

THE HEART
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Major Function:
Propulsion of blood through the body
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Size:
Approximately the size of a fist, weighs less than a pound
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Location:
The mediastinum (the medial cavity of the thorax)
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Orientation:
Apex points towards the left hip; base points towards the right shoulder
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Tissue Composition:
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PERICARDIUM Covers
the heart
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Fibrous pericardium
superficial portion
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Composed of dense
connective tissue
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Protects and
anchors the heart; prevents overfilling of heart
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Serous pericardium
deep portion
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Composed of
squamous epithelium and areolar connective tissue
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Two layers of
serous pericardium:
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Parietal layer
lines internal face of fibrous pericardium
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Visceral layer (Aka,
epicardium) lines the external heart surface
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Between the
parietal and visceral layer is the pericardial cavity, containing the
serous fluid that reduces friction.
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LAYERS OF THE HEART WALL
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Epicardium
superficial layer infiltrated with adipose tissue
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Myocardium
middle layer
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Composed of:
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Cardiac muscle
contraction
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Connective
tissue fibers reinforces cardiac muscles; provides structural
support and resists stretching; limits the direct spread of action
potentials across the heart to specific pathways (the intrinsic
conduction system)
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Endocardium
innermost layer
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Composed of
squamous epithelium and connective tissue
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Lines the heart
chambers and covers the fibrous skeleton of valves
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Continuous with
the endothelial linings of the blood vessels
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Chambers of the Heart
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The heart has four chambers: 2 receiving and 2 discharging
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Receiving Chambers
The atria
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Relatively small
and thin-walled
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Atria are
separated by the interatrial septum (the fossa ovalis is found here)
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Each atrium is
covered by an auricle, which increases the volume of the chambers
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The anterior walls
of each atrium is contains the ridged pectinate mucles
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Discharging Chambers
The ventricles
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The ventricular
walls are thicker due to their role in blood propulsion
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Right ventricle
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Relatively
smaller than the left ventricle
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Forms most of
the hearts anterior surface
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Left ventricle
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Larger than
the right ventricle
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Forms most of
the hearts posterorinferior surface
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Walls are
thicker because it must pump blood to the systemic circulation
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The ventricles
make up most of the heart volume
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Ventricles are
separated by the interventricular septum
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Ventricular walls
contain:
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Trabeculae
carnea irregular ridges of mucle
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Papillary
muscles fingerlike projections of muscle that aid in valve function
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Heart Valves
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The major function of heart valves is to prevent the backflow of blood.
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The heart contains two sets of valves: atrioventricular valves and semilunar
valves.
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Atrioventricular (AV)
valves
located at the atrial-ventricular junctions
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The heart has two AV
valves:
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Tricuspid valve
located on the right
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Bicuspid (mitral)
valve
located on the left
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When the heart is
relaxed, the AV valves are open; when the heart contracts, the AV valves
are closed
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Semilunar (SL) valves
located at the bases of the large arteries issuing from the ventricles
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The heart has two
semilunar valves:
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Pulmonary
semilunar (SL) valve
guards the entrance of the pulmonary trunk
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Aortic semilunar
(SL) valve
guards the entrance of the aorta
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When the heart is
relaxed, the SL valves are closed; when the heart contracts, the SL valves
are open
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Coronary circulation
the functional blood supply of the heart
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Provides the nourishment to heart tissue
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Divided into the left and right coronary arteries and veins
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The coronary arteries deliver blood when the heart is relaxed.
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The coronary sinus delivers poorly oxygenated blood from the myocardium to
the right atrium.
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Pulmonary vs. Systemic
Circulation
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Pulmonary circulation right side of the heart; responsible for gas
exchange
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Systemic circulation left side of the heart; it is responsible for
transporting blood to and from the tissues of the body.
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Walls of the left
ventricle are thicker and can generate high pressure
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Pathway of Blood through
the Heart
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The right atrium receives poorly oxygenated blood from the inferior and
superior vena cava and the coronary sinus.
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The blood from the right atrium drains into the right ventricle. (Tricuspid
valve open/Pulmonary SL valve closed)
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Following ventricular filling, the blood is forced through the pulmonary
trunk. (Tricuspid valve closed/Pulmonary SL valve open)
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The blood flows from the pulmonary trunk to the lungs where it is
oxygenated.
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Oxygenated blood is delivered to the heart via the pulmonary arteries.
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The pulmonary arteries deliver blood to the left atrium.
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The blood in the left atrium drains into the left ventricle. (Biscupid (mitral)
valve open/Aortic SL valve closed)
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Following ventricular filling, the blood is forced through the aorta.
(Bicuspid (mitral) valve closed/Aortic SL valve open)
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Once the blood leaves the aorta, it is carried to the rest to the body.
- Once
depleted of the oxygen and nutrients it contains, the blood leaves the
tissues and eventually drains into the superior or inferior vena cava or the
coronary sinus.
- Properties of
Cardiac Muscle Fibers
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Microscopic Anatomy
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Cardiac cells are
short, fat, branched, interconnected, and striated
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Each cardiac muscle
fiber contains one or two large, centrally located nuclei.
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The sarcomeres of
cardiac cells contain actin and myosin microfilaments
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Intercellular spaces
are filled with loose connective tissue and capillaries
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Cardiac cells are
connected by specialized cell junctions, called intercalated discs.
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Intercalated discs
contain:
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Desmosomes
prevent adjacent cells from separating during contraction
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Gap junctions
allow ions to pass from cell to cell
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Causes the myocardium to act as a functional syncytium (a single
coordinated unit).
- Energy requirements
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Cardiac cells are highly dependent on oxygen for metabolic needs
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Cardiac muscle relies almost exclusively on aerobic respiration
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Cardiac muscle is able to utilize multiple fuel sources (ex. Glucose, fatty
acids, and even lactic acid for a short period of time)
- Mechanisms and
Events of Contraction
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The autorhythmic cells of the heart are able to initiate their own
depolarization.
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The action potential
in cardiac muscle cells:
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Normally cardiac
cells have a resting membrane potential of approximately 90mV.
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The action potential
in cardiac muscle cells begins when the membrane potential is brought down
to approximately 75mV.
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The stimulus of an
action potential is usually the excitation of an adjacent muscle cell.
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Once threshold has
been reached, the action potential proceeds as follows:
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RAPID
DEPOLARIZATION - Voltage-regulated sodium channels open, and the
membrane becomes permeable to sodium ions. This results in the rapid
depolarization of the sarcolemma.
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The sodium
channels are called fast channels because they open quickly and remain
open for only a few milliseconds.
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THE PLATEAU
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As the
transmembrane potential approaches +30mV, the voltage-regulated sodium
channels close. They will remain closed and inactivated until the
membrane potential reaches 60mV.
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As the sodium
channels are closing, calcium channels begin to open and calcium
enters the cardiac cells. The calcium channels are called slow
channels because they open slowly and remain open for a relatively
long period (~175 ms). This causes the transmembrane potential to
remain near 0mV for an extended period of time this is called the
plateau.
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This increase
in calcium ions around the myofibrils (from the calcium ions
entering the cell and the release of additional calcium ions from
the sarcoplasmic reticulum) generates a contraction.
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RAPID
REPOLARIZATION - As the plateau continues, slow calcium channels begin
closing and slow potassium channels begin opening. This restores the
resting membrane potential.
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REFRACTORY PERIOD
For some time after an action potential begins, the membrane will not
respond to a second stimulus. The length of this refractory period is
approximately 250ms.
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In cardiac
muscle the refractory period continues until the muscle begins to
relax. Summation of action potentials is not possible at this point
and this prevents tetanic contractions in cardiac cells.
- Intrinsic
Conduction System of the Heart
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The cardiac conduction system coordinates and synchronizes heart activity
and forces the heart to beat faster
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The intrinsic conduction system of the heart consists of noncontractile
cardiac cells that are able to generate and distribute electrical
impulses.
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The autorhythmic
cells of the heart do not have a stable resting potential. Instead, they
have spontaneously changing membrane potentials called pacemaker
potentials.
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The influx of
calcium ions generates the action potential, not sodium ions
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The rate of
spontaneous depolarization varies in different portions of the
conduction system
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Sinoatrial node
generates action potentials at a rate of 75-100 per minute
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Atrioventricular
node generates action potentials at a rate of 40-60 per minute
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Most cells of
the AV bundle and Purkinje fibers do not depolarize spontaneously.
Those that do depolarize at the rate of about 30 times per minute
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Components of the
intrinsic conduction system:
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The sinoatrial (SA)
node cells of the SA node reach threshold first, so they establish the
heart rate
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Aka, the cardiac
pacemaker
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Located in the
posterior wall of the right atrium
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Contains pacemaker
cells which establish the heart rate
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Generates impulses
about 75 times every minute (~100 per minute, in the absence of neural
and hormonal factors) this is called the sinus rhythm
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The atrioventricular
(AV) node
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Connected to the
SA node via the internodal pathway
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Located in the
inferior portion of the interatrial septum, immediately above the
tricuspid valve
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The impulse is
delayed for about 100ms to allow for completion of the atrial
contraction before ventricular contraction
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The delay is due
to the smaller diameter of the fibers and the presence of fewer gap
junctions
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The atrioventricular
(AV) bundle
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Aka, the Bundle of
His
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Impulse travels
from here to the right and left bundle branches
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The only
electrical connection between the atria and the ventricles
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The Bundle branches
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Divide into right
and left bundle branches
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Run along the
interventricular septum toward the heart apex
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The Purkinje fibers
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Penetrate into the
heart apex and into the ventricular walls
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The Purkinje
fibers are more elaborate in the left side of the heart
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Directly supply
the papillary muscles
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Ventricular
contraction follows depolarization by the Purkinje fibers
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Electrocardiography
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An electrocardiogram is a graphic recording of heart activity.
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Aka, ECG or EKG
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3 distinguishable
deflection waves are present:
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P wave
depicts movement of the depolarization wave from the SA node to the
atria.
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The atria begin
to contract approximately 100ms after the start of the P wave.
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QRS complex
depicts ventricular depolarization.
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The ventricles
begin contracting shortly after the peak of the R wave.
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Atrial
repolarization takes place at this time, but the wave is obscured by
the QRS complex.
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T wave
depicts ventricular repolarization.
- The Cardiac Cycle
All of the events associated with blood flow through the heart during one
complete heartbeat.
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2 phases:
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Systole
Contraction
- Diastole
- Relaxtion
- Atrial Systole
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Atria contract;
increase in atrial pressures push residual blood into ventricles through
the open right and left AV valves.
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At the end of atrial
systole, each ventricle contains the maximum amount of blood that it will
hold in this cardiac cycle. This quantity is called the end-diastolic
volume (EDV).
- Ventricular
Systole
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As the pressure
inside the ventricles rise above those in the atria, the AV valves swing
shut.
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The ventricles
contract, but blood flow does not occur because the pressure isnt high
enough to force open the semilunar valves this is the period of
isometric contraction.
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During isometric
contraction, all of the heart valves are closed, the volume of the
ventricle remains constant, and the ventricular pressure rises.
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Once ventricular
pressure exceeds that in the arterial trunks, the semilunar valves open
and push blood into the pulmonary and aortic trunks this is the
beginning of the period of ventricular ejection.
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At the end of
ventricular systole, ventricular pressures fall rapidly. Blood starts to
flow back toward the ventricles and it is this backward movement that
closes the semilunar valves.
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When the semilunar
valves close, this increases the pressure in the arterial walls and they
recoil.
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The blood
remaining in the ventricle when the semilunar valves close, is the
end-systolic volume.
- Ventricular
Diastole
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The ventricular
myocardium is resting at this point and all the heart valves are closed.
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When ventricular
pressures fall bellow those of the atria, the atrial pressure forces the
AV valves to open. Blood flows from the atria to the ventricles and both
the atria and ventricles are in diastole.
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The ventricular
pressures continue to fall as the chambers expand.
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Because of this
passive filling, the ventricles will be nearly Ύ full before the cardiac
cycle ends.
- Heart Sounds (lub-dup)
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1st sound (lub) closing of the AV valves
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Louder and longer
than the second sound
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2nd sound (dup) closing of the semilunar valves
- Cardiodynamics
the movements and forces generated during cardiac contractions.
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Important Terms
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End-diastolic volume
The amount of blood in each ventricle at the end of ventricular diastole
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End-systolic volume
The
amount of blood remaining in each ventricle ate the end of ventricular
systole
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Stroke volume
The amount of
blood pumped out of each ventricle during a single beat. (SV = EDV ESV)
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Ejection fraction
The
percentage of the EDV represented by the SV.
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Stroke volume (SV) is the most important factor in an examination of a
single cardiac cycle. SV is relatively constant in healthy individuals
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Factors Controlling
Stroke Volume
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The EDV
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EDV is affected
by 2 factors:
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Filling time
during ventricular diastole
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Entirely
dependent upon heart rate.
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TREND:
Increase in heart rate = Decrease in the available filling time;
Decrease in heart rate = Increase in the available filling time
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Venous return
the rate of blood flow over this period
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Changes in
venous return can be caused by exercise, alterations in blood
volume, skeletal muscle activity, patterns in peripheral
ciruclation
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The ESV
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ESV is affected
by 3 factors:
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Preload the
degree of stretching experienced during ventricular diastole
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The greater
the EDV, the larger the preload
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EDV is
lowest during period of rest; highest during exercise
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The greater
the stretch, the greater the force of contraction (Frank-Starling
law of the heart)
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Cardiac
muscle cells are stretched more when there is more blood in the
chambers
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Contractility
the amount of force produced during a contraction, at a given
preload
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Positive
inotropic agents increase contractility
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Ex.,
increase in calcium ion concentration, glucagons, thyroxine,
epinephrine (sympathetic nervous system stimulation), digitalis
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Negative
inotropic agents decrease contractility
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Ex.
Acidosis, elevated potassium ion levels, calcium channel
blockers, parasympathetic nervous system
stimulation
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Afterload
the amount of tension the contracting ventricle must produce to
force open the semilunar valve and eject blood.
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Relatively
constant in health individuals
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Individuals
with hypertension reduced ability to eject blood
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Cardiac output (CO) the amount of blood pumped by each ventricle in 1
minute.
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Examination of
cardiac function over time
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CO = Stroke Volume x
Heart Rate
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Factors affecting
heart rate
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Autonomic
Nervous System Regulation
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Sympathetic
stimulation increases heart rate
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Parasympathetic stimulation decreases heart rate
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Chemical
Regulation
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Hormones
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Epinephrine
& thyroxine increase heart rate
- Ions