Cardio - electrical activation of heart + contraction + cardiac cycle Flashcards

1
Q

what is the main difference between cardiac and skeletal muscle

A

cardiac muscle can contract on its own and doesn’t get tired

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2
Q

what are the key features of cardiac myocytes

A

branched tubular cells
central nucleus
striated
high mitrochondrial density

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3
Q

what connects cardiac myocyte cells

A

intercalated discs with desmosomes and gap junctions

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4
Q

what gives the striated appearance of muscle cells

A

overlap of myosin and actin in sacromere

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5
Q

what maintains the reseting membrane potential in cardiac myocytes (-90mV in cell )

A

active membrane pumps
Na and Ca out with ATP and K in
ion channel- K out (permeable to K) passive

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6
Q

describe the steps when an action potential is initiated and activated

A

Phase 0- rapid depolarisation
Na+ inflow

Phase 1- partial depolarisation.
Na+ inflow stops
K+ outflow

Phase 2- plateau
Ca 2+ slow inflow

Phase 3- repolarisation
K+ outflow
inflow of Ca 2+ stops

Phase 4- resting potential-
K+ outflow down Conc Grad
Na/K ATPase
Ca ATPase (out of cell) pumps

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7
Q

what is the absolute refractory period

A

between phase 1 and 2, another action potential cannot be stimulated

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8
Q

what is the relative refractory period

A

(after phase 3) a stimulus could stimulate another action potential but likelihood is relative to the magnitude of the stimulus and number of reactivated NA channels

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9
Q

what are pacemaker cells

A

cells not dependent on an external stimulus to depolarise, they depolarise spontaneously and self initiate waves of depolarisation.

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10
Q

where are pacemaker cells in the heart

A

SA node, AV node and conducting tissue

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11
Q

how is automaticity possible with pacemaker cells

different to action potential of a non-pacemaker myoctye

A

they express different ion channels- funny Na channels, T type Ca and L type ca channels.

and phase 4 is less negative and constantly drifts towards the threshold (no true resting potential)

these channels constantly allow a slow influx of Na+ and Ca2+ into the cell- so it eventually reaches threashold to depolarize by itself.

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12
Q

what factors influence the rate of action potentials in the pacemaker cells (therefore heart rate)

A

automatic nervous system
external factors
the rate is determined by the rate of inward Na and Ca during phase 4.

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13
Q

what happens to pacemaker myocyte when the sympathetic nervous system is stimulated

A

adrenaline and noradrenaline are released
act on type 1 beta adrenoreceptors in the cell membrane of pacemaker cell
increase enzyme adenyly cyclase ATP –> cAMP
cAMP activates Na and Ca ion channels, leading to influx of Na and Ca, leads to positive threshold being reached

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14
Q

what does an increased sympathetic stimulation lead to

A

increases heart rate
inc force of contraction (inc Ca into cell)
large inc in cardiac volume

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15
Q

effect of parasympathetic stimulation on heart rate

why

A

decreased heart rate

acetylcholine acts on M2 receptors which inhibit adenyly cyclase, reduced cAMP, reduced ion channels

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16
Q

increased parasympathetic stimulation

A

decreased heart rate ]decreased force of contraction

decreased cardiac output

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17
Q

what do chronotropic and inotrophic relate to

A

chronotrophic- heart rate

inotrophic- contraction

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18
Q

describe the route of conduction tissue in the heart

A
sinoatrial node 
internodal pathway 
atrioventricular node 
bundle of His 
purkinje fibres (at apex)
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19
Q

where is the sinoatrial node located

A

posterior wall of right ventricle

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20
Q

what is bundle called that the wavefront travels through in left atrium

A

bachmanns bundle

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21
Q

how are the atria and ventricles electrically insulated from each other

A

fibroannular rings surrounding tricuspid valve and mitral valve

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22
Q

what makes a faster pacemaker

A

steeper the drift towards threashold value

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23
Q

true or false

A

spontaneous discharge rate of heart muscle decreases down heart rate

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24
Q

how and why does the AV node delay impulse

A

why- allows atria to empty blood into ventricles

how- less gap junctions and AV fibres are smaller than atrial fibres

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25
describe features of the bundle of his and purkinje fibres for rapid conduction
very large fibres high permeability at gap junctions spread from endocardium to pericardium (to allow coordinated ventricular contraction)
26
is the SA node the only pacemaker cells
no- many areas of the heart can serve as potential pacemaker sites so the heart can keep beating if the natural pacemaker fails
27
does a faster or slower pacemaker cell assume overall control?
faster | faster suppresses a slower
28
in terms of phases, what is the main difference between myocardial AP and skeletal AP
``` plateau phase (2) Ca channels open and Ca ions come into cell causes refractory period and allows heart to fill ``` (myocardial contraction is 15x longer)
29
what is excitation- contraction coupling
electrical activation triggers myocardial contraction
30
Describe the effect of Ca influx during phase 2 of AP
inc of IC Ca concentration triggers release of Ca from SR Ca binds to troponin C molecules on actin molecules -> conformational change -> exposing myosin binding heads increases force of contraction as more ca molecules so more bridges end of phase 2- Ca is pumped back to SR
31
describe what happens when cardiac muscles contract
wave of depolarisation spreads into myocytes via T tubules Ca 2+ enter into the cytosol from interstitial fluid this triggers the release of more Ca2+ from SR (Ca2+ induced Ca2+ release) Ca2+ binds with troponin C which uncoveres active site on tropomyosin
32
how does the wave of depolarisation spread in cardiac muscle
through T tubulea
33
process name where contractile proteins are activated
signalling process called excitation- contracting coupling
34
what shows that excitation- contraction coupling has begun and ended
begins- when the action potential depolarizes the cell ends- Ca2+ that appears within the cytosol binds to Ca2+ of the contractile apparatus
35
is the movement of Ca2+ into the cytosol passive or active
passive | mediated by Ca2+ channels
36
when does the heart relax
when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol
37
what does myocardial metabolism rely on
free fatty acids during aerobic metabolism
38
A band
the region of the sacromere occupied by the thick filaments (myosin and actin)
39
I band
occupied by thin filaments that extend toward the centre of the sacromere from the Z lines
40
sacromere
functional unit of the contractile apparatus region between a pair of Z lines
41
what does the sacromere contain
two half I bands and one A band
42
sarcoplasmic reticulum
membrane network that surrounds contractile proteins
43
what lines T tubule
membrane that is continuous with the sarcolemma | lumen of T tubules carries extracellular space toward centre of myocardial cell
44
define contraction
sliding of actin over myosin by ATP hydrolyisis through the action of ATPase in the head of the myosin molecule these heads form the crossbridges that interact with actin, after linkage between calcium and TnC and deactivation of tropomyosin and TnI
45
what is troponin
part of tropomyosin that can bind Ca2+
46
describe structure of myosin
2 heavy chains ( dual head) | 4 light chains
47
which was do the myosin bend during contraction | heads are perpendicular on the thick filament at rest
towards centre of sacromere
48
describe actin
globular protein | double stranded macromolecular helix
49
what is tropomyosin
elongated molecule made of two helical peptide chains it occupies the longitudinal grooves between the two actin strands (so myosin can't bind unless tropomyosin moves)
50
what is troponin
bound to tropomyosin
51
different types of troponin
I- inhibits actin and myosin interaction T- binds troponin complex to tropomyosin C- high affinity calcium binding sites, signalling contraction
52
what happens when Ca2+ binds to troponin C
drives TnI away from actin, allowing its interaction with myosin
53
purpose of tropomyosin
regulates actin-myosin interaction
54
does myosin or actin hydrolyse ATP
myosin
55
what opens the Ca2+ channels in the T- tubules into myocytes
wave of depolarisation/ Na+ influx through Na+ channels
56
what is the H zone in sarcomere
myosin ONLY
57
what is role of titin
molecular spring which connects myosin to Z line
58
p wave
atrial depolarisation SAN to AVN
59
P-R interval
slow conduction through AVN
60
Q wave
interventricular septum depolarisation
61
R wave
ventricular depolarisation (apex of heart)
62
S wave
depolarisation of ventricles (towards base)
63
QRS complex
depolarisation of ventricles
64
ST segment
period of time where myocardium of ventricles is still depolarised
65
T wave
reploarisation of ventricles
66
where is repolarisation of atria shown
masked by QRS complex
67
what are the 12 ECG leads
6 precordial leads (V1-V6) 3 bipolar leads I, II, III 3 unipolar limb leads avF avR avL
68
what plane do the precordial leads record in
transverse plane
69
what plane do bipolar and unipolar limb leads record in
coronal plane
70
what does an elevated ST segment mean
STEMI | st elevation myocardial infarction
71
what does T wave inversion mean
ischaemia (decreased blood flow to myocardial tissue)
72
describe what happens in systole
``` wave of depolarisation arrives opens the L-calcium Tubule (R wave) Ca2+ arrive at the contractile proteins LVp rises > LAp MV closes LVp rises (isovolumetric contraction)> Aop AoV opens and ejection starts ``` look at wiggers diagram :?
73
how long is the cardiac cycle systole diastole
cardiac cycle= 0.8s systole= 0.3s diastole= 0.5s
74
define preload
the load present before LV contraction has started
75
define afterload
the load after the ventricle starts to contract
76
what is starlings law of the heart
Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction.
77
define contractility
the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractibility is increased
78
elasticity
myocardial ability to recover its normal shape after removal of systolic stress
79
compliance
relationship between the change in stress and the resultant strain
80
diastolic distenibilty
pressure required to fill the ventricle to the same diastolic volume