Download Phys Chapter 10 [4-20

Phys Chapter 10: Rhythmical Excitation of the Heart
The heart has a system to generate rhythmical electrical impulses to cause rhythmical contraction of the
heart muscle, and conduct these impulses rapidly through the heart
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This system causes the atria to contract before the ventricles, which allows the ventricles to fill
before they pump the blood
This system also allows all the parts of the ventricle to contract almost simultaneously, which is
essential to create the pressure needed
This system is very susceptible to ischemia of the heart tissues from poor coronary blood flow
o This often leads to a bizarre heart rhythm, or abnormal sequence of contraction of the
heart chambers, & the pumping ability of the heart is often bad, which can lead to death
Normal rhythmical impulses are generated by the sinus (sinoatrial, SA) node
The atrioventricular (A-V) node delays signals from the atria before they pass into the ventricles
A-V bundle – conducts impulses from the atria into the ventricles
Bundle branches of Purkinje fibers – conduct heart impulses to all parts of the ventricles
The SA node is a small strip of specialized heart muscle found in the superior posterolateral wall fo the
right atrium, right below and lateral the opening of the superior vena cava – page 116
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The fibers of the SA node have almost no contractile muscle filaments, and the few that are
there are way thinner than surrounding atrial muscle fibers
The fibers of the SA node connect directly with the atrial muscle fibers so that any action
potential that begins in the SA node spreads immediately into the atrial muscle wall
Some heart fibers are able to excite themselves, which causes automatic rhythmical discharge and
contraction
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This includes the fibers of the heart’s specialized conducting system, including the SA node
The resting membrane potential of the SA node fibers is about -55 to -60 mV, compared to -85
to -90 for ventricular muscle fibers
o This is because the cell membranes of SA node fibers are naturally leaky to sodium &
calcium, so the “+” charges of the entering sodium & calcium decrease the negativity
Heart muscle has 3 kinds of membrane ion channels (fast sodium, slow sodium-calcium, and
potassium channels)
o Opening of the fast sodium channels causes the rapid upstroke spike of action potential
in ventricular muscle, because of the rapid influx of positive sodium into the fiber
o Then then the slower opening sodium-calcium channels open and stay open for 0.3
seconds, causing the plateau of the ventricle action potential
o Opening of the potassium channels allows diffusion of lots of positive potassium out of
the muscle fiber, returning membrane potential to its resting level
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In the SA node muscle fiber, it’s already less negative than normal heart muscle
o So at -55 mV, the fast sodium channels have already been “inactivated” meaning they
are blocked
 Any time the membrane potential remains less negative than about -55 mV for
more than a few miliseconds, the inactivation gates on the inside of the cell
membrane that close fast sodium channels become closed and stay closed
o So only the slow sodium-calcium channels can open (be “activated”), so they cause the
action potential
o This means the SA node action potential is slower to develop than the action potential
of ventricle muscle
o Also, after the action potential happens, return of the potential to its resting state is
slower as well
o Because of the high sodium concentration in the ECF outside the SA node fiber, and
moderate # of already open sodium channels, “+” sodium ions leak into the SA node
 So in between heartbeats, influx of sodium causes a slow rise in resting
membrane potential towards being positive
 So the resting potential gradually rises and becomes less negative between each
heartbeat
 When the potential reaches a threshold voltage of about -40 mV, the sodiumcalcium channels become “activated” causing the action potential
 So inherent leakiness of the SA node fibers to sodium and calcium causes their
self excitation
 The leakiness doesn’t cause them to remain depolarized all the time though,
because two things happen during the action potential to prevent that
 The sodium-calcium channels become inactivated (close) within 150 ms
after opening
 At about the same time, a lot more potassium channels open
 So influx of calcium and sodium stops, while lots of potassium leaves
 This decreases intracellular potential back to resting, ending the action
potential
 The potassium channels also stay open for a few tenths of a second,
causing excess negativity in the fiber, called hyperpolarization
o Hyperpolarization carries the potential to -55 to -60 mV
 Then the potassium channels close, & sodium and calcium start leaking
in again, decreasing potential towards starting another action potential
The ends of SA node fibers connect directly with the surrounding atrial muscle fibers
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So action potentials from the SA node travel out into the atrial muscle fibers, and spreads
through the entire atrial muscle mass, eventually to the AV node
Most atrial muscle conducts at a velocity about 0.3 m/sec, but some fibers conduct quicker
o The anterior interatrial band is a quicker fiber that connects the two atria
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The anterior, middle, and posterior intermodal pathways are quicker fibers that connect
to the AV node
The AV node and its conductive fibers delay the atrial impulses from getting into the ventricles
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The AV node is in the posterior wall of the right atrium immediately behind the tricuspid valve
The atrial impulse from the SA node gets to the AV node in about 0.03 seconds
It’s then delayed for another 0.09 seconds in the AV node, before the impulse enters the AV
bundle and goes into the ventricles
The signal then delays another 0.04 seconds in the AV bundle
o The AV bundle is made of many small fascicles passing through the fibrous tissue
separating the atria and ventricles
So the total delay in the AV node and AV bundle is 0.13 seconds
o This plus the 0.03 seconds it took to get there, means it takes 0.16 seconds to get from
the SA node to the ventricles
The slow conduction by the AV nodal and AV bundle fibers is due to decreased #’s of gap
junctions between cells in the conducting pathways, so there is a lot of resistance to
conduction of excitatory ions from one conducting fiber to the next
Purkinje fibers lead from the AV node through the AV bundle into the ventricles
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Purkinje fibers are very large fibers, bigger than the normal ventricular muscle fibers
Purkinje fibers transmit action potentials at a faster velocity than normal ventricular muscle
o This allows almost instantaneous transmission of the heart impulse throughout the rest
of the ventricular muscle
Purkinje fibers can transmit signals so quickly because they have very permeable gap junctions
at the intercalated discs between the cells of the Purkinje fibers
o So ions are transmitted easily from one cell to the next
Purkinje fibers have very few myofibrils, so they contract little or not at all during impulse
transmission
AV bundle fibers are unique in that they won’t let action potentials travel backwards from the
ventricles into the atria
Everywhere except the AV bundle, the atrial muscle is separated from the ventricular muscle by a
continuous fibrous barrier – page 117
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This barrier normally acts as an insulator to prevent impulses from going from the atria to
ventricles, so that the only way into the ventricles is the AV bundle
If for some reason this barrier doesn’t work and there is a way to transfer impulses between the
atria and ventricles, you get a serious arrhythmia
After penetrating the fibrous tissue between the atria and ventricle muscle, the distal part of the AV
bundle passes down the ventricular septum towards the apex of the heart
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The bundle then divides into left and right bundle branches that go under the endocardium on
each side of the ventricular septum
Each branch spreads down toward the apex of the ventricle, progressively dividing into smaller
branches
These branches turn sideways to go to the back of the heart
The ends of the Purkinje fibers penetrate about 1/3 of the way into the muscle mass, and then
become continuous with the heart muscle fibers
The time it takes from when the heart impulse enters the bundle branches in the ventricular
septum, until it reaches the ends of the Purkinje fibers, is only 0.03 seconds, so it’s almost
immediate
Once the impulse reaches the ends of the Purkinje fibers, it’s transmitted through the ventricle by the
ventricle muscle fibers
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This transmission takes up to 0.5 seconds, so much longer than the Purkinje fibers
The heart muscle wraps around the heart in a double spiral with a fibrous septa between the 2
spiral layers
So the heart impulse doesn’t travel directly out to the surface of the heart, and instead twists
and turns its way to the surface along the directions of the spirals
So transmission from the endocardial surface to the epicardial surface of the ventricle needs
another 0.03 seconds
So total time for transmission of the heart impulse from the initial bundle branches to the last
ventricle muscle fibers, is about 0.06 seconds
Quick summary of heart conduction – page 118
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The impulse spreads at moderate velocity through the atria, and is then delayed more than 0.1
seconds in the AV node, before appearing in the ventricular septal AV bundle
Once it enters the bundle, it spreads very quickly through the Purkinje fibers to the entire
endocardium of the ventricles
Then the impulse spreads less quickly through the ventricle mass to the epicardial surface of the
ventricles
The SA node is the normal pacemaker, and discharges 70-80 times per minute
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The AV node can discharge at 40-60 times per minute, and the Purkinje fibers at 15-40 times per
minute
The discharge rate of the SA node is faster than the natural self-excitatory discharge rate of the
AV node or Purkinje fibers
So each time the SA node discharges, its impulse goes into the AV node and Purkinje fibers,
causing them to discharge
o Every time the SA node discharges, it does so faster than the other two causing them to
discharge before they reach their own threshold
Sometimes, another part of the heart starts rhythmically discharging faster than the SA node
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Often this is the AV node or Purkinje fibers acting abnormally
So the faster site becomes the new pacemaker
A pacemaker that is not the SA node is called an ectopic pacemaker
An ectopic pacemaker causes an abnormal sequence of contraction of the different parts of the
heart, and can impair heart pumping
Another reason for shift of the pacemaker is blockage of transmission of the heart impulse from
the SA node to other parts of the heart
o So the next fastest site becomes the new pacemaker, so next is AV node, and then
Purkinje fibers
o AV block – when the impulse can’t get into the ventricles through the AV nodal or
bundle system
 So the atria beat at normal rhythm of the sinus node, while a new pacemaker
develops in the Purkinje system of the ventricles
 After sudden AV block, the Purkinje’s won’t start to emit impulses until 5-20
seconds later, because once the suppression is released, you have to wait for
the Purkinje pace to kick in
 During these 5-20 seconds, the ventricles don’t pump blood, so the person
faints after 4-5 seconds because of lack of blood flow to the brain
 This delayed pickup of the heartbeat is called Stokes-Adams syndrome
 If the delay period is too long, it can lead to death
The Purkinje fibers make it so that the impulse travels through the ventricles quickly, and there’s only a
0.03-0.06 second gap between the first ventricle fiber being stimulated, & the last ones being stimulated
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So the ventricle is able to contract all together at the same time
If the impulse travels slow through the ventricles, parts of the ventricle would contract before
the rest of it, which decreases the pumping effect
The parasymps go to the SA node and the AV node, a little bit to the atria, and very little to the
ventricles
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Stimulating the vagus to the heart causes acetylcholine to be released from the vagal endings
Acetylcholine decrease the rate of rhythm of the SA node, and decrease the excitability of the
AV junctional fibers between the AV node and atria muscle, slowing transmission of the heart
impulse into the ventricles
Weak to moderate vagal stimulation slows the rate of heart pumping
Strong vagal stimulation can stop discharge form the SA node, or cause an AV block
o This can cause Stoke-Adams, & then the Purkinje fibers kick in, called ventricular
escape
The acetylcholine greatly increase the permeability of the heart fiber membranes to potassium,
allowing rapid leakage of potassium out of the conductive fibers
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This causes increased negativity inside the fibers, called hyperpolarization, which makes
the tissue less excitable
In the SA node, the hyperpolarization changes the resting membrane potential of the SA
node to be more negative than usual
This makes it so that it takes longer to trigger an action potential, because more
sodium and calcium need to come in to offset the negative
This slows the rate of rhythm of the SA node fibers
In the AV node, the hyperpolarization makes it hard for atrial fibers entering the node to
generate enough electricity to excite the AV node fibers
 This decreases transmission from the AV node into the ventricles
 A large amount of acetylcholine can block conduction entirely
The symps are spread all throughout the heart, and innervate the ventricles well
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Symps increase the rate of SA node discharge, increase rate of conduction, and increase level
of excitability in all parts of the heart
Symps also increase the force of contraction of both the atrial and ventricular heart muscle
Stimulating symp nerves releases norepinephrine at the symp nerve endings
Norepinephrine stimulates β1 adrenergic receptors to regulate heart rate (β1 ↑ HR & SV = ↑CO)
o This increases the permeability of the membrane to sodium and calcium
In the SA node, an increase in permeability to sodium and calcium gives it a more positive
resting potential and also increases the rate of going towards the threshold for excitement
o So it accelerates excitation and heart rate
In the AV node and AV bundles, increased sodium-calcium permeability makes it easier for the
action potential to excite each succeeding part of the conducting fiber bundles, which
decreases the conduction time from the atria to the ventricles
The increase in permeability to calcium also causes the increase in contractile strength