lecture 2: 9/10 guyton Flashcards
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 devlops 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 valvues
A
pulmonary and aortic
10
Q
why is there a backflow of blood that develops the insura
A
blood bounces off of the peripheral ressitance
11
Q
whatt is the prupose 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 childrena nd highly trained individuals
13
Q
true or false: during the period of filling the ventricles, pressure increases significantly?
A
false, no it stays oretty 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 indidualss 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 thte heart needs to work harder
19
Q
true or false: end sytolic volume is the systolic bp
A
false, systlic 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 systlic volume), what happens to the ventricles
A
isovolumic relaxation and pressure starts to decrease
22
Q
why would an indivual get an incrased preload
A
because of an increase venous retrun (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 ifIf 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 sarcomers are stretched
there are more sites available for cross bridge interacteion
26
what happens if sarcomeres are stretched too much
there will no longer be optimal crossbirdged, pressure will will plateau, decrease in stroke volume
27
explain why the frank starlic mecahism is good
beacuse if you get an icnrease venous return, the heart will be able to eject the blood more forcefully (rubber band mecahnist) 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 measn there is more blood left in the ventricles, which will decrase storke volume
30
if you increase afterload, you increase or decrease stroke volume
stroke volume decreases
31
wnhat happens to BP with an increased afterload
if there is an icnreaase afterload that measn there is more blood left in the heart which means the ventricle must build higher pressure to which makes it harder for the hear 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 icnrease contractility
causes an increase in pressure since there heart needs to contract more forcefully
34
what happens to end systolic volume with an icnreased contractility
it will decrease
| less blood left in the haart since more was ejectred due to incrase contractility
35
how can you icnrease contractlity (2 ways)
1) hormones
| 2) 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 potention
39
what gives the resting membrame potential
The electro-chemical equilibrium
40
what are the 3 factors that affect permeability to diff ions of the mebrane
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
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 syncitum
47
since the SA node has no contractile filalnets, 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 cotnractile filaments, how are they self excibtable
because of the inherent leakiness of the SA node to sodium and calcium
52
what is the resting membrane potentation of the sinus nodal fiber
-55 to -60 mV
53
what is the resting membrane potential for the ventricular mucle fiber
-85 to -90 mV
54
which ap develps 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 postiive resting membrane potential and leakyiness, it is the first to be depolarized and spread because of the syncitum
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 rhytm
yes, Under abnormal conditions, few other parts of the heart can exhibit intrinsic rhythmical excitation in the same way like the sinus nodal fibers (A-V node and Purkinje fibers).
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/abnomral pacemake
61
where do Action potentials originating in the sinus node travel
outward into the atrial muscle fibers and to the A-V node.
62
what happens to the impluse (AP) afrter 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 syaus 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 portteial 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 noe
This happens because the A-V node has less gap junctions
66
what is the only fiber that connects the atrial to the ventrical
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 impuse
towards the apex of the heart
70
was is another name for the AV bundle
this His nundle
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 conduction of excitatory ions from one conducting fiber to the next.
74
what happens to the impluse at the termination of the purkine 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 proparge of the cardac impulse through the purkinje fibers and ventricles
importtant 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 heartt
because it allows max blood to be ejected
78
why is the 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 sense 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 new 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 depolarixed
82
the refrcatory period is short in BLANK muscles but long is BLANK MUSCLE
shoet in skeletal
| long in cardiac
83
what does it mean for the sketal 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 imporatnt for the heart muscle to have a long refractory periof
allows the atrium anf 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 soonwer and generate the AP faster
2) change the normal resting potential so you can reach the AP faster
86
what neurotranmitter to parasympathetic nerves release
acetylcholine
87
true or false, the parasympatheic increases or decrease the heart rhythem and excitability
decreases
88
what nerves make it so the excitatory signals are no longer transmitted into the ventricles
parasympahtetic
89
expalin how parasympathetic nerves decrease heart rhythem and excitability
because of Increased permeability of the fiber membranes to potassium ions
(longer to reach threshold)
90
what NT do sympathtic nerves release
noreipineprhine
91
true or false: sympathetic nerves increase or decrease the rate of sinus nodal discharge
increase
92
what happens to the heart activity when sympathttic nevres are stimulated
increases overall heart activity
93
explain how sympathetic nerves effect basic rhythem
increases the permibility to the NA and Ca ions, faster to reacher AP tthreshold
94
what modulates the frquence of depolizsaation of pacemaker
autonomic nervous system
95
where does the noepinephrine bind for sympathetic stimulation
binds to beta1 receptors on the SA nodal membranes
96
where does acetylcholine bind for parasymtphathic 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 meass there is a HIGHER OR LOWER resting membrane potential
higher (more postive) easier to reach threshold
98
parasympathetic stimulation meass there is a HIGHER OR LOWER resting membrane potential
lower (more negative0
| harder to reach threshold
99
what does atrial fibrilation mean
not just one cell initiating the signal causing irregular beat
100
what are 4 examples of abnormal heart rhytmes
atrial fibrilation
supraventrical tachycardia
ventricular tachycardia
bradycardia
101
what does supraventricular tahycardia mean
electic 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 putput
104
what is brady cardia
slow heart beat
105
where do they implant the pacemaker
connected to the SA node and apex
106
what do artificual pacemakers do
generate electrical signal when SA node doesnt work
