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Phys Chapter 9: Cardiac Muscle: The Heart as a Pump and Function of the Heart Valves
The heart is 2 separate pumps: right heart, which pumps blood through the lungs, and left heart, that
pumps blood through the body
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Each side of the heart is a 2 chambered pump with an atrium and a ventricle
Each atrium is a weak primer pump for the ventricle, helping to move blood into the ventricle
The ventricles then are the main pump to move blood either into the lungs by the right
ventricle, or body by the left ventricle
The heart is made of 3 major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized
excitatory and conductive muscle fibers
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Atrial and ventricular muscle contract like skeletal muscle, except the duration of their
contraction is much longer – page 101 – pic of the heart
The excitatory and conductive fibers contract weakly because they have few contractile fibrils
o Instead they either have automatic rhythmical electrical discharge as action potentials,
or conduction of the action potentials through the heart, providing an excitatory system
that controls the rhythmical beating of the heart
Heart muscle is striated, and have myofibrils that contain actin and myosin filaments that lie
side by side, and slide along one another during contraction, all just like skeletal muscle
Intercalated discs – cell membranes that separate individual heart muscle cells from each other
o They look like dark areas crossing the heart muscle fibers – page 102
Heart muscle fibers is are made of many individual cells connected in series and in parallel with
each other
At each intercalated disc, the cell membranes fuse with each other to form permeable
“communicating” junctions called gap junctions, which allow rapid diffusion of ions
o So ions move easily in the intracellular fluid (ICF) along the longitudinal axes of the heart
muscle fibers so that action potentials travel easily from one heart muscle cell to the
next
o So heart muscle is a syncytium of many heart muscle cells that are so interconnected,
that when one of the cells gets excited, the action potential spreads to all of the cells
The heart is made of 2 syncytiums:
o Atrial syncytium – makes up the walls of the 2 atria
o Ventricular syncytium – makes up the walls of the 2 ventricles
The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (AV) valves between the atria and ventricles
Normally, potentials are not conducted from the atrial syncytium to the ventricular directly
through the fibrous tissue
o Instead, they’re conducted through the specialized conductive system called the A-V
bundle
The separation of the heart muscle into 2 different syncytiums lets the atria contract before the
ventricles do, which is needed for heart pumping to work
When ventricular muscle has an action potential, it’s intracellular potential goes from very negative (-85
mV) between beats, to slightly positive (20 mV) during each beat – page 102 top right pic
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After the initial spike, the membrane remains depolarized for about 0.2 seconds, seen as a
plateau
o The plateau in ventricle action potentials causes ventricular cardiac muscle contraction
to last much longer than skeletal muscle does
The plateau ends in abrupt repolarization
2 major differences between the membranes of heart and skeletal muscle is why heart muscle
has a prolonged action potential and plateau
o The action potential of skeletal muscle is caused almost entirely by sudden opening of
lots of fast sodium channels, that allow lots of sodium to enter the skeletal muscle fiber
from the ECF
 They’re called fast because they stay open for only a few thousandths of a
second, and then quickly close
 At the end of closure, repolarization happens, and the action potential is over
quickly
 In heart muscle, the action potential is caused by opening of both the fast
sodium channels, and also slow calcium channels (calcium-sodium channels)
 Slow calcium channels open slower than fast sodium channels, and they
remain open for several tenths of a second, letting lets of calcium and
sodium through them into the heart muscle fiber, causing a prolonged
period of depolarization, which causes the plateau
 The calcium that enters during the plateau activate muscle contraction
o Unlike skeletal muscle, which gets its calcium for muscle
contraction from its sarcoplasmic reticulum (SR)
o Immediately after the action potential, the permeability of the heart muscle membrane
for potassium decreases, which doesn’t happen in skeletal muscle
 This decreases the outflux of potassium during the action potential plateau,
which prevents early return of the action potential voltage to its resting value
 When the slow calcium-sodium channels finally close, influx of calcium &
sodium stops, & the membrane permeability for potassium increases quickly,
returning the membrane potential to resting level, ending the action potential
Heart muscle conducts action potentials in the atria and ventricles at a velocity that is less than
nerves and skeletal muscle
o The conduction velocity is much faster in the Purkinje fivers, allowing rapid conduction
of excitatory signal to the different parts of the heart
Heart muscle, like all excitable tissue, is refractory to restimulation during the action potential
o So the refractory period of the heart is the time period where a normal heart impulse
can’t re-excite an already excited area of heart muscle
o The normal refractory period of heart muscle is just about as long as the heart muscle
plateau
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There is also a shorter relative refractory period, where the muscle is more difficult than
normal to excite, but still could be excited by a very strong excitatory signal
 Ex: premature contractions
The refractory period of the atrial muscle is much shorter than the ventricles
Excitation-contraction coupling – the way action potential causes myofibrils to contract
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When an action potential passes over the heart muscle membrane, it spreads into the heart
muscle fiber along the membranes of the transverse (T) tubules
T tubule action potentials get to the membranes of the longitudinal sarcoplasmic tubules to
cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum (SR)
The calcium then quickly diffuses into the myofibrils and catalyzes sliding of the actin and
myosin filaments along one another to cause muscle contraction
So far this works just like skeletal muscle
Unlike skeletal muscle though, calcium also diffuses into the sarcoplasm from the T tubules
themselves during the action potential, which opens voltage-dependent calcium channels in
the membrane of the T tubule – page 104
Calcium entering the cell then activates calcium release channels called ryanodine receptor
channels, in the SR membrane, triggering release of calcium into the sarcoplasm
Calcium in the sarcoplasm then interacts with troponin to initiate cross-bridge formation and
contraction, just like in skeletal muscle
Without the calcium from the T tubules, heart muscle contraction is much weaker, because the
SR of heart muscle is less developed than skeletal muscle, and doesn’t store enough calcium to
provide a full contraction
o The T tubules of heart muscle though have a much bigger volume than skeletal muscle,
and has lots of mucopolysaccharides that are negatively charged and bind lots of
calcium, keeping it always available for diffusion into the heart muscle fiber when an
action potential gets to it
The strength of heart muscle contraction depends on the concentration of calcium in the ECF
o The openings of the T tubules pass directly through the heart muscle cell membrane
into the extracellular spaces, letting that same fluid get into the T tubules
o So the amount of calcium in the T tubules to be used for heart muscle contraction,
depends on the ECF calcium concentration
o The strength of skeletal muscle contraction is hardly affected by moderate changes in
ECF calcium, because skeletal muscel contraction is caused almost entirely by calcium
ions released from the SR inside the skeletal muscle fiber
At the end of the plateau of the heart action potential, the influx of calcium inside the muscle is
lost, and calcium in sarcoplasm is rapidly pumped back out of the muscle fibers into both the SR
and T tubule/ECF
o Calcium is moved back into the SR by the calcium-ATPase pump (SERCA)
o Calcium is also removed from the cell by a sodium-calcium exchanger
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The sodium that enters the cell during this exchange is then transported out of
the cell by the sodium-potassium ATPase pump
o This makes it so that contraction stops until a new action potential comes along
Heart muscle begins to contract a few milliseconds after the action potential begins, and
continues to contract a few milliseconds after the action potential ends
o So the duration of contraction of heart muscle is mainly due to the duration of the
action potential, including the plateau
o Contraction in atrial muscle lasts about 0.2 seconds, in the ventricle 0.3 seconds
Cardiac cycle – events from the beginning of one heartbeat to the beginning of the next
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Each heart cycle is initiated by spontaneous generation of an action potential in the sinus-atrial
(SA) node
o The SA node is found in the superior lateral wall of the right atrium near the opening of
the superior vena cava
The action potential rapidly travels from the SA node through both atria, and then through the
AV bundle into the ventricles
There is a delay of about 0.1 seconds when the impulse passes from the atria into the ventricles
o This allows the atria to contract into the ventricles first, before the ventricles contract
The heart cycle has a period of relaxation (diastole) where the heart fills with blood, followed by
a period of contraction (systole)
The total duration of the cardiac cycle (systole and diastole) is the reciprocal of the heart rate
o Ex: if heart rate is 72 bpm, the duration of the cardiac cycle is 1/72 bpms (less than a
second)
Page 105 – graph of everything happening in the cardiac cycle
When heart rate increases, the duration of each cardiac cycle decreases, so diastole and systole
both don’t last as long
o Diastole decreases more though than systole and the duration of the action potential
o Ex: at normal heart rate of 72 bpm, systole is about 40% the cardiac cycle, but at 3 times
the normal heart rate, systole becomes 2/3 the cardiac cycle
o So when the heart beats at a fast rate, it doesn’t remain relaxed long enough to allow
complete filling of the heart chambers before the next contraction
The electrocardiogram (ECG) shows electrical voltages generated by the heart
o They are recorded by the ECG from the surface of the body
o P wave – depolarization of the atria
 This is followed by atrial contraction, which causes a slight rise in atrial pressure
immediately after the ECG P wave
o QRS complex – depolarization of the ventricles
 Happens 0.16 seconds after the P wave
 The QRS depolarization of the ventricles initiates contraction of the ventricles,
and causes the ventricle pressure to start rising
 So the QRS starts slightly before ventricular systole starts
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T wave – ventricle repolarization
 This is when the ventricles begin to relax
 So the T wave happens slightly before the end of ventricular contraction
When blood comes from the veins into the atria, 4/5 of the blood flows directly from the atria
into the ventricle, without any contraction
o Atrial contraction then moves the last 1/5 into the ventricles
o So the atria act as primer pumps that increase the effectiveness of ventricle pumping
by 20%
o The heart can work without that 20% though, because it is normally able to pump 300400% more blood than is needed by the resting body
o So when the atria fail and don’t work, you probably won’t notice a difference unless the
person exercises
 Then you get acute signs of heart failure, like shortness of breath
o Atrial pressure waves – a, c, and v waves
 a wave – atrial contraction
 Usually the left atrial pressure increases more than the right
 c wave – happens when the ventricles contract, because of mainly the bulging of
the AV valves backward toward the atria due to increased pressure in the
ventricles
 Also caused a little by slight backflow fo blood into the atria at the onset
of ventricular contraction
 v wave – happens towards the end of ventricular contraction, from slow flow of
blood into the atria from the veins while the AV valves are closed during
ventricular contraction
 When ventricular contraction is over, the AV valves open, allowing this
stored atrial blood to flow rapidly into the ventricles, causing the v
wave to disappear
Filling of the ventricles during diastole:
o During ventricular systole, lots of blood accumulates in the atria because the AV valves
are closed
o Once systole is over and ventricular pressures fall again to diastolic levels, the atrial
pressure is slightly higher, so the AV valves open, letting blood flow rapidly into the
ventricles
 This is called the period of rapid filling of the ventricles
 The period of rapid ventricular filling lasts for the first 1/3 of diastole
o In the middle 1/3 of diastole, only a small amount of blood flows into the ventricles
from the atria
o In the last 1/3 of diastole, the atria contract to move the rest of the blood into the
ventricles
Emptying of the ventricles during systole – page 108
o Period of isovolumic (isometric) contraction:
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Immediately after the ventricular contraction begins, the ventricular pressure
increases quickly, causing the AV valves to close
 The ventricles then take another 0.02-0.03 seconds to build up enough pressure
to push the semilunar (aortic and pulmonary) valves open against the pressures
in the aorta and pulmonary artery
 So in the isovolumic period, the ventricles contract, but they don’t empty their
blood
 This increases tension in the muscle, but it’s isometric, so the muscle doesn’t
shorten
Period of ejection:
 When left ventricular pressure rises slightly above 80 mm Hg, and right
ventricular pressure slightly above 8 mm Hg, the ventricular pressures push the
semilunar valves open
 Immediately blood begins to pour out of the ventricles, with about 70% of the
blood emptying happening in the first 1/3 of ejection, so the first 1/3 is called
the period of rapid ejection, and the last 2/3 the period of slow ejection
Period of isovolumic (isometric) relaxation:
 At the end of systole, ventricular relaxation starts suddenly, allowing both the
right and left intraventricular pressures to decrease rapidly
 The increased pressures in the arteries that were just filled, immediately push
blood back toward the ventricles, which snaps the aortic and pulmonary valves
closed
 For another 0.03-0.06 seconds, the ventricular muscle continues to relax, even
though the ventricular volume doesn’t change
 This is the period of isovolumic (isometric) relaxation
 During this period, the intraventricular pressures decreases rapidly back to their
low diastolic levels
 Then the AV valves open to begin a new cycle of ventricular pumping
During diastole, normal filling of the ventricles increases the volume of each ventricle to
about 110-120 mL, called the end-diastolic volume
As the ventricles empty during systole, the volume decreases about 70 mL, called the
stroke volume output
The remaining volume in each ventricle is about 40-50 mL, and called the end-systolic
volume
The fraction of the end-diastolic volume that is ejected is called the ejection fraction
 Usually the ejection fraction is about 60%
When the heart contracts strongly, the end-systolic volume can be decreased more than
normal
When lots of blood flows into the ventricles during diastole, the ventricular end-diastolic
volumes can be higher than normal
By both increasing the end-diastolic volume and decreasing the end-systolic volume, the
stroke volume output can be increased to more than normal
Heart valves – page 107
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Heart valves open and close passively
o They close when a backward pressure gradient pushes blood backward
o They open when a forward pressure gradient forces blood forward
o The thin AV valves need almost no backflow to cause closure, while the heavier
semilunar valves need rapid backflow for a few milliseconds to close
Atrioventricular (A-V) valves – tricuspid and mitral valves, which prevent backflow of blood from
the ventricles into the atria during systole
Semilunar valves – aortic and pulmonary artery valves, which prevent backflow from the aorta
and pulmonary arteries into the ventricles during diastole
Papillary muscle attaches to the AV valves by chordae tendineae
o The papillary muscles contract when the ventricle walls contract, but they don’t help
the valves close
o Instead, papillary muscle pulls the valves inward toward the ventricles, to prevent
bulging too far backward toward the atria during ventricle contraction
o If a chorda tendinea ruptures, or one of the papillary muscles doesn’t work, the valve
bulges so far backward during ventricle contraction, that it leaks and can cause severe
or lethal heart incapacity
The semilunar valves work different from the AV valves
o The high pressures in the arteries at the end of systole cause the semilunar valves to
snap closed, unlike the much softer closing of the AV valves
o The semilunar valves have smaller openings than the AV valves, so the velocity of blood
ejection through them is much higher than through the AV valves
o Due to rapid closure and more forceful ejection through them, the semilunar valves
face more stress than the AV valves
o Semilunar valves are not supported by chordae tendineae, like the AV valves are
When the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve
opens
o After the valve opens, the pressure in the ventricle rises much less rapidly, because
blood immediately flows out of the ventricle into the aorta
o When blood flows into the arteries, it causes the walls of the arteries to stretch, and the
pressure to increase to about 120 mm Hg, which is your systolic blood pressure
o At the end of systole, when the aortic valve closes and no more blood comes out, the
elastic walls of the arteries maintain a high pressure in the arteries, even during diastole
o An indentation happens in the aortic pressure curve when the aortic valve closes
 This is caused by a short period of backward flow of blood immediately before
closing of the valve, followed by a sudden stop in backflow
o After the aortic valve has closed, the pressure in the aorta decreases slowly throughout
diastole because the blood stored in the elastic arteries flows through the system to the
veins
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Before the ventricle contracts again, the aortic pressure has fallen to about 80 mm Hg,
which is your diastolic blood pressure
The same events happen in the right ventricle and pulmonary artery, but the pressures
involved are 1/6 of these
When you listen to the heart with a stethoscope, you’re hearing the heart valves close
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S1 – first heart sound
o When the ventricles contract, you hear a sound due to the AV valves closing
S2 – second heart sound
o When the aortic and pulmonary valves close at the end of systole
Stroke work output of the heart – amount of energy the heart converts to work during each heartbeat
while pumping blood into the arteries
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Minute work output – total amount of energy converted to work by the heart in a minute
o Minute work output = stroke work output x heart rate per minute
Work output of the heart is in two forms
o Most of the work output is used to move the blood from the low pressure veins to the
high pressure arteries
 This is called volume-pressure work (aka external work)
o A minor amount of energy is used to accelerate the blood to its velocity of ejection
through the aortic and pulmonary valves
 This is the kinetic energy of blood flow part of work output
Right ventricle volume-pressure work is usually 1/6 the work output of the left ventricle
The amount of work output of each ventricle needed to create kinetic energy of blood flow is
proportional to the mass of blood ejected times the square of velocity ejection
o Normally, the work output of the left ventricle needed to create kinetic energy of blood
flow is only about a % of the total work output of the ventricle, so it’s ignored when you
calculate total stroke work output
o But in abnormal states, like aortic stenosis, which has blood flow with a lot of velocity
through the stenosed valve, a lot more of the work output may be needed to create
kinetic energy of blood flow
Graphing left ventricle pumping – page 108
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The diastolic pressure curve is determined by filling the heart with more and more blood, and
measuring the diastolic pressure right before the ventricles contract (the end-diastolic pressure
of the ventricle)
The systolic pressure curve is determined by measuring the systolic pressures reached during
ventricle contraction at each volume of filling
Until the volume of the noncontracting ventricle rises to about 150 mL, the diastolic pressure
doesn’t increase much
o So up to this volume, blood can flow easily into the ventricle from the atrium
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Above 150 mL, the diastolic pressure increases rapidly, partly because the fibrous tissue in the
heart won’t stretch anymore, and partly because the pericardium surrounding the heart won’t
allow any more expansion
During ventricular contraction, the systolic pressure increases even at low ventricular volumes,
and reaches a max at a ventricular volume of 150-170 mL
As the volume increases even more, the systolic pressure decrease, seen as a falling systolic
pressure curve
o This is because at volumes this great, the actin and myosin filaments of the heart muscle
fibers are pulled far enough apart that the strength of each heart fiber contraction is
less than optimal
Max systolic pressure for the left ventricle is between 250-300 mm Hg, while max for the right
ventricle is 60-80 mm Hg
Volume-pressure diagram – red lines in pic on 108, and more detailed pic on page 109
o There are 4 phases to the volume-pressure diagram of the left ventricle
o Phase 1 – period of filling
 Starts at a ventricle volume of about 50 mL and diastolic pressure of 2-3 mm Hg
 The amount of blood left in the ventricle after the previous heartbeat is about
50 mL, called the end-systolic volume
 As venous blood flows into the ventricle from the left atrium, the ventricle
volume increases to about 120 mL, the end-diastolic volume
 So in phase 1 (ventricle filling) the volume increases from 50120, and diastolic
pressure rises from 2-3 mm Hg  5-7 mm Hg
o Phase 2 – period of isovulumic contraction
 During isovolumic contraction, the volume of the ventricle doesn’t change,
because all the valves are closed
 The pressure increases though to equal the pressure in the aorta, and rises to
80 mm Hg
o Phase 3 – period of ejection
 During ejection, the systolic pressure rises even higher because of even more
contraction of the ventricle
 At the same time, the volume of the ventricle decreases because the aortic
valve has opened, and blood flows out of the ventricle into the aorta
o Phase 4 – period of isovolumic relaxation
 At the end of the period of ejection, the aortic valve closes, and the ventricular
pressure falls back to the diastolic pressure level
 The volume doesn’t change though
 So you’re back where you started in the ventricle, with 50 mL of blood left in the
ventricle, and an atrial pressure of 2-3 mm Hg
o The area in between the lines graphed out for the volume-pressure diagram (tan area in
pic) is the net external work output of the ventricle during its contraction cycle
o Volume-pressure diagrams are used to calculate cardiac work output
o When the heart pumps lots of blood, the area of the work diagram gets much larger:
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It extends to the right - because the ventricle fills with more blood during
diastole
 It rises higher - because the ventricle contracts with greater pressure
 It goes farther left - because the ventricle contracts to a smaller volume,
especially if stimulated by symps
Preload – the degree of tension on the muscle when it begins to contract
o Preload is considered the end-diastolic volume, when the ventricle is filled
Afterload – the load the muscle has to contract against
o Afterload is the pressure in the aorta, which will be the systolic pressure
o So afterload is the resistance in circulation
Heart muscle uses chemical energy to provide the work for contraction
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Most (70-90%) of this energy is gotten from oxidative metabolism of fatty acids
o The rest comes from other nutrients, like lactate or glucose
So the rate of oxygen use by the heart is a good way to measure the chemical energy released
when the heart performs work
Oxygen use of the heart and chemical energy expended during contraction, are directly related
to external work (shaded part of volume-pressure diagram) and potential energy
o Potential energy – additional work that could be done by contraction if the ventricle
emptied completely
Oxygen use by the heart is proportional to the tension that happens in the heart muscle during
contraction times the duration of time the contraction happens, called the tension-time index
o Tension is high when systolic pressure is high, so more oxygen is used the higher
systolic pressure is
o More chemical energy is expended even at normal systolic pressures, when the
ventricle is abnormally dilated, because the heart muscle tension during contraction is
proportional to pressure times the diameter of the ventricle
 This is important in heart failure, where the heart ventricle is dilated, so the
amount of chemical energy needed for a given amount of work output is more
than normal, even though the heart is already failing
During heart muscle contraction, most of the expended chemical energy is converted into heat,
and a smaller amount is converted into work output
o The ratio of work output to total chemical energy expenditure is called the efficiency of
heart contraction, or just efficiency of the heart
o Max efficiency of the normal heart is 20-25%
o In heart failure, the efficiency decreases below normal
Regulation of heart pumping:
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The heart pumps more blood when you’re exercising than when you’re resting
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Heart pumping is regulated by intrinsic cardiac regulation of pumping in response to changes in
volume of blood going into the heart, and control of heart rate and strength of heart pumping
by the autonomic nervous system
Frank-Starling mechanism – ability of heart to adapt to increasing volumes of incoming blood
o Under normal conditions, the amount of blood pumped by the heart each minute is
normally determined almost entirely by the rate of blood flow into the heart from the
veins, called venous return
 Each peripheral tissue of the body controls its own local blood flow, and the
blood then drains into veins into the right atrium
 The heart then automatically pumps this incoming blood into the arteries
o Frank-Starling mechanism means the greater the heart muscle is stretched during
filling, the greater the force of contraction and the greater the amount of blood
pumped into the arteries
 The heart pumps all the blood that returns to it through the veins
o More blood into the ventricles stretches the heart muscle more than usual
 This causes the muscle to contract stronger than normal, because the actin and
myosin filaments are brought to a more optimal degree of overlap for force
generating
 So since the ventricle will increase its pumping ability, it automatically pumps
out any extra blood put into it
 This is a feature that is characteristic of all striated muscle, not just heart muscle
Also, stretch of the right atrial wall directly increases the heart rate, which increases the amount
of blood pumped each minute, but this doesn’t contribute as much as Frank-Starling does
Ventricular function curves – express functional ability of the ventricles to pump blood
o Page 110 – top graph – stroke work output curve
 As atrial pressure for each side of the heart increases, the stroke work output
for that side increases until it reaches the limit of the ventricles pumping ability
o Page 110 – bottom graph – ventricular volume output curve
 As atrial pressures increase, the volume output per minute of that ventricle
increases
o So as the ventricles fill in response to higher atrial pressures, each ventricular volume
and strength of muscle contraction increase, causing the heart to pump more blood into
the arteries
Pumping effectiveness of the heart is also controlled by symps & parasymps (vagus) to the heart
o Cardiac output – amount of blood pumped each minute
o Symps increase cardiac output, by increasing heart rate and force of contraction
 Increasing force of contraction increases volume of blood pumped and
increases the ejection pressure
 Inhibiting symps to the heart can moderately decrease heart pumping
 Normally, the heart receives symps that keep it pumping about 30%
higher than it would if symps didn’t work
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So removing the symps decreases the heart rate and force of
contraction up to 30%
o Parasymps decrease cardiac output
 Strong parasymp stimulation to the heart through the vagus can stop the heart
from beating for a few seconds, until the heart “escapes” when the purkinje
fibers kick in as pace makers and make it beat at 20-40 bpm
 Parasymps also slightly decrease the strength of heart muscle contraction
 Vagal fibers mainly go to the atria and not much to the ventricles
 This is why parasymps are way better at decreasing heart rate than
force of contraction
 Symps go to both the atria and ventricles – page 111 left pic
o At any given right atrial pressure, the cardiac output is increased by symps, and
decreased by parasymps – page 111 right pic
Potassium effects on the heart:
o Excess potassium in the ECF causes the heart to become dilated and flaccid, also slows
the heart rate
 Lots of potassium can block conduction of the cardiac impulse from the atria to
the ventricles through the AV bundle (AV block)
 Potassium levels 2-3 times normal can cause the heart to have an abnormal
rhythm and get so weak it leads to death
 High potassium in the ECF decreases the resting membrane potential in the
heart muscle fibers, by partially depolarizing the cell membrane, causing the
membrane potential to be less negative
 As the membrane potential decreases, the intensity of the action potential also
decreases, which makes contraction of the heart progressively weaker
Calcium effects on the heart – acts the opposite of potassium
o Excess calcium causes the heart to start having spastic contractions, due to calcium
directly initiating heart contraction
o Decreased calcium causes the heart to be flaccid
o Calcium is so closely regulated in the blood that calcium effects on the heart are rare
Increased body temperature, like in fever, increases the heart rate
Decreased body temperature decreases heart rate
Heat increases the permeability of the heart muscle membrane to ions that control heart rate,
resulting in acceleration of the self-excitation process
Contractile strength of the heart increases temporarily when there’s an increase in body
temperature, like in exercise
Increasing the pressure in the aorta does not decrease the cardiac output until the pressure gets
to be above 160 mm Hg
o So in normal working hearts with normal systolic blood pressures, the cardiac output is
determined almost entirely by the ease of blood flow through the body, which controls
venous return of blood to the heart