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Electrical Properties of the Heart
Chapters 9 and 10
Review of Heart Muscle• Cardiocytes, myocardium• Branched cells• Intercalated discs- (desmosomes)
and electrical junctions (gap junctions).
• Has actin and myosin filaments
• Has low resistance (1/400 the resistance of cell membrane)
• Atrial syncytium• Ventricular syncytium• Fibrous insulator exists between
atrium and ventricle (what would this do to any electrical activity trying to go through?)
Figure 9-1; Guyton & Hall
• If the electrical signals from the atria were conducted directly into the ventricles across the AV septum, the ventricles would start to contract at the top (base). Then the blood would be squeezed downward and trapped at the bottom of the ventricle.
• The apex to base contraction squeezes blood toward the arterial opening at the base of the heart.
• The AV node also delays the transmission of action potentials slightly, allowing the atria to complete their contraction before the ventricles begin their contraction. This AV nodal delay is accomplished by the naturally slow conduction through the AV node cells. (Why are they slow conductors? Small diameter cells, fewer channels. Refer to text)
Fibers within the heart• Specialized Fibers
– are the fibers that can spontaneously initiate an AP all by themselves!
– The AP will spread to all other fibers via gap junctions
– AKA “leading cells”– But they are also muscle, so they do contract, albeit
feebly!– They are not nerves!!!!
• Contractile Fibers– These maintain their RMP forever, unless brought to
threshold by some other cell– They cannot generate an AP by themselves– AKA “following cells”– But they do have gap junctions, so once they’re
triggered, they will help spread the AP to neighbors.
Pathway of Heartbeat• Begins in the sinoatrial (S-A)
node• Internodal pathway to
atrioventricular (A-V) node • Impulse delayed in A-V node
(allows atria to contract before ventricles)
• A-V bundle takes impulse into ventricles
• Left and right bundles of Purkinje fibers take impulses to all parts of ventricles
KEY Red = specialized cells;
all else = contractile cells
Sinus Node• Specialized cardiac muscle
connected to atrial muscle.• Acts as pacemaker
because membrane leaks Na+ and membrane potential is -55 to -60mV
• When membrane potential reaches -40 mV, slow Ca++ channels open causing action potential.
• After 100-150 msec Ca++ channels close and K+channels open more thus returning membrane potential toward -55mV.
Internodal Pathways
• Transmits cardiac impulse throughout atria• Anterior, middle, and posterior internodal
pathways• Anterior interatrial band carries impulses to left atrium.
A-V Node
• Delays cardiac impulse• Most delay is in A-V node• Delay AV node---0.09 sec.• Delay AV bundle--0.04 sec.
A-V Bundles
• Only conducting path between atria and ventricles
• Divides into left and right bundles
• Time delay of 0.04sec
Purkinje System
• Fast conduction; many gap junctions at
intercalated disks
SA Node
AV Node
AV Bundle
Left Bundle Branch
Right Bundle Branch
(0.0)
(0.03) (0.12)
(0.19)
(0.21)
(0.22)
(0.19)
(0.18)
(0.17)
(0.18)
(0.16)
Time of Arrival of Cardiac Impulse
Main Arrival TimesS-A Node 0.00 secA-V Node 0.03 sec A-V Bundle 0.12 sec Ventricular Septum 0.16 secBase 0.22 sec
Copyright © 2006 by Elsevier, Inc.
How can these Specialized fibers spontaneously “fire?”
• Can’t hold stable resting membrane potential
• Potentials drift (gradual depolarization) –”prepotential” or “pacemaker potential”
• During this time, they have a gradually increasing perm to Na+ and less leaky to K+ (more “+” inside causes cell to depolarize, remember?)
Na+
Specialized fibers
Notice slow rise from rest to threshold.
This is called the “prepotential” or “pacemaker potential”
Only specialized fibers of the heart can do this.
This is what gives the heart it’s rhythm.
-100
-80
-40
-60
+20
0
-20
2 3 40 1
Seconds
Mem
bra
ne
Pot
enti
al (
mV
)
Threshold
Sinus Nodal Fiber
Na+ LeakAnd less leaky to potassium
Slow Ca++
Channels Open
K+ ChannelsOpen more
Ventricular Muscle fiber
}
“Pre- Potential”
Rhythmical Discharge of Sinus Nodal Fiber
Specialized fibers of conductive system
• Each region generates its own rhythm.• If cells didn’t touch, then….• Faster at SA vs AV node, etc.• SA is faster than AV- “pacemaker”
– SA 60-80 depol/min – AV 40-60 depol/min– Purkinje 15-30 depol/min
• Draw it!
Time (min)
SA
AV
PurBecause SA node has the highest intrinsic rhythm, it is called the cardiac pacemaker. What if damaged…?
Specialized fibers of conductive
system• These rhythms can
ALSO be modified by the ANS
• NTS can change slope of prepotentials…faster or slower rise to threshold (bringing them closer or further from threshold.) by altering ion permeability.
• ACh (psymp postganglionic); NE (symp postganglionic)
K+ efflux
• Sympathetic – speeds heart rate by Ca++ & Na+ channel influx and K+ permeability/efflux (positive chronotropy)
• Parasympathetic – slows rate by K+ efflux & Ca++ influx (negative chronotropy)
Sympathetic and Parasympathetic
Figure 14-17: Modulation of heart rate by the nervous system
Other effect of ANS
• Symp (NE) also affects inotropy in ALL fibers, specialized and contractile
• Inotropy is the “force of contraction” or the tension development in the muscle fiber (strength of the contraction.)
• Sympathetic firing causes positive inotropy! (the pounding heart)
• Parasympathetics have little effect on inotropy
Terminology: Chrono, Inotropy Symp (+,+) Parasym ( -, )
http://www.phschool.com/science/biology_place/biocoach/cardio1/electrical.html
Regulators of the Heart: Reflex Controls of Rate
• Your HR at any moment is the balance between symp and parasym discharge rates. (“tone”/ reserve)
• Tonic discharge• How to speed up? Two ways
(faucet analogy)• How to slow down? Two ways• Range: about 50 – near 200• Typical resting HR: near 70 --
SA would normally beat at 60-80 bpm- but vagal tone slows it down. Parasympathetic slows-down (20bpm or even stop)-
• Sympathetic speeds-speed up (230bpm)
K+
Contractile Fibers of Heart• Bulk of heart mass• Review APs
– Still need calcium to initiate contraction
• Differences from Skeletal Muscle and neurons– Nature of AP – Source of calcium (EC
vs. SR)– Duration of contraction– Resting potential
EC Coupling – how it works (skeletal muscle)
AP
Ca2+ pump
calsequestrin
Sequence of Events:1. AP moves along T-tubule2. The voltage change is sensed
by VONa+ Channels3. Is communicated to the
(VOCC) (voltage operated calcium channel; VOCR) how much calcium released depends on voltage
4. Contraction occurs.5. Calcium is pumped back into
SR. Calcium binds to calsequestrin to facilitate storage.
6. Contraction is terminated.
EC Coupling –
AP
Ca2+ pump requires ATP
calsequestrin
Sequence of Events:1. AP moves along T-tubule.2. Activation – voltage sensors
that release a small amount of Ca into the fiber.3. Ca then binds to a receptor
which opens, releasing a large amount of Ca. (Calcium
Activated Calcium Release) How much calcium released depends on how much calcium gets through cell membrane
4. Calcium is pumped (a) back into SR, and (b) back into T tubule. 5. Contraction is terminated.
Ca2+/Na+ exchanger (Ca2+ out / Na+ in)
Cardiac Muscle
Ventricular Muscle Action Potential-RMP -85mV;
-100
-80
-40
-60
+20
0
-20
2 3 40 1
Mem
bra
ne
Pot
enti
al(m
V)
Seconds
Fast Na+
Channels Open
0
1
2
3
4
phase
Fast Na+ close
phase 0- Fast Na+ channels open phase 1- Fast Na+ channels closephase 2- slow Ca++ open and decreased K+ permeability phase 3- K+ channels openphase 4- Resting membrane potential
K+ Channels Open
Slow Ca++ Channels open and decreased K+ permeability
Copyright © 2006 by Elsevier, Inc.
Important things to consider
• Cardiac muscle cells have a long absolute refractory period
• Twitches can not summate• Tetanus not possible (this is
good!)• If average heart beats 72bpm;
what does the heart do for the rest of the time?
• Answer : It “rests” and fills
Spread of Depolarization
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Direction of Depol
Resting Cell
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
Depolarizing Current!+ + +
+
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Direction of Depol
Stim microelectrode
Depolarizing Current!
+
+
+
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Direction of Depol
Stim microelectrode
Depolarizing Current!
++ +
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
Depol = spread of surface NEG charge
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Direction of Repolarization
Stim microelectrode
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Begin Repolarization
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Repolarization= spread of positive surface charge
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Repolarization= spread of POS surface charge
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Depolarization/Repolarization Cycle in the Atria
=Resting cell
=Depol cell
Depolarization Begins
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
Depolarization Complete
=Resting cell
=Depol cell
Repolarization Begins
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
Repolarization Complete
Depolarization/Repolarization Cycle in the Ventricles
=Resting cell
=Depol cell
Depolarization Begins
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
Depolarization Complete
=Resting cell
=Depol cell
Repolarization Begins
=Resting cell
=Depol cell
=Resting cell
=Depol cell
=Resting cell
=Depol cell
Repolarization Complete