Chapter 10 Rhythmical Excitation Of The Heart Flashcards

1
Q

Where is the sinoatrial node located?

A) Right atrium
B) Left atrium
C) Superior vena cava
D) Caudal vena cava

A

A) Right atrial wall, below and slightly lateral to the opening of the superior vena cava.

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2
Q

Is the resting membrane potential of the sinus nodal fibers more or less negative than that of the ventricular muscle fibers?

What causes this difference?

A

The sinus nodal fibers are less negative than that of the ventricular muscle fibers. This is because the cell membranes are naturally leaky to sodium and calcium ions, neutralizing some of the intracellular negativity.

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3
Q

Which ion channel causes the difference in atrial nodal action potential when compared to that of the action potential in ventricular muscle.

A) Fast sodium channels
B) L-type calcium channels
C) Potassium channels
D) Slow sodium channels

A

A) Fast sodium channels.

The atrial node fibers resting membrane is much less negative than that of the ventricular fibers. This may have already inactivated the fast sodium channels, essentially causing them to be blocked. Only slow sodium-calcium channels can open and cause the action potential. This is the reason that the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. The atrial nodal action potential also returns to its negative state slower than that of the ventricular fiber.

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4
Q

What ion channels influence the prevention of the sinus nodal fibers from constant depolarization?

A) Fast sodium channels
B) L-type calcium channels
C) Potassium channels 
D) Slow sodium channels
E) A & C
F) B & D
G) A & D
H) B & C
A

H) B & C

The L-type calcium channels close mere milliseconds after opening and a large number of potassium channels open about the same time. This prevents the influx of positive ions and allows the rapid efflux of positive ions out. This reduces the intracellular potential back to its negative resting level, terminating the action potential.

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5
Q

Who is responsible for delaying the cardiac impulse from the atria into the ventricles?

A) Sinus node
B) AV node
C) Right bundle branch
D) Left bundle branch

A

B) AV node and its adjacent conductive fibers delay transmission.

This allows time for the atria to empty their blood into the ventricles.

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6
Q

What causes the slow conduction throughout the transition, nodal and penetrating AV bundle?

A

Diminished numbers of gap junctions between successive cells in the conducting pathways, so there is great resistance to conduction fo the excitatory ions from one conducting fiber to the next.

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7
Q

Once the action potentials have crossed the AV bundle into the ventricles, what causes the rapid transmission of the AP by the Purkinje fibers?

A

There is a high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers. These Purkinje fibers also have very little myofibrils meaning they contract little or not at all during times of impulse transmission.

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8
Q

Why does the sinus node rather than the AV node or the Purkinje fibers control the heart’s rhythmicity?

A

Discharge rate of the sinus node is considerably faster than the natural self-excitatory discharge rate of either the AV node or the Purkinje fibers. The sinus node then discharges again before either the AV node or the Purkinje fibers can reach their own thresholds for self-excitation.

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9
Q

Define an ectopic pacemaker.

A

A pacemaker elsewhere than the sinus node.

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10
Q

Where are the parasympathetic nerves in the heart distributed?
(There may be more than one answer)

A) SA nodes
B) AV nodes
C) Muscle of the atria
D) Muscle of the ventricles

A

A, B, C and very little to D.

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11
Q

Where are the sympathetic nerves in the heart distributed?
(There may be more than one answer)

A) SA nodes
B) AV nodes
C) Muscle of the atria
D) Muscle of the ventricles

A

A-D, but very strong distribution to the ventricular muscle

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12
Q

Stimulation of the parasympathetic nerves in the heart causes what hormone to be released?

A) Norepinephrine
B) Acetylcholine
C) Bradykinin
D) Adenosine

A

B) Acetylcholine

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13
Q

Stimulation of the sympathetic nerves in the heart causes what hormone to be released?

A) Norepinephrine
B) Acetylcholine
C) Bradykinin
D) Adenosine

A

A) Norepinephrine

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14
Q

Which of the following is NOT caused by stimulation of parasympathetic nerves in the heart?

A) Release of acetylcholine
B) Increase the permeability of the fiber membranes to potassium ions.
C) Decrease the rate of rhythm of the sinus node
D) Increased rate of upward drift of the diastolic membrane potential

A

D) Increased rate of upward drift of the diastolic membrane potential

Stimulation of the parasympathetic nerves in the heart cause release of acetylcholine. This release at the vagal nerve endings causes increased permeability of the fiber membranes to potassium ions, allowing an increased negative inside the fibers. This is also known as hyperpolarization. Subsequently, there is a longer rise to reach the threshold potential for needed for self-excitation. This ultimately decreases the rate of rhythm of the sinus node and decreases the excitability of the AV junctional fibers, slowing transmission to the ventricles.

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15
Q

Which of the following is NOT caused by excitation of the sympathetic nerves in the heart?

A) Hyperpolarization
B) Stimulation of the beta-1 adrenergic receptors
C) Increase permeability to sodium and calcium ions
D) Increase in contractile strength of the cardiac muscle

A

A) Hyperpolarization DOES NOT occur with stimulation of sympathetic nerves

Sympathetic stimulation causes release of norepinephrine, which stimulates beta-1 adrenergic receptors. This is thought to increase the fiber membrane’s permeability to sodium and calcium ions, allowing a more positive resting potential and an increased rate of upward drift of the diastolic membrane potential toward the threshold level for self-excitation. There is an increase in the rate of sinus nodal discharge and an increase in the rate of conduction. The force of contraction of all the cardiac musculature is increased as well.

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