lecture 2: 9/10 guyton Flashcards
(106 cards)
1
Q
what happens to aortic pressure during systole after the aortic valve opens?
A
aortic pressure increases
2
Q
when does aortic pressure decrease
A
towards the end of the ejection phase
3
Q
what develops after the aortic valve closes and why
A
insura develops due to a sudden back flow towards the left ventricle
4
Q
why does aortic pressure decrease slowly during diastole
A
because of the elasticity of the aorta
5
Q
why do we get heart sounds
A
because of the closing of heart values
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
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
8
Q
what are the atrioventricular valves
A
tricuspid and mitral
9
Q
what are the semilunar valves
A
pulmonary and aortic
10
Q
why is there a backflow of blood that develops the insura
A
blood bounces off of the peripheral resistance
11
Q
what is the purpose of the valves
A
to prevent backflow
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
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
14
Q
what is another name for preload
A
end-diastolic volume
15
Q
when the end-diastolic volume is reached, what happens
A
isovolumic contraction
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
17
Q
what is the minimum blood pressure needed to eject blood called?
A
diastole
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
19
Q
true or false: end systolic volume is the systolic bp
A
false, systolic BP is highest pressure in the ventricles
20
Q
what is another name for afterload?
A
end-systolic volume
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
22
Q
why would an individual get an increased preload
A
because of an increase venous return (more blood comes into the heart)
23
Q
what are 2 ways to increase venous return?
A
slow heart rate
make better posture
24
Q
what happens if cardiac muscle sarcomeres are stretched, within limits?
A
they contract more forcibly without increase in heart work
25
why do cardiac muscles contract more forcefully if the sarcomeres are stretched
there are more sites available for cross-bridge interaction
26
what happens if sarcomeres are stretched too much
there will no longer be optimal cross-bridge, pressure will plateau, decrease in stroke volume
27
explain why the frank starlic mechanism is good
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
28
if you increase preload, you get a larger or smaller stroke volume
larger
29
what happens if there is an increased after load>
increase afterload means there is more blood left in the ventricles, which will decrease stroke volume
30
if you increase afterload, you increase or decrease stroke volume
stroke volume decreases
31
what happens to BP with an increased afterload
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
32
if you have an increased contractility what happens to the stroke volume (increase or decrease)
increase
33
what happens to BP if there is an increase contractility
causes an increase in pressure since there heart needs to contract more forcefully
34
what happens to end-systolic volume with an increased contractility
it will decrease
| less blood left in the haart since more was ejectred due to incrase contractility
35
how can you increase contractility (2 ways)
hormones and sympathetic activation (epinephrine)
36
The concentrations of K+ (and organic anions) are BLANK inside a myocyte but very BLANK outside the sarcolemma.
high inside
| low outisde the sarcolemma
37
Na+ (and Ca2+ & Cl-) are more concentrated outside or inside the cell
outside
38
what is the potential difference between the inside and outside is called
diffusion potential
39
what gives the resting membrane potential
The electro-chemical equilibrium
40
what are the 3 factors that affect permeability to different ions of the membrane
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
41
membrane potential is a potential?
false, it is the difference between two potentials so it is a voltage
42
what does SA node stand for
sinoatrial node
43
what is the SA node made of
Specialized cardiac muscle
44
what is the SA node and where is it
a flattened ellipsoid strip of cells in the right atrium.
45
true or false: there are no contractile filaments in the sinus node
true
46
what are sinus nodal fibers are electrically connected to
atrial muscle fibers through syncytium
47
since the SA node has no contractile filaments, it is not excitable.
false, there are highly excitable
48
what is the inherent rate of the SA node
100 bpm
49
true or false: The SA node sets the rate and rhythm of your heartbeat
true
50
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
dampening
51
if the SA node has no contractile filaments, how are they self excitable
because of the inherent leakiness of the SA node to sodium and calcium
52
what is the resting membrane potentiation of the sinus nodal fiber
-55 to -60 mV
53
what is the resting membrane potential for the ventricular muscle fiber
-85 to -90 mV
54
which ap develops slower, the atrial nodal or the ventricular muscle
atrial nodal
55
true or false: there is a slow depolarization for sinus nodal
true
56
why does the Sinus Node Controls Heart Rhythmicity
because of its more positive resting membrane potential and leakiness, it is the first to be depolarized and spread because of the syncytium
57
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.
false, it is much faster
58
can other parts of the heart ever control heart rhythm
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
what other types of parts of the hear can exhibit rhythmical excitation?
av node and purkinje fibers
60
what is a pacemaker elsewhere than the sinus node is called ...
an ectopic pacemaker/abnormal pacemaker
61
where do action potentials originating in the sinus node travel
outward into the atrial muscle fibres and to the A-V node.
62
what happens to the impulse (AP) after it travels through the internodal pathways
it reaches the A-V node about 0.03 second after its origin in the sinus node.
63
true or false: the impulse/AP stays the same speed travelling from the SA node to the AV node
false, it gets delayed
64
what is the reason for the delay of action potential from reaching the ventricles
allowing the atria to empty blood into the ventricles before the ventricles contract.
65
why does the delay happen at the AV node
This happens because the A-V node has less gap junctions
66
what is the only fiber that connects the atrial to the ventricle
the av bundle
67
true or false: the Ap only delays at the AV node
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
the AV bundle has one way or 2 way conduction
one way
69
where do the right bundle branch and left bundle branch carry the impulse
towards the apex of the heart
70
was is another name for the AV bundle
His bundle
71
how does the impulse transmit to the ventricular
Purkinje System
72
where do the special purkinje fibers lead
lead from the A-V node through the A-V bundle into the ventricles.
73
what is the effect of the diminished numbers of gap junctions between successive cells in the conducting pathways within the A-V node?
induce resistance to the conduction of excitatory ions from one conducting fibre to the next.
74
what happens to the impulse at the termination of the Purkinje fibers
the impulse rapidly travels through the ventricle muscle fibers via gap junctions, from the inside (endocardium) to the outside (epicardium).
75
why is it necessary for rapid propagare of the cardiac impulse through the Purkinje fibers and ventricles
important for an effect contraction
76
true or false: the impulse rapidly travels through the ventricle muscle fibers via gap junctions, from the inside (endocardium) to the outside (epicardium).
true
77
why does the signal/impulse go to the apex of the heart
because it allows max blood to be ejected
78
why is the SA and AV node action potential is slower to develop than the action potential of the atrial or ventricular muscles?
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
can fast responses (like in the atria and ventricles) ever be converted to the slow responses?
yes
Fast responses may be converted to slow responses either spontaneously or under certain experimental conditions (lack of blood supply)
80
what does ERP stand for and what does it mean
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
what is the RRp
relative refractory period
period where under certain circumstances, it can be depolarized
82
the refractory period is short in BLANK muscles but long is BLANK MUSCLE
short in skeletal
long in cardiac
83
what does it mean for the skeletal muscle to have short refractory periods and cardiac muscle to have long refractory periods?
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
why is it important for the heart muscle to have a long refractory period
allows the atrium and ventricle to refill with blood
| prevent artyhmias
85
what are 2 ways to change the frequence of pacemaker firing
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
what neurotransmitter to parasympathetic nerves release
acetylcholine
87
true or false, the parasympathetic increases or decrease the heart rhythm and excitability
decreases
88
what nerves make it so the excitatory signals are no longer transmitted into the ventricles
parasymphathetic
89
explain how parasympathetic nerves decrease heart rhythm and excitability
because of the Increased permeability of the fiber membranes to potassium ions
(longer to reach threshold)
90
what NT do sympathetic nerves release
norepinephrine
91
true or false: sympathetic nerves increase or decrease the rate of sinus nodal discharge
increase
92
what happens to the heart activity when sympathetic nerves are stimulated
increases overall heart activity
93
explain how sympathetic nerves effect basic rhythm
increases the permeability to the NA and Ca ions, faster to reacher AP threshold
94
what modulates the frequency of depolarization of pacemaker
autonomic nervous system
95
where does the norepinephrine bind for sympathetic stimulation?
binds to beta1 receptors on the SA nodal membranes
96
where does acetylcholine bind for parasympathetic stimulation and what does that do
binds to muscarinic receptors on nodal membranes; increases conductivity of K+ and decreases conductivity of Ca2+
97
sympathetic stimulation means there is a HIGHER OR LOWER resting membrane potential
higher (more positive) easier-to-reach threshold
98
parasympathetic stimulation means there is a HIGHER OR LOWER resting membrane potential
lower (more negative)
| harder to reach threshold
99
what does atrial fibrillation mean
not just one cell initiating the signal causing irregular beat
100
what are 4 examples of abnormal heart rhythms
atrial fibrillation
supraventricular tachycardia
ventricular tachycardia
bradycardia
101
what does supraventricular tachycardia mean
electric impulses travel from ventricle to atria
102
what is ventricular tachycardia
ventricles do not have enough time to fill up properly
103
what is the effect on stroke volume and cardiac output of ventricular tachycardia
decreased stroke volume and decreased cardiac output
104
what is bradycardia
slow heart beat
105
where do they implant the pacemaker
connected to the SA node and apex
106
what do artificial pacemakers do
generate electrical signal when SA node doesn't work
