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CARDIO > Force of Contraction > Flashcards

Force of Contraction Flashcards

1
Q

can nerve activation modify activity of striated cardiac muscles

A

No

only ANS has effect on activity

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2
Q

what does cell-to-cell conduction mean

A

occurs due to gap junctions low resistance electrical communication between neighbouring myocytes

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3
Q

what 2 types of junction occur between intercalated discs

A

desmosomes

gap junctions

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4
Q

what is the purpose of desmosomes between intercalated discs of myocytes

A

provide tension

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5
Q

by what means do myocytes contract after excitation

A

All or none

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6
Q

what are muscle fibres (cells) made up of

A

myofibrils (contractile units)

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7
Q

what myofibrils made up of

A

actin: thin filaments, light
myosin: thick filaments, dark

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8
Q

what forms the scaromere of muscle fibres

A

actin + myosin

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9
Q

how is muscle tension produced

A

by sliding actin filaments on myosin filaments

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10
Q

what is muscle tension dependant on

A

Calcium

ATP

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11
Q

what proteins are present on actin filament

A

tropomyosin

troponin

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12
Q

what is the troponin-tropomyosin complex’s role

A

binding site of myosin forming cross bridges

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13
Q

what binds to troponin

A

calcium

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14
Q

what doe action potentials that excite cardiac muscle depend on

A

entry of Ca into cell triggers the release of Ca from the sarcoplasmic rectiulum (calcium induced calcium release)

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15
Q

where is Calcium stored in myocytes

A

sarcoplasmic reticulum

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16
Q

when does Ca enter the sarcoplasmic reticulum

A

in plateau

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17
Q

why is there a long refractory period

A

prevents generation of tetanic contraction

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18
Q

what is the refractory period

A

period following an AP where it is not possible to produce an AP

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19
Q

what happens during the plateau phase of the ventricles

A

Na channels are depolarised closed state so can’t open

20
Q

what happens during the descending phase of myocytes

A

K channels open

K efflux

21
Q

how can SV be calculated

A

end diastolic volume (EDV) - End systolic volume (ESV)

22
Q

how is the heart regulated intrinsically

A

due to diastolic lenght and stretch of myocardial fibres

more stretch = bigger SV

23
Q

what is diastolic length/stretch determined by

A

the volume of blood in each ventricle at the end of diastole

24
Q

what does the EDV determine

A

cardiac preload

25
Q

what is EDV determined by

A

venous return

26
Q

what does Frank Starlings Curve show

A

Relationship between venous return, END DIASTOLIC VOLUME and STROKE VOLUME

27
Q

the more the ventricle is fulled with blood during diastole (EDV) the greater/less the volume of ejected blood will be during the resulting systolic contraction (SV)

A

greater

28
Q

if venous return of the right ventricle increases what else is increased and what does this lead to

A

EDV of the right ventricle

therefore increased SV to the pulmonary artery

29
Q

if venous return of the left ventricle increases what else is increased and what does this lead to

A

EDV of the left ventricle therefore increased SV into aorta

30
Q

what is afterload

A

resistance into which the heart is pumping

31
Q

what happens if after load increases

A

at first the heart is unable to eject full SV so EDV increases
force of contraction increases by Frank Starling mechanism

32
Q

how does the heart compensate for a prolonged continued increased after load eg. untreated hypertenion

A

ventricular increased muscle mass (ventricular hypertrophy) overcomes resistance

33
Q

other than increasing SV what other effect does stretch have

A

increases affinity of troponin for Ca

34
Q

what 2 extrinsic mechanisms effect the heart

A

neves - ANS

hormones

35
Q

what nerves affect the ventricles

A

Sympathetic

noradrenaline increases HR acts on B1

36
Q

what 2 effects does the sympathetic NS have on the heart

A

Positive chronotropic effect

Positive Inotropic effect

37
Q

as well as increasing rate of contraction what other effect does the sympathetic NS have on heart contraction

A

increases force

38
Q

why does the force of contraction increase by action of the sympathetic NS

A

due to activation of Ca channels

peak ventricular pressure rises: rate of pressure change during systole increases (reducing duration of systole)

39
Q

what mediates the activation of Ca channels

A

cAMP

40
Q

how does the rate of ventricular relaxation increase

A

by the increasing rate of Ca pumping reducing the duration of systole

41
Q

what direction does a positive inotropic effect have on Frank Starlings Law and why

A

shift to the left

increased SV therefore peak ventricular pressure rises, contractility of the heart at a given EDV rises

42
Q

what direction does a negative inotropic effect eg in heart failure have on Frank Starlings Law

A

shift to right

43
Q

what 2 hormones effect the heart by having chronotropic and inotropic effects

A

adrenaline and noradrenaline (minor compared with sympathetic NS)

44
Q

define cardiac output

A

volume fo blood pumped by each ventricle per minute

45
Q

equation to calculate CO

A

CO = SV x HR

CARDIO (14 decks)

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