Physio Ch 10; Rhythmical Excitation Of The Heart

Front 1

The SA node is located

Back 1

in the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava

Front 2

The resting membrane potential of the sinus nodal fiber between discharges has a negativity of about

Back 2

-55 to -60 mV in comparison with -85 to -90 mV for the ventricular MUSCLE fiber. The reason for this is the SA nodal fibers are naturally leaky to Na+ and Ca+ ions and positive charges of the entering Na+ and Ca+ neutralize much of the intracellular negativity.

Front 3

Cardiac muscle has three types of membrane ion channels:

Back 3

1) fast Na+ channels; 2) slow Na+ Ca+ channels and 3) K+ channels.

Front 4

The plateau of the ventricular action potential is caused primarily by slower opening of the

Back 4

slow Na+Ca+ channels which lasts for about 0.3 second. Finally opening of Ka+ channels allows diffusion of large amounts of K+ outward and returns the membrane potential to its resting level

Front 5

Resting potential of sinus nodal fiber

Back 5

-55 mV

Front 6

Resting potential of the ventricular muscle fiber

Back 6

-90 mV

Front 7

The fast Na+ channel really doesn't play a part in the SA fiber because the fibers resting potential (-55 mV) is too positive for it to open. But the slow Na+Ca+ channels can open and thereby cause the action potential of the ventricular muscle. As a result

Back 7

the SA action potential is slower to develop than the action potential of the ventricular muscle. The return of the potential to negative state is slow as well.

Front 8

Between heartbeats, ___ tend to leak into the inside of the SA fibers, causing a slow rise

Back 8

in the resting membrane potential in the positive direction. The resting potential gradually rises between heartbeats to about -40 mV. Therefore basically, the inherent leakiness of the sinus nodal fibers to Na+ and Ca+ causes their self-excitation

Front 9

Ending the depolarization of SA node:

Back 9

1) Na+Ca+ channels become inactivated soon; 2) greatly increased numbers of K+ channels open. Therefore, influx of positive Ca+ and Na+ through the Na+Ca+ through their channel cease which at the same time K+ diffuse OUT. Terminates action potential

Front 10

Hyperpolarization

Back 10

The hyperpolarization caused by the K+ channels to remain open, carries the resting membrane down to -55 to -67 mV. The K+ channels close and once again, the inward leaking Na+Ca+ causes the upward drift once more

Front 11

anterior interatrial band

Back 11

The sinus nodal fibers of the anterior interatrial band, passes through the anterior walls of the atria to the left atrium. There is also the anterior, middle and posterior internodal pathways which terminate in the AV node.

Front 12

delayed transmission into the ventricles

Back 12

It is primarily the AV node and its adjacent conductive fibers that delay transmission into the ventricles

Front 13

The AV node is located

Back 13

in the posterior wall of the right atrium immediately behind the tricuspid valve

Front 14

The impulse from the SA node to the AV node is ___ second

Back 14

0.03 second

Front 15

The delay of ___ second in the AV node

Back 15

0.09 second in the AV node itself before the impulse enters the penetrating portion of the AV bundle

Front 16

A final delay of another ___ second occurs mainly in the penetrating AV bundle

Back 16

0.04 second

Front 17

The total delay from SA node to finally reaching the contracting muscle of the ventricles is

Back 17

0.16 second

Front 18

The cause of the slow conduction in the transitional, nodal and penetrating AV bundle fibers is caused mainly by

Back 18

diminished numbers of gap junctions between successive cells

Front 19

Purkinje fibers

Back 19

lead from the AV node through the AV bundle into the ventricles. They are very large fibers and they transmit 1.5 to 4.0 m/sec. Almost instantaneous transmission of the impulse throughout the entire remainder of the ventricular muscle. Lots of gap junctions at the intercalated disks

Front 20

The left and right bundle branches lie beneath

Back 20

the endocardium on the two respective sides of the ventricular septum.

Front 21

From the time the cardiac impulse enters the bundle branches in the ventricular septum until it reaches the terminations of the Purkinje fibers, the total elapsed time averages only

Back 21

0.03 second

Front 22

Transmission from the endocardial surface to the epicardial surface of the ventricle requires __ second

Back 22

0.03 second.

Front 23

The total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about ___ second

Back 23

0.06 second

Front 24

The AV nodal fibers intrinsic rhythmical rate is

Back 24

40-60 times per minute

Front 25

The Purkinje fibers discharge at a rate between

Back 25

15 and 40 times per minute

Front 26

Ectopic pacemaker

Back 26

is a pacemaker elsewhere than the sinus node

Front 27

Stokes-Adams syndrome

Back 27

After sudden AV bundle block, Purkinje system does not begin until 5-20 seconds later, the ventricles fail to pump blood and the person faints after the first 4-5 seconds because of lack of blood flow to the brain

Front 28

All portions of the ventricular muscle in both ventricles begins contracting at almost the same time and then continues contracting for about another

Back 28

0.3 seconds

Front 29

Stimulation of the parasympathetic nerves to the heart causes the hormone ___ to be released at the vagal endings

Back 29

acetylcholine. which 1) decreases the rate of rhythm of the SA node and 2) it decreases the excitability of the AV junctional fibers thereby slowing transmission of the cardiac impulse into the ventricles

Front 30

Strong vagal stimulation can

Back 30

completely block impulse from the atria to the ventricles

Front 31

The acetylcholine released at the valgal nerve endings greatly increases the permeability of the fiber membranes to

Back 31

K+ which allows rapid leakage of potassium out of the conductive fibers. This causes increased negativity inside the fibers called "hyperpolarization" which makes this excitable tissue MUCH LESS EXCITABLE

Front 32

In the sinus node, the state of hyperpolarization decreases the resting membrane potential of the sinus nodal fibers to -65 to -75 mV (rather than -55 to -60 mV) . Therefore,

Back 32

the initial rise caused by the leaky Na+ and Ca+ requires much longer to reach the threshold potential for excitation. Greatly slows rate of rhythmicity of these nodal fibers

Front 33

In the AV node, a state of hyperpolarization caused by vagal stimulation

Back 33

decreases the safety factor for transmission of the cardiac impulse through the transitional fibers into the AV nodal fibers

Front 34

Sympathetic stimulation

Back 34

1) increases the rate of sinus nodal discharge. 2) increases the rate of conduction as well as the level of excitability in all portions of the heart. 3) increases greatly the force of contraction of all the cardiac musculature both atrial and ventricular

Front 35

Stimulation of the sympathetic nerves releases the hormone

Back 35

norepinephrine at the sympathetic nerve endings. In the AV node and AV bundles, increased Na+Ca+ permeability makes it easier for the action potential to excite each succeeding portion of the conducting fiber bundles thereby decreasing the conduction time from the atria to the ventricles. An increase in permeability to calcium ions is at least partially responsible for the increase in contractile strength of the cardiac muscle under the influence of sympathetic stimulation.