Chapter 20
THE CARDIOVASCULAR SYSTEM: THE HEART
I. INTRODUCTION
A. The cardiovascular system consists of the blood, heart, and blood vessels.
B. The heart is the pump that circulates the blood through an estimated 60,000 miles of blood vessels.
C. The study of the normal heart and diseases associated with it is known as cardiology.
II. LOCATION AND SURFACE PROJECTION OF THE HEART
A. The heart is situated between the lungs in the mediastinum with about two-thirds of its mass to the
left of the midline.
B. Determining an organ’s surface projection involves outlining its dimensions with respect to
landmarks on the surface of the body.
C. Because the heart lies between two rigid structures, the vertebral column and the sternum, external
compression on the chest can be used to force blood out of the heart and into the circulation.
III. STRUCTURE AND FUNCTION OF THE HEART
A. Pericardium
1. The heart is enclosed and held in place by the pericardium.
a. The pericardium consists of an outer fibrous pericardium and an inner serous
pericardium.
b. The serous pericardium is composed of a parietal layer and a visceral layer.
c. Between the parietal and visceral layers of the serous pericardium is the pericardial
cavity, a potential space filled with pericardial fluid that reduces friction between the
two membranes.
d. A fibrous pericardium made up of dense irregular connective tissue. It functions
to:
1)To hold the heart in place.
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2)To prevent over distension.
3)To protect the heart.
2. An inflammation of the pericardium is known as pericarditis. Associated bleeding into the
pericardial cavity compresses the heart (cardiac tamponade) and is potentially lethal.
B. Layers of the Heart Wall
1. The wall of the heart has three layers: epicardium, myocardium, and endocardium.
2. The epicardium consists of mesothelium and connective tissue, the myocardium is composed
of cardiac muscle, and the endocardium consists of endothelium and connective tissue.
Three layers of tissue
3. Epicardium: This serous membrane of smooth outer surface of heart
4. Myocardium: Middle layer composed of cardiac muscle cell and responsibility for heart
contracting
5. Endocardium: Smooth inner surface of heart chambers
C. Chambers of the Heart
1. The chambers of the heart include two upper atria and two lower ventricles.
2. On the surface of the heart are the auricles and sulci.
a. The auricles are small pouches on the anterior surface of each atrium that slightly
increase the capacity of each atrium.
b. The sulci are grooves that contain blood vessels and fat and separate the chambers.
The Chambers
•
The heart has four chambers.
•
The right and left atria receive blood flowing to the heart. Each atrium has a small, earlike
extension called an auricle that slightly increases its volume.
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The two inferior chambers, the left and right ventricles, pump the blood into the arteries for
distribution elsewhere.
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Other features of the heart include the atrioventricular sulcus, the anterior and posterior
interventricular sulci, the interatrial septum, and the interventricular septum.
3. Right Atrium
a. The right atrium receives blood from the superior and inferior vena cava and the
coronary sinus.
b. In the septum separating the right and left atria is an oval depression, the fossa ovalis,
which is the remnant of the foramen ovale.
c. Blood passes from the right atrium into the right ventricle through the tricuspid valve.
4. Right Ventricle
a. The right ventricle forms most of the anterior surface of the heart.
b. Blood passes from the right ventricle to the pulmonary trunk via the pulmonary
semilunar valve.
5. Left Atrium
a. The left atrium receives blood from the pulmonary veins.
b. Blood passes from the left atrium to the left ventricle through the bicuspid (mitral)
valve.
6. Left Ventricle
a. The left ventricle forms the apex of the heart.
b. Blood passes from the left ventricle through the aortic semilunar valve into the aorta.
c. During fetal life the ductus arteriosus shunts blood from the pulmonary trunk into the
aorta. At birth the ductus arteriosus closes and becomes the ligamentum arteriosum.
D. Myocardial Thickness and Function
1. The thickness of the myocardium of the four chambers varies according to the function of
each chamber.
2. The atria walls are thin because they deliver blood to the ventricles.
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3. The ventricle walls are thicker because they pump blood greater distances.
a. The right ventricle walls are thinner than the left because they pump blood into the
lungs, which are nearby and offer very little resistance to blood flow.
b. The left ventricle walls are thicker because they pump blood through the body where
the resistance to blood flow is greater.
E. The fibrous skeleton of the heart forms the foundation for which the heart valves attach, serves as
points of insertion for cardiac muscle bundles, prevents overstretching of the valves as blood passes
through them, and acts as an electrical insulator that prevents direct spread of action potentials from
the atria to the ventricles.
Fibrous Skeleton
•
Muscle fibers are bound together by a fibrous skeleton that
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provides support for the heart,
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gives the muscle something to pull against, and
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limits the routes by which electrical activity can travel through the heart.
F. Operation of Heart Valves
1. Valves open and close in response to pressure changes as the heart contracts and relaxes.
2. Atrioventricular Valves
a. Atrioventricular (AV) valves prevent blood flow from the ventricles back into the
atria.
b. Back flow is prevented by the contraction of papillary muscles tightening the chordae
tendinae which prevent the valve cusps from everting.
3. Semilunar Valves
a. The semilunar (SL) valves allow ejection of blood from the heart into arteries but
prevent back flow of blood into the ventricles.
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b. Semilunar valves open when pressure in the ventricles exceeds the pressure in the
arteries.
c. Certain infectious diseases, such as rheumatic fever, can damage or destroy heart
valves.
The Valves
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Valves prevent the backflow of blood into the heart.
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The pulmonary valve guards the opening from the right ventricle to the pulmonary
trunk. The aortic valve guards the opening from the left ventricle to the aorta. Both
of these valves are called semilunar valves because of the moonlike shape of their
three cusps. Their function is to prevent backflow from the aorta and pulmonary
trunk into the ventricles.
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An atrioventricular (AV) valve guards the opening between each atrium and
ventricle. The right AV valve is also known as the tricuspid valve; the left is also
called the bicuspid or mitral valve. Stringlike chordae tendineae attach the valve
cusps to papillary muscles. Their function is to prevent backflow of blood from the
ventricles into the atria.
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The opening and closing of the heart valves is the result of pressure gradients from
one side of the valve cusps to the other.
IV. CIRCULATION OF BLOOD
A. Systemic and Pulmonary Circulations
1. The left side of the heart is the pump for the systemic circulation. It pumps oxygenated blood
from the lungs out into the vessels of the body.
2. The right side of the heart is the pump for the pulmonary circulation. It receives
deoxygenated blood from the body and sends it to the lungs for oxygenation.
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B. Coronary Circulation
1. The flow of blood through the many vessels that pierce the myocardium of the heart is called
the coronary (cardiac) circulation; it delivers oxygenated blood and nutrients to and removes
carbon dioxide and wastes from the myocardium.
2. The principal arteries, branching from the ascending aorta and carrying oxygenated blood,
are the right and left coronary arteries.
3. Deoxygenated blood returns to the right atrium primarily via the principal vein, the coronary
sinus.
The Coronary Circulation
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Although the heart accounts for a tiny fraction of the body’s weight, it uses 5% of its output to
supply its own needs.
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The myocardium has an extensive network of coronary arteries to ensure an adequate blood
supply to itself.
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The first branches off the aorta are the left and right coronary arteries.
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The left coronary artery supplies blood to the left side of the heart and divides into the
anterior interventricular and circumflex arteries.
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The right coronary artery supplies blood to the right side of the heart and divides into
the marginal and posterior interventricular arteries.
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A myocardial infarction occurs when any of the coronary arteries become occluded with plaque
and a portion of the heart muscle dies from lack of blood flow. Partial obstruction of blood
flow to the heart may result in myocardial ischemia. This is can be accompanied by angina
pectoris which is a severe pain brought about by myocardial ischemia.
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V. CARDIAC MUSCLE AND THE CARDIAC CONDUCTION SYSTEM
A. Histology of Cardiac Muscle
1. Compared to skeletal muscle fibers, cardiac muscle fibers are shorter in length, larger in
diameter, and squarish rather than circular in transverse section. They also exhibit
branching.
2. Cardiac muscles have the same arrangement of actin and myosin, and the same bands,
zones, and Z discs as skeletal muscles.
3. They do have less sarcoplasmic reticulum than skeletal muscles and require Ca+2 from
extracellular fluid for contraction.
4. They form two separate functional networks in the heart: the atrial and the ventricular
networks.
a. Fibers within the networks are connected by intercalated discs, which consist of
desmosomes and gap junctions.
b. The intercalated discs allow the fibers in the network to work together so that
each network serves as a functional unit.
Cardiac Muscle and the Cardiac Conduction System
•
Structure of Cardiac Muscle
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Cardiac muscle cells (myocytes or cardiocytes) are different from skeletal muscle fibers
in that they are relatively short, thick, branching cells that have one nucleus.
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The sarcoplasmic reticulum (SR) is less developed and lacks terminal cisternae, but T
tubules are larger than in skeletal muscle.
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Each myocyte is surrounded by a connective tissue endomysium, which allows access to
blood capillaries.
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The myocytes are joined end-to-end by intercalated discs, which have three
distinct features: The plasma membranes of the adjacent cells display
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interdigitating folds; two forms of mechanical junctions tightly join the cells; and
there are electrical gap junctions between the cells.
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Mitochondria are larger and more numerous in cardiac muscle compared to skeletal
muscle.
Metabolism of Cardiac Muscle
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At rest, the heart gets 60% of its energy from fatty acids, 35% from glucose, and 5% from
other fuels such as ketones, lactic acid, and amino acids. Cardiac muscle is more vulnerable
to oxygen deficiency than it is to a lack of fuel.
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Heart muscle is not prone to fatigue because it makes little use of anaerobic fermentation or the
oxygen debt mechanism.
B. Autorhythmic Cells: The Conduction System
1. Cardiac muscle cells are autorhythmic cells because they are self-excitable. They repeatedly
generate spontaneous action potentials that then trigger heart contractions.
a. These cells act as a pacemaker to set the rhythm for the entire heart.
b. They form the conduction system, the route for propagating action potential
through the heart muscle.
2. Components of this system are the sinoartrial (SA) node (pacemaker), atrioventricular (AV)
node, atrioventricular bundle (bundle of His), right and left bundle branches, and the
conduction myofibers (Purkinje fibers).
3. Signals from the autonomic nervous system and hormones, such as epinephrine, do modify
the heartbeat (in terms of rate and strength of contraction), but they do not establish the
fundamental rhythm.
The Cardiac Conduction System
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Vertebrate hearts are myogenic because the pacemaker is in the heart itself, and the autonomic
nervous system can only modify heart rate.
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Cardiac myocytes are autorhythmic. Some of them lose their ability to contract and become
specialized for generating and transmitting action potentials. These make up the cardiac
conduction system.
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The cardiac conduction system begins with the sinoatrial (SA) node, which serves as the
pacemaker. Signals from the SA node spread throughout the atria and on to the atrioventricular
(AV) node near the lower interatrial septum. The AV node is an electrical gateway to the
ventricles. The AV bundle leaves the AV node and divides into right and left bundle branches
leading into the interventricular septum. Next the impulse is spread to the Purkinje fibers.
C. Timing of Atrial and Ventricular Excitation
1. From the SA node, a cardiac action potential travels throughout the atrial muscle and down to
the AV node where it slows considerably because the fibers there have a smaller diameter.
This gives the atria time to completely contract before ventricular contraction begins.
2. An artificial pacemaker may be used to restore cardiac rhythm due to disruption of
components of the conduction system.
Electrical and Contractile Activity of the Heart
•
The Cardiac Rhythm
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The normal heartbeat generated by the SA node is called the sinus rhythm, and shows a
resting rate of 70–80 bpm. The SA node tends to speed up, and the vagus nerve keeps a
brake on heart rate.
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Sometimes regions other than the SA node fire spontaneously; these are called ectopic
foci.
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Any abnormal cardiac rhythm is called arrhythmia.
Impulse Conduction to the Myocardium
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SA nodes fires and the atria depoarize.
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The Atria contract.
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The wave of depolarization reaches the AV node and is delayed one tenth of a second.
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The AV bundle depolarized.
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The right and left bundle branches depolarize.
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The Purkinje fibers depolarize.
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The ventricles depolarize.
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The ventricles contract.
D. Physiology of Cardiac Muscle Contraction
1. An impulse in a ventricular contractile fiber is characterized by rapid depolarization, plateau,
and repolarization.
2. The refractory period of a cardiac muscle fiber (the time interval when a second contraction
cannot be triggered) is longer than the contraction itself.
Electrical Behavior of the Myocardium
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Contractile myocytes exhibit action potentials that are different from neurons or skeletal muscle.
They have a stable RMP of –90 mV and depolarize only when stimulated. The influx of sodium
ions and depolarization of the myocytes is similar to that seen in neurons.
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Depolarization of a myocyte, with its sparse SR, causes release of supplemental calcium ions
from the ECF. Unlike cardiac muscle, the SR of skeletal muscle contains sufficient calcium.
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In skeletal muscle and neurons, an action potential falls back to RMP within 2 msec, but in
cardiac muscle, slow calcium channels remain open longer (after sodium channels close),
prolonging the depolarization of the cell (250 msec). As long as the action potential is in its
plateau and calcium is entering the myocytes, the myocytes contract. These plateaus are more
pronounced in the ventricles.
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Cardiac muscle has an absolute refractory period of 250 msec, compared with 1–2 msec in
skeletal muscle.
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There is no tetany in cardiac muscle.
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VI. ELECTROCARDIOGRAM
A. Impulse conduction through the heart generates electrical currents that can be detected at the surface
of the body. A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is
called an electrocardiogram (ECG or EKG).
1. The ECG helps to determine if the conduction pathway is abnormal, if the heart is
enlarged, and if certain regions are damaged.
B. In a typical Lead II record, three clearly visible waves accompany each heartbeat.
1. A normal ECG consists of a P wave (atrial depolarization - spread of impulse from SA
node over atria), QRS complex (ventricular depolarization - spread of impulse through
ventricles), and T wave (ventricular repolarization).
2. The P-Q (PR) interval represents the conduction time from the beginning of atrial
excitation to the beginning of ventricular excitation.
3. The S-T segment represents the time when ventricular contractile fibers are fully
depolarized, during the plateau phase of the impulse.
D. An arrhythmia is an abnormality or irregularity in the heart rhythm resulting from a disturbance in
the conduction system of the heart, due either to faulty production of electrical impulses or to poor
conduction of impulses as they pass through the system. Examples of arrhythmias include heart
block (most commonly atrioventricular block), flutter, fibrillation, and premature ventricular
contraction (PVC).
VII. THE CARDIAC CYCLE
A. A cardiac cycle consists of the systole (contraction) and diastole (relaxation) of both atria, rapidly
followed by the systole and diastole of both ventricles .
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Blood Flow, Heart Sounds, and the Cardiac Cycle
•
The cardiac cycle consists of one complete cycle of contraction and relaxation. Its major events,
in order of occurrence, are: atrial systole, atrial diastole, ventricular systole, ventricular
diastole, and a quiescent period.
Principles of Pressure and Flow
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Pressure is often measured by observing how high it can push a column of mercury (Hg) up a
manometer—e.g., blood pressure is usually measured with a sphygmomanometer.
•
Any change in the volume of a container creates a pressure gradient. Pressure gradients cause the
alternate opening and closing of heart valves.
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There is always a positive blood pressure in the aorta, and if it is greater than the pressure in the
ventricle, it holds the aortic valve closed and prevents the backflow of blood. When continuing
ventricular contraction causes its internal pressure to rise above aortic pressure, the valve is
forced open, and blood enters the aorta.
B. The phases of the cardiac cycle are (1) the relaxation (or quiescent) period, (2) ventricular filling,
and (3) ventricular systole.
C. The act of listening to sounds within the body is called auscultation, and it is usually done with a
stethoscope. The sound of a heartbeat comes primarily from the turbulence in blood flow caused by
the closure of the valves, not from the contraction of the heart muscle.
1. The first heart sound (lubb) is created by blood turbulence associated with the closing of the
atrioventricular valves soon after ventricular systole begins.
2. The second heart sound (dupp) represents the closing of the semilunar valves close to the end
of the ventricular systole.
3. A heart murmur is an abnormal sound that consists of a flow noise that is heard before,
between, or after the lubb-dupp or that may mask the normal sounds entirely. Some murmurs
are caused by turbulent blood flow around valves due to abnormal anatomy or increased
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volume of flow. Not all murmurs are abnormal or symptomatic, but most indicate a valve
disorder.
Phases of the Cardiac Cycle
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Quiescent period. The cardiac cycle begins with the quiescent period in which the heart is at
rest (all chambers in diastole). Blood is flowing into the atria, and AV valves are open, allowing
blood to passively flow through to the ventricles (90ml)
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Atrial systole. The SA nodes fires and atrial systole (contraction) results. 40 ml of blood is
pumped into the ventricles. The total amount of blood in the ventricles is 130ml. This is
known as the end diastolic volume (the amount of blood in the ventricles at the end of
ventricular diastole).
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Isovolumetric contraction of the ventricles occurs after the ventricles depolarize. The AV
valves close as ventricular blood surges back against the cusps. The first heart sound is heard.
This phase is called isovolumetric because the ventricles do not yet eject blood and there is no
change in their volume even though they are contracting.
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Ventricular ejection. Next comes ventricular ejection, in which the amount known as stroke
volume passes into the major vessels on top of the heart. Stroke volume is the amount of
blood pumped by each ventricle with each contraction (70 ml). The 60 ml of blood left in
the ventricles is known as the end systolic volume.
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Isovolumetric relaxation. Isovolumetric relaxation and ventricular filling follow, completing
one cardiac cycle. All valves are closed. Note the dicrotic notch.
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Ventricular filling. Ventricular diastole occurs, the atrioventricular valves are open, and blood
flows into the ventricles. Rapid ventricular filling, diastasis, and atrial systole.
Overview of Volume Changes
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Viewing the balance sheet, it is evident that the ventricle pumps out as much blood as it received
during diastole.
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The two ventricles eject the same amount of blood, but pressure is less in the right ventricle than
in the left.
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The left ventricle contracts with greater force to overcome the arterial pressure of the systemic
circuit.
VIII. CARDIAC OUTPUT
A. Since the body’s need for oxygen varies with the level of activity, the heart’s ability to discharge
oxygen-carrying blood must also be variable. Body cells need specific amounts of blood each minute
to maintain health and life.
B. Cardiac output (CO) is the volume of blood ejected from the left ventricle (or the right ventricle)
into the aorta (or pulmonary trunk) each minute.
1. cardiac output equals the stroke volume, the volume of blood ejected by the ventricle with
each contraction, multiplied by the heart rate, the number of beats per minute.
2. Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and
the cardiac output at rest.
Cardiac Output
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Cardiac output (CO) is the volume pumped by each ventricle per minute. A person's
cardiac reserve is the difference between maximum and resting cardiac output. Typical cardiac
reserve for is four or five times the resting cardiac output. For top endurance athletes this
increases to 7 or 8 times the resting cardiac output. Agents that raise and lower the heart rate are
called positive and negative chronotropic agents; agents that alter the stroke volume of the
ventricles are called inotropic agents.
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CO
=
SV
X
Hr
(ml/min)
(ml/beat)
(beats/min)
5.25 L/min
70 ml/beat
75 beats/min
C. Regulation of Stroke Volume
1. Three factors regulate stroke volume: preload, the degree of stretch in the heart before it
contracts; contractility, the forcefulness of contraction of individual ventricular muscle
fibers; and afterload, the pressure that must be exceeded if ejection of blood from the
ventricles is to occur.
a. Preload: Effect of Stretching
1) According to the Frank-Starling law of the heart, a greater preload (stretch)
on cardiac muscle fibers just before they contract increases their force of
contraction during systole.
Preload (End diastolic Volume (EDV)
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Preload is the amount of tension in the ventricular myocardium immediately before it begins to
contract.
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As more blood enters the heart, it stretches the myocardium. Due to the length-tension
relationship, moderate stretch enables myocytes to generate more tension during contraction. If
the ventricles contract more forcefully, they expel more blood, thus adjusting cardiac output to
the increase in venous return.
•
This relationship is summarized by the Frank-Starling law of the heart, which states, in
essence, that the ventricles tend to pump out all the blood that entered them.
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Preload is determined by two factors: (1) the duration of ventricular diastole and (2)
venous return.
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2) The Frank-Starling law of the heart equalizes the output of the right and left
ventricles and keeps the same volume of blood flowing to both the systemic
and pulmonary circulations.
b. Myocardial contractility, the strength of contraction at any given preload, is affected
by positive and negative inotropic agents.
1) Positive inotropic agents increase contractility and negative inotropic
agents decrease contractility.
2) Thus, for a constant preload, the stroke volume increases when positive
inotropic agents are present and decreases when negative inotropic agents
are present.
Contractility
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The contractility of the myocardium refers to its strength of contraction for a given preload.
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Contractility can increase as a result of inotropic factors that make the myocytes more
responsive to stimulation, such as calcium, epinephrine, norepinephrine, glucagon and
sympathetic stimulation.
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Negative inotropic agents include myocardial hypoxia, hypercapnia, acidosis, and
barbiturates.
c. The pressure that must be overcome before a semilunar valve can open is the
afterload.
Afterload
The blood pressure in the arteries just outside the semilunar valves is called the
afterload.
Afterload opposes the opening of these valves, so an increased afterload reduces stroke
volume. Anything that impedes arterial circulation (scar tissue in the lungs, for example)
can increase the afterload.
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As the ventricle works harder to overcome the resistance, it hypertrophies. Stress and
hypertrophy of a ventricle can eventually cause it to weaken and fail. Look up
hypertension.
2. In congestive heart failure, blood begins to remain in the ventricles increasing the preload
and ultimately causing an overstretching of the heart and less forceful contraction.
D. Regulation of Heart Rate
1. Cardiac output depends on heart rate as well as stroke volume. Changing heart rate is the
body’s principal mechanism of short-term control over cardiac output and blood pressure.
Several factors contribute to regulation of heart rate.
2. Nervous control of the cardiovascular system stems from the cardiovascular center in the
medulla oblongata.
a. Proprioceptors, baroreceptors, and chemoreceptors monitor factors that influence the
heart rate.
b. Sympathetic impulses increase heart rate and force of contraction; parasympathetic
impulses decrease heart rate.
3. Heart rate is also affected by hormones (epinephrine, norepinephrine, thyroid hormones),
ions (Na+, K+, Ca+2), and other factors such as age, gender, physical fitness, and temperature.
Factors Affecting Heart Rate
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The resting heart rate of an adult is 64–72 in males and 72–80 in females. In infants, it is 120
bpm or more.
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Tachycardia is a persistent, resting heart rate above 100 bpm. This can be caused by anxiety,
drugs, heart disease, or elevated body temperature.
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The opposite condition, bradycardia, is a persistent resting adult heart rate of less than 60 bpm.
This can be seen in well-conditioned athletes, but can also indicate hypothermia and occurs with
immersion of the face in water.
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•
The autonomic nervous system can have chronotropic effects on the heart rate, both positive
and negative.
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The cardiac center of the medulla oblongata receives input from the cerebral cortex,
limbic system, and hypothalamus; many sensory and emotional stimuli can alter heart
rate.
•
The cardiac center also monitors the condition of the body through input received from
proprioceptors, chemoreceptors, and baroreceptors, and can adjust heart rate
accordingly.
•
The cardiac center is divided into a cardioacceleratory center and a cardioinhibitory
center that connect by nerves to the SA node.
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Certain chemicals also have chronotropic effects.
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Sympathetic neurotransmitters and adrenal gland hormones can accelerate heart rate,
as can arousal and stress.
•
Chemicals that lower heart rate include sodium (in hypernatremia) and potassium (in
hyperkalemia), the latter of which can kill.
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Hypercalcemia reduces heart rate, and hypocalcemia increases it.
.
IX. EXERCISE AND THE HEART
A. Sustained exercise increases oxygen demand in muscles.
B. Among the benefits of aerobic exercise (any activity that work large body muscles for at least 20
minutes, preferably 3-5 times per week) are increased cardiac output, increased HDL and decreased
triglycerides, improved lung function, decreased blood pressure, and weight control.
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Exercise and Cardiac Output
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The act of exercise increases cardiac output because proprioceptors signal the cardiac center that
the muscles are active and need more oxygen delivery and carbon dioxide removal. During
exercise, venous return to the heart increases, which increases preload on the heart.
•
A sustained program of exercise causes hypertrophy of the ventricles, which increases their
stroke volume and lowers heart rate. Athletes have greater cardiac reserve, so they can tolerate
more exertion than a sedentary person can.
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Other benefits of exercise include:
•
An increased hematocrit.
•
An increase in the number of capillaries to tissues.
•
Increased HDL levels.
•
Decreased triglyceride levels.
•
Decreased blood pressure.
•
Reduced stress, depression, and anxiety.
•
Increased fibrinolytic activity.
DEVELOPMENTAL ANATOMY OF THE HEART
A. The heart develops from mesoderm before the end of the third week of gestation.
B. The endothelial tubes develop into the four-chambered heart and great vessels of the heart.
XI. DISORDERS: HOMEOSTATIC IMBALANCES
A. Coronary artery disease (CAD), or coronary heart disease (CHD), is a condition in which the heart
muscle receives an inadequate amount of blood due to obstruction of its blood supply. It is the
leading cause of death in the United States each year. The principal causes of obstruction include
atherosclerosis, coronary artery spasm, or a clot in a coronary artery.
1. Risk factors for development of CAD include high blood cholesterol levels, high blood
pressure, cigarette smoking, obesity, diabetes, “type A” personality, and sedentary lifestyle.
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2. Atherosclerosis is a process in which smooth muscle cells proliferate and fatty substances,
especially cholesterol and triglycerides (neutral fats), accumulate in the walls of the mediumsized and large arteries in response to certain stimuli, such as endothelial damage.
3. Diagnosis of CAD includes such procedures as cardiac catherization and cardiac
angiography.
4. Treatment options for CAD include drugs and coronary artery bypass grafting.
B. Myocardial Ischemia and Infarction
1. Partial obstruction of blood flow in the coronary arteries may cause myocardial ischemia.
a. Ischemia usually causes hypoxia which may weaken cells without killing them.
b. Angina pectoris is a severe pain that usually, but not always, accompanies
myocardial ischemia.
2. A complete obstruction to blood flow may result in myocardial infarction (MI), commonly
called a heart attack.
a. Infarction means death of an area of tissue because of an interrupted blood supply.
b. The resulting damage may be so extensive that death results.
C. Congenital Heart Defects
1. A congenital defect is a defect that exists at birth, and usually before birth.
2. Congenital defects of the heart include coarctation of the aorta, patent ductus arteriosus,
septal defects (interatrial or interventricular), valvular stenosis, and tetralogy of Fallot.
a. Some congenital defects are not serious or remain asymptomatic; others heal
themselves.
b. A few congenital defects are life threatening and must be corrected surgically.
Fortunately, surgical techniques are highly refined for most of the defects listed.
D. Congestive heart failure is a chronic or acute state that results when the heart is not capable of
supplying the oxygen demands of the body.
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