This is the pump of the cardiovascular
system. At rest, the heart pumps about 10 qts. of
blood per minute and the volume increases with exercise.
Cardiology is the study of the heart.
Your heart is about the same size as your
closed fist. It rests on the diaphragm in the mediastinum, with about 2/3 of
its mass to the left of the midline. The pointed bottom end is the apex and the
top is the base.
The pericardium is a sac that surrounds
the heart. Layers:
1. Fibrous pericardium---outer layer of tough fibrous CT
(dense irregular) that protects and anchors in position
2. Serous pericardium---inner layer of thinner membrane that
consists of:
a. Outer parietal layer fused to the inside of the fibrous
pericardium
b. Inner visceral layer that adheres to the outside of the
heart muscle (also called epicardium)
Between the 2 layers of the serous
pericardium is a space, the pericardial cavity. It contains a small amount of
serous fluid for lubrication---reduces friction as the heart beats.
The heart wall is made of 3 layers:
1. Epicardium---same thing we just called the visceral layer
of the serous pericardium
2. Myocardium—cardiac muscle tissue---involuntary, striated,
branching fibers. Responsible for the pumping action of the heart. The fibers
form 2 networks, an upper atrial network and a lower ventricular network. All
fibers in the same network contract together as a unit.
3. Endocardium---thin layer of endothelium over a thin layer
of CT. It provides a smooth lining and covers the valves.
The inside of the heart is divided into
4 compartments called chambers:
2 superior atria (R & L), each with a pouchlike extension called an
auricle (to increase capacity)---the atria are
collecting chambers.
2 inferior ventricles (R & L)—pumping chambers
Inside:
Interatrial septum separates the 2 atria—thin partition
Interventricular septum separates the 2 ventricles--thicker
Right atrium has a smooth posterior wall, but the anterior wall and the
inside of the auricle have muscular ridges called pectinate muscles
Left atrium—interior wall is all smooth but auricle has pectinate
muscles
Both ventricles—ridges on inside wall formed by bundles of muscle fibers
are called trabeculae carnae. Cone-shaped trabeculae carnae known as papillary
muscles provide a point of attachment for chordae tendineae.
Grooves on the outer surface of the
heart contain coronary blood vessels and mark the external boundaries between
chambers.
Coronary sulcus—groove between atria and ventricles
Anterior interventricular sulcus—groove between right and left
ventricles on anterior surface
Posterior interventricular sulcus—groove between ventricles on posterior
aspect
Mixed in with the cardiac muscle, the
heart wall contains dense fibrous CT that forms a framework called the fibrous
skeleton of the heart. Rings of CT surround and support the valves of the
heart, which themselves consist of more fibrous CT
covered by endocardium. CT separates the atrial network from the ventricular
network, so action potentials do not spread directly from atria to ventricles.
The thickness of the walls of the
chambers varies:
Both atria---thinnest
Right ventricle---somewhat thicker
Left ventricle---2-4X thicker than right
1. Right atrium---receives deoxygenated blood from tissues
(all of body except lungs)
BLOOD ENTERS FROM:
a. Superior vena cava—from all of body above the heart
b. Inferior vena cava—from body below the heart
c. Coronary sinus—from the myocardium
BLOOD LEAVES THROUGH:
Right AV (tricuspid) valve going to right ventricle
2. Right ventricle---pumps deoxygenated blood to the lungs
BLOOD ENTERS FROM:
Right atrium through right AV valve
BLOOD LEAVES THROUGH:
Pulmonary trunk (an artery) which soon divides into
the R & L pulmonary arteries which go to each lung. There, in lung
capillaries, blood gives off CO2 and picks up O2.
3. Left atrium---receives oxygenated blood from the lungs
BLOOD ENTERS FROM:
4 pulmonary veins, 2 from each lung
BLOOD LEAVES THROUGH:
Left AV (bicuspid,
mitral) valve going to left ventricle
4. Left ventricle---pumps oxygenated blood to tissues of the
body
BLOOD ENTERS FROM:
Left atrium through left AV valve
BLOOD LEAVES THROUGH:
Aorta (largest artery in the body)
These are the arteries and veins
attached directly to the heart:
Aorta Both
vena cavae
Pulmonary trunk
Pulmonary veins
The heart requires valves (like any
pump) to prevent backflow. The valves are made of thick CT covered by
endocardium. There are 4 major valves:
1. Atrioventricular (AV) valves---lie between atria and
ventricles
a. Right AV valve---tricuspid
b. Left AV valve---bicuspid, mitral
These valves consist of 2 or 3 flaps
(cusps) attached to the heart wall. When open, these cusps drop down into the
ventricles so blood flows freely from atrium to ventricle. When
pressure in the ventricle rises higher than pressure in the atrium, the AV
valves close. Now little fibrous cords called chordae tendineae, which
are connected to the cusps and to the papillary muscles in the ventricle walls,
allow the cusps to rise just high enough to close the opening but no further.
2. Semilunar (SL) valves---these prevent backflow from the
arteries leaving the heart
a. Pulmonary SL valve in pulmonary trunk
b. Aortic SL valve in the aorta
These consist of 3 half-moon shaped
cusps attached just inside the artery with the free edges of the cusps
projecting on into the artery. These valves permit blood flow only one
way---out of the heart.
Rheumatic fever is a complication of a
streptococcal throat infection that can damage heart valves as well as joints
and other CT of the body.
The myocardium has its own network of
blood vessels called the coronary (cardiac) circulation. Two coronary arteries
(R & L) arise from the ascending aorta and carry oxygenated blood to the
myocardium.
1. Left coronary artery---2 main branches
a. Left anterior descending (LAD), also known as anterior
interventricular---both ventricles and IV septum
b. Circumflex---LA and
2. Right coronary artery---right atrium and then branches into :
a. Posterior interventricular artery—both ventricles and IV septum
b. Marginal branch---RV
The myocardium contains many
anastomoses---connecting branches that extend between different coronary
arteries and provide alternate routes for blood to reach the tissue.
Blood from the
myocardium drains into veins which unite to form larger and larger veins. Eventually all blood drains into one
large vein on the posterior surface of the heart called the coronary sinus,
which empties into the right atrium. It is formed from the union of the great
cardiac vein and the middle cardiac vein.
Compared to skeletal muscle, cardiac
muscle fibers are shorter and larger in diameter. They have one centrally
located nucleus, and branch and interconnect with each other. They have
abundant sarcoplasm and numerous mitochondria.
Fibers have the same crosswise
compartments, called sarcomeres, with the same bands, zones, etc. SR is scanty
in cardiac muscle.
The fibers of the myocardium
interconnect to form 2 separate networks, the upper atrial and the lower
ventricular. The ends of fibers within a network connect to each other by
thickenings of the sarcolemma called intercalated discs. Gap junctions in the
discs allow muscle action potentials to spread rapidly across the network, so
that all fibers in the network contract together as a unit.
The cardiac muscle contracts
independently from the nervous system---autorhythmicity. Signals from the
autonomic nervous system and hormones can modify the rate but do not establish
the fundamental rhythm.
During embryonic development, a small fraction (1%) of the cardiac muscle fibers become
autorhythmic—able to generate impulses. Some of these fibers act as the heart’s
natural pacemaker and set the rhythm. The rest form the conduction system and
spread the action potentials over the heart muscle. This assures that the
chambers contract in a coordinated manner for effective pumping. Conduction
system:
1. Sinoatrial (SA) node
2. Atrioventricular (AV) node
3. Atrioventricular (AV) bundle
4. Right & left bundle branches
5. Conduction myofibers (Purkinje fibers)
1. SA node—this is the heart’s natural pacemaker. It is
located in the right atrial wall just below the opening of the superior vena
cava. The action potentials that cause each heartbeat originate here and spread
through gap junctions to all atrial fibers, causing the 2 atria to contract.
The action potential then reaches the AV node.
2. AV node—located in the interatrial septum. It receives
action potentials from the SA node and passes them on to the AV bundle.
3. AV bundle (bundle of His)—only connection between atria
and ventricles
4. Right and left bundle branches—run down the
interventricular septum toward the apex
5. Purkinje fibers—penetrate into the ventricular muscle and
actually carry the MAP (muscle action potential) to the fibers of the
ventricles.
On their own, fibers of the SA node
initiate MAPs 90 - 100 times per minute (faster than other autorhythmic
fibers), so the SA node acts as the natural pacemaker of the heart. If a
different rate is needed, the autonomic nervous system can act through the SA
node and modify the rate. Sympathetic impulses speed the depolarization rate of
the SA node; parasympathetic impulses slow it.
If the SA node is unable to function,
the AV node can become the pacemaker, although the rate will be slower. If the
AV node fails, the remaining conduction fibers may initiate an even slower
beat, too slow to supply blood to the brain. An artificial pacemaker can
correct this.
Muscle action potential---occurs in all
3 types of muscle---a change in charge of the inside of a cell from negative to
0 to positive (depolarization) and back to negative (repolarization). The
result is a muscle contraction.
Remember, in the heart there are 2
kinds of muscle fibers:
1. Conduction myofibers—modified to become
autorhythmic—concerned with starting and spreading a MAP over the heart.
2. Contractile fibers---contract forcefully in response to a
MAP and do the pumping
The structure of cardiac muscle
contractile fibers is almost exactly the same as that of skeletal muscle
fibers, with the same arrangement of sarcomeres containing thick and thin
myofilaments. Contraction occurs in the same way (pulling of thin myofilaments
by the myosin cross bridges of the thick myofilaments).
In order for a muscle contraction to
occur, the muscle cell must depolarize (this is the beginning of a muscle
action potential). Skeletal muscle fibers only do this when stimulated by a
motor neuron. In conduction myofibers of the heart, depolarization occurs automatically
at regular time intervals.
About 100 times per minute the fibers
of the SA node automatically become highly permeable to Na+ (for no reason
except that nature made them this way---no stimulus required). This rate can be
modified up or down by the autonomic nervous system and hormones. The action
potential spreads to contractile fibers (atrial network first, then ventricular
network). Events in contractile fibers then proceed:
1. Voltage-gated fast Na+ channels open and Na+ rushes into
the cell (due to a conc. gradient and a charge gradient). The net charge inside
the cell goes rapidly from negative to 0 to positive and this is
depolarization. After a few milliseconds, the Na+ channels close.
2. Voltage-gated slow Ca2+ channels in both the
sarcolemma and SR membrane open and Ca2+ enters
the cytosol from both ECF and the SR. During this time in cardiac muscle, the
sarcolemma is relatively impermeable to K+ and the Ca2+ channels remain
open---this is called the plateau. The cardiac muscle remains depolarized all
this time (different from skeletal muscle, where the sarcolemma immediately
becomes highly permeable to K+ as soon as the Na+ channels close).
Depolarization lasts about 250 milliseconds in cardiac muscle compared to 1
millisecond in skeletal.
3. Voltage-gated K+ channels finally open, increasing
permeability of the membrane to K+ and allowing it to diffuse out of the cell
due to a conc. gradient. As many positive K+ ions leave, the net charge inside
goes from positive back to negative (repolarization). The Na+ and K+ are in the
wrong place, but that is quickly fixed by the Na+/K+ pump. Repolarization
causes the Ca2+ channels to close and active transport pumps remove
the Ca2+ from the sarcoplasm. The contraction ends.
The refractory period is the time interval when a second contraction
cannot be triggered. It is prolonged in cardiac muscle to insure that tetanus
cannot occur.
ECG
HANDOUT
CARDIAC CYCLE
This is all the events associated with
one heartbeat. We are aware only of ventricular systole. In a normal cardiac
cycle the 2 atria contract together, each pumping an equal amount of blood,
while the ventricles are relaxed. While chambers are relaxed, they fill with
the blood they will pump with the next contraction. Then the
2 ventricles contract together, also each pumping an equal amount of blood,
while the atria relax. Systole is contraction of any chamber; diastole
is relaxation. Pressure rises inside a chamber that is contracting; pressure
drops as a chamber relaxes.
At rest, with a heart rate of 75 beats
per minute, each cardiac cycle lasts about .8 seconds.
Relaxation period .4 sec
Atrial contraction
.1 sec
Ventricular " .3 sec
As the heart rate speeds up the
relaxation period becomes shorter, but the others change very little.
Events in the cardiac cycle:
1. Relaxation period
a. At the end of a cycle, all 4 chambers are briefly relaxed. The
ventricles have just finished contracting. As they relax, pressure inside them
drops and the SL valves close to prevent backflow from the aorta and pulmonary
trunk. The AV valves, which were already closed during ventricular contraction,
remain closed. Since all 4 valves are closed, volume of blood in the ventricles
does not change, and this is called the period of isovolumetric relaxation.
b. All 4 chambers continue to be relaxed, but the atria continue to fill
with blood. As the pressure in the atria rises above pressure in the
ventricles, the AV valves open and allow flow of blood down into the
ventricles. This flow at first is due to gravity and the pressure differential
(atria are not contracting yet), but most of the blood that will enter the
ventricles moves down at this time. This begins the ventricular filling period.
2.Atrial systole—both atria now contract; both
ventricles continue to be relaxed. Depolarization of the SA node causes
depolarization and contraction of the atria—(P wave on the ECG.) As atria begin to
contract pressure inside them rises, causing whatever blood remains in them to
be forced down into the ventricles. At the end of atrial systole, both
ventricles contain approximately 130 ml of blood (the end-diastolic volume or
EDV). Only about 25 ml of this is due to atrial systole. During this phase of
the cycle, the AV valves are open and the SL valves remain closed.
3. Ventricular systole--the impulse
that initiated atrial contraction reaches the ventricles—(QRS on the ECG).
Atria repolarize and relax. Ventricular systole begins and the AV valves close
(SL valves are already closed). For about .05 seconds all 4 valves are closed.
Since all the valves are closed the volume of blood remains the same in the
ventricles, so this is the period of isovolumetric contraction. Pressure is
building in the ventricles. Then the SL valves open and blood is ejected from
both ventricles--period of ventricular ejection. As the ventricular contraction
ends, the SL valves close and another relaxation period begins—this would be
the T wave on the ECG. At the end of the contraction, both ventricles still
contain about 60 ml of blood (end-systolic volume or ESV). During this phase,
the AV valves are closed and the SL valves are open.
At rest, the stroke volume (amount of
blood ejected from each ventricle) is about 70 ml---just slightly over half of
the blood the ventricle contained when systole began.
Auscultation is listening to sounds within
the body. A stethoscope is used. Sounds are primarily blood turbulence caused
by closing of the heart valves. 2 heart sounds are normally heard:
Lubb---as AV valves close (also called the S1 sound)
Dupp---as SL valves close (also called the S2 sound)
Each sound is best heard in a slightly
different location on the chest surface. An abnormal sound is called a
murmur and usually indicates a valve disorder.
Insufficiency---valve doesn’t close tightly and allows backflow
Stenosis---valve opening is narrowed and
it is hard for blood to flow through
The amount of blood the heart pumps
each minute is frequently adjusted to meet the needs of the cells at the time.
Cardiac output is the amount of blood ejected from the left ventricle into the
aorta each minute. The 2 factors that determine cardiac output are stroke
volume and the number of beats per minute.
Stroke volume X Rate
= Cardiac Output
70 ml X 75
= 5250 ml (5.25 liters)
Both stroke volume and rate increase
with exercise or decrease during sleep. They are constantly adjusted. Cardiac reserve is the ratio between maximum
possible cardiac output and output at rest. On the average, it is 4-5 times the
resting value. Athletes may increase 7-8 times. With severe heart disease there
may be little or no cardiac reserve.
3 factors regulate stroke volume in
different circumstances and ensure that the right and left ventricles pump
equal amounts of blood:
1. Preload--the stretch on cardiac
muscle fibers just before they contract. The greater the
stretch (due to filling with blood) the greater the force of contraction.
This is the Frank—Starling law of the heart, and its 2
major effects are:
a. Causes both ventricles to pump harder when increased cardiac output
is needed
b. Equalizes output of left and right
ventricles
Preload is proportional to the EDV, so:
c. When the resting heart rate is slow, stroke volume may increase as
the prolonged filling time allows greater amounts of blood to collect
d. Heart rate over 160—stroke volume decreases due to shortened filling
time
2. Contractility of myocardium
a. Positive inotropic agents increase contractility--increased blood Ca2+
level, sympathetic stimulation, epinephrine, digitalis
b. Negative inotropic agents decrease contractility--inhibitors of
sympathetic nervous system, anoxia, acidosis, certain
anesthetics, increased blood K+ level, calcium channel blockers
(type of blood pressure medication)
3. Afterload--pressure in the pulmonary
trunk and aorta that must be exceeded by pressure in the ventricles before any
blood can be pumped. When afterload increases (high BP, narrowed arteries)
stroke volume decreases and the heart must work harder.
1. Autonomic nervous control--from the
cardiovascular center of the medulla oblongata, which receives input from
sensory receptors and higher brain regions such as the limbic system and the
cerebral cortex:
a. Limbic system can increase rate even before activity begins—anxiety
or anticipation
b. Proprioceptors report movement of muscles and joints
c. Chemoreceptors monitor chemical changes in blood
d. Baroreceptors monitor blood pressure
All of this input is evaluated and the
cardiovascular center can send 2 types of output to the heart:
a. Sympathetic fibers extend from the medulla to the spinal cord. From
there, cardiac
accelerator nerves extend to the SA node, AV node and most of the myocardium.
Norepinephrine is released and binds to b receptors on cardiac muscle fibers. This speeds up the
rate of autorhythmic depolarization of the SA node and also increases
contractility.
b. Parasympathetic nerve impulses travel on the vagus nerve (X) to the
SA node, the AV node and atrial myocardium. They release acetylcholine, which
slows the rate of autorhythmic depolarization.
With no nerve stimulation of either
kind, the SA node would set a rate of about 100 beats/minute.
Most of the time, we send enough parasympathetic stimulation to slow the rate
to an average of 75 beats/minute. When we need to increase the rate, we can
reduce parasympathetic and also use sympathetic to increase the speed to a rate
above 100. Maximum vagal (parasympathetic) stimulation can even stop the heart
temporarily.
2. Chemical regulation
a. Hormones can increase rate and contractility--epinephrine,
norepinephrine, thyroid hormones
b. Ions
1) Decreased rate and contractility--elevated Na or K
2) Increased rate and contractility--elevated Ca
c. Miscellaneous---hypoxia and
acidosis/alkalosis all depress rate and contractility
3. Other factors
a. Age--up to 120 beats/minute normal in newborn, slows during
childhood, may increase in old age
b. Sex--females slightly higher rate than males
c. Physical condition--fitness decreases resting rate
d. Body temp--increase also increases heart rate. Considerable decrease
(hypothermia) slows heart rate and all metabolic activities.
HEART DISEASE is the number one cause of death in
this country. One in 5 persons who reach age 60 will have a heart attack, and
other disorders are also very common. Risk factors in heart disease are:
1. High blood cholesterol 5. Lack of regular exercise
2. High blood pressure 6. Diabetes mellitus
3. Cigarette smoking 7. Heredity
4. Obesity 8. Male
gender
Some
of these can be modified.
BLOOD CHOLESTEROL---we all know high blood cholesterol
is bad for your heart—but what specifically does it do? It can promote growth
of fatty plaques in the walls of arteries. In addition to deposits of
cholesterol, cells of the artery wall can react by increasing in number and
further contribute to narrowing the lumen of the artery. All of this also
increases the chance of an inappropriate clot (thrombus) forming, and can
contribute to heart attacks or strokes.
When
you have your blood cholesterol checked, if the result is given to you as one
number, this is your total blood cholesterol. While this is a good indication
of your status, additional information is also important. Levels of several
different kinds of cholesterol are added together to get that total, and just
what percentage of the total each kind represents is significant. A more
complete test is called a lipid profile.
To
understand the next section, you need to know that all lipids are insoluble in
water (and also in blood plasma). In order to transport lipids from one part of
the body to another, the lipid must be combined with a special protein called a
transport protein. The combination is water-soluble even though the lipid alone
is not. The combination is called a lipoprotein and we are concerned with 3
types:
1.
Low-density
lipoprotein (LDL)—this type delivers cholesterol to body cells for use in
making plasma membranes (all cells need it for this) and in some cells for use
in synthesizing steroids and bile salts. Unfortunately, on the way to cells
this type is likely to drop some of its cholesterol, which then forms a deposit
on the artery wall. This type is called “bad cholesterol.”
2.
High-density
lipoprotein (HDL)—this type removes excess cholesterol from cells and
transports it to the liver, which can remove it from the body. This prevents accumulation
of excess cholesterol in the blood. HDLs may even pick up deposited cholesterol
from artery walls and carry it away. This is called “good cholesterol.”
3.
Very
low-density lipoprotein (VLDL)—transport triglycerides from the liver to
adipose cells for storage. VLDLs may be converted to LDLs.
Cholesterol
may either be taken in as such (eggs, dairy products, red meat, etc. are high
in it) or synthesized by the liver from fats, especially saturated fats. Blood
cholesterol is measured in milligrams per deciliter (1/10 of a liter).
Desirable levels are:
Total cholesterol below
200. Above 200 the risk of heart attack doubles with every 50 mg
increase.
¨
LDLs
under 130
¨
HDLs
over 40
¨
Triglycerides
10-190
The
risk ratio compares the total cholesterol number to the HDL number. The HDL
number is divided into the total number and the result should be below 4. For
example:
Total 180 divided by an HDL of 60 = Risk
ratio of 3 (very good)
Blood
cholesterol may be reduced by improved diet, weight loss and increased exercise
in many cases. Medications are also available. Increased exercise has these
beneficial effects also:
1. Increase in maximum cardiac output—this
strengthens the heart and increases stroke volume while resting heart rate
decreases
2. Decrease in triglycerides and LDLs
3. Increase in HDLs
4. Improved lung function
5. Reduced blood pressure
6. Less anxiety and depression
7. Weight loss
8. Increased ability to dissolve clots
9. Increased levels of endorphins (natural
painkillers)
10. Stronger bones
1. Angina pectoris---chest pain due to
cardiac ischemia (insufficient blood flow to cardiac muscle). This results in
hypoxia of cells, which weakens them but does not kill them. This pain usually
appears during exertion and disappears with rest.
2. Myocardial infarction (heart attack)---this is death of tissue due to loss of blood flow. It
may result from a thrombus, an embolus or a spasm of a coronary artery. Heart
muscle is replaced by scar tissue. If the infarction disrupts the conduction
system, sudden death may result due to ventricular fibrillation or cardiac
arrest. If a large area of the heart muscle is affected, the attack may also be
fatal.
3. Heart murmurs---abnormal heart
sounds—some are harmless
a. Mitral valve stenosis---narrowing of
mitral valve
b. Mitral insufficiency---valve allows
backflow into atrium
c. Aortic stenosis---narrowing of aortic
SL valve
d. Mitral valve prolapse---portion of
mitral valve is pushed back too far into the atrium during ventricular
contraction
4. Congestive heart failure---heart fails
due to problems such as coronary artery disease, congenital defects, long-term
high BP, valve disorders, myocardial infarctions. The ventricles are not able
to pump effectively enough to meet needs. Fluid accumulated in tissues as blood
backs up—in lungs if
5. Arrhythmias (dysrhythmias)---abnormality or irregularity of heart rhythm. They result
from a disturbance in the conduction system, either in the generation of
impulses or their conduction. Causes include excess caffeine, nicotine,
alcohol, certain drugs, hyperthyroidsim, and K+ deficiency. Serious arrhythmias
could result in cardiac arrest.
a.
Heart
block—BE SURE TO NOTE THAT THIS CONCERNS THE CONDUCTION SYSTEM, NOT THE FLOW OF
BLOOD!!!---most common in the AV node but is a blockage of impulses anywhere
between the SA node and the ventricular myocardium. Effects vary due to
location and severity of the block.
b.
Atrial
flutter---rapid inefficient atrial contractions
c.
Atrial
fibrillation---atrial muscle fibers contract out of rhythm so no effective
pumping occurs. An otherwise healthy heart can continue to function
d.
Ventricular
fibrillation---most serious arrhythmia. Causes death rapidly unless corrected.
Muscle fibers of the ventricles do contract, but not together and not at the
proper time. The result is that the heart is unable to pump blood.
Defibrillation is passage of a strong electrical current across the chest. It
temporarily stops all contractions and the idea is that when ventricular
contraction begins again it will be normal.
Be sure to look over the treatments for “unblocking”
coronary arteries on p. 728.