Physiology Chapter 10

Front 1

The normal rhythmical impulse of the heart is generated in the ___.

Back 1

sinus node aka sinoatrial node aka SA node

Front 2

The SA node is located ___.

Back 2

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

Front 3

Ventricular contraction in the normal heart has a delayed onset of ___ after the atrial contraction.

Back 3

1/6 sec

Front 4

The ___ conduct the impulse from the sinus node to the atrioventricular (A-V) node.

Back 4

internodal pathways

Front 5

The ___ conducts the impulse from the atria into the ventricles

Back 5

A-V bundle

Front 6

The ___ conduct the cardiac impulse to all parts of the ventricles.

Back 6

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

Front 7

Does the sinus node tissue contract?

Back 7

No, the fibers of this node have almost no contractile muscle filaments

Front 8

the resting membrane potential of the sinus nodal fiber between discharges has a negativity of about ___, in comparison with ___ for the ventricular muscle fiber.

Back 8

negative 55 to negative 60 millivolts / negative 85 to negative 90 millivolts

Front 9

What is the natural permeability of sinus fibers?

Back 9

leaky to sodium and calcium ions, these positive charges neutralize much of the intracellular negativity

Front 10

What types of channels are gound in cardiac muscle fiber?

Back 10

1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels.

Front 11

Opening of the ___ channels is responsible for the action potential observed in ventricular muscle

Back 11

fast sodium

Front 12

Then the plateau of the ventricular action potential is caused primarily by ___ channels

Back 12

slower opening of the slow sodium-calcium

Front 13

At this level of -55 millivolts or less, the fast sodium channels mainly have become ____.

Back 13

inactivated, therefore, only the slow sodium-calcium channels can open to cause the action potential.

Front 14

When the potential reaches a threshold voltage of about ___, the sodium-calcium channels become activated, thus causing the action potential.

Back 14

negative 40 millivolts

Front 15

Why does the leakiness to sodium and calcium ions not cause the sinus nodal fibers to remain depolarized all the time?

Back 15

sodium-calciuminflux is inactivated about 100 to 150 milliseconds after the channel opens, then greatly increased numbers of potassium channels openallowing potassium efflux

Front 16

How is hyperpolarization caued in cardiac muscle?

Back 16

potassium channels remain open for another few tenths of a second after negative resting level is reached, temporarily continuing movement of positive charges out of the cell, with resultant excess negativity inside the fiber

Front 17

The velocity of conduction in most atrial muscle is about ___, but can be as fast as ___, in several small bands of atrial fibers.

Back 17

0.3 m/sec, 1 m/sec

Front 18

The anterior, middle, and posterior internodal pathways are bands that ___.

Back 18

are located in the atrium, have faster contractility, and terminate in the AV node

Front 19

The anterior interatrial band passes ___.

Back 19

through the anterior walls of the atria to the left atrium

Front 20

The A-V node is located ____.

Back 20

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

Front 21

The impulse, after traveling through the internodal pathways, reaches the A-V node about ___ after its origin in the sinus node.

Back 21

0.03 second

Front 22

There is a delay of ___ in the A-V node itself before the impulse enters the penetrating portion of the A-V bundle, where it passes into the ventricles.

Back 22

0.09 second

Front 23

A final delay of ___ occurs in the penetrating A-V bundle

Back 23

0.04 second

Front 24

The total delay in the A-V nodal and A-V bundle system is about ___.

Back 24

0.13 second

Front 25

There is a total delay of ___ before the excitatory signal finally reaches the contracting muscle of the ventricles.

Back 25

0.16 second

Front 26

Purkinje fibers transmit action potentials at a velocity of ___.

Back 26

1.5 to 4.0 m/sec

Front 27

Can action potentials to travel backward from the ventricles to the atria?

Back 27

not under normal circumstances

Front 28

The distal portion of the A-V bundle passes downward in the ventricular septum and divides into ___ in the ___.

Back 28

left and right bundle branches that lie beneath the endocardium on the two respective sides of the ventricular septum.

Front 29

The total elapsed time of transduction from the bundle branches in the ventricular septum to the terminations of the Purkinje fibers is ___.

Back 29

0.03 second

Front 30

The velocity of transmission in the ventricular muscle fibers themselves is ____.

Back 30

0.3 to 0.5 m/sec

Front 31

Transmission from the endocardial surface to the epicardial surface of the ventricle requires ___.

Back 31

0.03 second

Front 32

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 ___.

Back 32

0.06 second

Front 33

Impulse spreads at moderate velocity through the atria but is delayed ___ in the A-V nodal region before appearing in the ventricular septal A-V bundle.

Back 33

0.1 second

Front 34

The A-V nodal fibers, when not stimulated from some outside source, discharge at an intrinsic rhythmical rate of ___, and the Purkinje fibers discharge at a rate between ___.

Back 34

40 to 60 times per minute / 15 and 40 times per minute

Front 35

The pacemaker of the heart is the ___.

Back 35

the sinus node because its rate of rhythmical discharge is faster than that of any other part of the heart

Front 36

A pacemaker elsewhere than the sinus node is called an ___.

Back 36

ectopic pacemaker

Front 37

When A-V block occurs a new pacemaker usually develops in the Purkinje system of the ventricles and drives the ventricular muscle at a new rate of ___.

Back 37

15 and 40 beats per minute

Front 38

What is Stokes-Adams syndrome?

Back 38

An AV block of 5 to 20 seconds when the ventricles fail to pump blood- person faints after the first 4 to 5 seconds

Front 39

Stimulation of the parasympathetic nerves to the heart (the vagi) causes the hormone ___ to be released at the vagal endings.

Back 39

acetylcholine

Front 40

What is the effect of parasympathetic innervation on the heart?

Back 40

decreases the rate of rhythm of the sinus node, andt decreased excitability of the A-V junctional fibers between the atrial musculature and the A-V node

Front 41

What is ventricular stimulation?

Back 41

Strong vagal stimualtion causes the ventricles stop beating for 5 to 20 seconds, but then some point in the Purkinje fibers, usually in the ventricular septal portion of the A-V bundle, develops a rhythm of its own and causes ventricular contraction at a rate of 15 to 40 beats per minute.

Front 42

What does acetylcholine do to potassium channels in the heart?

Back 42

it increases the permeability of the fiber membranes to potassium ions, which allows rapid leakage of potassium out of the conductive fibers causing hyperpolarization

Front 43

In the sinus node, the state of hyperpolarization decreases the resting membrane potential of the sinus nodal fibers to a level of ___.

Back 43

negative 65 to negative 75 millivolts

Front 44

Stimulation of the sympathetic nerves to the heart (the vagi) causes the hormone ___ to be released at the vagal endings.

Back 44

increases the rate of sinus nodal discharge, rate of conduction, and level of excitability in all portions of the heart

Front 45

Stimulation of the sympathetic nerves releases the hormone ___ at the sympathetic nerve endings.

Back 45

norepinephrine

Front 46

What does norepinephrine so to sodium-potassium channels?

Back 46

increases the permeability of the fiber membrane to sodium and calcium ions accelerating self-excitation