force generation by the heart Flashcards

1
Q

how is striation achieved

A

regular arrangement of contractile protein

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2
Q

what is missing in cardiac muscle

A

neuromuscular junctions

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3
Q

cardiac myocytes are electrically coupled by

A

gap junctions

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4
Q

what are gap junctions

A

protein channels which forms low resistance electrical communication pathways between neighbouring myocytes

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5
Q

what do gap junctions do

A

they ensure that each electrical excitation has reaches all the cardiac myocytes

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6
Q

what do desmosomes do

A

provide mechanical adhesion between cardiac cells

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7
Q

what are myofibrils

A

contractile units of muscle

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8
Q

within myofibrils, the actin and myocin is arranged into

A

sarcomeres

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9
Q

what does force generation depend upon

A

ATP dependent interaction between myosin and actin

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10
Q

ATP is required for both

A

contraction and relaxation

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11
Q

Ca++ is required for

A

cross bridge formation

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12
Q

actin potential switches on

A

cardiac muscle contraction

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13
Q

Ca++ is released from

A

sarcoplasmic reticulum

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14
Q

in cardiac muscle, the release of Ca++ from SR is dependent on

A

the presence of extracellular Ca++

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15
Q

diastole

A

ventricular muscle relaxes

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16
Q

systole

A

ventricular muscle contracts

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17
Q

when muscle fiber is relaxed

A

no cross bridge binding because the cross bridge binding site on actin is physically covered by the troponintropomyosin complex

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18
Q

binding of actin and myosin cross bridge

A

triggers power strokes that pulls thin filament inward during contraction

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19
Q

when muscle fiber is excited

A

Ca++ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross bridge binding site
cross bridge binding occurs

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20
Q

long refractory period prevents

A

generation of tetanic contraction

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21
Q

refractory period

A

a period following an action potential in which it is not possible to produce another action potential

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22
Q

during the plateau phase of ventricular action potential the Na+ channels are

A

in depolarised closed state

ie sodium channels closed

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23
Q

during the descending phase of action potential

A

the K+ channels are open and the membrane can not be depolarised

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24
Q

the long refractory period is protective for the heart as

A

it prevents generation of tetanic contractions

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25
contraaction of ventricular muscle
ejects the stroke volume
26
stroke volume
the volume of blood ejected by EACH ventricle PER heartbeat
27
SV =
end diastolic volume - end systolic volume
28
how is the stroke volume regulated
intrinsic and extrinsic mechanisms
29
intrinsic
within heart
30
extrinsic
hormonal and nervous control
31
changes in stroke volume are brought about by
changes in the diastolic length/diastolic stretch of myocardial fibers
32
the diastolic length and stretch is determined by
the volume of blood within each ventricle at the end of diastole. this is caked END DIASTOLIC VOLUME
33
the end diastolic volume determines
the cardiac preload (the diastolic length/stretch of myocardial fibers)
34
the end diastolic volume is determined by
the venous return to the heart
35
the frank starling curve describes
the relationship between venous return, end diastolic volume and stroke volume
36
the more the ventricle is filled with blood during diastole
the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)
37
stretch also increases the affinity of troponin for
Ca++
38
optimal length in cardiac muscle is achieved by
stretching the cardiac muscle
39
if venous return to right atrium increases
EDV of right ventricle increases
40
starling law leads to
increased SV into pulmonary artery
41
venous return to left atrium from pulmonary vein increases
EDV of left ventricle increases
42
starlings law leads to
increased SV into aorta
43
afterload means the
resistance into which heart is pumping
44
the extra load is imposed
after the heart has contracted
45
if afterload increases, at first
heart unable to eject full SV, so EDV increases
46
force of contraction rises by
frank- stark mechanism
47
if increased afterload continue to exist, eg, untreated hypertension eventually the
ventricular muscle mass increases (ventricular hyertrophy) to overcome resisitance
48
extrinsic control of stroke volume involves
nerves and hormones
49
the ventricular muscle is supplied by
sympathetic nerve fibers
50
the neuro transmitter in extrinsic control is
noradrenaline
51
stimulation of sympathetic nerves
increases the force of contraction
52
this is known as
positive inotropic effect
53
stimulation of sympathetic nerves also causes
positive chronotropic effect
54
force of contraction increases
greater Ca++ influx
55
the effect is ____ mediated
cAMP
56
the peak ventricular pressure
rises
57
rate of pressire change during systole
increases
58
this reduces the duration of
systole
59
rate of ventricular relaxation
increases (increased rate of Ca++)
60
this reduces the duration of
diastole
61
peak ventricular pressure rises
contractility of heart at a given EDV rises
62
parasympathetic nerves have
no direct effect on SV
63
vagal stimulation (parasympathetic) has major influence on
rate, not force of contraction
64
adrenaline and noradrenaline released from adrenal medulla have
inotropic and chronotropic effect
65
cardiac output
the volume of blood pumped by EACH ventricle per MINUTE
66
CO =
SV x HR
67
the resting CO in a healthy adult is approcx
5 litres per minute
68
how to regulate the CO
regulate stroke volume and heart rate