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259 - physiology > lecture 2: 9/10 guyton > Flashcards

lecture 2: 9/10 guyton Flashcards

1
Q

what happens to aortic pressure during systole after the aortic valve opens?

A

aortic pressure increases

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2
Q

when does aortic pressure decrease

A

towards the end of the ejection phase

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3
Q

what develops after the aortic valve closes and why

A

insura develops due to a sudden back flow towards the left ventricle

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4
Q

why does aortic pressure decrease slowly during diastole

A

because of the elasticity of the aorta

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5
Q

why do we get heart sounds

A

because of the closing of heart values

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6
Q

when does the first hear sound occur

A

First sound occurs as the atrioventricular (Tricuspid and Mitral) valves close and signifies beginning of systole

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7
Q

when does the second heart sound occur

A

Second sound occurs when the semilunar (Pulmonary & Aortic) valves close at the beginning of ventricular diastole

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8
Q

what are the atrioventricular valves

A

tricuspid and mitral

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9
Q

what are the semilunar valves

A

pulmonary and aortic

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10
Q

why is there a backflow of blood that develops the insura

A

blood bounces off of the peripheral resistance

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11
Q

what is the purpose of the valves

A

to prevent backflow

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12
Q

why do we sometimes hear a 3rd heart sound and who do we hear it in

A

sometimes when the blood flowing back into the ventricles is so rapid it produces a third sound

can happen in children and highly trained individuals

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13
Q

true or false: during the period of filling the ventricles, pressure increases significantly?

A

false, no it stays pretty constant because the heart is elastic and expanding

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14
Q

what is another name for preload

A

end-diastolic volume

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15
Q

when the end-diastolic volume is reached, what happens

A

isovolumic contraction

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16
Q

when is the blood from the ventricles ejected

A

when the pressure in the ventricle is equal or greater than the systemic pressure so that the valve can open

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17
Q

what is the minimum blood pressure needed to eject blood called?

A

diastole

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18
Q

what do hypertensive individuals hearts need to work harder

A

since they have a higher systemic pressure, the heart must have a higher pressure in the ventricles to combat that which means the heart needs to work harder

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19
Q

true or false: end systolic volume is the systolic bp

A

false, systolic BP is highest pressure in the ventricles

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20
Q

what is another name for afterload?

A

end-systolic volume

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21
Q

when all the blood has been ejected (end systolic volume), what happens to the ventricles

A

isovolumic relaxation and pressure starts to decrease

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22
Q

why would an individual get an increased preload

A

because of an increase venous return (more blood comes into the heart)

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23
Q

what are 2 ways to increase venous return?

A

slow heart rate

make better posture

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24
Q

what happens if cardiac muscle sarcomeres are stretched, within limits?

A

they contract more forcibly without increase in heart work

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25
Q

why do cardiac muscles contract more forcefully if the sarcomeres are stretched

A

there are more sites available for cross-bridge interaction

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26
Q

what happens if sarcomeres are stretched too much

A

there will no longer be optimal cross-bridge, pressure will plateau, decrease in stroke volume

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27
Q

explain why the frank starlic mechanism is good

A

because if you get an increased venous return, the heart will be able to eject the blood more forcefully (rubber band mechanism) without extra heart work and that will increase the stroke volume

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28
Q

if you increase preload, you get a larger or smaller stroke volume

A

larger

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29
Q

what happens if there is an increased after load>

A

increase afterload means there is more blood left in the ventricles, which will decrease stroke volume

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30
Q

if you increase afterload, you increase or decrease stroke volume

A

stroke volume decreases

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31
Q

what happens to BP with an increased afterload

A

if there is an increased afterload that means there is more blood left in the heart which means the ventricle must build higher pressure to which makes it harder for the heart to eject the blood

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32
Q

if you have an increased contractility what happens to the stroke volume (increase or decrease)

A

increase

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33
Q

what happens to BP if there is an increase contractility

A

causes an increase in pressure since there heart needs to contract more forcefully

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34
Q

what happens to end-systolic volume with an increased contractility

A

it will decrease

less blood left in the haart since more was ejectred due to incrase contractility

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35
Q

how can you increase contractility (2 ways)

A

hormones and sympathetic activation (epinephrine)

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36
Q

The concentrations of K+ (and organic anions) are BLANK inside a myocyte but very BLANK outside the sarcolemma.

A

high inside

low outisde the sarcolemma

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37
Q

Na+ (and Ca2+ & Cl-) are more concentrated outside or inside the cell

A

outside

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38
Q

what is the potential difference between the inside and outside is called

A

diffusion potential

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39
Q

what gives the resting membrane potential

A

The electro-chemical equilibrium

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40
Q

what are the 3 factors that affect permeability to different ions of the membrane

A

1) Polarity of the electrical charge of each ion (compare Na+ to Ca2+)
2) Permeability of the membrane
3) Concentrations of the respective ions on the inside and outside of the membrane

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41
Q

membrane potential is a potential?

A

false, it is the difference between two potentials so it is a voltage

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42
Q

what does SA node stand for

A

sinoatrial node

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43
Q

what is the SA node made of

A

Specialized cardiac muscle

44
Q

what is the SA node and where is it

A

a flattened ellipsoid strip of cells in the right atrium.

45
Q

true or false: there are no contractile filaments in the sinus node

A

true

46
Q

what are sinus nodal fibers are electrically connected to

A

atrial muscle fibers through syncytium

47
Q

since the SA node has no contractile filaments, it is not excitable.

A

false, there are highly excitable

48
Q

what is the inherent rate of the SA node

A

100 bpm

49
Q

true or false: The SA node sets the rate and rhythm of your heartbeat

A

true

50
Q

since the SA node controls HR and has a rate of 100 bpm, that means something is BLANK these cells to get it to resting HR

A

dampening

51
Q

if the SA node has no contractile filaments, how are they self excitable

A

because of the inherent leakiness of the SA node to sodium and calcium

52
Q

what is the resting membrane potentiation of the sinus nodal fiber

A

-55 to -60 mV

53
Q

what is the resting membrane potential for the ventricular muscle fiber

A

-85 to -90 mV

54
Q

which ap develops slower, the atrial nodal or the ventricular muscle

A

atrial nodal

55
Q

true or false: there is a slow depolarization for sinus nodal

A

true

56
Q

why does the Sinus Node Controls Heart Rhythmicity

A

because of its more positive resting membrane potential and leakiness, it is the first to be depolarized and spread because of the syncytium

57
Q

true or false The discharge rate of the sinus node is considerably slow than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers.

A

false, it is much faster

58
Q

can other parts of the heart ever control heart rhythm

A

yes, under abnormal conditions, few other parts of the heart can exhibit intrinsic rhythmical excitation in the same way as the sinus nodal fibres (A-V node and Purkinje fibres).

59
Q

what other types of parts of the hear can exhibit rhythmical excitation?

A

av node and purkinje fibers

60
Q

what is a pacemaker elsewhere than the sinus node is called …

A

an ectopic pacemaker/abnormal pacemaker

61
Q

where do action potentials originating in the sinus node travel

A

outward into the atrial muscle fibres and to the A-V node.

62
Q

what happens to the impulse (AP) after it travels through the internodal pathways

A

it reaches the A-V node about 0.03 second after its origin in the sinus node.

63
Q

true or false: the impulse/AP stays the same speed travelling from the SA node to the AV node

A

false, it gets delayed

64
Q

what is the reason for the delay of action potential from reaching the ventricles

A

allowing the atria to empty blood into the ventricles before the ventricles contract.

65
Q

why does the delay happen at the AV node

A

This happens because the A-V node has less gap junctions

66
Q

what is the only fiber that connects the atrial to the ventricle

A

the av bundle

67
Q

true or false: the Ap only delays at the AV node

A

false The impulse is delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal A-V bundle.

68
Q

the AV bundle has one way or 2 way conduction

A

one way

69
Q

where do the right bundle branch and left bundle branch carry the impulse

A

towards the apex of the heart

70
Q

was is another name for the AV bundle

A

His bundle

71
Q

how does the impulse transmit to the ventricular

A

Purkinje System

72
Q

where do the special purkinje fibers lead

A

lead from the A-V node through the A-V bundle into the ventricles.

73
Q

what is the effect of the diminished numbers of gap junctions between successive cells in the conducting pathways within the A-V node?

A

induce resistance to the conduction of excitatory ions from one conducting fibre to the next.

74
Q

what happens to the impulse at the termination of the Purkinje fibers

A

the impulse rapidly travels through the ventricle muscle fibers via gap junctions, from the inside (endocardium) to the outside (epicardium).

75
Q

why is it necessary for rapid propagare of the cardiac impulse through the Purkinje fibers and ventricles

A

important for an effect contraction

76
Q

true or false: the impulse rapidly travels through the ventricle muscle fibers via gap junctions, from the inside (endocardium) to the outside (epicardium).

A

true

77
Q

why does the signal/impulse go to the apex of the heart

A

because it allows max blood to be ejected

78
Q

why is the SA and AV node action potential is slower to develop than the action potential of the atrial or ventricular muscles?

A

because of the leaky channels

since the atrial/ventricular muscles are already at their resting membrane potential, when the impulse is sensed the AP gets sent fast

79
Q

can fast responses (like in the atria and ventricles) ever be converted to the slow responses?

A

yes
Fast responses may be converted to slow responses either spontaneously or under certain experimental conditions (lack of blood supply)

80
Q

what does ERP stand for and what does it mean

A

effective refractory period

The effective refractory period (ERP) is the amount of time in which the cell cannot respond to a newly conducted stimulus. This period is how the heart stays in rhythm and prevents arrhythmias

81
Q

what is the RRp

A

relative refractory period

period where under certain circumstances, it can be depolarized

82
Q

the refractory period is short in BLANK muscles but long is BLANK MUSCLE

A

short in skeletal
long in cardiac

83
Q

what does it mean for the skeletal muscle to have short refractory periods and cardiac muscle to have long refractory periods?

A

This means that skeletal muscle can undergo summation and tetanus, via repeated stimulation

Cardiac muscle CAN NOT sum action potentials or contractions and CAN NOT be tetanized

84
Q

why is it important for the heart muscle to have a long refractory period

A

allows the atrium and ventricle to refill with blood

prevent artyhmias

85
Q

what are 2 ways to change the frequence of pacemaker firing

A

1) increase HR (increase sodium in the cell)
you will reach the threshold sooner and generate the AP faster

2) change the normal resting potential so you can reach the AP faster

86
Q

what neurotransmitter to parasympathetic nerves release

A

acetylcholine

87
Q

true or false, the parasympathetic increases or decrease the heart rhythm and excitability

A

decreases

88
Q

what nerves make it so the excitatory signals are no longer transmitted into the ventricles

A

parasymphathetic

89
Q

explain how parasympathetic nerves decrease heart rhythm and excitability

A

because of the Increased permeability of the fiber membranes to potassium ions

(longer to reach threshold)

90
Q

what NT do sympathetic nerves release

A

norepinephrine

91
Q

true or false: sympathetic nerves increase or decrease the rate of sinus nodal discharge

A

increase

92
Q

what happens to the heart activity when sympathetic nerves are stimulated

A

increases overall heart activity

93
Q

explain how sympathetic nerves effect basic rhythm

A

increases the permeability to the NA and Ca ions, faster to reacher AP threshold

94
Q

what modulates the frequency of depolarization of pacemaker

A

autonomic nervous system

95
Q

where does the norepinephrine bind for sympathetic stimulation?

A

binds to beta1 receptors on the SA nodal membranes

96
Q

where does acetylcholine bind for parasympathetic stimulation and what does that do

A

binds to muscarinic receptors on nodal membranes; increases conductivity of K+ and decreases conductivity of Ca2+

97
Q

sympathetic stimulation means there is a HIGHER OR LOWER resting membrane potential

A

higher (more positive) easier-to-reach threshold

98
Q

parasympathetic stimulation means there is a HIGHER OR LOWER resting membrane potential

A

lower (more negative)

harder to reach threshold

99
Q

what does atrial fibrillation mean

A

not just one cell initiating the signal causing irregular beat

100
Q

what are 4 examples of abnormal heart rhythms

A

atrial fibrillation
supraventricular tachycardia
ventricular tachycardia
bradycardia

101
Q

what does supraventricular tachycardia mean

A

electric impulses travel from ventricle to atria

102
Q

what is ventricular tachycardia

A

ventricles do not have enough time to fill up properly

103
Q

what is the effect on stroke volume and cardiac output of ventricular tachycardia

A

decreased stroke volume and decreased cardiac output

104
Q

what is bradycardia

A

slow heart beat

105
Q

where do they implant the pacemaker

A

connected to the SA node and apex

106
Q

what do artificial pacemakers do

A

generate electrical signal when SA node doesn’t work

259 - physiology (21 decks)

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