Transcript Chapter 18 The Cardiovascular System

Chapter 18 --The Heart
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Use the video clip, CH 18 Heart Anatomy for a
review of the gross anatomy of the heart
J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G.R. Pitts, Ph.D.
Pericardium
The sac containing the heart
3 Layers Form the Heart’s Wall -
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Epicardium (outer)
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Myocardium (middle)
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Endocardium (inner)
Pericarditis
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inflammation of the
pericardium
painful
may damage the lining
tissues
may damage myocardium
fibrinous pericarditis
Cardiac Tamponade
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a buildup of pericardial fluid, or
bleeding into the pericardial cavity
may result in cardiac failure
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Elizabeth, Empress of Austria (d. 1898) by
assassination with a hat pin
Chambers of the Heart
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Internally - 4
compartments
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LA
RA
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RV
LV
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R/L atria with auricles
R/L ventricles
Interatrial septum
separates atria
Interventricular
septum separates
ventricles
Left ventricular wall
is much thicker
because it must pump
blood throughout the
body and against
gravity
Blood Flow through the Heart
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SVC
Right atrium (RA) receives
deoxygenated blood
from three sources
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(CS
RA
IVC
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superior vena cava
(SVC)
inferior vena cava
(IVC)
coronary sinus (CS)
Blood Flow through the Heart
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Right ventricle (RV)
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PA
PA
PT
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Pulmonary Trunk (PT) from RV branches into the
pulmonary arteries (PA)
Pulmonary arteries
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RA
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RV
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receives blood from RA
pumps to lungs via Pulmonary
Trunk (PT)
deoxygenated blood from
the heart to the lungs for
gas exchange
right and left branches for
each lung
blood gives up CO2 and picks
up O2 in the lungs
Pulmonary veins (PV) oxygenated blood from
the lungs to the heart
Pulmonary Circulation
Blood Flow through the Heart
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Left atria
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Aortic
arch
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Left ventricle (LV)
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PV
LA
receives blood from PV
pumps to left ventricle
PV
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sends oxygenated blood
to the body via the
ascending aorta
aortic arch
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LV
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curls over heart
three branches off of it
feed superior portion of
body
thoracic aorta
abdominal aorta
Schematic of Circulation
Know the names
of the valves
indicated here.
Schematic of
Circulation
Review
Routes
Myocardial Blood Supply
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Myocardium has its own
blood supply
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coronary vessels
simple diffusion of
nutrients and O2 into the
myocardium is impossible
due to its thickness
Collateral circulation =
duplication of supply
routes and anastomoses
(crosslinked connections)
Heart can survive on 1015% of normal arterial
blood flow
Myocardial Blood Supply
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Arteries
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first branches off the
aorta
blood moves more easily
into the myocardium
when it is relaxed
between beats  during
diastole
blood enters coronary
capillary beds
[note the collateral
circulation]
Myocardial Blood Supply
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Coronary veins
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deoxygenated blood
from cardiac muscle is
collected in the
coronary veins and then
drains into the
coronary sinus
deoxygenated blood is
returned to the right
atrium
Coronary Circulation Pathologies
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Compromised coronary
circulation due to:
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emboli: blood clots, air,
amniotic fluid, tumor
fragments
fatty atherosclerotic
plaques
smooth muscle spasms
in coronary arteries
Problems
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ischemia (decreased
blood supply)
hypoxia (low supply of
O2)
infarct (cell death)
Pathologies (cont.)
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Angina pectoris - classic chest pain
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pain is due to myocardial ischemia – oxygen
starvation of the tissues
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tight/squeezing sensation in chest
labored breathing, weakness, dizziness,
perspiration, foreboding
often during exertion - climbing stairs, etc.
pain may be referred to arms, back,
abdomen, even neck or teeth
silent myocardial ischemia can exist
Pathologies (cont.)
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Myocardial infarction
(MI) - heart attack
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thrombus/embolus in
coronary artery
some or all tissue distal
to the blockage dies
if pt. survives, muscle is
replaced by scar tissue
Long term results
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size of infarct, position
pumping efficiency?
conduction efficiency,
heart rhythm
Pathologies (cont.)
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Treatments
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clot-dissolving agents
angioplasty (bypass surgery)
Reperfusion damage
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re-establishing blood flow may damage tissue
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oxygen free radicals - electrically charged oxygen
atoms with an unpaired electron
radicals indiscriminately attack molecules: proteins
(enzymes), neurotransmitters, nucleic acids, plasma
membrane molecules
further damage to previously undamaged tissue
or to the already damaged tissue
Valve Structure
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Dense connective
tissue covered by
endocardium
AV valves
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chordae tendineae thin fibrous cords
connect valves to
papillary muscles
Valve Function
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Opening and closing a
passive process
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when pressure low,
valves open, flow occurs
with contraction,
pressure increases
papillary muscles
contract pull valves
together
Valves of the Heart
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Tricuspid
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Bicuspid
(Mitral)
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Semi-lunar
Function to prevent
backflow of blood
into/through heart
Open and close in
response to changes in
pressure in heart
Four key valves: tri- and
bi-cuspid (mitral) valves
between the atria and
ventricles and semi-lunar
valves between ventricles
and main arteries
Valves also close the
entry points to the atria
Atrioventricular (AV) valves
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anterior
Separate the
atria from the
ventricles
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bicuspid
tricuspid
bicuspid (mitral)
valve – left side
tricuspid valve –
right side
note the feathery
edges to the
cusps
Semilunar valves
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in the arteries that
exit the heart to
prevent back flow of
blood to the ventricles
pulmonary semilunar
valves
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aortic semilunar valves
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Pathologies
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Incompetent – does not
close correctly
Stenosis – hardened,
even calcified, and does
not open correctly
Normal Action Potential
Review in Chapter 11
Cardiac Muscle Action Potential
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Contractile cells
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near instantaneous
depolarization is
necessary for
efficient pumping
much longer
refractory period
ensures no summation
or tetany under
normal circumstances
Cardiac Muscle Action Potential
electrochemical
events
Cardiac Muscle Action Potential
sarcolemma’s
ion permeabilities
 opening fast Na+ channels initiates
depolarization near instantaneously
 opening CA++ channels
while closing K+ channels
sustains depolarization and
contributes to sustaining
the refractory period
 closing Na+ and
Ca++ channels while
opening K+ channels
restores the
resting state
repolarization
Cardiac Muscle Action Potential
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long absolute
refractory period
permits forceful
contraction
followed by
adequate time for
relaxation and
refilling of the
chambers
inhibits summation
and tetany
Pacemaker Potentials
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leaky membranes
spontaneously
depolarize
creates
autorhythmicity
the fact that the
membrane is more
permeable to K+ and
Ca++ ions helps
explain why
concentration
changes in those
ions affect cardiac
rhythm
Conduction System and Pacemakers
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Autorhythmic cells
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cardiac cells repeatedly fire
spontaneous action potentials
Autorhythmic cells: the
conduction system
pacemakers
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SA node
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origin of cardiac excitation
fires 60-100/min
AV node
conduction system
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AV bundle (Bundle of His)
R and L bundle branches
Purkinje fibers
It’s as if the heart had only two motor units: the atria and the ventricles!
Conduction System and Pacemakers
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Arrhythmias
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Fibrillation
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rapid, fluttering, out of phase contractions – no
pumping
heart resembles a squirming bag of worms
Ectopic pacemakers (ectopic focus)
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irregular rhythms: slow (brady-) & fast (tachycardia)
abnormal atrial and ventricular contractions
abnormal pacemaker controlling the heart
SA node damage, caffeine, nicotine, electrolyte
imbalances, hypoxia, toxic reactions to drugs, etc.
Heart block
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AV node damage - severity determines outcome
may slow conduction or block it
Conduction System and Pacemakers
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SA node damage (e.g., from an MI)
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AV node can run things (40-50 beats/min)
if the AV node is out, the AV bundle, bundle
branch and conduction fibers fire at 20-40
beats/min
Artificial pacemakers - can be activity
dependent
Atrial,Ventricular Excitation Timing
Atrial,Ventricular Excitation Timing
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Sinoatrial node to Atrioventricular node
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about 0.05 sec from SA to AV, 0.1 sec to
get through AV node – conduction slows
allows atria time to finish contraction and to
better fill the ventricles
once action potentials reach the AV bundle,
conduction is rapid to rest of ventricles
Extrinsic Control of Heart Rate
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basic rhythm of the
heart is set by the
internal pacemaker
system
central control from
the medulla is routed
via the ANS to the
pacemakers and
myocardium
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sympathetic input norepinephrine
parasympathetic input
– acetylcholine
Electrocardiogram
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measures the sum
of all electrochemical activity in
the myocardium at
any moment
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P wave
QRS complex
T wave
Electrocardiogram
Cardiac Cycle
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Relationship between electrical and mechanical
events
Systole
Diastole
Isovolumetric
contraction
Ventricular
ejection
Isovolumetric
relaxation
Cardiac Output
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Amount of blood pumped by each
ventricle in 1 minute
Cardiac Output (CO) = Heart Rate x
Stroke Volume
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HR = 70 beats/min
SV = 70 ml/beat
CO = 4.9 L/min *
*Average adult total body blood volume = 4-6 L
Cardiac Reserve
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Cardiac Output is variable
Cardiac Reserve = maximal output (CO) –
resting output (CO)
average individuals have a cardiac
reserve of 4X or 5X CO
trained athletes may have a cardiac
reserve of 7X CO
heart rate does not increase to the same
degree
Regulation of Stroke Volume
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SV = EDV – ESV
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EDV
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ESV
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End Diastolic Volume
Volume of blood in the heart after it fills
120 ml
End Systolic Volume
Volume of blood in the heart after contraction
50 ml
Each beat ejects about 60% of the blood in
the ventricle
Regulation of Stroke Volume
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Most important factors in regulating SV:
preload, contractility and afterload
Preload – the degree of stretching of cardiac
muscle cells before contraction
Contractility – increase in contractile strength
separate from stretch and EDV
Afterload – pressure that must be overcome
for ventricles to eject blood from heart
Preload
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Muscle mechanics
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Length-Tension relationship?
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fiber length determines number of cross bridges
cross bridge number determines force
increasing/decreasing fiber length
increases/decreases force generation
Cardiac muscle
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How is fiber length determined/regulated?
Fiber length is determined by filling of heart – EDV
Factors that effect EDV (anything that effects
blood return to the heart) increases/decreases
filling
Increases/decreases SV
Preload
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Preload – Frank-Starling Law of the
Heart
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Length tension relationship of heart
Length = EDV
Tension = SV
As the ventricles become
overfilled, the heart
becomes inefficient and
stroke volume declines.
“cardiac reserve”
Contractility
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Increase in contractile strength
separate from stretch and EDV
Do not change fiber length but increase
contraction force?
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What determines force?
How can we change this if we don’t change
length?
Sympathetic
Stimulation
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Increases the number of
cross bridges by
increasing amount of Ca++
inside the cell
Sympathetic nervous
stimulation (NE) opens
channels to allow Ca++ to
enter the cell
Positive Inotropic Effect
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increase the
force of
contraction
without
changing
the length
of the
cardiac
muscle cells
Afterload
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if blood pressure is high, it is difficult
for the heart to eject blood
more blood remains in the chambers
after each beat
heart has to work harder to eject blood,
because of the increase in the
length/tension of the cardiac muscle
cells
Regulation of Heart Rate
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Intrinsic
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Pacemakers
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Bainbridge effect
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Increase in EDV increases HR
Filling the atria stretches the SA node
increasing depolarization and HR
Regulation of Heart Rate
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Extrinsic
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Autonomic Nervous System
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Sympathetic - norepinephrine
Parasympathetic – acetyl choline
hormones – epinephrine, thyroxine
ions (especially K+ and Ca++)
body temperature
age/gender
body mass/blood volume
exercise
stress/illness
Regulation of Heart Rate
Overview
End Chapter 18