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
Q

describe features of the bundle of his and purkinje fibres for rapid conduction

A

very large fibres
high permeability at gap junctions
spread from endocardium to pericardium

(to allow coordinated ventricular contraction)

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26
Q

is the SA node the only pacemaker cells

A

no- many areas of the heart can serve as potential pacemaker sites so the heart can keep beating if the natural pacemaker fails

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27
Q

does a faster or slower pacemaker cell assume overall control?

A

faster

faster suppresses a slower

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28
Q

in terms of phases, what is the main difference between myocardial AP and skeletal AP

A
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)

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29
Q

what is excitation- contraction coupling

A

electrical activation triggers myocardial contraction

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30
Q

Describe the effect of Ca influx during phase 2 of AP

A

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

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31
Q

describe what happens when cardiac muscles contract

A

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

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32
Q

how does the wave of depolarisation spread in cardiac muscle

A

through T tubulea

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33
Q

process name where contractile proteins are activated

A

signalling process called excitation- contracting coupling

34
Q

what shows that excitation- contraction coupling has begun and ended

A

begins- when the action potential depolarizes the cell

ends- Ca2+ that appears within the cytosol binds to Ca2+ of the contractile apparatus

35
Q

is the movement of Ca2+ into the cytosol passive or active

A

passive

mediated by Ca2+ channels

36
Q

when does the heart relax

A

when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol

37
Q

what does myocardial metabolism rely on

A

free fatty acids during aerobic metabolism

38
Q

A band

A

the region of the sacromere occupied by the thick filaments (myosin and actin)

39
Q

I band

A

occupied by thin filaments that extend toward the centre of the sacromere from the Z lines

40
Q

sacromere

A

functional unit of the contractile apparatus

region between a pair of Z lines

41
Q

what does the sacromere contain

A

two half I bands and one A band

42
Q

sarcoplasmic reticulum

A

membrane network that surrounds contractile proteins

43
Q

what lines T tubule

A

membrane that is continuous with the sarcolemma

lumen of T tubules carries extracellular space toward centre of myocardial cell

44
Q

define contraction

A

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
Q

what is troponin

A

part of tropomyosin that can bind Ca2+

46
Q

describe structure of myosin

A

2 heavy chains ( dual head)

4 light chains

47
Q

which was do the myosin bend during contraction

heads are perpendicular on the thick filament at rest

A

towards centre of sacromere

48
Q

describe actin

A

globular protein

double stranded macromolecular helix

49
Q

what is tropomyosin

A

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
Q

what is troponin

A

bound to tropomyosin

51
Q

different types of troponin

A

I- inhibits actin and myosin interaction
T- binds troponin complex to tropomyosin
C- high affinity calcium binding sites, signalling contraction

52
Q

what happens when Ca2+ binds to troponin C

A

drives TnI away from actin, allowing its interaction with myosin

53
Q

purpose of tropomyosin

A

regulates actin-myosin interaction

54
Q

does myosin or actin hydrolyse ATP

A

myosin

55
Q

what opens the Ca2+ channels in the T- tubules into myocytes

A

wave of depolarisation/ Na+ influx through Na+ channels

56
Q

what is the H zone in sarcomere

A

myosin ONLY

57
Q

what is role of titin

A

molecular spring which connects myosin to Z line

58
Q

p wave

A

atrial depolarisation

SAN to AVN

59
Q

P-R interval

A

slow conduction through AVN

60
Q

Q wave

A

interventricular septum depolarisation

61
Q

R wave

A

ventricular depolarisation (apex of heart)

62
Q

S wave

A

depolarisation of ventricles (towards base)

63
Q

QRS complex

A

depolarisation of ventricles

64
Q

ST segment

A

period of time where myocardium of ventricles is still depolarised

65
Q

T wave

A

reploarisation of ventricles

66
Q

where is repolarisation of atria shown

A

masked by QRS complex

67
Q

what are the 12 ECG leads

A

6 precordial leads (V1-V6)
3 bipolar leads I, II, III
3 unipolar limb leads avF avR avL

68
Q

what plane do the precordial leads record in

A

transverse plane

69
Q

what plane do bipolar and unipolar limb leads record in

A

coronal plane

70
Q

what does an elevated ST segment mean

A

STEMI

st elevation myocardial infarction

71
Q

what does T wave inversion mean

A

ischaemia (decreased blood flow to myocardial tissue)

72
Q

describe what happens in systole

A
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
Q

how long is the cardiac cycle
systole
diastole

A

cardiac cycle= 0.8s
systole= 0.3s
diastole= 0.5s

74
Q

define preload

A

the load present before LV contraction has started

75
Q

define afterload

A

the load after the ventricle starts to contract

76
Q

what is starlings law of the heart

A

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
Q

define contractility

A

the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractibility is increased

78
Q

elasticity

A

myocardial ability to recover its normal shape after removal of systolic stress

79
Q

compliance

A

relationship between the change in stress and the resultant strain

80
Q

diastolic distenibilty

A

pressure required to fill the ventricle to the same diastolic volume