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Phys Ch 10
Rhythmical Excitation of the Heart
 Atria contract about 1/6 of a second ahead of ventricles
 Susceptible to damage by heart disease, especially ischemia
Specialized Excitatory and Conductive System of Heart
 SA node – flattened, ellipsoid strip of specialized cardiac muscle about 3 mm wide, 15 mm long, and 1 mm thick
o Immediately below and slightly lateral to the opening of the superior vena cava
 Ventricular muscle fibers have a more negative resting potential than SA node’s resting potential
o Cell membrane of SA node cells naturally leaky to Na+ and Ca2+, allowing more positive charges
 Opening of the fast sodium channels for a few 10,000ths of a second is responsible for rapid upstroke spike of
AP observed in ventricular muscle, because of rapid influx of Na+ to interior of fiber
 Plateau of ventricular action potential caused primarily by slower opening of slow sodium-calcium channels,
which lasts for about 0.3 sec
 Opening of potassium channels allows diffusion of large amounts of K+ in outward direction through fiber
membrane and returns membrane potential to its resting level
 At SA node (higher resting potential), fast sodium channels mainly have already become inactivated (blocked)
o Any time membrane potential remains less negative than about -55 mV for more than a few
milliseconds, inactivation gates on inside of PM that close fast sodium channels become closed and
remain so
o Only slow sodium-calcium channels open (i.e., can become "activated") and thereby cause AP
 Atrial nodal AP slower to develop than AP of ventricular muscle; after AP does occur, return of potential to its
negative state occurs slowly, rather than abrupt return that occurs for ventricular fibers
Excitation of SA Node
 Because of high Na+ concentration in extracellular fluid outside nodal fiber, as well as moderate number of
already open sodium channels, Na+ from outside fibers normally tend to leak inside
 Between heartbeats, influx of Na+ causes slow rise in resting membrane potential in positive direction (resting
potential gradually becomes less negative between heartbeats)
o When potential reaches threshold voltage of about -40 mV, sodium-calcium channels become
"activated," thus causing AP
o Therefore, inherent leakiness of SA nodal fibers to Na+ and Ca2+ causes their self-excitation
 2 events occur during course of AP to prevent SA node depolarization at all times
o Sodium-calcium channels become inactivated (i.e., they close) within about 100-150 ms after opening
o At about same time, greatly increased numbers of potassium channels open, so influx of Na+ and Ca2+
through the sodium-calcium channels ceases, while large quantities of K+ diffuse out of fiber; both of
these effects reduce intracellular potential back to its negative resting level and therefore terminate AP
o K channels remain open for another few tenths of a second, temporarily continuing movement of
positive charges out of the cell, with resultant excess negativity inside (hyperpolarization)
 During next few tenths of second after AP is over, progressively more and more potassium channels close, and
inward-leaking Na+ and Ca2+ once again overbalance outward flux of K+, and this causes "resting" potential to
drift upward once more, finally reaching threshold level for discharge
Internodal Pathways and Transmission of Cardiac Impulse through Atria
 Ends of SA nodal fibers connect directly with surrounding atrial muscle fibers, so APs originating in SA node
travel outward into these atrial muscle fibers – AP spreads through atria until it reaches AV node
o Velocity of conduction in most atrial muscle is about 0.3 m/sec, but conduction is more rapid (about 1
m/sec) in several small bands of atrial fibers
o Anterior interatrial band – passes through anterior walls of atria to left atrium (rapid band)
o 3 other small bands curve through anterior, lateral, and posterior atrial walls and terminate in AV node
(anterior, middle, and posterior internodal pathways)
o Cause of more rapid velocity of conduction in these bands is presence of specialized conduction fibers
similar to even more rapidly conducting Purkinje fibers of ventricles
AV Node and Delay of Impulse Conduction from Atria to Ventricles
 Primarily AV node and its adjacent conductive fibers that delay transmission to ventricles
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AV node located in posterior wall of right atrium immediately behind tricuspid valve
Impulse, after traveling through internodal pathways, reaches AV node about 0.03 sec after its origin in SA node;
delay of another 0.09 sec in AV node itself before impulse enters penetrating portion of AV bundle, where it
passes to ventricles; delay of another 0.04 sec occurs mainly in this penetrating A-V bundle, which is composed
of multiple small fascicles passing through fibrous tissue separating atria from ventricles
 Slow conduction caused by diminished numbers of gap junctions between successive cells in conducting
pathways, so there is great resistance to conduction of excitatory ions from one conducting fiber to the next
Rapid Transmission in Ventricular Purkinje System
 Purkinje fibers lead from AV node through AV bundle into ventricles - except for initial portion of these fibers
where they penetrate AV fibrous barrier, they are very large fibers (even larger than normal ventricular muscle
fibers), and they transmit APs at 1.5-4.0 m/sec (6x faster than that in usual ventricular muscle and 150x that in
some AV nodal fibers)
 Rapid transmission caused by very high level of permeability of gap junctions at intercalated discs between
successive cells that make up Purkinje fibers; ions are transmitted easily from one cell to the next, thus
enhancing velocity of transmission
 Purkinje fibers have very few myofibrils, which means that they contract little or not at all during impulse
transmission
One Way Conduction through AV Bundle
 Except in pathological conditions, AV bundle prevents re-entry of cardiac impulses from ventricles to atria
 Fibrous barrier separates atria from ventricles except at AV node
o In rare instances, abnormal muscle bridge does penetrate fibrous barrier elsewhere, causing ability of
cardiac impulse to re-enter atria from ventricles and cause serious cardiac arrhythmia
Distribution of Purkinje Fibers in Ventricles
 Distal portion of AV bundle passes downward in ventricular septum for 5-15 mm toward apex of heart, where it
divides into left and right bundle branch that lie beneath endocardium on sides of ventricular septum
 Each branch spreads downward toward apex of ventricle, progressively dividing into smaller branches, that in
turn course sidewise around each ventricular chamber and back toward base of heart
 Ends of Purkinje fibers penetrate about 1/3 of way into the muscle mass and finally become continuous with the
cardiac muscle fibers
 Average time from release from AV bundle until end of Purkinje fibers is 0.03 sec (essentially instantaneous)
Transmission of Cardiac Impulse in Ventricular Muscle
 Once impulse reaches ends of Purkinje fibers, it is transmitted through ventricular muscle mass by ventricular
muscle fibers themselves at velocity of 0.3-0.5 m/sec (1/6 that in Purkinje fibers)
 Cardiac muscle wraps around the heart in a double spiral, with fibrous septa between spiraling layers; therefore,
cardiac impulse does not travel directly outward toward surface of heart, but instead goes toward surface along
directions of spirals
 Transmission from endocardial surface to epicardial surface of ventricle requires 0.03 sec
Sinus Node as Pacemaker of the Heart
 AV nodal fibers have intrinsic rate of 40-60 bpm, and Purkinje fibers have intrinsic rate of 15-40 bpm
o Lower foci conduct the SA impulse (hence sending a signal) and SA node fires again before any of them
have a chance to depolarize to their own threshold (overdrive suppression)
 Ectopic pacemaker – one of the other foci starts discharging faster than SA node or grows irritable and does so
 Ectopic pacemaker can take over if SA node transmissions are blocked – can take 5-20 seconds to realize what
happened and take over (Purkinje fibers are in suppressed state because of rapid SA firing before)
o Person faints after 4-5 seconds because of lack of blood flow to brain
o Stokes-Adams syndrome – delayed pickup of heartbeat
Control of Heart Rhythmicity and Impulse Conduction by Cardiac Nerves: SNS and PNS
 PNS nerves (vagi) distributed mainly to SA and AV nodes, to a lesser extent to muscle of atria, and very little
directly to ventricular muscle
 SNS nerves well distributed to all parts of heart, with strong representation to ventricular muscle
 Stimulation of PNS to heart causes hormone acetylcholine to be released by vagal endings
o
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Decreases rate of rhythm of SA node and decreases excitability of AV junctional fibers, slowing
transmission of cardiac impulse to ventricles
o Strong stimulation by vagi can stop completely rhythmical excitation by SA node or block completely
transmission of cardiac impulse from atria to ventricles through AV node – can cause ventricular escape
o Acetylcholine released at vagal nerve endings greatly increases permeability of fiber membranes to K+,
which allows rapid leakage of K+ out of conductive fibers (hyperpolarization)
o In SA node, hyperpolarization alters resting potential of SA fibers, so initial rise of SA nodal membrane
potential caused by inward Na+ and Ca2+ leakage requires much longer to reach threshold potential
o In AV node, hyperpolarization caused by vagal stimulation makes it difficult for small atrial fibers
entering node to generate enough electricity to excite nodal fibers, so safety factor for transmission of
cardiac impulse through transitional fibers into AV nodal fibers decreases
o Moderate decrease delays conduction of impulse, but large decrease blocks conduction entirely
SNS stimulation causes increase of SA node discharge rate and increases rate of conduction as well as level of
excitability in all portions of heart; increases greatly force of contraction of all cardiac musculature
o Maximal stimulation can almost triple frequency of heartbeat and double strength of contraction
o Stimulation of SNS nerves releases norepinephrine at SNS nerve endings
o Norepinephrine stimulates β-1 adrenergic receptors, which mediate effects on heart rate (increases
permeability of fiber membrane to Na+ and Ca2+)
o In SA node, increase of sodium-calcium permeability causes more positive resting potential and
increased rate of upward drift of diastolic membrane potential toward threshold level for self-excitation,
accelerating self-excitation and thus increasing heart rate
o In AV node and AV bundles, increased Na-Ca permeability makes it easier for Aps to excite each
succeeding portion of conducting fiber bundles, thereby decreasing conduction time from atria to
ventricles
o Increase in permeability to Ca2+ is at least partially responsible for increase in contractile strength of
cardiac muscle under influence of SNS stimulation because Ca2+ play powerful role in exciting contractile
process of myofibrils