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Physiology Chap10 (Rhythmical Excitation of the Heart)

Physiology Chap10 (Rhythmical Excitation of the Heart)

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Published by: Man Dejelo on Feb 07, 2011
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10/12/2013

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10 Rhythmical Excitation of theHeart
y
 
HEART is endowed with a special systemfor (1) generating rhythmical electricalimpulses to cause rhythmical contraction of the heart muscle and (2) conducting theseimpulses rapidly through the heart
 
y
 
allows all portions of the ventricles tocontract almost simultaneously
 
Sp
ecialized Excitatory andConductive
S
ystem of the Heart
y
 
sinus node - normal rhythmical impulses aregenerated
 
y
 
internodal pathways - conduct impulses fromthe sinus node to the atrioventricular (A-V)node
 
y
 
 A-V node - impulses from the atria aredelayed before passing into the ventricles
 
y
 
 A-V bundle - conducts impulses from theatria into the ventricles
 
y
 
Purkinje fibers - conduct the cardiacimpulses to all parts of the ventricles
 
S
inus (
S
inoatrial) Node
y
 
small, flattened, ellipsoid strip of specializedcardiac muscle
 
y
 
superior posterolateral wall of the rightatrium immediately below and slightly lateralto the opening of the superior vena cava
 
y
 
no contractile muscle filaments
 
y
 
connect directly with the atrial muscle fibersso that any action potential that begins in thesinus node spreads immediately into theatrial muscle wall.
 
A
utomatic Electrical Rhythmicity of the
S
inus Fibers
y
 
self-excitation -
process that can causeautomatic rhythmical discharge andcontraction
 
y
 
controls the rate of beat of the entire heart
 
Mechanism of Sinus Nodal Rhythmicity 
y
 
"resting membrane potential" of the sinusnodal fiber between discharges has anegativity of about -55 to -60 millivolts, incomparison with -85 to -90 millivolts for theventricular muscle fiber.
 
y
 
cause of this lesser negativity is that the cellmembranes of the sinus fibers are naturallyleaky to sodium and calcium ions, andpositive charges of the entering sodium andcalcium ions neutralize some of theintracellular negativity
 
y
 
Opening of the fast sodium channels isresponsible for the rapid upstroke spike of the action potential observed in ventricular muscle
 
y
 
"plateau" of the ventricular action potential iscaused primarily by slower opening of theslow sodium-calcium channels, which lastsfor about 0.3 second
 
y
 
Opening of potassium channels allowsdiffusion of large amounts of positivepotassium ions in the outward direction
 
y
 
 At this level of -55 millivolts, the fast sodiumchannels mainly have already become"inactivated," / blocked
 
y
 
inactivation gates on the inside of the cellmembrane that close the fast sodiumchannels become closed and remain so
 
y
 
only the slow sodium-calcium channels canopen
 
Self-Excitation of Sinus Nodal Fibers
y
 
high sodium ion concentration in theextracellular fluid outside the nodal fiber 
 
y
 
positive sodium ions from outside the fibersnormally tend to leak to the inside
 
y
 
slow rise in the resting membrane potentialin the positive direction
 
y
 
When the potential reaches a thresholdvoltage of about -40 millivolts, the sodium-calcium channels become "activated," thuscausing the action potential
 
y
 
inherent leakiness of the sinus nodal fibersto sodium and calcium ions causes their self-excitation.
 
 
y
 
Why does this leakiness to sodium andcalcium ions not cause the sinus nodalfibers to remain depolarized all the time?- the sodium-calcium channels becomeinactivated (i.e., they close) within about100 to 150 milliseconds after opening,and second, at about the same time,greatly increased numbers of potassiumchannels open. Therefore, influx of positive calcium and sodium ionsthrough the sodium-calcium channelsceases
 
- reduce the intracellular potential back toits negative resting level and thereforeterminate the action potential
 
-
hyp
er 
 p
olarization
- continuingmovement of positive charges out of thecell, with resultant excess negativityinside the fiber; "resting" membranepotential down to about -55 to -60millivolts at the termination of the actionpotential
 
y
 
Why is this new state of hyperpolarizationnot maintained forever?- inward-leaking sodium and calcium ionsonce again overbalance the outward fluxof potassium ions, and this causes the"resting" potential to drift upward oncemore, finally reaching the threshold levelfor discharge at a potential of about -40millivolts
 
- Then the entire process begins again:self-excitation to cause the actionpotential, recovery from the actionpotential, hyperpolarization after theaction potential is over, drift of the"resting" potential to threshold, andfinally re-excitation
 Internodal Pathways and Transmission of the Cardiac Impulse Through the Atria
y
 
ends of the sinus nodal fibers connectdirectly with surrounding atrial muscle fibers
 
y
 
action potentials originating in the sinusnode travel outward into these atrial musclefibers
 
y
 
The velocity of conduction in most atrialmuscle is about 0.3 m/sec, but conduction ismore rapid, about 1 m/sec, in several smallbands of atrial fibers
 
 Atrioventricular Node and Delay of Impulse Conduction from the Atria to theVentricles
y
 
this delay allows time for the atria to emptytheir blood into the ventricles beforeventricular contraction begins
 
y
 
posterior wall of the right atrium immediatelybehind the tricuspid valve
 
y
 
after traveling through the internodalpathways, reaches the A-V node about 0.03second after its origin in the sinus node.Then there is a delay of another 0.09second in the A-V node itself before theimpulse enters the penetrating portion of the A-V bundle, where it passes into theventricles. A final delay of another 0.04second occurs mainly in this penetrating A-Vbundle
 
y
 
total delay in the A-V nodal and A-V bundlesystem is about 0.13 second
 
y
 
This, in addition to the initial conductiondelay of 0.03 second from the sinus node tothe A-V node, makes a total delay of 0.16second before the excitatory signal finallyreaches the contracting muscle of theventricles
 
ause of the Slow 
onduction
y
 
caused mainly by diminished numbers of gap junctions between successive cells inthe conducting pathways
 
y
 
great resistance to conduction of excitatoryions from one conducting fiber to the next
 Rapid Transmission in the Ventricular Purkinje
S
ystem
y
 
lead from the A-V node through the A-Vbundle into the ventricles
 
y
 
functional characteristics that are quite theopposite of those of the A-V nodal fibers
 

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