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unit 4 youtube -https://youtu.be/eslA6rU55To – cooresponds to week 4
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The heart
Dr. S. Glaser
Bio 12
19-1
The Heart- an overview
• Overview of Cardiovascular System
• Gross Anatomy of the Heart
• Cardiac Conduction System and Cardiac
Muscle
• Electrical and Contractile Activity of Heart
• Blood Flow, Heart Sounds, and Cardiac
Cycle
• Cardiac Output
19-2
What are the functions of the
circulatory system?
• Let’s list some……
• What does the circulatory system need to
do to accomplish these tasks?
19-3
Circulatory System: The Heart
• cardiology – the study of the heart and the
treatment of its disorders
• major divisions of circulatory system
– pulmonary circuit – begins at right side of heart
• carries blood to lungs for gas exchange and then returns
to heart
– systemic circuit – begins at left side of heart
• supplies oxygenated blood to all tissues of the body and
returns it to the heart
19-4
Cardiovascular System Circuit
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
left side of heart
– fully oxygenated
blood arrives from
lungs via
pulmonary veins
– blood sent to all
organs of the body
via aorta
right side of heart
– blood with lower
oxygen content
arrives from inferior
and superior vena
cava
– blood sent to lungs
via pulmonary
19-5
trunk
Position, Size, and Shape of Heart
• heart located in
mediastinum (central
compartment of the
thoracic cavity), between
lungs
• base – wide, superior
portion of heart, blood
vessels attach here
• apex – inferior end, tilts to
the left, tapers to point
• The heart is roughly the
size of your clenched fist.
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”.
WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-6
pericardium – doublewalled sac
(pericardial sac) that
encloses the heart
-allows heart to beat
without friction,
provides room to
expand, yet resists
excessive expansion
-anchored to diaphragm
inferiorly and sternum
anteriorly
parietal pericardium
– outer wall of sac
superficial fibrous layer
of connective tissue
a deep, thin serous
layer
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-7
visceral
pericardium
(epicardium) –
heart covering
serous lining of sac
turns inward at base
of heart to cover the
heart surface
pericardial cavity space inside the
pericardial sac filled
with 5 – 30 mL of
pericardial fluid
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-8
endocardium
smooth inner lining of
heart and blood
vessels covers the
valve surfaces and
continuous with
endothelium of blood
vessels
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-9
myocardiumlayer of cardiac muscle
proportional to work load
muscle spirals around
heart which produces
wringing motion
fibrous skeleton of the
heart – framework of
collagenous and elastic
fibers
provides structural support
and attachment for cardiac
muscle and anchor for
valve tissue
electrical insulation
between atria and
ventricles important in
timing and coordination of
contractile activity
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-10
Cardiac Muscle
cardiocytes striated, short, thick,
branched cells, one
central nucleus
surrounded by light
staining mass of
glycogen
– electrical junctions gap junctions allow
ions to flow between
cells – can stimulate
neighbors
• entire myocardium of
either two atria or two
ventricles acts like
single unified cell
BruceBlaus [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]
19-11
Cardiac Muscle
BruceBlaus [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]
• intercalated discs – join cardiocytes
– interdigitating folds – folds interlock with each other, and increase
surface area of contact
– mechanical junctions tightly join cardiocytes
• fascia adherens – broad band in which the actin of the thin myofilaments is
anchored to the plasma membrane
– each cell is linked to the next via transmembrane proteins
• desmosomes – weld-like mechanical junctions between cells
– prevents cardiocytes from being pulled apart
19-12
Metabolism of Cardiac Muscle
• cardiac muscle depends almost exclusively on
aerobic respiration to make ATP
– rich in myoglobin and glycogen
– huge mitochondria – fill 25% of cell
• adaptable to organic fuels used
– fatty acids (60%), glucose (35%), ketones, lactic acid
and amino acids (5%)
– more vulnerable to oxygen deficiency than lack of a
specific fuel
• fatigue resistant since makes little use of
anaerobic fermentation or oxygen debt
mechanisms
– does not fatigue for a lifetime
19-13
Coronary
Circulation
BruceBlaus [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• 5% of blood pumped by heart is pumped to the heart itself through the
coronary circulation to sustain its strenuous workload
• left coronary artery (LCA) branch off the ascending aorta
– anterior interventricular branch
• supplies blood both ventricles and anterior two-thirds of the interventricular
septum
– circumflex branch
• passes around left side of heart in coronary sulcus
• supplies left atrium and posterior wall of left ventricle
• right coronary artery (RCA) branch off the ascending aorta
– supplies right atrium and sinoatrial node (pacemaker)
19-14
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1
(2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
Venous Drainage
of Heart
– great cardiac vein
• travels along side of anterior interventricular artery
• collects blood from anterior portion of heart and empties into coronary sinus
– middle cardiac vein (posterior interventricular)
• found in posterior sulcus
• collects blood from posterior portion of heart and drains into coronary sinus
coronary sinus
• large transverse vein in coronary sulcus on posterior side of heart
• collects blood and empties into right atrium
19-15
Heart Chambers
four chambers
– right and left atria
• two superior
chambers
• receive blood
returning to heart
• auricles (seen on
surface) enlarge
chamber
– right and left
ventricles
• two inferior
chambers
• pump blood into
arteries
ZooFari [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]
19-16
Heart Structures
• interatrial
septum- wall that
separates atria
• pectinate
muscles
– internal ridges of
myocardium in
right atrium and
both auricles (an
auricle is a muscular
pouch of an atrium
which permits it to
receive more blood)
• interventricular
septum
– muscular wall that
separates
ventricles
ZooFari [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]
19-17
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• trabeculae carneae
– internal muscular ridges in both ventricles
• papillary muscles pull on the chordae tendineae, preventing
inversion of the mitral (bicuspid) and tricuspid valves and backflow of
blood into the atria.
19-18
Valves ensure a oneway flow of blood
through the heart
Heart Valves
atrioventricular (AV)
valves – controls
blood flow between
atria and ventricles
-right AV valve has 3
cusps (tricuspid
valve)
-left AV valve has 2
cusps (mitral or
bicuspid valve)
-chordae tendineae cords connect AV
valves to papillary
muscles on floor of
ventricles
-prevent AV valves
from flipping inside
out or bulging into the
atria when the
ventricles contract
Blausen Medical Communications, Inc. [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-19
semilunar valves – control
flow into great arteries – open
and close because of blood
flow and pressure
pulmonary semilunar valve – in
opening between right ventricle
and pulmonary trunk
aortic semilunar valve in
opening between left ventricle
and aorta
19-20
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
AV Valve Mechanics
ventricles relax
– pressure drops inside the ventricles
– semilunar valves close as blood
attempts to back up into the
ventricles from the vessels
– AV valves open
– blood flows from atria to ventricles
ventricles contract
– AV valves close as blood attempts
to back up into the atria
– pressure rises inside of the
ventricles
– semilunar valves open and blood
flows into great vessels
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”.
WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-21
Valvular Insufficiency
• valvular insufficiency (incompetence) – any failure of a
valve to prevent reflux (regurgitation) the backward flow
of blood
– valvular stenosis – cusps are stiffened and opening is
constricted by scar tissue
• result of rheumatic fever autoimmune attack on the mitral and aortic
valves
• heart overworks and may become enlarged
• heart murmur – abnormal heart sound produced by regurgitation of
blood through incompetent valves
– mitral valve prolapse – insufficiency in which one or both mitral
valve cusps bulge into atria during ventricular contraction
• hereditary in 1 out of 40 people
• may cause chest pain and shortness of breath
19-22
Heart Sounds
• auscultation – listening to sounds made by body
• first heart sound (S1), louder and longer “lubb”,
occurs with closure of AV valves, turbulence in
the bloodstream, and movements of the heart
wall
• second heart sound (S2), softer and sharper
“dupp” occurs with closure of semilunar valves,
turbulence in the bloodstream, and movements of
the heart wall
• exact cause of each sound is not known with
certainty
19-23
Blood Flow Through Heart
1 Blood enters right atrium from superior
and inferior venae cavae.
2 Blood in right atrium flows through right
AV valve into right ventricle.
3 Contraction of right ventricle forces
pulmonary valve open.
4 Blood flows through pulmonary valve
into pulmonary trunk.
5 Blood is distributed by right and left
pulmonary arteries to the lungs, where it
unloads CO2 and loads O2.
6 Blood returns from lungs via pulmonary
veins to left atrium.
7 Blood in left atrium flows through left AV
valve into left ventricle.
8 Contraction of left ventricle (simultaneous with
step 3 ) forces aortic valve open.
9 Blood flows through aortic valve into
ascending aorta.
10 Blood in aorta is distributed to every organ in
the body, where it unloads O2 and loads CO2.
11 Blood returns to heart via venae cavae.
Blausen Medical Communications, Inc. [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-24
Nervous system influence of
heart rate
• ***The central nervous system only influences the RATE of heart
beats, it is not responsible for telling the heart to beat each
time.***
• sympathetic nerves (raise heart rate)
– sympathetic pathway to the heart originates in the lower cervical to
upper thoracic segments of the spinal cord
– cardiac nerves to the heart
• increase heart rate and contraction strength
• dilates coronary arteries to increase myocardial blood flow
• parasympathetic nerves (slows heart rate)
– Cardiac nerves to the heart
– fibers of right vagus nerve lead to the SA node
– fibers of left vagus nerve lead to the AV node
19-25
We’re about to discuss the action potentials in the
heart… let’s first do a brief review of neuronal
action potentials and the sarcomere.
19-26
Neuronal action potential review
Voltage-gated calcium channels on T
tubules open (due to depolarization),
resulting in calcium entering the
sarcomeres.
Calcium binds troponin, resulting in that
protein changing shape, and pulling
tropomyosin. This reveals the binding site
for myosin on actin.
Actin and myosin bind, resulting in
sarcomere contraction.
OpenStax [CC BY 4.0
(https://creativecommons.org/licenses/by/4.0)]
19-28
Cardiac Rhythm
• cycle of events in heart – special names
– systole – atrial or ventricular contraction
– diastole – atrial or ventricular relaxation
• sinus rhythm – normal heartbeat triggered by
the SA node
– set by SA node at 60 – 100 bpm
– adult at rest is 70 to 80 bpm (vagal tone)
• ectopic focus – another parts of heart fires before
SA node
– caused by hypoxia, electrolyte imbalance, or caffeine,
nicotine, and other drugs
19-29
Cardiac Conduction System
• coordinates the heartbeat
Madhero88 [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
– composed of an internal pacemaker and
Nerve-like conduction pathways through myocardium
– generates and conducts rhythmic electrical signals
in the following order:
• sinoatrial (SA) node – modified cardiocytes
– pacemaker in right atrium near base of superior vena cava
– initiates each heartbeat and determines heart rate
– signals spread throughout atria
19-30
SA Node Potentials
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
Note: There is no stable resting membrane potential. Instead,
cardiocytes are leaky and depolarize without outside stimulation.
19-31
Cardiac Conduction System
• atrioventricular (AV) node
Madhero88 [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
– located near the right AV valve at lower end of interatrial septum
– electrical gateway to the ventricles
– fibrous skeleton acts as an insulator to prevent currents from getting to the
ventricles from any other route
• atrioventricular (AV) bundle (bundle of His)
– bundle forks into right and left bundle branches
– these branches pass through interventricular septum toward apex
• Purkinje fibers
– nervelike processes spread throughout ventricular myocardium
• signal pass from cell to cell through gap junctions
19-32
Impulse Conduction to Myocardium
Madhero88 [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• signal from SA node stimulates all myocardial cells of the atria
to depolarize and contract almost simultaneously
– reaches AV node in 50 msec
• signal slows down through AV node
– thin cardiocytes have fewer gap junctions
– delays signal 100 msec which allows the ventricles to fill
19-33
Impulse Conduction to Myocardium
Madhero88 [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• signals travel very quickly through AV bundle and
Purkinje fibers
– entire ventricular myocardium depolarizes and contracts in near
unison
• papillary muscles contract an instant earlier than the rest, tightening
slack in chordae tendineae
• ventricular systole progresses up from the apex of the
heart
– spiral arrangement of cardiocytes twists ventricles slightly
– like someone wringing out a towel
19-34
Cardiomyocyte action potential
1- Voltage-gated Na+ channels open.
Membrane potential (mV)
+30
-90
2- Na+ enters the cell and depolarizes
3
the membrane, triggering the opening
of more Na+ channels. This suddenly
increases membrane voltage.
4
5
3- Na+ channels close when the cell
depolarizes, and the voltage peaks at
nearly +30 mV.
2
4- Ca2+ entering through slow Ca2+
Channels maintains depolarization of
membrane, as some K+ leakage
repolarize the cell. The net effect is a
plateau. The plateau phase lasts 200250 ms.
1
5- Ca2+ channels close and Ca2+ is
0
0.15
time (s)
0.30
transported out of cell. K+ channels
open, with K+ outflow reducing the
cell’s membrane potential back to its
resting potential.
Following repolarization, there is a long
absolute refractory period of 250 msec
– prevents wave summation
and tetanus which would
stop the pumping action of
the heart
19-35
ECG Deflections
• P wave
– SA node fires, atria
depolarize and
contract
– atrial systole begins
100 msec after SA
signal
• QRS complex
– ventricular
depolarization
– complex shape of
spike due to different
thickness and shape
of the two ventricles
Created by Agateller (Anthony Atkielski), converted to svg by atom. [Public domain]
19-36
ECG Deflections
• ST segment ventricular systole
– plateau in myocardial
action potential
• T wave
– ventricular
repolarization and
relaxation
Created by Agateller (Anthony Atkielski), converted to svg by atom. [Public domain]
19-37
Electrical Activity
of Myocardium
1)
SA node
depolarizes
(ventricles
relaxed)
2)
atrial
depolarization
begins
3)
atrial
depolarization
complete (atria
contracted)
ventricles
depolarize
atria repolarize
(atria relaxed).
4)
5)
ventricles
contract
6)
ventricles
repolarize
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-38
Cardiac Cycle
• cardiac cycle – one complete contraction and
relaxation of all four chambers of the heart
• atrial systole (contraction) occurs while
ventricles are in diastole (relaxation)
• atrial diastole occurs while ventricles in
systole
• quiescent period all four chambers relaxed at
same time
• questions to solve – how does pressure affect
blood flow? and how are heart sounds
produced?
19-39
Principles of Pressure and Flow
• two main variables that
govern fluid
movement:
• pressure – causes a
fluid to flow (fluid
dynamics)
– pressure gradient pressure difference
between two points
– measured in mm Hg
with a manometer or
sphygmomanometer
By pressing on the plunger
of a syringe, you are
increasing the pressure of
the fluid within the syringe.
19-40
Principles of Pressure and Flow
• two main variables that
govern fluid movement:
• resistance – opposes
fluid flow
– great vessels have
positive
blood pressure
– ventricular pressure
must rise
above this resistance for
blood to flow into great
vessels
The needle of the syringe is
very narrow, and therefore
provides a lot of resistance.
You must depress the plunger
and increase pressure in
order for fluid flow to
overcome that high
resistance.
19-41
Principles of Pressure and Flow
• Syringes come with
needles of different
diameters.
• Do you think it is more
difficult to depress the
plunger and force liquid
to flow through a
narrow needle or a
wide needle?
19-42
Pressure
Gradients and
Flow
• Fluid flows only if it is
subjected to more
pressure at one point
than another which
creates a pressure
gradient
– fluid flows down its
pressure gradient
from high pressure to
low pressure
19-43
Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”.
WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.
[CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
Phases of Cardiac Cycle
• ventricular filling
• isovolumetric contraction
• ventricular ejection
• isovolumetric relaxation
• all the events in the cardiac
cycle are completed in less
than one second!
19-44
Ventricular Filling
• during diastole, ventricles expand
– their pressure drops below that of the atria
– AV valves open and blood flows into the
ventricles
• ventricular filling occurs in three phases:
– rapid ventricular filling – first one-third
• blood enters very quickly
– diastasis – second one-third
• marked by slower filling
• P wave occurs at the end of diastasis
– atrial systole – final one-third
• atria contract
• end-diastolic volume (EDV) – amount of
blood contained in each ventricle at the end
of ventricular filling
– 130 mL of blood
19-45
Isovolumetric Contraction
• atria repolarize and relax
– remain in diastole for the rest of the cardiac cycle
• ventricles depolarize, create the QRS complex, and
begin to contract
• AV valves close as ventricular blood surges back
against the cusps
• heart sound S1 occurs at the beginning of this phase
• ‘isovolumetric’ because even though the ventricles
contract, they do not eject blood
– because pressure in the aorta (80 mm Hg) and in
pulmonary trunk (10 mm Hg) is still greater than in the
ventricles
• cardiocytes exert force, but with all four valves closed,
the blood cannot go anywhere
19-46
Ventricular
Ejection
• ejection of blood begins when the ventricular
pressure exceeds arterial pressure and forces
semilunar valves open
– pressure peaks in left ventricle at about 120 mm Hg
and 25 mm Hg in the right
• blood spurts out of each ventricle rapidly at first –
rapid ejection
• then more slowly under reduced pressure – reduced
ejection
• ventricular ejections last about 200 – 250 msec
– corresponds to the plateau phase of the cardiac
action potential
• T wave occurs late in this phase
19-47
Ventricular Ejection
• stroke volume (SV)
• Prior to ventricular ejection, the ventricles
each contain about 130 ml of blood.
• At the end of ventricular ejection, about 70
mL of blood has been ejected.
• ejection fraction of about 54%
– as high as 90% in vigorous exercise
• end-systolic volume (ESV) – the 60 mL of
blood left behind
19-48
Isovolumetric Relaxation
• early ventricular diastole
– when T wave ends and the ventricles begin to
expand
• elastic recoil and expansion would cause
pressure to drop rapidly and suck blood into the
ventricles
– blood from the aorta and pulmonary briefly flows
backwards
– filling the semilunar valves and closing the cusps
– creates a slight pressure rebound that appears as
the dicrotic notch of the aortic pressure curve
19-49
Isovolumetric Relaxation
• early ventricular diastole
– heart sound S2 occurs as blood rebounds from the
closed semilunar valves and the ventricle expands
– ‘isovolumetric’ because semilunar valves are closed
and AV valves have not yet opened
• ventricles are therefore taking in no blood
– when AV valves open, ventricular filling begins again
19-50
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
19-51
Timing of Cardiac Cycle
• in a resting person
– atrial systole last about 0.1 sec
– ventricular systole about 0.3 sec
– quiescent period, when all four chambers
are in diastole, 0.4 sec
• total duration of the cardiac cycle is
therefore 0.8 sec in a heart beating 75 bpm
19-52
Overview of Volume Changes
end-systolic volume (ESV)
-passively added to ventricle
during atrial diastole
-added by atrial systole
total: end-diastolic volume (EDV)
stroke volume (SV) ejected
by ventricular systole
leaves: end-systolic volume (ESV)
60 ml
+30 ml
+40 ml
130 ml
-70 ml
60 ml
both ventricles must eject same amount of blood
19-53
Isovolumetric Isovolumetric
relaxation
contraction
Ventricular
ejection
Ventricular filling
1st
2nd
19-54
Unbalanced Ventricular Output
Cmglee [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]
When the right
ventricle is pumping
more blood than the
left ventricle, blood
backs-up in the
pulmonary
circulation. This
results in fluid
accumulating in the
lungs (pulmonary
edema).
19-55
Unbalanced Ventricular Output
When the left ventricle is
pumping more blood than the
right ventricle, blood backs-up
in the systemic circulation.
This results in fluid
accumulating in the body
(peripheral edema).
•congestive heart failure
(CHF) – results from the failure
of either ventricle to eject
blood effectively
Cmglee [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]
– usually due to myocardial
infarction, chronic
hypertension, valvular
insufficiency, or congenital
defects in heart structure.
19-56
Cardiac Output (CO)
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• cardiac output (CO) – amount ejected by ventricle in 1 min
• cardiac output = heart rate x stroke volume
– about 4 to 6 L/min at rest
– a RBC leaving the left ventricle will return to the left ventricle in about 1 min
– vigorous exercise increases CO to 21 L/min for fit person and up to 35 L/min
19-57
for world class athlete
Cardiac Output (CO)
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
• cardiac reserve – the difference between a person’s
maximum and resting cardiac output.
– increases with fitness, decreases with disease
• to keep cardiac output constant as we increase in age, the
heart rate increases as the stroke volume decreases
19-58
Heart Rate
• pulse – surge of pressure produced by each heart beat
that can be felt by palpating a superficial artery with the
fingertips
– infants have HR of 120 bpm or more
– young adult females avg. 72 – 80 bpm
– young adult males avg. 64 to 72 bpm
– heart rate rises again in the elderly
• tachycardia – resting adult heart rate above 100 bpm
– stress, anxiety, drugs, heart disease, or fever
– loss of blood or damage to myocardium
• bradycardia – resting adult heart rate of less than 60 bpm
– in sleep, low body temperature, and endurance trained athletes
• positive chronotropic agents – factors that raise the heart rate
• negative chronotropic agents – factors that lower heart rate
19-59
Chronotropic Effects of the
Autonomic Nervous System
• autonomic nervous system does not initiate the
heartbeat, it modulates rhythm and force
• cardiostimulatory effect – some neurons of the cardiac
center transmit signals to the heart by way of
sympathetic pathways
• cardioinhibitory effect – others transmit
parasympathetic signals by way of the vagus nerve
19-60
Chronotropic Effects of the Sympathetic
Nervous System
– Norepinephrine is released and
binds to β-adrenergic fibers in the
heart which leads to opening of Ca2+
channels in plasma membrane of
cardiocytes and nodal cells
– increased Ca2+ inflow accelerates
depolarization of SA node to
threshold
– cAMP accelerates the uptake of
Ca2+ by the sarcoplasmic reticulum
allowing the cardiocytes to relax
more quickly
– At high heart rates, diastole becomes
too brief for adequate filling and both
stroke volume and cardiac output are
reduced.
From: https://opentextbc.ca/anatomyandphysiology/chapter/19-4-cardiac-physiology/#fig-ch20_04_03
19-61
Chronotropic Effects of the
Parasympathetic Nervous System
parasympathetic vagus
nerves have inhibitory effects
on the SA and AV nodes
– acetylcholine (ACh) binds to
muscarinic receptors
– opens K+ gates in the SA and
AV node cells
– as K+ leaves the cells, they
become hyperpolarized. This
results in the cell taking a longer
time to reach threshold.
– heart slows down
Without influence from the CNS,
the heart has a intrinsic “natural”
firing rate of 100 bpm.
From: https://opentextbc.ca/anatomyandphysiology/chapter/19-4-cardiac-physiology/#fig-ch20_04_03
vagal tone – holds down this heart
rate to 70 – 80 bpm when a person is
at rest.
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Inputs to CNS cardiac center
• cardiac centers in the medulla receive input from many
sources and integrate it into the ‘decision’ to speed or
slow the heart
• higher brain centers (cerebral cortex, limbic system,
hypothalamus) -sensory or emotional stimuli affect heart rate
• medulla also receives input from muscles, joints, arteries,
and brainstem
– proprioceptors in the muscles and joints
• inform cardiac center about changes in activity, HR increases before
metabolic demands of muscle arise
– baroreceptors signal cardiac center
• pressure sensors in aorta and internal carotid arteries affected by blood
pressure
– chemoreceptors
• in aortic arch, carotid arteries and medulla oblongata
• sensitive to blood pH, CO2 and O2 levels
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Chronotropic Chemicals
• chemicals affect heart rate as well as
neurotransmitters from cardiac nerves
– blood born adrenal catecholamines (NE and
epinephrine) are potent cardiac stimulants
• drugs that stimulate heart
– nicotine stimulates catecholamine secretion
– thyroid hormone increases number adrenergic
receptors on heart so more responsive to sympathetic
stimulation
– caffeine inhibits cAMP breakdown prolonging
adrenergic effect
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Chronotropic Chemicals: electrolytes
– K+ has greatest chronotropic effect
• hyperkalemia – excess K+ in cardiocytes
– myocardium less excitable, heart rate slows and
becomes irregular
– Cardiocyte resting membrane potential is elevated
(because excess K+ is retained in cells /
concentration gradient maintaining resting potential
is reduced due to high extracellular levels)
– For more info, watch video beginning at 9 min point:
– https://www.youtube.com/watch?v=tyl4Ob522Bw
– At very high K+ levels, heart rate slows due to fewer
Na+ channels opening, resulting in bradycardia.
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Chronotropic Chemicals: electrolytes
– K+ has greatest chronotropic effect
• hypokalemia – deficiency K+ in cardiocytes
– K deficiency results in SA node cardiocytes
depolarizing more quickly (channels become more
leaky), resulting in a faster heart rate and
ventricular fibrillation.
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Chronotropic Chemicals
• electrolytes
– calcium
• hypercalcemia – excess of Ca2+
– decreases heart rate and contraction strength
• hypocalcemia – deficiency of Ca2+
– increases heart rate and contraction strength
19-67
Cardiac output
OpenStax College [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
•
•
the other factor that in cardiac output, besides heart
rate, is stroke volume
Stroke volume is the amount of blood the ventricle
19-68
moves with one contraction.
Preload
• preload – the amount of tension in ventricular
myocardium immediately before it begins to
contract
– increased preload causes increased force of contraction
– exercise increases venous return and stretches myocardium
– cardiocytes generate more tension during contraction
– increased cardiac output matches increased venous return
• Frank-Starling law of heart –
stroke volume end diastolic volume
– ventricles eject as much blood as they receive
– the more they are stretched, the harder they contract
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Contractility
• contractility refers to how hard the myocardium contracts
for a given preload
• positive inotropic agents increase contractility
– hypercalcemia can cause strong, prolonged contractions and even
cardiac arrest in systole
– catecholamines increase calcium levels
– glucagon stimulates cAMP production
– digitalis raises intracellular calcium levels and contraction strength
• negative inotropic agents reduce contractility
– hypocalcemia can cause weak, irregular heartbeat and cardiac
arrest in diastole
– hyperkalemia reduces strength of myocardial action potentials and
the release of Ca2+ into the sarcoplasm
19-70
Afterload
• afterload – the blood pressure in the aorta and
pulmonary trunk immediately distal to the semilunar
valves
– opposes the opening of these valves
– limits stroke volume
• hypertension increases afterload and opposes
ventricular ejection
• anything that impedes arterial circulation can also
increase afterload
– lung diseases that restrict pulmonary circulation
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Exercise and Cardiac Output
• exercise makes the heart work harder and increases cardiac
output
• proprioceptors signal cardiac center
– at beginning of exercise, signals from joints and muscles reach the
cardiac center of brain
– sympathetic output from cardiac center increases cardiac output
• increased muscular activity increases venous return
– increases preload and ultimately cardiac output
• increase in heart rate and stroke volume cause an increase
in cardiac output
• exercise produces ventricular hypertrophy
– increased stroke volume allows heart to beat more slowly at rest
– athletes with increased cardiac reserve can tolerate more exertion
than a sedentary person
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Coronary Artery Disease
Blausen.com staff (2014). “Medical gallery of Blausen Medical
2014”. WikiJournal of Medicine 1 (2).
DOI:10.15347/wjm/2014.010. ISSN 2002-4436. [CC BY 3.0
(https://creativecommons.org/licenses/by/3.0)]
coronary artery disease (CAD) – a constriction of the coronary arteries
– usually the result of atherosclerosis – accumulation of lipid deposits that degrade
the arterial wall and obstruct the lumen
– endothelium damaged by hypertension, virus, diabetes or other causes
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Coronary Artery Disease
Blausen.com staff (2014). “Medical gallery of Blausen Medical
2014”. WikiJournal of Medicine 1 (2).
DOI:10.15347/wjm/2014.010. ISSN 2002-4436. [CC BY 3.0
(https://creativecommons.org/licenses/by/3.0)]
– Monocytes penetrate walls of damaged vessels and transform into macrophages
• absorb cholesterol and fats (foam cells)
– look like fatty streak on vessel wall
– can grow into atherosclerotic plaques (atheromas)
– Platelets adhere to damaged areas and secrete platelet-derived growth factor
• attracting immune cells and promoting mitosis of muscle and fibroblasts, and the
deposition of collagen
• Bulging mass grows to obstruct arterial lumen- reduces vessel diameter
and blood flow
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Affects of Atheromas
• causes angina pectoris, intermittent chest pain,
by obstructing 75% or more of the blood flow
• immune cells of atheroma stimulate inflammation
– may rupture – traveling clots or fatty emboli
may result
• cause coronary artery spasms due to lack of
secretion of nitric oxide (vasodilator)
• inflammation transforms atheroma into a
hardened complicated plaque called
arteriosclerosis
19-75
Skeletal outline to your lecture notes:
Unit 4: The h
