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The Heart
The Heart
Martini Chapter 20
Heart
Anatomy
Approximately
the size of
your fist
Location
 Superior surface
of diaphragm
 Left of the midline
 Anterior to the vertebral column, posterior to the
sternum
3
Position in Thorax
Base: Where
the Great
Vessels enter
and exit
Apex: points
inferiorly,
anteriorly and
to the left
4
Position in Thorax
Base
Normal chest
X-Ray
Apex
5
Position of Heart
Hint: Nipples are at the
4th intercostal space
Apex at 5th
intercostal space
during ventricular
systole (contraction)
Point of Maximum Impulse: PMI is the apex on surface anatomy
6
Pericardium
Pericardium: a double-walled
sac around the heart
 A superficial fibrous pericardium
 A deep two-layer serous pericardium
The parietal layer lines the internal surface of
the fibrous pericardium
The visceral layer or epicardium lines the
surface of the heart
They are separated by the fluid-filled
pericardial cavity
7
Pericardial Layers of the
Heart
Outer balloon wall: superficial
fibrous pericardium, the inside
is lined by the parietal layer of
the serous pericardium
Air: The Pericardial cavity which
contains the pericardial fluid
Inner balloon wall is the visceral
layer of the serous pericardium
Figure 18.2
8
Pericardium: 3 Layers
Visceral Pericardium
touches the heart
(aka: epicardium)
Parietal Pericardium
Pericardial
Fluid is
between the
two layers
Parietal Pericardium
Parietal Pericardium: Lines
the internal surface of the
outer layer of fibrous dense
connective tissue
9
Pericardium
Visceral Pericardium:
Appears as a shiny surface
Parietal Pericardium:
Inside the sack around the heart
10
Layers of the Heart
Myocardium: Heart
muscle is thickest in the left
ventricle because this area
of the heart needs to
generate the most force.
(Think about where blood
in this chamber is going)
Endocardium:
simple squamous
epithelium lines the
chambers of the heart
11
Medical Examples
Pericarditis: Inflammation of the
pericardium
Pericardial Tampanade: Compression of
the heart caused by blood or fluid
accumulation in the space between the
heart and the fibrous pericardium
12
Cardiac tamponade
radiographics.rsna.org/.../g07nv13g04x.jpeg
www.beliefnet.com
13
Heart Wall – 3 layers
Epicardium: Visceral layer of the serous
pericardium on the outside
 Exposed layer of simple squamous epithelium
underlain by loose connective tissue
Myocardium: Cardiac muscle layer
 Contains blood vessels and nerves
 Fibrous skeleton of the heart: crisscrossing,
interlacing layer of connective tissue that
provides the origins and insertions for the
cardiac muscle cells
14
Heart Wall
Endocardium: Endothelial layer of the
inner myocardial surface (the
chambers)
 Simple squamous epithelium
 Is continuous with the endothelial lining of the
blood vessels
15
Heart Wall
16
Great Vessels of the Heart
Vessels returning blood to the heart include:
 Superior and inferior venae cavae
 Right and left pulmonary veins
Vessels conveying blood away from the heart
include:
 Pulmonary trunk, which splits into right and left
pulmonary arteries
 Ascending aorta, which curves into the aortic arch that
has three vessels branching from it – brachiocephalic,
left common carotid, and subclavian arteries
17
Great Vessels of the Heart
Superior Vena
Cava
Right Pulmonary
Artery
Pulmonary
Artery Trunk
Aortic Arch
Ascending
Aorta
Left
Pulmonary
Artery
Inferior Vena Cava
18
Ascending Aorta
Coronary
Artery
The coronary arteries
are the only vessels
that branch off the
Ascending Aorta
19
Aortic Arch
Right Common
Carotid Artery
Left Common
Carotid Artery
Right Subclavian
Artery
Brachiocephalic
Trunk
Left
Subclavian
Artery
Aortic Arch
Right Pulmonary
Artery
Left Pulmonary A.
20
Right Common
Carotid Artery
Left
Common
Carotid
Artery (2)
Right
Subclavian
Artery
Brachiocephalic
Trunk (1)
1
2
3
Aortic Arch
Left
Subclavian
Artery (3)
21
Chambers of the Heart: External
Left Atrium
Right
Atrium
Right Ventricle
Left Ventricle
22
Outer Surface Landmarks
Left Ventricle
Superior &
Inferior Vena
Cava enter the
Right Atrium
Right Ventricle
connects with the
pulmonary trunk
Left Ventricle
connects with the
Aorta, it fits
behind the
pulmonary trunk
23
Heart Chambers
24
Double Pump
The basic job of the heart is to pump blood.
Blood is actually pumped through 2 separate
circuits.
Pulmonary circuit: Runs between the heart and
the gas exchange surfaces of the lungs.
 Right ventricle-pulmonary arteries-pulmonary
capillaries-pulmonary veins-left atrium
Systemic Circuit: Runs between the heart and
the tissues of the rest of the body.
 Left ventricle-aorta-arteries-capillaries-veinsvena cava or coronary sinus-right ventricle.
25
26
Atria of the Heart
Atria are the receiving chambers of the
heart
 They are superior and mostly posterior to the
ventricles
Each atrium has a protruding auricle
which slightly increases its volume
Blood enters right atria from superior and
inferior venae cavae and coronary sinus
Blood enters left atria from pulmonary
veins
27
Atria of the Heart
The right atrium receives deoxygenated
blood from the systemic circuit and
passes it into the right ventricle, which
discharges it into the pulmonary circuit.
The left atrium receives oxygenated blood
from the pulmonary circuit and passes it
into the left ventricle, which discharges
it into the systemic circuit.
28
Atria of the Heart
Atria have thin, flaccid walls
corresponding to their light workload.
 Serve as receptacles for the blood
returning from the systemic and
pulmonary circuits. Most of this blood
flows into the ventricles due to gravity.
The right and left atrium are separated by
the interatrial septum.
29
Ventricles of the Heart
Ventricles are the discharging chambers
of the heart
Papillary muscles and trabeculae carneae
(create the waffle pattern) muscles mark
ventricular walls
Right ventricle pumps blood into the
pulmonary trunk
Left ventricle pumps blood into the aorta
30
Ventricles of the Heart
Interventricular septum: Separates the left
and right ventricles.
The left ventricle is 2-4x as thick as the
right ventricle
 LV has a greater workload (The LV and
RV pump EQUAL amounts of blood, but
the LV has to pump it against greater
resistance)
31
Consist of 2-3 flaps of
connective tissue
covered by
endothelium
Valves
32
Right Side of Heart
Tricuspid: Between
Right Atrium and
Right Ventricle
Pulmonic
Semilunar:
Between Right
Ventricle and
Pulmonary Trunk
Valves
Left Side of Heart
Mitral: Between
Left Atrium and
Left Ventricle
Aortic Valve:
Between Left
Ventricle and
Aorta
Chordae Tendineae are only on the Tricuspid and
Mitral Valves (valves between atrium and ventricle)
33
AV Heart Valves
Heart valves ensure one-way blood flow
through the heart
Atrioventricular (AV) valves lie between
the atria and the ventricles
 Right: Tricuspid Valve
 Left: Mitral Valve
AV valves prevent backflow into the atria
when ventricles contract
34
AV Heart
Valves
Chordae tendineae
anchor AV valves to
papillary muscles
 Made of strings
of collagen
Prevent valve flaps
from flipping
upward into the
atria
35
Tricuspid Valve: Between RA & RV
The leaflets are thin and delicate, and have thin
chordae tendineae that attach the leaflet margins to
the papillary muscles of the ventricular wall below.
36
AV Valves: Tricuspid &
Mitral
When the ventricles contract they are pressed
closed from the ventricular side.
37
AV Valves: Tricuspid &
Mitral
When the heart is relaxed the flaps hang open.
38
AV Valves
Figure 18.8c,
39 d
Semilunar Heart Valves
Aortic semilunar valve lies between the left
ventricle and the aorta
Pulmonary semilunar valve lies between
the right ventricle and pulmonary trunk
Semilunar valves prevent backflow of
blood into the ventricles
40
Semilunar Heart Valves
When the
ventricle
contracts blood
is pushed
against the AV
valve and
blood is
expelled
through the SL
valve into the
artery
41
Semilunar Heart Valves
When the
ventricle
relaxes blood
pressure is
higher in the
vessels,
which closes
the valve.
42
Pathway of Blood Through
the Heart and Lungs
Superior & Inferior Vena Cava - Right atrium 
tricuspid valve  right ventricle  pulmonary
semi lunar valve  pulmonary trunk  pulmonary
arteries  lungs
Lungs  pulmonary veins  left atrium mitral
valve  left ventricle  aortic semilunar valve 
aorta  systemic circulation
43
44
45
Pathway of Blood Through the Heart and Lungs
Figure4618.5
Blood Flow Through the Heart
1. Right Atrium
Blood arrives at the heart from the body
(systemic circuit)
Blood from the systemic circuit is high in
carbon dioxide and low in oxygen and will
arrive in the right atrium from 3 vessels.
 Superior vena cava: Drains head, torso, and
upper arms.
 Inferior vena cava: Drains abdomen, pelvis,
and legs.
 Coronary sinus: Drains the coronary
circulation.
47
Blood Flow Through the Heart
2. Right Ventricle
From the right atrium, blood passes the
tricuspid valve and enters the right
ventricle
Blood leaves from the right ventricle and
enters the pulmonary trunk to begin the
pulmonary circuit.
48
Blood Flow Through the Heart
3. Pulmonary Circuit
The pulmonary trunk splits into the right and left
pulmonary arteries.
Arteries branch into capillaries in the lungs
 The capillary beds are the place where O2 and CO2 are
exchanged.
Capillaries lead to the pulmonary veins (the
blood is now oxygen rich)
Pulmonary veins lead back to the heart with
oxygenated blood
49
50
Blood Flow Through the Heart
4. Left Atrium
Blood arrives at the
left atrium from the
4 pulmonary veins:
right superior,
right inferior, left
superior, and left
inferior pulmonary
veins
Left Atrium
Posterior View
51
Blood Flow Through the Heart
4. Left Ventricle
From the left atrium, blood passes the
mitral valve and enters the left ventricle
Blood leaves the left ventricle and enters
the aorta to begin the systemic circuit.
52
Blood Flow Through the Heart
4. Systemic Circuit
The aorta branches into arteries
Arteries lead into capillaries
Capillaries in the body exchange O2 and
CO2
Oxygen poor blood then enters veins
Veins converge into the inferior and
superior vena cava
53
54
Coronary Circulation
Coronary circulation is the functional
blood supply to the heart muscle itself
Collateral routes ensure blood delivery to
heart even if major vessels are occluded
These are the vessels that get blocked
during a heart attack
55
Coronary Circulation: Arterial Supply
Posterior descending Left anterior
descending (LAD)
artery (PDA)
56
Coronary Circulation: Venous Return
•20% drains directly into right ventricle
•80% returns to right atrium
57
Figure 18.7b
Coronary Blood Flow
When the heart relaxes high pressure of
blood in aorta pushes blood into
coronary vessels
Reduced during ventricular contraction
Increased during ventricular relaxation
 Blood flows into coronary arteries during
ventricular diastole
58
Coronary Artery Disease
(CAD)
Heart muscle receiving
insufficient blood supply
Narrowing of vessels:
atherosclerosis, artery spasm
or clot
 Atherosclerosis: smooth
muscle proliferation & fatty
deposits in walls of arteries
Treatment
 Drugs, bypass graft,
angioplasty, stent
59
Clinical Problems: CAD
MI: Myocardial infarction
 Death of area of heart muscle from lack of O2
 Replaced with scar tissue
 Results depend on size & location of damage
Blood clot
 Use clot dissolving drugs streptokinase or t-PA &
heparin
 Balloon angioplasty
Angina pectoris: heart pain from ischemia of
cardiac muscle
60
Coronary Artery Bypass Graft
(CABG)
61
Angioplasty
Thread a catheter
through the arteries
(like a maze) –
usually the femoral
artery
Once in position,
blow up the balloon
to push open the
blockage
62
Stent in an Artery
Same situation as angioplasty, but you put in this stent
to keep it open.
63
Cardiac Physiology
Major concepts:
1.
2.
3.
4.
5.
Contraction physiology
Electrical system
Cardiac cycle
Cardiac output
Health issues
Microscopic Anatomy of
Heart Muscle
Cardiac muscle is striated, short, fat,
branched, and interconnected
The connective tissue endomysium acts
as both tendon and insertion
Intercalated discs anchor cardiac cells
together and allow free passage of ions
Heart muscle behaves as a functional
syncytium
65
Functional Syncytium
The thousands of cardiac muscle cells behave
as if they were one giant cell.
All Cells are connected electrically and
mechanically.
This allows the heart to beat in an organized
fashion
Scar tissue from a heart attack interrupts the
functional syncytium and causes fibrillation
(we will examine this issue more later)
66
Microscopic Anatomy of Heart Muscle
67
Figure 18.11
Cardiac Muscle Histology
Branching cells
Once central nucleus
Intercalated disc: contains
many gap junctions
connecting the adjacent cell
cytoplasm, creates a
functional syncytium
68
Cardiac Muscle Metabolism
Aerobic respiration
 Minimal anaerobic respiration
Rich in myoglobin and glycogen
Large mitochondria
Organic fuels: fatty acids, glucose,
ketones
Fatigue resistant
69
Physiology of Contraction
Compare to
skeletal muscle
70
Physiology of Contraction:
Depolarization
Myocytes have stable resting potential of -90
mV
Depolarization (very brief)
 Stimulus opens voltage regulated Na+ gates, (Na+
rushes in) membrane depolarizes rapidly
 Excitation spreads through gap junctions
 Fast Na+ channels open for rapid depolarization
 Action potential peaks at +30 mV
 Na+ gates close quickly
 Ca+2 rushes into cytoplasm from SR and extracellular
fluid and binds to troponin to allow for actin-myosin
cross-bridge formation & tension development
71
Physiology of Contraction:
Plateau Phase & Repolarization
Plateau phase
 Period of maintained depolarization
 250 msec (only 1msec in neuron)
 Slow Ca+2 channels open, let Ca+2 enter from
outside cell and from storage in sarcoplasmic
reticulum
Repolarization
 Ca+2 channels close and K+ channels open
 Rapid K+ out returns to resting potential of
-90mv
72
Physiology of Contraction
Refractory period (from plateau to beginning of
repolarization
 Very long so heart can fill
 Absolute refractory period continues until
relaxation has started (200 msec)(relative
refractory is another 50 msec)
Tetanus (continuous contraction) and wave
summation cannot happen
• Why is this a good thing???
Skeletal muscle refractory period 0.4 to 1
msec
• Ends before peak tension develops so tetanus
can occur
73
Action Potential in Cardiac Muscle
Absolute refractory period
Changes in cell membrane permeability.
74
Terminology
An inotrope is an agent which increases
or decreases the force or energy of
muscular contractions.
A Chronotropic effects are those that
change the heart rate
75
Medical Example:
Calcium Channel Blockers
Keep in mind, there are many different types of CCB,
they can work on arterial smooth muscle, cardiac
contractile cells or the electrical system
The negative inotropic (decrease force of
contraction) effect is due to reduced inward
movement of Ca++ during the action potential
plateau phase
 Good for patients with HTN
 We will see later how contractility effects cardiac output
76
Cardiac Physiology
Cardiac Electrical
System
Cardiac Myocytes
99% are the contractile cardiac muscle
cells.
 Generate the force that pumps blood
through the systemic and pulmonary
circuits.
1% are the autorhythmic cells of the heart
 Lack the elaborate sarcomeres and other
contractile machinery
78
Autorhythmic Cells
Autorhythmic cells have the ability
to spontaneously depolarize to
threshold and generate action potentials
These cells set the rhythm of the heart
without any input from any external
organs, tissues, or signals.
(Keep in mind, the ANS does modify the
rate and strength of contraction, this is
just the baseline rhythm)
79
Spontaneous Depolarization
These cells are characterized as having no true
resting potential because they generate
regular, spontaneous action potentials.
Depolarizes because Ca2+ leaks in without help
from neural stimulation
Contrast to voltage gated Na+ channels in
muscle and neurons that must be activated
SA node depolarizes 100 times per minute
AV node depolarizes 40-60 times per minute
All other pacemaker cells: 20-35 times per
minute
80
Autorhythmic Cells
Sinoatrial Node (SA node) - Adjacent to the
SVC opening in the right atrium.
Atrioventricular Node (AV node) - Near the
right AV valve at the bottom of the
interatrial septum.
Atrioventricular Bundle (AV bundle or
Bundle of His) - Inferior interatrial septum.
Left & Right Bundle Branches Interventricular septum.
Purkinje Fibers - Distributed throughout the
right and left ventricle.
81
82
Sinoatrial Node (SA Node)
Pacemaker of the heart because they
have the fastest rate of depolarization
Depolarization begins in the SA node
travels throughout the atria to all the
contractile cells as well as to the cells in
the AV node.
The atrial contractile cells will respond to
the depolarization by contracting.
83
84
The purple
corresponds to the
path of the electrical
impulse and the
wave of contraction
85
At this point the
atria are
contracting and
the electrical
impulse is
traveling through
the
interventricular
septum
86
Atrioventricular Node (AV node)
At the AV node, the impulse is delayed
momentarily to allow the atria to
complete their contraction before the
ventricles begin to contract.
 This delay is due to the smaller diameter of
the fibers
 Takes about 50 msec
From the AV node, the impulse travels to
the AV bundle.
87
AV Bundle
The AV bundle is the only electrical
connection between the atria and the
ventricles.
The position ensures that the electrical
signal goes down the septum before
going to the myocardium
 This causes the ventricles begin
contracting at the septum then the
bottom (the apex) rather than the top.
88
AV Bundle
Bundle Branches
89
Bundle Branches &
Purkinje Fibers
The impulse travels on to the left and right
bundle branches and then onward to the
purkinje fibers
The Purkinje fibers direct the wave of
depolarization through the myocardium so it
can start contracting
 Depolarization travels to the ventricular
contractile cells via the gap junctions in the
intercalated discs.
 The ventricular contractile cells respond by
contracting.
90
91
Summary – conduction system
1.
2.
3.
4.
Sino-atrial node
Atrio-ventricular node
AV bundle (Bundle of His)
Perkinje fibres.
Atrial
contract
Ventricle
contract
92
Medical Example:
Calcium Channel Blockers (Again)
Negative chronotropic effects (slow rate) are also
seen with some of the Ca++ channel blockers
Decrease the rate of recovery of the slow channel
in AV conduction system and SA node, and
therefore act directly to depress SA node
pacemaker activity and slow conduction
 These ones are good for patients with HTN and
arrhythmias
 ? Why would you choose this type of drug over a BBlocker to slow the rate?
93
Extrinsic Influences on Heart Rate
The autonomic nervous system provides a large
influence on the activity of the heart.
 Sympathetic nervous system increases both
the rate and the force of heartbeat
The cardio-acceleratory center of the
medulla is the source of the sympathetic
output to the heart. Sympathetic nerve fibers
project to the SA node, AV node, and the
bulk of the myocardium
94
Extrinsic Influences on Heart Rate
 Parasympathetic nervous system decreases
heart rate but has little effect on the force of
contraction.
The cardio-inhibitory center of the medulla
is the source of the parasympathetic output
to the heart the vagus nerve (CN X) to the
SA and AV nodes.
Dominant during rest
Endocrine system plays a role as various
hormones (e.g., epinephrine, thyroid
hormone) can exert an effect on the heart's
rhythm.
95
96
Conduction Problems
Arrhythmia: An irregular heart rhythm.
Fibrillation: A condition of rapid and out-of-phase
contractions.
 In ventricular fibrillation, the depolarization and
contraction of the ventricular muscle cells is not
coordinated.
 Without a coordinated contraction as a unit, the
ventricles cannot generate enough force to propel blood
through the arterial system.
 This is the one they shock you for!
97
Cardiac Physiology
Cardiac Cycle
The Cardiac Cycle
Cardiac cycle: Everything that occurs between
the start of one heartbeat and the beginning of
the next.
For any one chamber in the heart, the cardiac
cycle can be divided into 2 phases:
 Systole = contraction.
 Diastole = relaxation.
Blood will only flow from point A to point B if the
pressure at point A is greater than at point B.
99
The Cardiac Cycle
The cardiac cycle can be broken down
into 4 phases:
Ventricular Filling
Isovolumetric Contraction
Ventricular Ejection
Isovolumetric Relaxation.
100
1. Ventricular Filling
AV valves are open
 Tricuspid and mitral (inflow from atria to
ventricles)
Semilunar valves are closed
 Aortic and pulmonary (outflow from ventricles)
Atrial pressure exceeds ventricular pressure
Both the atria and the ventricles are in diastole
 About 70% of the blood enters the ventricle passively
101
1. Ventricular Filling
Towards the end of ventricular filling, the SA
node will depolarize.
The resulting atrial depolarization will cause
atrial systole.
The contraction of the atria completes the
filling of the ventricles (final 30%).
The final ventricular volume (achieved just
prior to the beginning of ventricular systole)
is known as the end diastolic volume (EDV)
and is typically about 130mL.
102
2. Isovolumetric Contraction
The atria repolarize and remain in diastole
for the rest of the cardiac cycle.
Meanwhile, the ventricles depolarize and
begin to contract.
Blood surges upward and the AV valves
are forced shut
 This causes the first of the 2 heart sounds (S1)
that can be auscultated with a stethoscope
(phonetically it's given as LUB).
103
2. Isovolumetric Contraction
After the AV valves are closed, the heart
continues to contract as it tries to generate
enough pressure to open the semilunar valves.
During this time, the ventricular pressure is
rising (because the ventricles are contracting)
but the ventricular volume is not changing.
Thus this period is known as isovolumetric
contraction.
104
3. Ventricular Ejection
Ejection of blood begins when ventricular
pressure exceeds arterial pressure
 About 120mmHg in the left ventricle and 25mmHg in
the right ventricle.
 Blood spurts out of each ventricle rapidly at first and
then more slowly.
It's important to note that the ventricles do NOT
expel all their blood.
 The amount ejected (typically about 70mL) is known
as the stroke volume.
 The blood remaining in the ventricles is known as the
end systolic volume. ESV is typically about 60mL.
105
Stroke Volume
Stroke Volume=
End Diastolic Volume - End Systolic Volume
The stroke volume of the left ventricle
must equal the stroke volume of the
right ventricle.
106
Right sided
failure
Left sided
failure
107
4. Isovolumetric Relaxation
The ventricles now repolarize and enter
diastole. The ventricles begin to relax.
Pretty quickly, the pressure in the aorta
and pulmonary trunk exceeds ventricular
pressure and the semilunar valves shut
(this causes the 2nd heart sound (S2) the DUP).
108
4. Isovolumetric Relaxation
However, it takes a lot longer for ventricular
pressure to drop below atrial pressure.
 Remember, the blood will only flow from a
higher pressure area to a lower pressure area
Before this happens, the ventricles are relaxing
and pressure is dropping, but the volume is
not changing - thus we have isovolumetric
relaxation.
When ventricular pressure does drop below
atrial pressure, the AV valves open and
ventricular filling begins anew
109
110
111
Cardiac Cycle Summary
Atrial contraction begins
Atria ejects remaining 30% of blood into ventricles (S4)
Atrial systole ends, AV valves close (S1)
Isovolumetric ventricular contraction
Ventricular ejection occurs
Semilunar valves close (S2)
Isovolumetric relaxation occurs
AV valves open, rapid ventricular filling (70%)
(passive: this is atrial diastole) (S3)
Repeat ….
(keep in mind, there is a constant flow of blood into the
atria)
112
Cardiac Physiology
Cardiac Output
Cardiac Output
Cardiac Output is the volume of blood
ejected by each ventricle in one minute
Stroke Volume(mL/beat) x Heart
Rate(beats/minute) = Cardiac
Output(mL/minute)
Cardiac output varies with the body's state
of activity. For example, cardiac output
increases during exercise.
114
Example
Suppose Bob's heart rate was 1 beat per
second. His EDV was 140mL and his ESV
was 60mL. What was his cardiac output?
Heart Rate = (1 beat/second) x (60
seconds/minute) = 60 beats/minute
SV = EDV - ESV = 140 mL/beat - 60 mL/beat =
80mL/beat
CO = SV x HR = 80ml/beat x 60 beats/minute =
4800 mL/minute
115
Cardiac output will vary directly with
both heart rate and stroke volume
116
Factors Affecting Stroke
Volume
Stroke volume is primarily governed by 3
factors:
Preload: The amount of tension in the
ventricular myocardium just prior to
contraction
Contractility: The contraction force at any
given preload
Afterload: The blood pressure just outside the
semilunar valves (in the aorta and pulmonary
trunk).
117
Preload
Amount of tension in ventricular myocardium
before it contracts
↑ preload causes ↑ contraction strength
 exercise ↑ venous return, stretches myocardium
(↑ preload) , myocytes generate more tension during
contraction, ↑ CO matches ↑ venous return
Frank-Starling law of heart: Stroke volume is
proportional to EDV
 The more the heart fills during diastole, the greater the
force of contraction during systole (within limits)
118
Contractility
Contraction force for a given preload
Tension caused by factors that adjust myocyte’s
responsiveness to stimulation
 Factors that ↑ contractility are positive inotropic
agents
NE, hypercalcemia, catecholamines,
glucagon, digitalis
 Factors that ↓ contractility are negative inotropic
agents
Hyperkalemia (K+), hypocalcemia, hypoxia,
hypercapnia
119
Afterload
Pressure in arteries above semilunar valves
opposes opening of valves
 Basically, this is the pressure in the aorta or pulmonary
arteries that the heart needs to work against
↑ Afterload ↓ SV
 any impedance in arterial circulation ↑ afterload
Continuous ↑ in afterload (lung disease,
atherosclerosis, etc.) causes hypertrophy of
myocardium, may lead it to weaken and fail
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Cardiac Physiology
Health Issues
Valvular Pathologies
Murmur: Abnormal heart sound due to
turbulent blood flow. Not always
pathologic
Prolapse: Malfunction where one or more
valve flaps bulge backward. (valves are
leaky)
 Blood goes back from where it came (backflow)
because the door is left open
 Example Mitral valve prolapse: blood goes back
to the left atrium and can congest the lungs
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Valvular Pathologies
Stenosis: Narrowing of the opening of a
valve often caused by the stiffening of
valve cusps due to scar tissue formation.
 Greater force is needed to push blood through
 Mitral valve stenosis can cause ↑ left atrial
pressure, which leads to ↑ pulmonary venous
pressure → pulmonary edema
 Aortic stenosis, get left ventricular hypertrophy
and/or pulmonary edema
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Medical Example
Lowering arterial resistance (blood pressure) will
decrease cardiac afterload
Some calcium channel blockers:
 Decreased intracellular Ca++ in arterial smooth muscle
results in relaxation (vasodilatation)
 Little or no effect on venous beds (no effect on cardiac
preload
Alpha blockers: decrease sympathetic
vasoconstriction in arteries
Other blood pressure lowering agents also
decrease afterload
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Exercise and Cardiac Output
Effect of proprioceptors
 HR ↑ at beginning of exercise due to signals from
joints, muscles
Effect of venous return
 Muscular activity ↑ venous return causes ↑ SV
↑ HR and ↑ SV cause ↑CO
Effect of ventricular hypertrophy
 Caused by sustained program of exercise
 ↑ SV allows heart to beat more slowly at rest, 40-60bpm
 ↑ cardiac reserve, can tolerate more exertion
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Risk Factors for Heart
Disease
Risk factors in heart disease:
 High blood cholesterol level
 High blood pressure
 Cigarette smoking
 Obesity & lack of regular exercise.
Other factors include:
 Diabetes mellitus
 Genetic predisposition
 High blood levels of fibrinogen
 Left ventricular hypertrophy
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Plasma Lipids and Heart
Disease
Risk factor for developing heart disease is high blood
cholesterol level.
 Promotes growth of fatty plaques
 Most lipids are transported as lipoproteins
 HDLs (high-density lipoproteins) remove excess cholesterol from
circulation
 LDLs (low-density lipoproteins) are associated with the formation
of fatty plaques
 VLDLs (very low-density lipoproteins) contribute to increased fatty
plaque formation
There are two sources of cholesterol in the body:
 in foods we ingest & formed by liver
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Desirable Levels of Blood
Cholesterol for Adults
TC (total cholesterol) under 200 mg/dl
LDL under 130 mg/dl
HDL over 40 mg/dl
Normally, triglycerides are in the range of
10-190 mg/dl.
Among the therapies used to reduce
blood cholesterol level are exercise,
diet, and drugs.
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In these patients you want a positive inotrope
Congestive Heart Failure
When the pumping efficiency, i.e., the cardiac
output, is so low that the blood circulation is
inadequate to meet tissue needs
Causes: coronary artery disease, high BP, MI,
valve disorders, congenital defects
Left side heart failure
 Less effective pump so more blood remains in
ventricle (right side pumps more blood)
 Blood backs up into lungs as pulmonary edema
Right side failure
 Fluid builds up in tissues as peripheral edema
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The End