Electrical Properties of the Heart Chapters 9 and 10

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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Stim microelectrode

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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

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Direction of Depol

Stim microelectrode

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Direction of Depol

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Direction of Depol

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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

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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