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Chapter 20
Cardiovascular System:
The Heart
AP2 Chap. 20: Cardio Syst-Heart
1
Cardiovascular System: The Heart
I. Fxns of the heart
II. Size, Shape, & Location of the heart
III. Anatomy of the heart
IV. Route of blood flow thru the heart
V. Histology
VI. Electrical Properties
VII. Cardiac Cycle
VIII.Mean Arterial BP
IX. Regulation of the heart
X. Heart & Homeostasis
XI. FX of aging on the heart
AP2 Chap. 20: Cardio Syst-Heart
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Cardiovascular System
• Heart is actually
2 pumps:
 1st pump receives
O2 poor blood from
the body and
pumps it to the
lungs
–
Pulmonary
Circulation
 2nd pump receives
O2 rich blood from
the lungs and
pumps it to the
body
–
Systemic
Circulation
Fig. 20.1 pg 679
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I. Functions of the Heart
AP2 Chap. 20: Cardio Syst-Heart
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I. Fxns of the heart
1. Generating BP (blood
pressure)
–
Pg 680 Figure 20.2a
Contractions of the ♥ generate
the BP, wh/ is responsible for
blood mvment thru vessels
2. Routing Blood
–
♥ is the interchange between
pulmonary & systemic
circulation, thus insuring better
oxygenation of bld going to
tissues
3. Insuring One-Way blood flow
–
Valves of the heart are 1-way
thus insuring no backflow
4. Regulating Blood Supply
–
As metabolic needs of the
tissues D the heart can D rate &
force of contraction to aid the
AP2 Chap. 20: Cardio Syst-Heart
tissues
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II. Size, shape, & location of the ♥
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II. Size, shape, & location of
the ♥
• ~ size of a
closed fist,
shaped like a
blunt cone
• Lies obliquely
within the
mediastinum
with its base
directed back
and superior &
apex coming
forward inferiorly
to the left.
AP2 Chap. 20: Cardio Syst-Heart
Front View
Pg 684 Figure 20.5 a
Posterior View
Pg 685 Figure 20.5 c
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III. Anatomy of the ♥
A.
B.
C.
D.
Pericardium
Heart Wall
External Anatomy & Coronary Circulation
Heart Chambers & Valves
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III. Anatomy of the heart: Pericardium
• A sac surrounding the heart made of 2 layers that can also be
called the pericardial sac.
• It can D in size to accommodate more fluid or D in heart size
1. Fibrous Pericardium
–
Pg 681 Figure 20.3
Aids in holding the heart in
place
2. Serous Pericardium
–
Reduces friction as the heart
beats and is made up of 3
regions:
a) Parietal Pericardium
•
Lies just under & Lines #1
b) Pericardial Cavity
•
•
c)
Lies between a) & c) filled with
pericardial fluid
Helps reduce friction as heart
moves in the pericardial sac
Visceral Pericardium
•
Lines the exterior surface of the
heart
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III. Anatomy of the Heart: Heart Wall
• Has 3 main layers:
1. Epicardium
•
Outermost layer that protects from
friction
Pg 682 Figure 20.4
2. Myocardium
•
Middle layer responsible for
contraction
3. Endocardium
•
•
•
•
Atria (top chambers)
–
•
Innermost layer & protects from friction
created by flowing blood
Simple squamous epi over CT
Heart valves are modified
Endocardium
Mainly smooth w/some raised areas
called pectinate muscles that are
separated by smooth parts by a
ridge called cristae terminalis
Ventricles (bottom chambers)
–
Have large ridges called trabeculae
carneae
10
III. Anatomy of the Heart:
External Anatomy & Coronary Circulation
Right
Auricle
Left
Auricle
There is also a posterior
Interventricular Sulcus
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III. Anatomy of the Heart:
External Anatomy & Coronary Circulation
These veins come from the
body with O2 poor blood and
empty into the right atrium
+ Coronary Sinus
These veins come from the
lungs with O2 Rich blood and
empty into the left atrium.
12
III. Anatomy of the Heart:
External Anatomy & Coronary Circulation
These arteries exit the heart
carrying O2 poor blood to the
lungs
This major artery exits the heart
carrying O2 rich blood to the
body.
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III. Anatomy of the Heart:
External Anatomy & Coronary Circulation
Blood flow to the coronary
blood vessels isn’t
continuous.
• Cardiac Muscle
contracts blood vessels
get compressed & blood
doesn’t readily flow
• Cardiac Muscle relaxes 
Blood vessels aren’t
compressed & blood flow
thru the coronary blood
vessels resumes
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III. Anatomy of the Heart: External Anatomy & Coronary Circulation
Major Arteries (A) supplying heart tissue
• Lie within the coronary sulcus & interventricular sulci.
• Rt. & Lt. Coronary Arteries (CA)
– Major A’s supplying blood to heart
– Exit the aorta just as it leaves the heart and lie w/in the coronary sulcus
– Right is smaller in diameter than left
Branches of the Rt.CA
• Rt. Marginal A
• Supply bld to lat’l
wall of the rt
ventricle
• Post’r Interventricular
A.
• Supplies bld to
the posterior &
inferior region of
the heart
Pg 685 Figure 20.6a
Branches of the Lt.CA
• Ant. Interventricular A
– Supplies most of
the ant. heart
• Left Marginal A
– Supplies bld to the
lat. lt. ventricle
• Circumflex A
– supplies most of
the posterior
heart.
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III. Anatomy of the Heart: External Anatomy & Coronary Circulation
Major veins (V) draining the heart tissue
Pg 685 Figure 20.6a
• Great Cardiac V
– Major vein draining the
tissue on the left side of the
heart
• Small Cardiac Vein
– Drains the right margin of
the heart
• Both empty into the
Coronary Sinus
– Empties into the right
atrium
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hambers & Valves
III. Anatomy of the heart:
Interatrial Septum
• piece of tissue that
separates L from R atrium
• Foremen Ovale/ Fossa
Ovalis
• Ovale, an opening
between the atria in a
embryo & fetus to
bypass pulmonary
circulation that seals
and forms the Ovalis
Pg 686 Figure 20.7
Right Atrium
Left Atrium
– Upper R chamber
– 3 openings:
– Upper L chamber
– 4 uniform openings:
1. Superior Vena Cava
–
Drains upper body
2. Inferior Vena Cava
–
Drians Lower Body
3. Coronary Sinus
–

Pulmonary Veins
1.
2.
2 from each lung
Drains lungs after
getting O2
Drains the Heart
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hambers & Valves
III. Anatomy of the heart:
Interventricular Septum
• Thick muscular piece of
tissue that separates L
from R ventricle
• Each ventricle has 1
large, superiorly placed
outflow route near
midline
Pg 686 Figure 20.7
Right Ventricle
Left Ventricle
– Lower R chamber
– Opens to the
pulmonary trunk
– Lower L chamber
– Opens to the aorta
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Semilunar Valves
• Composed of 3 pocket like
semilunar cusps/flaps the
free inner borders meet in
the center of the arteries to
block blood flow.
Pulmonary Valve
Between the R
ventricle and the
Pulmonary Trunk
Aortic Valve
Between L ventricle
and the Aorta
III. Anatomy of the heart:
Chambers & Valves
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Atrioventricular Valves
– Composed of
cusps/flaps allow blood
to flow from atrium to
the ventricles but
because of design help
to prevent back flow
Tricuspid Valve
Between the R
atrium and R
ventricle
3 cusps/flaps
Bicuspid Valve
Between the
L atrium and
L ventricle
2 cusps/flaps
III. Anatomy of the heart:
Chambers & Valves
20
Pg 687 Figure 20.9
• Blood pushing out of the ventricle causes enough pressure to push the
semilunar valves open while at the same time causing the atrioventricular
valves to seal with the help of the chordae tendineae and the papillary
muscle. As the ventricle relaxes the semilunar valves get sucked back
effectively sealing them while the atrioventricular valves open
• Chordae Tendineae
• Strong CT strings that connect to the cusps of AV-valves
• Papillary Muscle
• Cone-shaped muscular pillars, that contract when V contract & prevent
flaps from protracting
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IV. Route of blood flow thru
the heart
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Figure 20.10
Pg 688
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Cardiac Cycle
• Arteries:
• BLUE:
– Carries blood away
from the heart
• Veins:
– Deoxygenated blood
• RED
– Oxygenated blood
– Carries blood toward
the heart
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Lung
Tissue
Body
Tissue
Left
Atrium
Right
Atrium
Right
Ventricle
Left
Ventricle
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Tricuspid
Valve
Pulmonary
Semilunar
Valve
Bicuspid
Valve
Aortic
Semilunar
Valve
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Pulmonary
Arteries
Coronary
Arteries
Inferior
Vena
Cava
Pulmonary
Veins
Superior
Vena
Cava
Coronary
Sinus
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Body
Tissue
Inferior
Vena
Cava
Superior
Vena
Cava
Coronary
Sinus
• Deoxygenated blood drains into the Right atrium via the:
– The inferior vena cava drains the lower body tissue
– The superior vena cava drains the upper body tissue
– The coronary sinus drains the heart tissue
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Right
Atrium
• The right atrium fills with deoxygenated blood
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Right
Atrium
Tricuspid
Valve
• Deoxygenated blood goes from the right atrium
thru the tricuspid valve into the right ventricle. 30
Right
Ventricle
• The right ventricle fills with deoxygenated blood
31
Pulmonary
Semilunar
Valve
Right
Ventricle
• Deoxygenated blood is squeezed from the right
ventricle thru the pulmonary semilunar valve into the
32
pulmonary trunk.
Pulmonary
Arteries
Lung
Tissue
• The pulmonary trunk splits into the right and left pulmonary arteries
carrying deoxygenated blood in to the right and left lungs
respectively to pick up oxygen and drop off carbon dioxide.
33
Lung
Tissue
• In the lungs CO2 is exchanged for O2
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Lung
Tissue
Left
Atrium
Pulmonary
Veins
• The right and left pulmonary veins carry the newly
oxygenated blood back to the left atrium from the
right and left lungs respectively.
35
Left
Atrium
• The left atrium fills with freshly oxygenated
blood.
36
Left
Atrium
Bicuspid
Valve
Left
Ventricle
• The oxygenated blood is pumped from the left atrium
thru the bicuspid valve into the left ventricle.
37
Left
Ventricle
• The left ventricle fills with freshly oxygenated
blood.
38
Aorta
Aortic
Semilunar
Valve
Left
Ventricle
• Oxygenated blood is squeezed from the left ventricle
thru the aortic semilunar valve into the aorta.
39
Coronary
Arteries
Aorta
Body
Tissue
Aortic
Semilunar
Valve
• The aorta splits into the right and left coronary
arteries carrying oxygenated blood to the heart
tissue.
40
Coronary
Arteries
Aorta
Body
Tissue
• Then the aorta continues to carry the oxygenated
blood to the body tissues.
41
V. Histology
A. Heart Skeleton
B. Cardiac Muscle
C. Conducting System
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V. Histology: Heart Skeleton
• Consists of a plate of
fibrous CT that serves 3
purposes:
1. Supports both the
semilunar &
atrioventricular valves to
insure they don’t collapse
2. Acts as electrical
insulation between the
atria & ventricles
3. Acts as a point of
attachment for cardiac
muscle
AP2 Chap. 20: Cardio Syst-Heart
Figure 20.11
Pg 690
43
V. Histology: Cardiac Muscle (CM)
Figure
20.11
Pg 690
• CM cells joined by intercalated
disks that allow action
potentials to move directly from
1 cell to the next, thus cardiac
muscle cells fxn as a unit
– Intercalated disks are a combo of
desmosomes (wh/hold cells
together) & gap junctions
(wh/allow for cell to cell
communication)
• Elongated, branching
cells w/ 1 or 2 centrally
located nuclei.
• Like skeletal muscle actin
& myosin are organized
to form sarcomeres.
Arrangement of both the
Smooth ER & transverse
tubules varies but fxns
essentially the same.
• CM cells have a slow onset as
well as period of contraction
due to Ca2+ mvmt along
myofibrils.
• Has a good blood supply to
support aerobic respiration
– ATP prod’d with:
• Glucose, Fatty Acids, Lactic Acid
• CM doesn’t develop O2-debt
44
V. Histology:
Conducting System (CS)
• Consists of modified CM-cells
that form 2 nodes & a conducting
bundle. (both of which are made
up of small diameter cells to slow
action potential)
1. SA-Node
2. AV-Node
•
•
•
SA-node initiates action
potentials that spread across the
atria & cause them to contract
At the AV-node action potential
slows allowing atria to complete
contraction & ventricles to fill
Next it follows along the AV
bundle, Rt & Lt bundle branches
& Purkinje fibers.
–
This causes the contraction of the
ventricles from the apex of the
heart toward the base
SA-node

AV-node

AV bundle

Rt & Lt Bundle braches

Purkinje fibers
45
V. Histology: Conducting System (CS)
• The CS of the heart consists
of modified CM-cells that
form 2 nodes & a
conducting bundle.
1. SA-Node medial to the
opening of the superior vena
cava
•
A.k.a. Pacemaker (generates
spontaneous action potentials)
2. AV-Node- medial to the
tricuspid valve
SA-node AV-node AV
bundle Rt & Lt Bundle
braches Purkinje fibers
46
VI. Electrical Properties
A. Action potentials
B. Autorhythmicity of cardiac muscle
C. Refractory periods of cardiac muscle
D. Electrocardiogram
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VI. Electrical Properties
• CM have a resting membrane potential
(RMP)
• Depends on the permeability of the PM
– Low permeability to Na+ and Ca2+
– Higher permeability to K+
• Once their threshold is reached….an
Action Potential results
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VI. Electrical Properties: Action Potentials
Permeability D’s during and action
potential in CM
1.
Depolarization Phase
–
Voltage-Gated (VG) Na+ channels open
(Na+ rushes in)
VG K+ channels close (K can’t get out)
VG Ca2+ channels begin to open (Ca2+
goes in)
–
–
2.
Early Repolarization & Plateau Phase
–
VG Na+ channels close (Na+ can’t get
in)
Some VG K+ channels open causing
“early” repolarization
–
•
–
3.
K+ goes out in a rush
VG Ca2+ channels are open, prod’ing
the plateau by further slowing
repolarization (Ca2+ coming in)
Final Repolarization Phase
–
–
VG Ca2+ channels close
Many VG K+ channels open
Action potentials in CM last longer
than in SM
SM 2 ms
CM 200-500ms
49
VI. Electrical Properties: Action Potentials
• Gap junctions w/in
intercalated disks do
allow action potentials
to transfer between
CM-cells, but they do
slow the rate of the
action potential
between them.
• Calcium-induced calcium
release (CICR)
– Movement of the Ca2+ into
the cell stimulates the
release of Ca2+ from the
sarcoplasmic reticulum
• Ca2+ binding facilitates the
interaction between actin &
myosin to produce the
contraction of CM.
AP2 Chap. 20: Cardio Syst-Heart
50
VI. Electrical Properties:
Autorhythmicity of the heart
• Autorhythmicity means at
regular intervals it is selfstimulating
• SA-node’s pacemaker
cells generate action
potentials spontaneously &
@ regular intervals.
– This is the initial step toward
full heart contraction.
– Prepotential is the beginning
of the spontaneously
developing local potential in
the pacemaker cells
• Unlike other CM-cells,
Ca2+ is primarily
responsible for the
depolarization phase in
pacemaker cells.
• Even with the SA-node
setting the rhythm of the
heart there are some
other CM-cells that can
generate spontaneous
AP’s, the SA node is just
quicker than the others
thus setting the pace.
These other regions are
called Ectopic Focuses.
– Ex/ AV-bundle
– Artificial EF’s can be
created by changing the
CM-cell membrane’s
permeability
51
VI. Electrical Properties
Refractory periods of CM
• Time it takes to begin another AP.
– Absolute
– Relative
• CM has a prolonged depolarization & thus a prolonged RP. This
allows time for cardiac muscle to relax b4 the next action potential
causes a contraction.
Electrocardiogram
• Records the electrical activities of the
heart.
• Can be used as a diagnostic tool.
• P-wave Depolarization of atria
• QRS-wave Depolarization
ventricles (AV-node R&L bindle
branches, & Purkinje fibers)
• T-wave repolarization of ventricles
52
VII. Cardiac Cycle
•Repetitive pumping process that
begins w/the onset of CM
contraction and ends with the
A. Events occurring during ventricular
systole
B. Events occurring during ventricular
diastole
C. Heart Sounds
D. Aortic Pressure Curve
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53
VII. Cardiac Cycle
Heart: 2 separate circuits in the same organ
RIGHT SIDE
O2 poor blood from body

R Atrium

Tricuspid Valve

R Ventricle

Pulmonary Valve

Lungs for O2 pick-up
LEFT SIDE
O2 rich blood from lungs

L Atrium

Bicuspid Valve

L Ventricle

Aortic Valve

Body to drop off O2 & pick-up CO2
The Atria
Each atria can be considered a primer pumps

The Ventricles
Each Ventricle can be considered a power pumps
Produce major force causing blood to flow thru
pulmonary & systemic arteries (respectively)
Movement from High to Low pressure
54
– Ventricular systole
– Atrial systole
• Diastole: to dilate
– Ventricular diastole
– Atrial diastole
• Without “reference” to V or
A. It is referring to V only
AP2 Chap. 20: Cardio Syst-Heart
V. Diastole
A. Systole
• Time frame between cycles
can vary widely from 0.25s
in newborns to 1s or more in
well trained athletes
• Systole: to contract
V. Systole
VII. Cardiac Cycle
55
• Period of isovolumic contraction
• Period of ejection
– Once the V’s have enough
pressure to cause the semilunar
valves of the aorta and pulmonary
arteries to open pushing the blood
through (Pressure in V’s is greater
than in the Pulmonary trunk or
aorta)
• Period of isovolumic relaxation
– As V’s relax pressure w/in
decreases below that in the
pulmonary trunk & aorta causing
the blood to flow back toward the
V’s wh/causes the semilunar valves
to close. When the valves close all
valves are closed and no blood
flows into relaxing V’s
VII. Cardiac Cycle
– Brief interval in which the V’s (filled
with blood) begin to contract but no
movement of blood occurs because
the pressure isn’t yet great enough
to open the valves
56
VII. Cardiac Cycle: 5 periods
1. Period of Isovolumic Contraction: heart is
contracting but vol isn’t Ding b/c valves are not
open
2. Period of Ejection: semilunar valves open &
blood is ejected
3. Period of Isovolumic Relaxation: heart muscle
is relaxing but vol doesn’t D b/c no valves are
open
4. Passive Ventricular Filling when blood flows
from higher pressure in veins & atria into the
lower pressured relaxed ventricles
5. Active Ventricular Filling results when atria
contract & pump blood into the ventricles
AP2 Chap. 20: Cardio Syst-Heart
57
Figure 20.18 pg 698
58
VII. Cardiac Cycle:
Events of:
Ventricular Systole
• Contraction of V closes AV
valves, opens semilunar
valves, & ejects blood from
the heart
• End diastolic volume: vol of
bld just b4 it contracts
• End Systolic Volume: vol of
bld after contraction
Ventricular Diastole
•
•
•
Relaxation of the V results in
closing of the semilunar valves,
opens the AV valves, &
movement of bld into V
Most bld mvmt occurs when bld
moves from higher pressure in
veins & atria to the lower
pressure (sucking) relaxing V’s
Contraction of the Atria
completes filling
Heart Sounds
• 1st Sound: “Lubb”  Closure of the AV Valves
• 2nd Sound  “Dupp” Close of the Semilunar Valves
• Possible 3rd sound  Turbulent blood flow
59
VIII. Mean Arterial Blood Pressure
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60
VIII. Mean Arterial Blood Pressure (MAP)
• Ave. bld pressure in the aorta
MAP= CO X PR
• Cardiac Output (CO)  amount of bld pumped thru the
heart per minute
– CO= heart rate X stroke volume
– Stroke Volume is the amount of bld pumped thru the heart
per beat
• Equal to ( end-diastolic volume – end-systolic volume)
• This can D based on 2 things
– Venus return (amount of bld coming into heart) increases SV
– Increased ventricular contraction can increase SV
• Peripheral Resistance (PR)  total resistance to bld
flow thru bld vessels
• Cardiac reserve  difference btwn resting & exercising
CO
61
Figure 20.21 Factors affecting MAP
pg 704
AP2 Chap. 20: Cardio Syst-Heart
62
IX. Regulation of the Heart
A. Intrinsic Regulation
B. Extrinsic Regulation
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63
IX. Regulation of the heart
To maintain homeostasis, the amount of blood pumped by
the heart must vary dramatically
• Intrinsic Regulation:
– Results from normal fxnal
characteristics of the heart
– Doesn’t depend on
neuronal or hormonal
regulation
• Extrinsic Regulation:
– Involves neural & hormonal
control
– Neural: sympathetic &
parasympathetic reflexes
– Hormonal: epi & norepi
from the adrenal medulla
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64
IX. Regulation of the heart
Intrinsic Regulation
• As venous return increases, end-diastolic volume
increases. The greater the end-diastolic volume, the
greater the stretch on the ventricular walls.
• Preload extent to wh/ventricular walls are stretched
• Cardiac muscle exhibits a length vs. tension
relationship. Meaning the longer it gets the more
power it contracts with.
• Venous Return:
– amount of bld returning to heart @ each cardiac cycle
• Starlings law of the heart
– Increased Preload causes the CM-fibers to contract w/greater
force & prod a greater stroke volume
– Afterload- pressure the contracting ventricles must overcome
to move bld.
65
IX. Regulation of the heart
Extrinsic Regulation
Nervous System Control
• Cardioregulatory center of the medulla oblongata regulates the
parasympathetic & sympathetic nervous control of the heart
– PNS
• Supplied by the vegus nerve
• Postganglionic neurons secrete Ach  increases membrane permeability to
K+  hyperpolarizes the membrane  slows down action potentials 
decreases heart rate
– SNS
• Supplied by cardiac nerves
• Postganglionic neurons secrete norepi  increases membrane permeability
to Na & Ca  depolarization of the membrane  speeds up action
potentials increases heart rate & force of contraction
Hormonal Control
• Epi & Norepi get released from the adrenal medulla into bld as
a result of SNS stimulation
– Long lasting FX compared to NS stimulation
– Increases the rate & force of CM contraction.
66
X. Heart & Homeostasis
A. Effect of BP
B. Effect of pH, CO2, & O2
C. Effect of Extracellular Ion [ ]
D. Effect of Body Temperature
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67
X. Heart & Homeostasis
Pumping efficiency of the heart plays an important role in the
maintenance of homeostasis. BP in systemic circulation must
be maintained at a level high enough to achieve any XD that
must occur. And conditions of metabolic activity may D thanks to
exercise & rest
FX of BP
FX of Extracellular ion [ ]
• Baroreceptors are those that
monitor BP (Stretch receptors)
• Decrease in BP
baroreceptor reflexes increase
SNS stimulation & decrease
PNS stimulation of heart. 
increase in heart rate & force
of contraction
• Increase or decrease in
extracellular K  decrease
in heart rate
• Increase in extracellular Ca
 increased force of
contraction & decrease
heart rate
– Decreased Ca opposite FX
FX of Body Temperature
• Increase in body temp  increase in heart rate
• Decrease in body temp  decrease in heart rate
68
Fig 20.23
Pg 708
AP2 Chap. 20: Cardio Syst-Heart
69
X. Heart & Homeostasis
FX of pH, CO2, & O2
Chemoreceptors (CR) monitor blood pH, CO2, and O2
Response:
• All regulatory
mechanisms fxning
• Medullary CR reflexes
together respond to:
–  CO2 &  pH
•  SNS &  PNS
stimulation of the heart
• Carotid body CR reflex
– Stimulated by  O2 levels
• Decreased heart rate &
vasoconstriction
–  blood pH
–  blood CO2 levels
–  blood O2 levels
• Produce an increase in
heart rate &
vasoconstriction
• Lowered O2 increases
respiratory rate wh/
activates the SNS
stimulation of the heart
AP2 Chap. 20: Cardio Syst-Heart
70
Fig 20.24
Pg 709
AP2 Chap. 20: Cardio Syst-Heart
71
XI. FX of Aging of the heart
AP2 Chap. 20: Cardio Syst-Heart
72
XI. FX of Aging of the heart
• Aging results in gradual changes to the heart that
are mostly seen when exercising
• Abnormal enlargement (Hypertrophy) of the L.
ventricle is common
• Max Heart rate may decrease
• Increase in abnormal valve fxn & arrhythmia
• Increased O2 consumption, req’d to pump same
amount of bld, make age-related coronary artery
disease more severe
• Exercise improves fxnal capacity of heart at all
ages
AP2 Chap. 20: Cardio Syst-Heart
73