Cardiac contraction Flashcards

(68 cards)

1
Q

sarcolemma permeability

A

more permeable to K+ than Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

sarcolemma definition

A

cardiac myocyte membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what happens in a sarcolemma when an AP arrives

A

Na VG ion channels open and Na entry depolarise cell - positive feedback as more VG Na channels triggered to open
Ca VG channels also open - slower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which opens faster - Na or Ca channels - when an AP arrives in a sarcolemma

A

Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens when cell potential is positive

A

VG Na channels close
VG K channels open
cell partially repolarises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what happens during partial repolarisation in sarcolemma

A

VG Ca channels open at T tubules leading to inflow of Ca into cell, balancing flow of K out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what type of Ca channels stay open for longer

A

L-type Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does the inflow of Ca do during partial repolarisation

A

balances flow of K+ out so keep membrane depolarised at plateau level of 0mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when does repolarisation occur

A

eventual closure of L-type Ca channels and reopening of K channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what ion does excitation-contraction coupling depend on

A

calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the role of Na channel during systole

A

depolarisation of sarcolemma, opens Ca2+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the role of Ca2+ channels during systole

A

AP plateau, trigger Ca2+ release - positive feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the role of Ca2+ pump during diastole

A

Ca2+ removal (PMCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the role of Na pump during diastole

A

repollarisation, Na+ for Na+/ Ca2+ exchanger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the general role of actin and myosin

A

contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the general role of TnC

A

Ca2+ receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does excitation-contraction coupling mean

A

how electrical impulse becomes muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what receptors does calcium bind to on sarcoplasmic reticuum

A

ryanodine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does binding of Ca2+ to ryanodine receptors do

A

causes sarcoplasmic reticulum to release stored ca2+ into cytoplasm and causing start of cross-bridge cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does Ca released from SR bind to

A

ca2+ binding sites on troponin protein on actin filament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what happens when ca binds to actin

A

tropin changes shape, displacing tropomyosin protein on actin filament and exposing myosin binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

where does myosin bind to actin

A

myosin binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does myosin contract

A

head drops ADP to contract and oull actin filament over myosin = power stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what happens when power stroke occurs (ultrastructure)

A

z line decreases, myocyte contracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what causes myosin head to detach from actin filament
binding of ATP to myosin head, returning head to start position
26
what happens to ATP that binds to myosin head
hydrolysed by ATPase in myosin head into ADP and Pi - ready for next contraction if myosin binding sites remain open
27
when does myocyte contraction stop
when cytosolic calcium concentration is restored to original low resting value
28
how is original calcium concentration restored in the cytosol
primary active Ca-ATPase pumps in SR and sarcolemma and Na/Ca counter-transporters in sarcolemma
29
brief summary of excitation-contraction coupling
AP arrives and travels down T tubule Depolarisation causes ca channels to open Ca binds to SR causing more Ca release Ca binds to sarcomere and allows contraction
30
describe the structure of actin
thin filament, polymerised globular protein with tropin and tropomyosin incorporated - double stranded macromolecular helix each actin molecule has myosin binding site
31
describe the structure of myosin
2 heavy chains (dual heads), 4 light chains - heads are perpendcilar on thick filament at rest, bend towards centre of sarcomere at contraction
32
describe the structure of tropomyosin
elongated molecule, 2 helical PP - occupies longitudional groove between 2 actin strand and overlies myosin binding sites on actin
33
what are the 3 types of troponin
TnI, TnT, TnC
34
what does TnI do
with tropomyosin, inhibits actin and myosin interaction
35
what does TnT do
binds troponin complex to tropomyosin
36
what does TnC do
high affinity with Ca2+ binding site; signals contraction - drives TnI away from actin when bonded with ca so allows interaction with myosin
37
what is titin
elastic filament that maintains alignment of sarcomere
38
what happens in P wave
depolarisation of SAN, atria activated so contraction | mitral valve open so blood moves from atria to ventricles
39
what happens in QRS complex
depolarisation of ventricle so ventricle contract, repolarisation of atria isovolemic contraction aortic valve opens so blood moves ventricle to aorta
40
what happens in T wave
repolarisation of V so contraction stops, aortic valve shuts
41
how much blood remains when ventricle contracts
1/3
42
what is the ejection fraction
blood that leaves ventricles during ventricular contraction
43
how long does systole last
0.3 seconds
44
what is isovolumic contraction
doesn't change volume of ventricle
45
what happens during systole
1. wave of depolarisation arrives 2. L-calcium tubule opens 3. calcium arrives at contractile proteins 4. LVp>Lap so mitral valve closes 5. LVp increases > aortic pressure - isovolumic contraction 6. aortic valve opens, ejection starts
46
what forms the 1st heart sound and where is it heard
mitral valve closing, 5th intercostal space
47
how long does diastole last
0.5s
48
what happens during diastole
1. LVp peaks then decreases 2. influence of phosphorylated phosopholambdan - cytostolic ca taken up into SR 3. phase of reduced ejection 4. Ao flow maintained by Ao distensibility LVp < Aop so Ao valve closes 5. isovolumic relaxation then mitral valve opens
49
what causes the 2nd heart sound
Ao valve closing
50
what happens during ventricular filling
1. isovolumic relaxation 2. LVp < Lap so mitral valve opens 3. rapid ejection (filling of V) 4. diastasis 5. filling renewed when atrial booster raises Lap >LVp
51
what is diastasis
Lap = LVp so filling temporarily stops
52
what happens in atrial booster
pressure suddenly increases due to atrial contraction - enables ventricles to be actively filled
53
what gives the 3rd heart sound
ventricular suction, active diastolic relaxation
54
what gives the 4th heart sound
only in pathology | aortic stenosis, filling of V as A contracts at end of diastole
55
what is Frank-starlings law
force of contraction is proportional to end diastolic length of cardiac muscle fibres
56
what does frank-starlings law mean
more the ventricle fills the harder it contracts - ventricular output increases as preload (end diastolic pressure) increases
57
why does stroke volume increase as end-diastolic volume (EDV) increases
length-tension relationship of muscle
58
how does increased VR lead to increased CO even with constant HR
increased EDV so increased preload so increased sarcomere length so increased force of contraction so increased SV
59
what happens to myocardial fibres when ventricular diastolic volume increases
stretched more during diastole so more tension in fibres so greater force of contraction
60
what can be said about cardiac muscle at rest
not at optimal length
61
what is the name given to something that increases HR
positively chronotropic
62
what is the name given to something that increases force
positively inotropic
63
describe sympathetic innervation of the heart
postganglionic fibres innervate the whole heart - sympathetic increase CO
64
what controls sympathetic innervation of the heart
adrenaline, noradrenaline, type 1 beta adrenoreceptors - increase adenylyl cyclase activation so increased cAMP, increased permeability to na so threshold potential reached faster
65
describe parasympathetic innervation of the heart
vagus nerve | decrease CO
66
what controls parasympathetic innervation of the heart
ACh; M2 receptors inhibit adenylyl cyclase so decrease cAMP, decreased na permeability so longer time to reach threshold
67
what are the mechanisms of altering rate of cardiac contraction
``` PACE preload afterload contractibility (h)eart rate ```
68
what is the percentage of potential the heart pumps at rest
60%