood. The iron may promote
atherosclerosis by increasing the accumulation of LDLs in arteries and causing
cell damage by promoting the formation of free radicals. If having relatively
high blood levels of iron is shown conclusively to be a significant risk
factor, steps to lower the levels might include reducing the consumption of
foods high in iron (e.g., red meat, liver, spinach, iron‑fortified
foods); not drinking water with a high iron content; taking iron supplements
only when absolutely necessary; and giving blood regularly.
Periodontal disease Periodontal
disease is associated with increased risk of atherosclerosis, heart attack, and
stroke. The mechanisms by which periodontal disease contributes to
atherosclerosis are not known. They may involve a genetic predisposition to
both periodontal disease and atherosclerosis; toxins and chemical signals
produced at the teeth; and effects from bacteria spreading from the teeth
throughout the body. Some of these mechanisms may affect endothelial function.
Congestive heart
failure (CHF) is another disease that becomes more
common and serious with age. Approximately three million people in the U.S. have
CHF, and there are approximately 400,000 new cases each year. More than 75
percent of cases are in people age 65 and over. Incidence rates double for each
decade over age 45, and approximately 10 percent of elders over age 80 have
CHF. Congestive heart failure is the leading cause of hospital admissions for
people 65 and over, and it is a major cause of disability, reduced
independence, and death. The number of cases is expected to double by the year
2040.
Main causes of CHF are
factors that weaken the heart. The most frequent causes are coronary artery
disease, high blood pressure, disease of the heart valves, obesity, and kidney
disease. The underlying problem is years of overworking the heart. An
overworked heart tends to strengthen itself by dilating and thickening. At
first these changes increase heart strength, but if the heart continues to be
overworked, it continues to dilate and thicken. Excessive amounts of these
changes weaken the heart. Then the heart chambers contain a great deal of blood
but cannot pump it effectively. The flow of blood diminishes and organs begin
to malfunction.
In addition, fluid
accumulates in the lungs (pulmonary edema). Affected individuals
have difficulty breathing and may feel out of breath after the slightest exertion
or even when resting. Poor circulation in other areas, especially the legs,
causes swelling and discomfort and promotes the formation of varicose veins.
Many ordinary activities become difficult or impossible.
The heart tends to solve
these problems by dilating and thickening even more, but this exacerbates the
situation. Unless steps are taken to strengthen the heart and reduce its
workload, the heart gradually becomes so weak that it fails completely and the
individual dies.
Untreated serious valvular
heart disease causes detrimental changes similar to those resulting
from congestive heart failure. This disease usually develops after coronary
artery disease or rheumatic fever, which can prevent the valves from closing
properly. Then some of the blood in the heart flows backward during each beat.
Rheumatic fever can also prevent the valves from opening properly, and so blood
does not flow forward as easily as it should. In either case the heart is
overworked.
Arteries
are flexible tubes that carry blood from the heart to every region of the body.
Arteries have special properties that ensure that they perform this task
effectively. These properties derive from the three layers composing the
arterial wall.
The innermost layer of an
artery is called the endothelium. It is supported by a thin
underlying layer that contains collagen and a mat of elastin fibers (Fig. 4.9a).
Like the endocardium in the heart, the endothelium provides smoothness by
forming a continuous glistening layer that coats the collagen and other materials
in the arterial wall. In so doing, it permits blood to flow easily without
clotting.
The endothelium also
secretes several signaling materials including nitric oxide (*NO);
prostacyclin, endothelin, and angiotensin
converting enzyme (ACE), and ACE inhibitors.
Nitric oxide and prostacyclin promote vasodilation in many arteries. Nitric
oxide also limits vessel thickening by inhibiting the growth of smooth muscle,
and it inhibits clot formation and plaque formation. Endothelin and ACE promote
vasoconstriction. ACE inhibitors reduce blood pressure by inhibiting
vasoconstriction, thus allowing natural vasodilators to have more effect. The
effects of *NO usually dominate, keeping vessels adequately dilated.
The middle layer of the
largest arteries consists mostly of elastic fibers that make the arteries
strong. Most of the elastic fibers in the aorta are produced before birth or
during childhood, but some new elastin is produced throughout life. Since these
arteries are closest to the heart, strength is necessary to withstand the high
blood pressure produced by each heartbeat.
This layer also provides
elasticity, which allows the arteries to be stretched outward somewhat each
time the ventricles pump blood into them. The extra space provided by the
stretching prevents the systolic pressure from rising too high, and the work
the heart must perform is kept reasonably low, just as it is easier to blow up
an easily stretched balloon than a stiff one. Preventing excessive pressure
also keeps the arteries from being injured by the accompanying extreme forces.
The elasticity of large
arteries helps to prevent blood pressure from rising too high in yet another
way. Unusually high blood pressure immediately causes normal arteries to be
stretched outward excessively. Nerve cells in the walls of arteries detect this
abnormal stretching and send signaling impulses to the blood pressure control
center in the brain. Other factors from the artery that influence the sensory
neurons include prostacyclin, which increases the signals, and reactive oxygen
species, which reduce them. The brain then sends impulses to the heart telling
it to pump less blood. It also tells blood vessels in various areas of the body
to dilate to provide more space for the blood coming from the heart. As a
result, blood pressure decreases and the large arteries return to their normal
size. The nerve cells are then no longer activated, and blood pressure
stabilizes at the normal level. Note that this is a negative feedback system
that maintains proper and fairly stable conditions in the body.
The nerves in blood
vessels send different impulses to the brain when blood pressure is too low and
arteries are not stretched enough. The result is the sending of norepinephrine
and related substances to the heart and vessels. These substances raise blood
pressure by several means, including stimulating the heart and causing the
smaller arteries to constrict.
Elasticity also causes
the arteries to snap back to their original diameters when the ventricles are
relaxing. This elastic recoil helps maintain diastolic pressure between beats
by squeezing the blood. Diastolic pressure keeps the blood moving forward
steadily while the heart rests briefly after each beat. Thus, elastic recoil
serves the same purpose as the spring that keeps a watch ticking between
windings.
Middle Layer: Smaller Arteries
The middle layer of smaller
arteries contains some elastic fibers but is composed mostly of smooth muscle (Fig. 4.9b).
When the muscle contracts, it causes the arteries to constrict, reducing the
flow of blood.
As a rule, the smooth
muscle in most smaller arteries contracts weakly, providing some resistance to
flow while allowing ample blood flow through the arteries. This resistance is
important because without it, blood would flow from the arteries into the
capillaries so quickly that blood pressure would drop too low, especially
between heartbeats. The same effect is observed with tires. A tire with a tiny
hole loses pressure so slowly that it can be reinflated before any harm is
done, while a tire with a large leak loses all its pressure and goes flat very
quickly.
In normal situations the
constriction of small arteries increases whenever blood pressure begins to drop
too far. This additional constriction increases resistance and raises blood
pressure back to the proper level. Conversely, if blood pressure rises too
high, the smooth muscle relaxes, the arteries dilate, resistance drops, and
blood pressure decreases back to normal levels.
In addition to regulating
blood pressure by constricting or dilating as a group, individual arteries can
constrict to reduce blood flow to organs that need little flow while others
dilate to increase flow to more active organs. Thus, the smaller arteries act
like a set of valves or traffic signals to make sure that each part of the body
receives only as much blood flow as it needs.
The constriction and
dilation of smaller arteries are controlled by negative feedback systems. The
arteries respond to several factors, including nerve impulses, hormones,
temperature, and chemical conditions in their vicinity. These mechanisms help
maintain normal blood pressure and blood flow to each body structure.
The outer layer of
arteries consists largely of loose connective tissue containing soft gel and
scattered fibers. This layer loosely attaches arteries to other structures,
enabling arteries to be shifted as parts of the body move while preventing the
arteries from moving too far out of position.
There are no important
age changes in the endothelial structure, its supporting layer, or the outer layer
of arteries. These layers function well regardless of age with one major
exception. There is an age-related decline in the ability of the endothelium to
regulate blood vessels and blood pressure. The cause is not clear. It may be
due to aging of endothelial cells, to free radical damage, or to age-related
increases in blood pressure. Nitric oxide reacts with superoxide radicals (*O2-),
producing toxic ONOO- (peroxynitrite).
This reaction reduces the amount of *NO available to regulate vessels and blood
clotting, and the ONOO- can slow *NO production further by injuring
endothelial cells. These changes may contribute to high blood pressure and to
atherosclerosis.
Numerous age changes
occur in the middle layer of large arteries. Age changes in elastic fibers
include breakage, glycation, accumulation of calcium and lipid deposits, and
faster breakdown by enzymes. Old damaged elastic fibers accumulate. The
increase in many substances, including smooth muscle, collagen, calcium
deposits, and cholesterol and other fatty materials, causes thickening and
stiffening of the arteries. These changes amplify the decline in elasticity
caused by the altered elastic fibers. Since the arteries are less able to be
stretched by each pulse of blood, systolic pressure tends to rise.
Since much elastin in the
aorta is produced before birth, children with low birth weights may have less
aortic elastin, resulting in less aortic strength and elasticity. This can
speed up aortic thickening and stiffening during childhood and adulthood,
resulting in a greater risk of high blood pressure and related diseases (e.g.,
atherosclerosis, congestive heart failure). These effects highlight the
importance of events in youth or even before birth to age-related changes and
disease later in life.
At the same time the
arteries are stiffening, years of containing blood under high pressure causes
them to gradually widen and lengthen. This is especially evident in the aorta.
These changes provide more space for blood. At first this compensates for the
declining ability of large arteries to be stretched, and consequently it keeps
the tendency toward increases in systolic pressure in check. Eventually,
however, the elastic fibers are stretched so much that they can yield no
further. Then each contraction of the heart produces a rapid and dramatic rise
in systolic blood pressure. This can increase cardiac oxygen demand by almost
30 percent. At the same time, the high blood pressure and thickening of the
heart reduce the amount of *NO in coronary vessels. This limits the vessel
dilation required to increase oxygen supply to the heart muscle.
Once the arteries no
longer stretch much with each heartbeat, sensory nerve cells that detect vessel
stretching are not activated as much. Age changes in the endothelium that
reduce prostacyclin and increase reactive oxygen species (ROS) also reduce the
nerve cell activation. The reflex to prevent abnormal increases in blood
pressure is suppressed, and the pressure remains high. In most cases sensory
nerve cells are fooled and respond as though blood pressure were too low. Age
changes in the brain's blood pressure control center amplify this effect. The
final result is the release of norepinephrine, which augments the high pressure
but also stimulates the heart. In this way, the extra norepinephrine seems to
be compensatory because it helps the aging heart maintain cardiac output.
As with all age changes, there
is much variation among individuals with respect to the rise in systolic
pressure. While the elevations are modest in most people, about 40 percent of
the elderly have systolic pressures above the safe maximum for those of
advanced age (140 mmHg). Recall that elevated blood pressure increases the
heart’s workload and oxygen needs and the risk of developing atherosclerosis.
Therefore, it is important for the elderly to have their blood pressure checked
and, when necessary, receive therapy to keep it within safe limits. However,
elevated blood pressure in older individuals must not be lowered too quickly or
too far, since the result can be weakness, fainting, or more serious damage to
the heart, the brain, and other parts of the body.
In addition to restricting
stretching, stiffening of the arteries diminishes their elastic recoil. The
slow decline in recoil does not cause a substantial change until about age 60,
after which diastolic pressure declines slightly. The result is a slowing of
blood flow through coronary arteries and other small arteries between heart
beats. Normally, this decline is not large enough to cause significant effects,
though it brings a person closer to having inadequate blood flow during each
diastole.
In a large longitudinal
study of people with no diseases of the circulatory system, systolic BP does
not change until approximately age 40 in women and age 50 in men. Then BP
increases approximately 5-8 mmHg per decade. In women, the systolic BP may stop
rising and may even begin to decrease after age 70, while in men the systolic
BP continues to rise throughout life. The overall increase in systolic pressure
averages 21 mmHg in women and 15 mmHg in men. Diastolic pressure in women
increases from ages 40 to 60, but then levels off or declines. Diastolic
pressure in men increases 1 mmHg per decade. Overall, diastolic pressures
increase 5 mmHg in women and 3.5 mmHg in men. Studies that include people with
diseases or who take medications show greater changes in BP, and the women may
not have the leveling and decline in BP after age 70.
Middle Layer: Smaller Arteries
Aging causes little if
any change in the overall resistance provided by the smaller arteries. Their
thickening seems to help prevent overstretching as systolic blood pressure
increases with age. Older arteries do not respond quite as well when conditions
such as chemical levels begin to change. This seems to be due in part to
decreased functioning of the nervous system and altered levels of the hormones
that control the vessels. The vessels also seem to have reduced sensitivity or
a reduced ability to respond to control signals. Therefore, the arteries do not
dilate as well when the areas they supply need more oxygen. This decrease in
supply tends to reduce the maximum rate of work that certain organs (e.g.,
muscles) can perform.
The decreased ability of
the arteries to respond to rising or falling body temperature is an even
greater problem, leaving older people less able to prevent themselves from
overheating or becoming chilled. For example, inadequate dilation of dermal
vessels prevents the extra heat produced during exercise from leaving the body
quickly. This can lead to excessively high body temperature, damage to body
molecules and cell parts, malfunctioning of organs such as the brain, illness,
or even death. Poor constriction by dermal vessels when a person is in a cold
environment can cause excessive loss of body heat and a drop in body
temperature. Not only will such an individual feel uncomfortably cold, but because
of slowing cell activities and malfunctioning of organs such as the muscles and
the heart, he or she may also become ill.
The declining ability to
maintain normal body temperature as age increases is due not only to age
changes in the middle layer of smaller arteries but also to age changes in the
integumentary system (e.g., sweat glands, fat tissue), the nervous system
(e.g., sensory neurons), and the muscle system (e.g., muscle mass).
Because of reduced
thermal adaptability, older individuals should avoid environments and
activities that tend to cause significant elevation or depression of body
temperature. Hot weather or very warm indoor areas, hot baths or showers, the
use of numerous blankets or electric blankets, and strenuous physical activity
tend to cause overheating. Cold weather or cool rooms, cool water for swimming
or bathing, exposure of the skin, inadequate clothing, and restricted physical
activity increase the risk of developing hypothermia.
The number of larger
arteries remains the same throughout life. The number of smaller arteries
remains about the same or increases slightly in some areas of the body (e.g.,
heart and brain). This slight increase helps sustain normal blood flow by
compensating for the development of somewhat irregular arteries. Other areas
(e.g., skin, kidneys) have decreasing numbers of smaller arteries with age.
Fortunately, the adverse
effects on blood flow caused by the aging of arteries can be largely overcome
through steps such as receiving proper medical care, pacing activities, and
avoiding situations that place a person in danger of overheating or chilling.
Unfortunately, for most individuals, aging arteries are affected not only by
age changes but also by arterial diseases.
ATHEROSCLEROSIS:
AN ARTERIAL DISEASE
By far the most common
arterial disease is atherosclerosis, which is one of a group of
arterial diseases called arteriosclerosis. Because
atherosclerosis is very common, some people mistakenly use these two terms
interchangeably. The incidence of atherosclerosis and the serious difficulties
it causes rise with age for the same reasons that cause the age‑related
increase in heart disease.
Some statistics on the
importance of atherosclerosis were presented earlier in this chapter. In
addition to causing most heart attacks, atherosclerosis causes most strokes. A stroke
is injury to or death of brain cells caused by low blood flow or bleeding
in the brain (Chap. 6). For those over age 65, strokes are now the fourth
leading cause of death, days in the hospital, and days in bed. Strokes also
cause many cases of dementia and other forms of disability.
Atherosclerosis is also a
major contributor to kidney disease, problems in the legs (e.g., weakening of
muscles and skin, pain during exertion), and male impotence. Such outcomes not
only affect an individual's health and survival, but also have an impact on all
other aspects of life. For example, dietary restrictions may become necessary,
demanding that occupational or recreational activities may have to be
curtailed, and interpersonal relations between affected men and their
spouses/partners can suffer dramatically.
Atherosclerosis begins as
small streaks of fatty tissue within the inner layer of arteries. Gradually,
the streaks widen and thicken as they accumulate a variety of other materials,
including smooth muscle cells, collagen fibers, cholesterol, and calcium
deposits. The resulting masses – plaques - protrude inward and
narrow the passageway in the artery (Fig. 4.7).
The plaques often grow completely through the endothelium and replace regions
of it. Both the roughness and the collagen fibers of the plaques cause the
blood to form clots. As a result, the narrowing of the artery leads to
reductions in or complete blockage of blood flow. In addition, pieces of the
plaque sometimes break off, move down the artery, and block the artery where it
branches to form smaller arteries.
These plaques usually
grow outward and infiltrate the middle layer of the artery, causing it to
stiffen. When this occurs in larger arteries, they are less able to be
stretched outward to accommodate pulses of blood from the heart, and systolic
pressure can skyrocket. Since the arteries are also less able to spring back
when the heart relaxes, diastolic pressure drops and the flow of blood becomes
less regular. When plaque grows outward in smaller arteries, the stiffening and
replacement of the smooth muscle prevent them from adjusting blood pressure and
blood flow to suit body needs. The cells do not receive adequate oxygen and
nutrients, and waste materials accumulate. The resulting loss of homeostasis
injures or kills cells, and the organs they compose malfunction.
The outward growth of
plaque also causes weakening of the middle layer, and affected arteries begin
to bulge outward from blood pressure. The outpocketings,
called aneurysms, can disturb nearby structures by pressing on
them (Fig. 4.10a).
Additionally, blood flowing past aneurysms tends to swirl and form clots (Fig. 4.10b).
Some arteries become so weak that they rupture, causing severe internal
bleeding that can lead to the most serious strokes (Fig. 4.10c).
Mechanism
promoting atherosclerosis
Several factors seem to
cause atherosclerosis or to promote its development. These include endothelial
dysfunction, free radicals, blood lipoproteins, elastase, glycation, heat shock
proteins, and insulin-like growth factors (IGFs). Some of these may interact
synergistically.
Endothelial dysfunction Endothelial
dysfunction may cause or result from endothelial aging, high blood pressure, or
atherosclerosis. Endothelial dysfunction increases the adverse effects from
high BP and from atherosclerosis. Part of the effect may be from an age-related
increase in *O2-, which reduces *NO by reacting with it
to form ONOO-. With less *NO, vessel dilation is reduced and vessel
smooth muscle growth and clot formation increase. At the same time, ONOO-
may initiate or promote plaque formation by injuring the vessel wall.
Free radicals Free
radicals may also contribute to atherosclerosis by increasing the formation of
lipid peroxides (LPs) from blood lipoproteins. Blood LPs increase with age and
after menopause, and also with increases in blood LDLs, blood pressure, stress,
diabetes mellitus, and smoking. Lipid peroxides may promote atherosclerosis in several
ways. Examples include increasing the absorption of LDLs by vessel macrophages,
converting them to cholesterol-filled foam cells; injuring vessel
cells directly; attracting monocytes and macrophages into vessel walls, which
promote inflammation and cell damage; promoting vessel constriction; and
promoting blood clot formation.
Blood LDLs Blood
LDLs may promote atherosclerosis by increasing LPs and by increasing elastase.
Elastase Elastase
is an enzyme that breaks down elastic fibers into elastin peptides. Elastin
peptides are also formed during elastin synthesis. Elastase increases with age
and with higher LDL levels. Elevated levels of elastin peptides seem to promote
more elastase production by promoting the binding of calcium and lipids to elastin
fibers.
Elastase may increase
atherosclerosis by reducing elastic fibers in arteries, making vessels more
susceptible to damage by blood pressure. The effects from the elastin peptides
produced seem to increase *NO. Results include benefits such as vasodilation,
and drawbacks such as vessel damage by stimulated monocytes. Research has
provided contradictory results regarding the effects from elevated elastin
peptides on promoting or reducing atherosclerosis.
Glycation Glycation
of proteins in arteries produces age-related glycation end-products (AGEs) and
*FRs. The *FRs may promote atherosclerosis directly.
The AGEs bind to fatty streaks and stimulate inflammation and *FR formation by
macrophages. Glycated collagen in arteries is distorted and stiffer, causing
adverse effects. These include reduced effectiveness of nitric oxide as a
vasodilator; detachments of endothelium from the vessel wall; and increased
clot formation.
Heat shock proteins Heat
shock proteins are produced when cells are stressed or injured. These
proteins received their name because they were first discovered in cells
subjected to abnormally high temperatures. Heat shock proteins seem to protect
cells from a variety harmful environmental factors. An
immune response to heat shock protein in damaged arteries may be the initial
event in atherosclerosis.
Insulin-like growth factors Insulin-like
growth factors (IGFs) from cells stimulate growth and regulate
other cell activities. The distribution and effectiveness of IGFs are altered
when they bind to insulin-like growth factor binding proteins (IGFBPs).
Research suggests that different ratios of IGFs and IGFBPs influence the
development of atherosclerosis, possible by altering blood levels of
lipoproteins and *NO and by affecting the growth of vessel smooth muscle.
The incidence and
seriousness of atherosclerosis can be greatly lowered by avoiding or reducing
the known risk factors, which were discussed in the section on coronary artery
disease.
The capillaries,
which receive blood from the smallest arteries, are often no more than 1 mm in
length. They are so narrow that blood cells can pass through only in single
file and often must actually fold to pass through. The capillaries run among
the body cells and are so numerous and so close together that no cell is very
far from a capillary (Fig. 4.11).
Capillaries are porous
vessels through which materials in the blood move out to the surrounding body
cells and many of the materials produced by body cells (e.g., wastes, hormones)
move back into the blood. Since materials are moving in both directions, this
process is called capillary exchange. However, a portion of the
material that moves out of the capillaries and some of the material produced by
the cells do not travel back into the capillaries. This material passes instead
into lymph capillaries, where it is known as lymph.
The lymph then passes through lymph vessels, which deliver it into large veins
near the heart.
The structure of
capillaries is well suited for capillary exchange (Fig. 4.12).
The wall of each capillary is composed of a single layer of thin cells that are
supported by a thin layer of material they secrete (basement membrane).
Many small atoms and molecules pass through the capillary wall quickly and
easily by the process of diffusion, which involves the movement
of materials from an area of higher concentration to an area of loser
concentration. Therefore, substances that are abundant in the blood diffuse
outward to the cells, while other substances diffuse from the cells into the
blood.
Capillary walls have
pores between the cells and through the cells that constitute them, making it
even easier for substances to diffuse between the blood and body cells. In
addition, blood pressure pushes many atoms, ions and small molecules out of the
capillaries through the pores, leaving large molecules and cells within the
blood. This separation of small substances from large ones by fluid pressure is
called filtration.
With increasing age, many
capillaries become narrower and irregular in shape, and this retards the flow
of blood. Some capillaries become so narrow that blood cells get stuck in them,
further inhibiting blood flow. In some organs (e.g., heart, muscles) blood
supply is further reduced because of a decrease in the number of capillaries. Finally,
capillary walls become thicker and have a decrease in the number of pores; both
changes inhibit capillary exchange.
Age changes reduce the
ability of capillaries to meet the needs of body cells quickly. Therefore,
while the cells may be able to function well at low levels of activity, both
the ability to sustain vigorous activity and the maximum rate of physical
activity may be lowered. This becomes evident when people tire more quickly
while performing vigorous work or experience a gradual drop in the maximum
speed of activity they can attain while performing vigorous activities such as
running or riding a bicycle.
Blood passing through
capillaries flows into very small veins. The small veins join to
form larger veins as they transport the blood back to the heart (Fig. 4.1).
Veins are made up of the
same three layers found in smaller arteries (Fig. 4.9a)
and (Fig. 4.9c).
The layers in veins are thinner and weaker, however, since venous blood
pressure is much lower than arterial pressure; therefore, there is no need for
thick strong walls in veins. Veins also tend to be somewhat larger in diameter
than arteries in the same area of the body. This extra internal space, along
with the greater ability of veins to expand outward, allows the veins to serve
as a reservoir for storing blood.
The inner layer provides
smoothness to prevent blood clots, and the middle layer contains smooth muscle
that regulates the diameter. When the muscle relaxes and the veins dilate, they
can hold a considerable amount of blood. When the muscle contracts and
constricts the veins, a great deal of blood is squeezed out and sent to the
heart. These changes in diameter are useful in regulating blood pressure. For
example, if blood pressure rises excessively, dilation allows the veins to
store much of the extra blood from the arteries. The blood pressure will then
return to normal. Conversely, if higher blood pressure is needed, the muscle
layer contracts, squeezing more blood back to the heart. The heart immediately
pumps this extra blood into the arteries, filling them further and increasing
blood pressure and blood flow to the desired levels.
Since the blood pressure in
veins is so low, blood flow tends to be sluggish. Gravity increases this
tendency by pulling blood in veins below the heart downward, away from the
heart. To prevent such backward flow, veins below the heart and in the arms
contain valves. These valves consist of flaps of tissue extending
from the walls of the veins into the blood (Fig. 4.9d).
The valves operate in the same way as do those in the heart.
The movement of blood in
veins is greatly aided by alternating contraction and relaxation of nearby
muscles, such as occurs during exercise involving body movement. During
contraction, muscles widen and press on neighboring veins, forcing blood to
move along the veins. During relaxation, the muscles become thinner, allowing
the veins to expand and fill with blood from below. Therefore, exercise
promotes blood flow in veins.
Several age changes occur
in veins, including accumulations of patchy thickenings in the inner layer and
fibers in the middle layer and valves. However, these changes do not alter the
functioning of veins because veins have such a large diameter to begin with that
slight narrowing is unimportant. Veins have thin walls and are able to expand
easily and compensate for narrowing, and there are often several veins draining
blood from each area of the body, which can provide ample alternative routes
for blood.
Some disease changes in
veins occur with increasing frequency and severity as age increases. One of the
most common is varicose veins, which now ranks as the tenth leading chronic
condition among people above age 64.
Varicose Veins
A varicose vein is
a vein that has developed a much larger diameter than normal because blood has
accumulated in the vein, stretching it outward. If the vein is stretched
frequently and for prolonged periods, it loses its elasticity and remains
permanently distended (Fig. 4.16).
Varicose veins frequently
develop in the legs. Conditions promoting their development in this area
include standing still for long periods, sitting in a posture that reduces
circulation, wearing tight clothing, and having certain diseases (e.g.,
congestive heart failure). Varicose veins are also found inside the abdomen;
for example, cirrhosis of the liver is a common cause of varicose veins in the
digestive system.
Varicose veins cause
several problems. Affected veins close to the skin can be cosmetically
undesirable because they appear as irregular bluish vessels. When veins remain
engorged with blood for long periods or become inflamed, they can be very
painful. They can even become sites of infection and, in extremely serious
cases, sites of bleeding. Bleeding is the main problem when a person has
varicose veins from cirrhosis. Very wide varicose veins also prevent the valves
from stopping backward blood flow, since the valve flaps are too far apart to
meet and blood slips back through the opening that remains between them. The
blood backs up into the capillaries, slowing flow there. When this happens in
the legs, swelling in the area below the varicose vein develops. Slow flow also
prevents the capillaries from serving the needs of body cells, and the cells
become weak and injured and may even die. Infection often adds to the resulting
skin, nerve, and muscle problems.
Another undesirable
result from varicose veins occurs because blood flow through these veins is
fairly sluggish and the blood tends to clot. A stationary blood clot inside a
vessel is called a thrombus. As in arteries, a thrombus in a vein
can block blood flow. Frequently, blood flow propels the thrombus within the
vein, in which case it is called a thromboembolus
or simply an embolus. An embolus can cause serious problems when
it moves to the heart and is pumped into the arteries, because as the arteries
branch into narrower ones, the embolus will finally reach an artery through
which it cannot pass and will block blood flow through that artery.
Almost all varicose veins
develop in systemic veins such as those in the legs and the digestive system.
Therefore, most emboli from varicose veins enter the right atrium and are
pumped by the right ventricle into the pulmonary arteries. Such emboli are
called pulmonary emboli.
A small pulmonary embolus
causes death of the area of the lung normally serviced by the artery that has
become blocked. If only a very small artery is blocked, the area that dies may
be so small as to go unnoticed. However, repetition of this type of event or
blockage of a larger pulmonary artery by a more substantial embolus may kill a
considerable portion of the lung, significantly reducing the ability of the
lung to serve the needs of the body. Dead lung tissue can become infected and
form a pocket of pus called a pulmonary abscess. These infections
and abscesses can make a person ill and can even be fatal.
A large pulmonary embolus
can obstruct blood flow from the right ventricle to the lungs to such an extent
that the right ventricle can no longer empty adequately and becomes overfull.
This overfilling, coupled with the high pressure developed as the right
ventricle attempts to pump blood through the artery. The result can be sudden death.
Since varicose veins
cause such a variety of undesirable and serious consequences, slowing or
preventing their formation can help maintain the quality and length of life.
When possible, people who stand or sit for long periods of time should move
about or change position frequently. When one is standing, alternately tensing
and relaxing the leg muscles periodically can help pump blood out of the veins.
Support stockings or tights that apply an even pressure over t veins. Elevating
the legs for short periods allows accumulated blood to drain out of the veins.
In addition, certain situations should be avoided. For example, sitting for
long periods with the legs crossed or in a tightly bent position inhibits blood
flow out of the veins. Clothing that is tight in the upper regions of the legs
should be avoided for the same reason. Excessive habitual consumption of
alcoholic beverages should be avoided because this is the most common cause of
liver cirrhosis. Individuals who have a weak heart or are developing congestive
heart failure should pay particular attention to these suggestions.
Hemorrhoids One type of varicose vein is singled out here
because of its location; it is found in the area of the anus and is called a hemorrhoid
(Fig. 4.13).
Hemorrhoids may remain small for long periods, may enlarge slowly, or may
become large in a short time. Some may reach the size of Ping‑Pong balls.
Like other types of
varicose veins, hemorrhoids can be painful and may bleed, become infected,
develop thrombi, and require surgery. These consequences can cause substantial
disability.
Factors that promote the
formation of hemorrhoids include chronic constipation, forced bowel movements,
chronic cough, and cirrhosis of the liver. The first two factors are often
found among disabled individuals and people whose occupations limit the
availability of toilet facilities. Chronic cough is associated with smoking and
other forms of air pollution, chronic bronchitis, and emphysema.
Several strategies can be
used to decrease the chance of developing hemorrhoids. Adequate amounts of
fiber and water in the diet help because these substances promote regular and
relatively easy bowel movements, as does exercise. Adequate access to toilet
facilities and timely use of those facilities are important. Smoking, breathing
polluted air, and consuming alcohol habitually should be avoided.
The structure and valves
of lymph vessels are very much like those of veins. Lymph flowing through lymph
vessels passes through lymph nodes, which are spongy structures
ranging up to the size of a large bean (Fig. 4.2).
Lymph nodes contain defense cells that neutralize or remove harmful chemicals
and microorganisms. By acting like purifying filters, lymph nodes reduce the
risk of spreading dangerous materials from a site of injury or infection in one
area of the body to another region.
Much lymph passes through
the spleen, which is toward the back of the abdominal cavity near
the lowest rib on the left side of the body. The spleen serves as a very large
lymph organ, stores blood, and removes old and damaged red blood cells from the
circulation.
Some defense cells in the
lymph nodes and spleen are called macrophages because they ingest
substances. Others are called lymphocytes. Macrophages and lymphocytes
are parts of the immune system.
Age Changes in Lymphatics and the Spleen
Aging seems to cause
little significant change in the structure and functioning of lymph vessels,
lymph nodes, and the spleen. However, there are important age changes in the immune
system.
Blood is a complex fluid
containing many different types of substances and cellular components.
Approximately 55 percent of the blood consists of a pale yellow liquid called plasma;
the other 45 percent is made up of the blood cells and platelets, which are
suspended in the plasma (Fig. 4.14).
A person maintains normal numbers of RBCs and platelets by balancing their
rapid destruction with rapid production in the red bone marrow.
About 90 percent of blood
plasma consists of water. The properties of water allow it to dissolve most
substances and flow easily through the circulatory system, transporting
materials and blood cells. Water also provides an excellent medium for
distributing heat from warmer to cooler areas. The water and buffers in the
plasma help maintain proper acid/base balance in body cells. Finally, plasma
contains substances (e.g., antibodies). Therefore, plasma contributes to all
four functions of the circulatory system.
Red blood cells
(RBCs) are the most numerous blood cells (Fig. 4.14).
They contain a great deal of a red material called hemoglobin.
Because hemoglobin can bind oxygen and carbon dioxide and can act as a buffer,
RBCs can transport much oxygen from the lungs to body cells, transport some
carbon dioxide from body cells to the lungs, and help regulate acid/base
balance.
Platelets
are cell fragments that form when small pieces break off from large parent
cells in the red bone marrow (Fig. 4.14).
Platelets start the formation of blood clots.
Because platelets are
fragments of cells, they are fragile and burst open when they come into contact
with rough spots, collagen, or unusual chemicals. This occurs, for example,
when blood leaks out of a damaged vessel (Fig. 4.15).
The bursting platelets release substances that help form a sticky fibrous
material called fibrin, which begins to plug the hole in the
vessel. As blood cells become trapped in the fibrin mesh, the spaces among the
fibrin threads are filled. The resulting blood clot forms a leakproof seal,
stopping the bleeding.
Unfortunately, platelets
burst open and start the clotting mechanism whenever roughness, collagen, or
unusual chemicals are encountered. When this happens on an atherosclerotic
plaque, the resulting clot may block the artery and lead to a heart attack or
stroke. In addition, since some platelets are bursting at all times, slow blood
flow, as occurs in varicose veins, permits the substances released by platelets
to accumulate at that location. When enough platelet material builds up, a
thrombus forms.
The white blood
cells (WBCs) are also called leukocytes,
which means "white cells." Blood contains only 1 WBC for every 500
RBCs (Fig. 4.14).
WBCs can be divided into
two main groups. The cells in one group are called polymorphonuclear
leukocytes (“many structured nucleus, white blood cell) (PMNs)
or granulocytes ("granular cells"). The other main
group of WBCs consists of the agranulocytes ("cells without
granules").
There are three types of
PMNs. The most numerous type by far are neutrophils,
which are important defense cells because they phagocytize
(ingest) undesirable materials. Because they can move about like amoebas and
can travel through capillary walls, they are found not only in the circulating
blood but also among body cells. These and other phagocytic WBCs resemble
vacuum cleaners as they move into every area of the body, sucking up debris.
Many neutrophils are
stored within blood vessels, especially in the bone marrow. Stored neutrophils
are mobilized into the circulating blood when there is a need for additional
defense activity, as occurs when an infection develops.
The other two types of
PMNs are basophils and eosinophils. Basophils
produce histamine, which initiates inflammation whenever body cells are injured
or killed. Eosinophils seem to help moderate inflammation. Eosinophils seem to
be defense cells, too, because their number increases in certain situations,
such as during an allergic reaction or when small parasites invade the body.
Eosinophils and basophils are thought to have several additional functions.
There are only two types
of agranulocytes in the blood. Lymphocytes are the more numerous
and function as part of the immune system. Monocytes function
like neutrophils and participate in immune responses. Lymphocytes and monocytes
are discussed in Chap. 15.
The total amount of blood
per unit of body mass and the relative amounts of plasma and cellular
components remain constant regardless of age. Though
some of the reserve capacity of the bone marrow to produce blood cells and
platelets declines with aging, the marrow always retains enough power to supply
as many blood cells and platelets as needed. Information about aging and blood
components follows.
Plasma Negligible
changes occur in the chemical composition of plasma, though there is an
increase in certain waste products (e.g., urea, creatinine). Increases in these
wastes are probably due to the decline in the ability of the kidney to remove
them from the blood.
There is an age-related
increase in the viscosity or "thickness" of blood. Reasons for the
increased viscosity include an increase in clotting factors and broken fibrin
strands; elevated norepinephrine, which promotes clot formation; and stiffening
of RBCs, especially in blood with high blood cholesterol. Certain clotting
factors increase dramatically at menopause, causing a rapid rise in blood
viscosity. Other factors that increase blood viscosity include reduced blood
oxygen; inadequate exercise; stress; and smoking, including secondhand smoke.
These factors can be reduced or eliminated. Effects from higher blood viscosity
include slower blood flow, increased risk of clot formation, and more rapid
development of atherosclerosis.
Red Blood Cells
No substantial changes occur in RBCs,
though there are some indications of a decrease in the concentration of
hemoglobin in men over age 65. Overall, however, aging causes no changes in the
ability of the RBCs to function.
Platelets The
number of platelets circulating in the blood remains essentially unchanged, and
the platelets retain the ability to initiate clot formation. An age‑related
increase in the tendency of platelets to clump together may cause a slight
increase in the risk of thrombus formation.
White Blood Cells
Age changes in PMNs include decreases in
the number and rate of release of stored cells, rate of movement, ability to be
chemically attracted to areas, and proportion of cells capable of performing
phagocytosis. The number of PMNs capable of performing phagocytosis seems to
decline especially rapidly after age 60. The net effect of age changes in PMNs
is a decrease in their ability to defend the body against infection, which
helps explain the age‑related increase in susceptibility to infections in
areas such as the respiratory, urinary, and integumentary systems.
Little has been reported
on age changes in monocytes that circulate in the blood. Age changes in
lymphocytes are discussed in Chap. 15.
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Copyright 2020: Augustine G. DiGiovanna, Ph.D.,
Salisbury University, Maryland
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