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Transcript
CARDIOVASCULAR DISEASE
The Nation’s #1 Killer
The Cardiovascular System
Cardio – the heart
Vascular – blood vessel system, circulation of nutrients.
STRUCTURE OF THE HEART
The heart weighs between 7 and 15 ounces and is a little larger than the
size of your fist. By the end of a long life, a person's heart may have beat
more than 3.5 billion times. In fact, each day, the average heart beats
100,000 times, pumping about 2,000 gallons of blood. It is almost all
muscle; made up of unique muscle tissue called the myocardium. Within
the heart there are four hallow chambers. Two collecting chambers, the
atria, and two pumping chambers, the ventricles. Between the
chambers of the heart there are valves that prevent the blood from flowing
in the wrong direction. The valve between the left atrium and the left
ventricle is the mitral valve. The valve between the right atrium and right
ventricle is the tricuspid. There are two other valves within the heart
where blood exits. When oxygen rich blood exits from the left ventricle it
passes through the aortic valve and into the aorta. When oxygen
depleted blood exits from the right ventricle it passes through the
pulmonary valve into the pulmonary artery.
STRUCTURE OF HEART
The heart is separated down the middle by a strong, muscular wall
called the septum. The heart is enclosed in a fibrous sac called the
pericardian (or pericardial sac).
The left side of the heart (left atria and left ventricle) are responsible for
pumping oxygen rich blood to all cells, tissues and organs. Conversely,
the right side of the heart is responsible for collecting and pumping oxygen
depleted blood back to the lungs to receive fresh O2. Oxygenated blood
enters the left atria and is passed to the left ventricle where it is pumped
through the aortic valve into the aorta. Oxygen depleted blood enters the
right atria of the heart through two large veins, the superior vena cava
(carrying all DeO2 above the heart) and the inferior vena cava (carrying
all DeO2) from below the heart. The heart muscle itself receives oxygen
and nutrients from the all important coronary arteries, which branch off
from the base of the aorta. There are four major branches off the
coronaries. These are the arteries where most heart issues occur.
STRUCTURE OF THE HEART
This is the external
appearance of a normal
heart. The epicardial
surface is smooth and
glistening. The amount of
epicardial fat is usual. The
left anterior descending
coronary artery extends
down from the aortic root
to the apex.
VASCULAR SYSTEM – BLOOD VESSELS AND CELLS
The circulatory (vascular) system is made up of arteries,
veins and capillaries. Blood (plasma) travels through
these vessels carrying nutrients, oxygen and waste products
to and from cells. Within blood plasma are three blood cells.
Red blood cells carry the oxygen within a pigment called
hemoglobin.
Arteries carry oxygen rich blood away from the heart
branching into smaller and smaller arteries then into the
arterioles which feed the capillary beds in tissues.
Diffusion occurs at the capillary bed level where oxygen is
diffused into tissue and carbon dioxide is picked up.
Capillary beds then drain waste blood into venules which
empty into veins and finally into the superior vena cava
(blood from above the heart) and inferior vena cava (blood
from below the hear).
Major arteries
and veins of
the circulatory
system
BLOOD CELLS
Plasma, the liquid portion of blood, is approximately 90%.
Over 100 different substances are dissolved in this fluid
including nutrients, salts (electrolytes, respiratory gases,
hormones, proteins and various wastes.
Red blood cells (erythrocytes) carry oxygen, inside
a pigment called hemoglobin, to all the cells of the body.
White blood cells (leukocytes), produce a variety of
antibodies to combat everything from the common cold
to tumors and viruses.
Platelets, responsible for clotting of blood, are not
really cells but fragments of bizarre multinucleate cells
called megakaryocytes.
CARDIOVASCULAR DISEASES (CVD’s)
Refers to diseases of all parts of the cardiovascular system, including
both the heart and blood vessels.
Atherosclerosis, or hardening of the arteries, is the most common
form of CVD. It begins early on with deposits of fat along the inner
walls of arteries. These deposits harden and form plaques. The
passageway narrows and blood supply lessens.
Atherosclerosis not only weakens the heart but it leads to HIGH
BLOOD PRESSURE. High blood pressure, hypertension, is a major
contributor to CVD. Hypertension damages artery walls.
Aneurysm occur when the pressure becomes so great a part of the
artery balloons out and can burst. When this happens to small vessel
it results in death to surrounding tissue. If it happens to a major
vessel like the aorta or coronary artery massive hemorrhage occurs
resulting in death.
CARDIOVASCULAR DISEASE (CVD’s)
cont.
Atherosclerosis can cause blockage of an artery in any of
three ways:
1. The plaques themselves can enlarge to block flow of
blood.
2. A blood clot may form, stick to a plaque, and grow until it
cuts off the blood supply like a plug. This is called a
thrombus. In the arteries of the heart it is called a
coronary thrombosis (a type of heart attack). In a
vessel that feeds the brain , the blockage is called a
cerebral thrombosis (a type of stroke).
3. A clot may also break loose, become a traveling clot, an
embolus and can circulate until it reaches an artery too
small to allow its passage. The sudden blockage of the
vessel is an embolism.
Strokes occur in the same way heart attacks do – by the
blockage of arteries – the cerebral arteries. Strokes do not
occur as often as heart attacks and many arise from the
bursting of an aneurysm in a small vessel.
CARDIOVASCULAR DISEASE (CVD’s)
cont.
Congestive Heart Disease – occurs because the heart muscle is damaged or
overworked. This can result from high blood pressure, artherosclerosis or
heart attack. The heart lacks strength to keep blood circulating throughout the
body. The result is congestion in the tissues resulting in swelling (edema) in
legs and ankles. Sometimes fluid collects in lungs and can interfer with
breathing.
Rheumatic Heart Disease – condition in which heart valves are damaged
by a disease process that begins with strep throat. If not treated it can
develop into rheumatic fever.
Bacterial Endocarditis – a bacterial infection of the heart lining or
valves. People with abnormal heart valves or congential heart defects
are at increased risk of developing this disease.
Congenital Heart Defects – malformation of the heart or of its major blood
vessels present at birth.
ATHEROSCLEROTIC CARDIOVASCULAR DISEASE
Some Pictures
This is the tricuspid valve. The leaflets thin
and delicate. Just like the mitral valve, the
leaflets have thin chordae tendineae that
attach the leaflet margins to the papillary
muscles of the ventricular wall below.
This is a normal coronary artery. The lumen is
large, without any narrowing by atherosclerotic
plaque. The muscular arterial wall is of normal
proportion.
The coronary artery shown here has
narrowing of the lumen due to build up of
atherosclerotic plaque. Severe narrowing can
lead to angina, ischemia, and infarction.
This is about as normal as an adult aorta in
America gets. The faint reddish staining is
from hemoglobin that leaked from RBC's
following death. The surface is quite smooth,
with only occasional faint small yellow lipid
streaks visible.
Put down that jelly doughnut and look
carefully at this aorta. The white arrow
denotes the most prominent fatty streak in
the photo, but there are other fatty streaks
scattered over the aortic surface. Fatty
streaks are the earliest lesions seen with
atherosclerosis in arteries.
These three aortas demonstrate mild,
moderate, and severe atherosclerosis from
bottom to top. At the bottom, the mild
atherosclerosis shows only scattered lipid
plaques. The aorta in the middle shows many
more larger plaques. The severe
atherosclerosis in the aorta at the top shows
extensive ulceration in the plaques.
Here is an example of an
atherosclerotic aneurysm
of the aorta in which a
large "bulge" appears just
above the aortic
bifurcation. Such
aneurysms are prone to
rupture when they reach
about 6 to 7 cm in size.
They may be felt on
physical examination as a
pulsatile mass in the
abdomen. Most such
aneurysms are
conveniently located below
the renal arteries so that
surgical resection can be
performed with placement
of a dacron graft.
This is severe atherosclerosis of the aorta in
which the plaques have undergone ulceration
along with formation of overlying mural
thrombus.
A coronary artery has been opened
longitudinally. The coronary extends from left
to right across the middle of the picture and is
surrounded by epicardial fat. Increased
epicardial fat correlates with increasing total
body fat. There is a lot of fat here, suggesting
one risk factor for atherosclerosis. This
coronary shows only mild atherosclerosis,
with only an occasional yellow-tan lipid plaque
and no narrowing.
This is the left coronary artery from the
aortic root on the left. Extending across the
middle of the picture to the right is the
anterior descending branch. This coronary
shows severe atherosclerosis with
extensive calcification. At the far right, there
is an area of significant narrowing.
This is coronary atherosclerosis with the
complication of hemorrhage into
atheromatous plaque, seen here in the
center of the photograph. Such hemorrhage
acutely may narrow the arterial lumen.
At high magnification, the dark red thrombus
is apparent in the lumen of the coronary. The
yellow tan plaques narrow this coronary
significantly, and the thrombus occludes it
completely.
The anterior surface of the
heart demonstrates an
opened left anterior
descending coronary artery.
Within the lumen of the
coronary can be seen a
dark red recent coronary
thrombosis. The dull red
color to the myocardium as
seen below the glistening
epicardium to the lower
right of the thrombus is
consistent with underlying
myocardial infarction.
A thrombosis of a coronary artery is shown
here in cross section. This acute thrombosis
diminishes blood flow and leads to ischemia
and/or infarction, marked clinically by the
sudden onset of chest pain.
MYOCARDIAL INFARCTION
HEART ATTACK
When the myocardium (heart
muscle) is deprived of oxygen the
result could be crushing chest pain
called anginas pectoris (anginas).
This pain is a warning that should
never be ignored because, if angina
is prolonged, the ischemic heart
cells may die, forming an infarct.
The resulting myocardial infarction
is commonly called a “heart attack”
or “coronary”.
Most heart attacks are brought on
by atherosclerosis.
WARNING SIGN OF HEART ATTACK
Even though not every heart attack is announced by clear
cut symptoms, you should get help immediately if you:
1. Feel uncomfortable pressure, fullness,
squeezing or pain in the center of the chest
lasting for more than two minutes.
2. Experience pain that spreads to the shoulders,
neck, or arms.
3. Become dizzy faint, sweats for no apparent
reason or have nausea or shortness of breath –
especially when other symptoms are present.
WARNING SIGN OF STROKE
Report to a physician immediately any of the following:
1. Sudden, temporary weakness or numbness in
any part of one side of the body.
2. Temporary loss of speech or of understanding
of speech.
3. Dizziness, unsteadiness, or unexplained falls.
4. Temporary dimness or loss of vision,
particularly one eye.
DIAGNOSIS AND TREATMENT FOR HEART DISEASE
Most patients, when symptoms of anginas appear, will have
diagnostic tests to determine what course of treatment is best.
There are also many who must first survive a heart attack before
determining best course of action.
HEART ATTACK – The most common of life-threatening events brought
on by lack of blood supply to the myocardium. It requires immediate
intervention with CPR (Cardio-Pulmonary Resuscitation) and Emergency
Medical Treatment (see handout on CPR performance.
DIAGNOSTIC TESTS
ELECTROCARDIOGRAM (ECG or EKG) – a graphic record of electrical
impulses by the heart.
ECHOCARDIOGRAPHY – sound waves are transmitted into the body and the
echoes returning record a picture of the heart’s silze, shape and movements.
ANGIOCARDIOGRAPHY – an X-ray picture of blood vessels or chambers of
the heart that show the course of dye injected into the bloodstream. The X-ray
pictures made are called angiograms.
ARTERIOGRAPHY - X-ray opaque dye shows pictures to show artery
damage.
CATHETERIZATION – examining an artery by introducing a thin tube
(catheter) into a vein or artery and passing it into the heart.
TREATMENT
CORONARY BYPASS SURGERY – surgery to improve blood supply to
the myocardium (heart muscle). This surgery is the most often performed
procedure when narrowed coronary arteries reduce the flow of oxygencontaining blood to the heart itself.
ANGOOPLASTY (Balloon Angioplasty) – a procedure sometimes used
to dilate (widen) narrowed arteries. A catheter with a deflated balloon on its
tip is passed into the narrowed artery segment, the balloon inflated, and the
narrowed segment widened. Often times a mesh stint is also put in to hold
the inflated artery open.
REPERFUSION THERAPY – if a victim gets to an emergency room fast
enough, a form of reperfusion therapy (called thrombolytic) sometimes
can be performed. It involves injecting a thrombolytic (clot-dissolving)
agent, to dissolve a clot in a coronary artery and restore some blood flow.
NITROGLYCERIN – a drug that causes dilation of blood vessels and is
often used in treating angina pectoris.
RISK FACTORS FOR HEART AND ARTERY DISEASE
Heredity (history of CVD prior to age 55 in family members.
Gender – males suffer more CVD’s than female although
current research shows that heart disease in females is
approaching males.
Smoking and use of other tobacco products.
High blood pressure – Hypertension
High blood cholesterol, high LDL, and/or low HDL.
Glucose intolerance – Diabetes
Lack of cardiovascular exercise.
Obesity – 30% or more overweight.
STRESS
BLOOD
CHOLESTEROL
CHART
HIGH BLOOD PRESSURE – THE “SILENT KILLER”
HYPERTENSION, the medical term for high blood pressure is called the
“silent killer” because it often has no recognizable symptoms.
Blood pressure is the measure of pressure within the walls of arteries. It
is read as a two number notation:
SYSTOLIC PRESSURE - a measure of pressure when the
ventricles contract and force more blood into the system.
DIASTOLIC PRESSURE – a measure of pressure when the
ventricles are refilling and the heart is in relaxation phase.
Normal blood pressure reading would be systolic in the 120-130 range
and diastolic in the 70-80 range. Systolic pressure over 140 and
diastolic over 90 would indicate pressure in the high range.
CONTRIBUTING FACTORS:
1.
2.
3.
4.
5.
Smoking
High Saturated Diet
Stress
Family History
Pregnancy – increase in
blood pressure
6.
7.
8.
BMI in the overweight range and
above
Age – pressure goes up with age
The Pill – two times greater in women
who use oral contraceptives
MYOCARDIAL INFARCTION – HEART ATTACK
Some Pictures
This is the left ventricular wall which has
been sectioned lengthwise to reveal a large
recent myocardial infarction. The center of
the infarct contains necrotic muscle that
appears yellow-tan. Surrounding this is a
zone of red hyperemia. Remaining viable
myocardium is reddish- brown.
This cross section through the heart
demonstrates the left ventricle on the left.
Extending from the anterior portion and into
the septum is a large recent myocardial
infarction. The center is tan with surrounding
hyperemia. The infarction is "transmural" in
that it extends through the full thickness of
the wall.
One complication of a
myocardial infarction is
rupture of the myocardium.
This is most likely to occur in
the first week between 3 to 5
days following the initial
event, when the myocardium
is the softest. The white
arrow marks the point of
rupture in this anteriorinferior myocardial infarction
of the left ventricular free
wall and septum. Note the
dark red blood clot forming
the hemopericardium. The
hemopericardium can lead
to tamponade.
The heart is opened to reveal the left
ventricular free wall on the right and the
septum in the center. There has been a
remote myocardial infarction that extensively
involved the anterior left ventricular free wall
and septum. The white appearance of the
endocardial surface indicates the extensive
scarring.
There has been a previous
extensive myocardial infarction
involving the free wall of the left
ventricle. Note that the thickness
of the myocardial wall is normal
superiorly, but inferiorly is only a
thin fibrous wall. The infarction
was so extensive that, after
healing, the ventricular wall was
replaced by a thin band of
collagen, forming an aneurysm.
Such an aneurysm represents
non-contractile tissue that
reduces stroke volume and
strains the remaining
myocardium. The stasis of blood
in the aneurysm predisposes to
mural thrombosis.
A cross section through the heart reveals a
ventricular aneurysm with a very thin wall at
the arrow. Note how the aneurysm bulges
out. The stasis in this aneurysm allows mural
thrombus, which is present here, to form
within the aneurysm.
This left ventricle is very thickened (slightly
over 2 cm in thickness), but the rest of the
heart is not greatly enlarged. This is typical
for hypertensive heart disease. The
hypertension creates a greater pressure load
on the heart to induce the hypertrophy.
This patient underwent coronary artery
bypass grafting with saphenous vein grafts.
The largest of these runs down the center of
the heart to anastomose with the left anterior
descending artery distally. Another graft
extends in a "Y" fashion just to the right of
this to branches of the circumflex artery. A
white temporary pacing wire extends from
the mid left surface.
The left ventricle is markedly thickened in this
patient with severe hypertension that was
untreated for many years. The myocardial
fibers have undergone hypertrophy.
This is a mechanical valve prosthesis of the more modern
tilting disk variety. Such mechanical prostheses will last
indefinitely from a structural standpoint, but the patient
requires continuing anticoagulation because of the exposed
non-biologic surfaces. The superior aspect (here the left
atrium) is seen at the left, while the outflow, with the two
leaflets tilted outward toward the left ventricle, is at the right
in this mitral valve prosthesis.
REDUCING THE RISK OF CVD
1. Learn about your heredity, and use the information. Control the
lifestyle factors that may affect you.
2. Don’t smoke. If you do smoke, STOP!
3. Keep your blood pressure below 125/80 if you are a teenage
girl; 130/80 if you are a teenage boy.
4. Keep; your blood cholesterol within the normal range (below
170 milligrams per deciliter for teenagers).
5. Keep your blood sugar under control.
6. Exercise vigorously for at least 20 minutes 4-6 times a week.
7. Maintain appropriate body weight.
8. Control stress. LEARN TO RELAX!!!.
TAKE CARE OF YOUR HEART
IT’S THE ONLY ONE YOU HAVE