Download Heart Anatomy (cont)

BIO 169
THE HEART
CHAPTER 20
created by Dr. C. Morgan
1
TOPICS
Introduction and Overview
Heart Anatomy
The Heartbeat
Cardiodynamics
Reference: IPCD
Cardiovascular System
2
Introduction and Overview Objectives
Discuss the work load placed on the heart.
Describe the circulatory plan with respect to
the heart and lungs.
Briefly discuss the definition of arteries,
veins, and capillaries.
3
Introduction and Overview
The function of the cardiovascular system depends on the
heart to develop the hydrostatic pressure which drives the
circulation of blood throughout the body.
Your heart beats around 100,000 times a day, pumping
enough blood to fill forty 55 gallon containers.
Multiply those statistics by a lifetime and you will see that
an astounding amount of work is accomplished by the
heart.
Blood flows through a network of vessels that are divided
into two circuits, pulmonary and systemic.
Vessels are arteries, veins, and capillaries.
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Introduction and Overview (cont)
HEART
HEART
LUNGS
TISSUES
HEART
HEART
veins carry
blood to the
heart
arteries carry
blood away from
the heart
Fig. 1
5
TOPICS
Introduction and Overview
Heart Anatomy
The Heartbeat
Cardiodynamics
6
Heart Anatomy Objectives
Describe the surface anatomy of the heart.
Describe the internal anatomy of the heart.
Discuss the heart valves, their location, and function.
Characterize the heart wall.
Describe the blood supply to the heart muscle tissue.
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Heart Anatomy
The fist size heart lies in the anterior thoracic cavity, slightly
left of the midline, where it is surrounded by connective
tissues of the mediastinum.
The heart is posterior to the sternum within its own
pericardial cavity and surrounded by the pericardium.
The parietal pericardium is a dense, irregular connective
tissue with an epithelial lining that secretes pericardial
fluid into the cavity.
Is the pericardium a mucous or serous membrane?
The epicardium is the visceral pericardium that adheres to
the surface of the heart muscle (myocardium).
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Heart Anatomy (cont)
base
apex
Fig. 3 c
Fig. 2 b
9
Heart Anatomy (cont)
Base
Apex
Fig. 2
(c)
10
Heart Anatomy (cont)
Surface
fat protects
vessels
Fig. 3
Left and right atria with auricles
Coronary sulcus: a depression
between atria and ventricles
Interventricular sulcus: between
left and right ventricles.
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11
Heart Anatomy (cont)
The heart wall has three concentric layers that wrap
around the atria and spiral within the wall of the ventricles.
3
2
1
squamous epithelium
Fig. 4 a
12
Heart Anatomy (cont)
The Myocardium
TABLE 1
Fig. 5 b, c
gap junction
communication
Ca2+ from ECF and SR
13
Heart Anatomy (cont)
Cardiac muscle cells are striated, branched, mononucleate,
with intercalated discs at intercellular junctions
composed of gap, tight, and desmosome junctions.
Gap junctions across intercalated disc allows fast, efficient
electrochemical communication to form a functional
synctium (contracts as one).
Cells have many mitochondria due to dependence on
aerobic metabolism with energy reserves as stored
glycogen and lipids.
Mitochondria make up 25% of the cardiac cell volume.
Autorhythmic pacemaker cells generate action potentials.
Motor neurons of the ANS division modify the heart rate.
14
Heart Anatomy (cont)
The wall structure of the right and left ventricles reflects the
different demands placed on them.
Right ventricle only has to move blood to nearby lungs.
Less vascular length = less pressure needed (thinner wall).
Left ventricle must move blood through all the vessels on
the arterial side of the systemic circuit which requires
much more pressure.
Left ventricle has a thicker myocardial wall than the right one.
Heart valves prevent backflow (regurgitation) of blood.
Papillary muscles and their chordae tendineae keep valve
cusps from being pushed into atria.
15
Heart Anatomy (cont)
ridges
Frontal section
Fig. 6 a
16
Heart Anatomy (cont)
Learn route
systemic
circuit
aorta
venae cavae
coronary sinus
Rt. atrium
tricuspid
valve
Lt. ventricle
Rt. ventricle
bicuspid
valve
pulmonary
semilunar
valve
pulmonary trunk
aortic
semilunar
valve
Lt. atrium
pulmonary arteries
lungs pulmonary veins17
Heart Anatomy (cont)
AV valves open
semilunar valves closed
diastole
Fig. 8 a
Semilunar valves are like 3 little pockets that
close the opening when they fill with blood.
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18
Heart Anatomy (cont)
systole
semilunar valves open
Fig. 8 b
AV valves closed
19
Heart Anatomy (cont)
Collagenous and elastic fibers in connective tissue wrap
around cardiac cells and are continuous with a branching
internal network of connective tissue that binds valves in
place to form a fibrous skeleton.
The fibrous skeleton consists of four bands around the
bases of the large vessels and valves to isolate the atria
from the ventricles.
Connective tissue fibers that bind the cells in place assists
in distributing the energy of contraction over the entire
myocardium.
The blood vessels and nerves are also bound in place by
the connective tissue.
The elastic fibers cause the myocardium to return to its
original size and shape after a contraction.
20
Heart Anatomy (cont)
1st branches from aorta are left and right coronary arteries
RA
Fig. 9 a, b
CAD results from restricted or blocked arteries.
2121
Heart Anatomy (cont)
Veins and
arteries
Fig. 9 c
22
TOPICS
Introduction and Overview
Heart Anatomy
The Heartbeat
Cardiodynamics
23
Heartbeat Objectives
Describe the two types of cardiac cells and their
role in contraction of cardiac muscle.
Discuss the action potential in cardiac muscle cells.
Learn the role of the conducting system of the heart.
Learn the components of the electrocardiogram.
Relate the electrocardiogram to the contraction cycle.
Discuss the origin of heart sounds.
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Heartbeat
Two types of cells communicate to produce a heartbeat.
Contractile cells shorten to pump blood out of the heart.
Conducting cells distribute the electrochemical signals
that trigger the contraction events in the contractile cells.
99% of the myocardium is composed of contractile cells.
Just like in skeletal muscle, an action potential travels along
the sarcolemma to trigger the appearance of Ca2+ ions
which bind to troponin to reveal actin sites to myosin.
Contraction follows but the depolarization-repolarization
cycle is 30 times longer in cardiac than skeletal muscle.
Because of a long refractory period, tetanus does not occur
and the maximum rate is about 200 beats / min.
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Heartbeat (cont)
-75 mv
250 – 300 msec
Fig. 15 a
26
Heartbeat (cont)
twitch
myogram
The plateau is a
major difference
between cardiac
and skeletal muscle
action potentials.
no summation
or tetanus
twitch
myogram
Fig. 15 b
27
Heartbeat (cont)
ECF source Ca2+ ions that enter the sarcoplasm during the
plateau phase of the action potential account for 20% of
the total.
The SR then releases its Ca2+ into the sarcoplasm.
Understanding that the initial ECF calcium source triggers
release of the subsequent SR source ions explains the
sensitivity of cardiac muscle to ECF calcium ion
concentration.
Active transport pumps restore the Ca2+ balance.
In cardiac muscle, relaxation is underway before the long
absolute refractory period ends – no summation or tetanus
possible.
28
Heartbeat (cont)
Cardiac muscle is able to initiate its own contractions—a
property known as autorhythmicity or automaticity.
During a normal contraction cycle, the atria contract before
the ventricles.
This coordination is possible because of electrochemical
signals from specialized muscle cells that do not contract
but instead, simply initiate and conduct action potentials to
contractile cells.
These cells are autorhythmic nodal (pacemaker) and
conducting cells respectively.
Nodal cells establish the rate; conducting cells distribute
action potentials to all of the contractile cells.
29
Heartbeat (cont)
tachycardia
= fast rate
80 -100
without
neural
input
40 - 60
no normal
spontaneous
depolarization
bradycardia
= slow rate
Fig. 12 a
30
Heartbeat (cont)
spontaneous SA depolarization  75 bpm
drift toward
threshold
Fig. 12 b
31
Heartbeat (cont)
Nodal cells are connected to conducting system cells which
in turn branch to all the muscle fibers in the heart.
Nodal cells depolarize spontaneously so they set the rate.
Pacemaker nodal cells in the sinoatrial (SA) node are
usually the first to depolarize at a rate of about 75 / min.
The SA node is the pacemaker of the heart.
The SA node conducts to the atria and to the AV node
located in the floor of the right atrium.
The action potential travels to the AV bundle, along the two
bundle branches in the interventricular septum, and then
are distributed to ventricular muscle cells via the Purkinje
system of branching, conducting fibers.
32
Heartbeat (cont)
SA node
AV node
AV bundle
bundle branches
Purkinje fibers
Fig. 13
3333
Heartbeat (cont)
The AV nodes slows the conduction rate which allows time
for the atria to contract.
The maximum rate of conduction from the AV node is 230
impulses per minute.
The right and left bundle branches are in the interventricular
septum.
Purkinje fibers conduct action potentials quickly, reaching
all ventricular cells within 75 msec.
There is a direct path (moderator band) to the papillary
muscles so they contract and apply tension to the chordae
tendineae before the myocardium contracts.
34
Heartbeat (cont)
P = atrial depolarization
ECG
tracing of
electrical
events in the
heart
QRS =
ventricular
depolarization
T = ventricular
repolarization
35
35
Heartbeat (cont)
ECG intervals
ECG leads in place
Fig. 14
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36
Heartbeat (cont)
Contraction follows the depolarization events.
Atria begin to contract 100 msec after P wave initiation.
An upward deflection is seen when the depolarization is
moving toward the sensing electrode (patch with attached
wire that is connected to the ECG machine).
A downward deflection is seen when the depolarization is
moving away from the sensing electrode.
When there are conduction defects (cardiac arrhythmias),
changes in the ECG may be apparent.
For example, scar tissue that forms after a heart attack
does not conduct so a “detour” occurs to produce an
altered tracing.
37
Heartbeat (cont)
Phases of the
cardiac cycle
Fig. 16
38
38
Heartbeat (cont)
One
Blood moves down hydrostatic pressure gradients.
3939
Heartbeat (cont)
Fig. 17
40
Heartbeat (cont)
The “lubb-dupp” sounds heard through a stethoscope are
due to valve closure.
The first sound (S1) is due to AV valve closure (ventricular
systole) and S2 is heard when the semilunar valves close.
Two additional sounds are difficult to hear.
S3 is heard as blood fills the ventricles and S4 is associated
with atrial contraction.
Murmurs are fluid sounds heard due to blood regurgitation
into the atria during ventricular systole.
Mitral (left AV valve) regurgitation is the most common
murmur heard.
41
Heartbeat (cont)
Sites for auscultation
of heart sounds
Fig. 18 a
42
Heartbeat (cont)
Fig. 18 b
43
TOPICS
Introduction and Overview
Heart Anatomy
The Heartbeat
Cardiodynamics
44
Cardiodynamics Objectives
Present an overview of factors affecting cardiac
output.
Discuss factors that affect the stroke volume.
Describe factors that affect the heart rate.
Discuss the cardiac responses to exercise.
Describe some abnormal conditions that affect
cardiac output.
45
Cardiodynamics
Cardiodynamics refers to the blood movements and forces
produced during each cardiac contraction cycle.
Both ventricles eject the same amount of blood during systole.
Terminology:
End-diastolic volume (EDV) = volume of blood in each
ventricle at the end of ventricular diastole.
End-systolic volume (ESV) = volume in each ventricle at
the end of systole.
Stroke volume (SV) = volume ejected by each ventricle
(SV = EDV – ESV)
Ejection fraction = SV as a % of EDV.
46
Cardiodynamics (cont)
Factors affecting CO
Fig. 23
CO = HR x SV
47
Cardiodynamics (cont)
Stroke volume is affected by changes in the EDV and ESV.
EDV is determined by filling time and volume of venous
return.
Faster heart rates decrease the filling time.
Venous return varies with heart rate, blood volume,
patterns of peripheral circulation, skeletal muscle activity,
and factors that affect venous flow patterns.
ESV is affected by preload, contractility of the ventricle,
and afterload.
*The preload is the volume of blood in the ventricle prior to
contraction.
Preload sets the length-tension relationship of muscle
myofilaments (overlap of actin and myosin).
48
Cardiodynamics (cont)
When the muscle is stretched little (at rest), the
myocardium develops a less powerful contraction and
the ESV is greater.
When you exercise, venous return increases, EDV
increases to stretch the myocardium more and ESV
decreases because contraction efficiency improves.
An overstretched myocardium is inefficient and the ESV is
very high (further decreasing venous return and EDV).
Within normal limits, the greater the EDV (preload), the
greater the stretch on the myocardium, the greater the SV,
and the less the ESV.
This is the Frank-Starling principle or Starling’s law.
49
Cardiodynamics (cont)
*Contractility is a measure of the force developed by the
ventricular myocardium at a given preload.
Contractility may be altered by inotropic factors.
Drugs that increase contractility exert positive inotropic
effects usually by stimulating Ca2+ movement into the
sarcoplasm or prolonging its presence there.
Drugs that decrease contractility exert negative inotropic
effects usually by blocking Ca2+ movement into the
sarcoplasm or decreasing metabolism.
The ANS, hormones, and ECF ion concentrations all affect
contractility.
50
Cardiodynamics (cont)
The ANS effects:
Sympathetic stimulation has a positive inotropic effect.
Neurotransmitters and adrenal medullae hormones, E
and NE, are released to act on alpha and beta receptors.
Parasympathetic stimulation has a negative effect.
ACh hyperpolarizes the SA and AV nodal cells and if
parasympathomimetic drugs are used, force of
contraction also decreases.
Additional hormones: glucagon and thyroid hormones both
have positive effects on contractility.
51
Cardiodynamics (cont)
Positive Inotropic Drugs: isoproterenol, dopamine,
dobutamine all mimic E and NE by stimulating beta-1
receptors.
Digitalis increases intracellular Ca2+ levels.
Negative Inotropic Drugs: propranolol and similar
derivatives, and several barbiturates block beta receptors
and alpha receptors to inhibit sympathetic stimulation.
*Afterload is the amount of contractile energy the ventricle
needs to develop in order to open the semilunar valve to
eject blood.
As afterload increases, SV decreases.
A damaged or a weakened myocardium has difficulty
coping with any increase in blood pressure.
52
Cardiodynamics (cont)
Factors affecting stroke volume
= increases
= decreases
Fig. 23
53
Cardiodynamics (cont)
Factors that affect the heart rate include the ANS, the atrial
reflex, and circulating hormones.
There is a cardioacceleratory center and a cardioinhibitory
center in the medulla oblongata.
These centers receive input from higher centers in the brain,
especially the hypothalamus.
Sensory information is carried to the CNS via the vagus (X)
and glossopharyngeal (IX) nerves.
Cardiac centers monitor baroreceptor and chemoreceptor
information.
The amount of CO2 in the blood is the most important
chemical factor (because it decreases pH).
54
Cardiodynamics (cont)
*ANS output
rate and
force of
contraction
Fig. 21
dual
innervation
rate and
force of
contraction
55
Cardiodynamics (cont)
Native rate of SA node is 80 – 100 bpm but parasympathetic
effects cause the resting rate to be about 70 – 80 bpm.
Dual innervation adjusts the autonomic tone to meet the
demands of your various systems on the body.
The ANS neurotransmitter substances result in a change in
the permeability of the conducting system cells, especially
the SA nodal cells.
ACh opens K+ channels which hyperpolarizes the cell.
NE binds to beta–1 receptors which opens Ca2+ channels
which increases the depolarization rate and shortens the
repolarization time (*hormonal effects are the same).
*The atrial reflex is a sympathetic response to increased
venous return which activates stretch receptors in the RA.
56
Cardiodynamics (cont)
In autorhythmic cells, when threshold is reached it is
an influx of ECF Ca2+ that causes depolarization.
SA
time in sec
Fig. 22 a
57
Cardiodynamics (cont)
Parasympathetic neurons release ACh which lengthens
the repolarization and slows depolarization by
hyperpolarizing cells in the SA region.
SA
time in sec
Fig. 22 b
58
Cardiodynamics (cont)
NE shortens repolarization and causes accelerated
depolarizations to increase the HR
SA
Atrial reflex
Fig. 22 c
59
Cardiodynamics (cont)
*The main circulating hormones that affect cardiac activity
include epinephrine and norepinephrine released from
the adrenal medullae as a component of the sympathetic
response.
E and NE increase rate and force of contraction.
Massive amounts of E and NE stimulation may cause
abnormal contractions and rhythms due to the
hypersensitivity of the cardiac cell membranes.
Thyroid hormones also increase contractility of the
myocardium.
60
Cardiodynamics (cont)
The cardiac output must be adequate to meet the needs of
tissues at any moment in time.
During strenuous exercise, CO may increase to 30 l / min.
Your cardiac reserve the the difference between your
resting CO and maximum CO.
Increasing CO during exercise is accomplished by
increasing rate and stroke volume.
Blood volume reflexes, the autonomic nervous system, and
hormones all have a role in matching CO to demand.
61
Cardiodynamics (cont)
Summary of factors affecting cardiac output.
Fig. 24
62
Cardiodynamics (cont)
Blood electrolyte levels are important in myocardial function.
Hypercalcemia  excitability and prolonged contractions
Hypocalcemia  weak contractions or cardiac arrest
Membrane potentials are affected by the K+ level.
Permeability to K+ establishes the resting potential.
Hyperkalemia  weak, irregular contractions and loss of the
chemical gradient for K+ leading to compromised function.
Hypokalemia  reduced HR due to hyperpolarized membrane
because of the enhanced gradient for K+ to move out of cells.
Often an analysis of blood chemistry gives clues to what may
underlie a cardiac problem.
63
Cardiodynamics (cont)
Text list (A-7) of normal electrolyte levels:
Na+ = 136 –142 mEq / l
(hypernatremia > 150) (hyponatremia < 130)
K+ = 3.8 – 5 mEq/l
(hyperkalemia > 8) (hypokalemia <2)
Ca2+ = 4.8 – 5.3 mEq/l (serum)
(hypercalcemia > 11) (hypocalcemia < 4)
64
Cardiodynamics (cont)
A myocardial infarction (heart attack) results in
damage to cardiac muscle which in turn may greatly
compromise cardiodynamics.
Evidence of an MI comes from many tests including
blood tests for enzymes coming from dead cardiac
cells.
Enzymes tested for are lactate dehydrogenase
(LDH), serum glutamic oxaloacetic transaminase
(SGOT), creatine phosphokinase (CK), and a
cardiac form (CK-MB).
About 1.3 million MIs occur in the US annually (see
text discussion on p. 704).
65
TOPICS
Introduction and Overview
Heart Anatomy
The Heartbeat
Cardiodynamics
66