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Cardiovascular: physiology > Force generation by the heart > Flashcards

Force generation by the heart Flashcards

1
Q

what type of muscle is cardiac muscle?

A

striated

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2
Q

what is the striation caused by?

A

reglular arrangement of contractile protein

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3
Q

what are the junctions in the heart like?

A

There is no neuromuscular junctions in the cardiac muscle

But, the cardiac myocytes are electrically coupled by gap junctions

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4
Q

what are gap junctions?

A

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

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5
Q

what does the presence of these gap junctions allow?

A

They ensure that each electrical excitation reaches all the cardiac myocyctes

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6
Q

what law is this?

A

all or none law

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7
Q

what are the other junctions in the heart?

A

desmosomes

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8
Q

what do the desmosomes do?

A

provide mechanical adhesion between adjacent cardiac cells

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9
Q

what do desmosomes ensure?

A

They ensure that the tension developed by one cell is transmitted to the next

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10
Q

where are the dermosomes located?

A

within the intercalated discs

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11
Q

what does each muscle fibre (one cell) contain many of?

A

myofibrils.

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12
Q

what are myofibrils ?

A

the contractile unit of the muscle

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13
Q

describe the myofibrils?

A

they have alternating segments of thick and thin protein filaments

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14
Q

what makes up the thin filaments and what do they look like?

A

The ACTIN (thin filaments) causes the lighter appearance in myofibrils and fibers

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15
Q

what makes up the thick filaments and what do they look like?

A

MYOCYIN (thick filaments) causes the darker appearance

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16
Q

what is the arrangement of actin and myocin called in myofibrils?

A

sarcomeres

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17
Q

what is a sarcomere?

A

the smallest functional unit of the heart

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18
Q

how is muscle tension generate?

A

by sliding the actin filaments on myocin filaments

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19
Q

what does force generation depend on ?

A

ATP dependent interaction between actin and myocin

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20
Q

Energy is stored in the myocin head but even if ADP and Pi are attached and the head is energised you need another component, what is this?

A

calcium

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21
Q

what other process involving cross bridges do you need ATP for?

A

breaking the bridges down

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22
Q

what complex is formed if the cells die?

A

rigor complex

23
Q

what does Ca do in the sliding theory?

A

Ca binds to troponin resulting in a conformational change which takes the troponin away. troponin normally covers the actin binding

24
Q

where is Ca released from?

A

the sarcoplasmic reticulum

25
Q

In cardiac muscle: what is the release of Ca from SR dependent on?

A

the presence of extra-cellular Ca

26
Q

in What phase is Ca influx in ventricular muscle AP?

A

THE PLATEAu phase - ca influx through voltage gated Ca channels

27
Q

give a summary of the events leading to muscle fibre contraction

A

Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs

28
Q

give a summary of the events leading to muscle fibre relaxation

A

no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin-
tropomyosin complex

29
Q

what effect does the long refractory period prevent?

A

generation of tetanic contraction

30
Q

why does the long refractory period not occur in skeletal muscle cells

A

because the AP do not have a the plateau

31
Q

what is the refractory period?

A

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

32
Q

what happens in the plateau phase to generate a refractory period?

A

the Na channels are in the depolarised closed state i.e. they are not available for opening

33
Q

what happens in the descending phase of the AP to generate a refractory period?

A

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

34
Q

what is the definition of SV?

A

the volume of blood ejected by each ventricle per heart beat

35
Q

SV =

A

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

36
Q

what intrinsic mechanisms regulate the SV?

A

mechanisms within the heart muscle itself

37
Q

what extrinsic mechanisms regulate the SV?

A

nervous and hormonal control

38
Q

Which intrinsic mechanisms change the SV?

A

they are brought about by changes in the diastolic length of myocardial fibres

39
Q

what is the diastolic length (end diastolic volume) defined as?

A

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

40
Q

what is the EDV dependent on?

A

venous return

41
Q

what does the Frank - Starling curve state

A

the more the ventricle is filled with blood during diastole (end diastolic volume) the greater the volume of ejected blood will be during the resulting systolic contraction (SV)

42
Q

which factor increases the affinity of troponin for Ca

A

stretch

43
Q

In skeletal muscle there is an optimum fibre length at resting muscle length. what happens in cardiac muscle?

A

this is not true. the optimal length in cardiac muscle is achieved by stretching the muscle (frank starling mechanism)

44
Q

what happens if the venous return to the right atrium is increased?

A

starlings law matched the stroke volume of RV and LV

45
Q

what is the afterload?

A

this refers to the resistance into which the heart is pumping. It is the extra load imposed after the heart has contracted

46
Q

what happens as a result of afterload?

A

at first the heart is unable to eject full SV, so the EDV increases

the force of contraction rises via the starling mechanism.

If increased afterload continues to exist, eventually the ventricular muscle mass increases to overcome the resistance

47
Q

what is an clinical reason for afterload?

A

hypertension

48
Q

what autonomic system innervates the ventricular muscle ?

A

sympathetic nerve fibres

49
Q

what is the increase in force by sympathetic innervation called?

A

positive inotropic effect

50
Q

how is the increase in force linked to the increase in rate?

A

the force of contraction increases - get an activation of Ca channels - greater Ca influx. The effect is cAMP mediated. it results in the rate of pressure chande dP/dt during systloe increasing. This reduces the duration of systole

The rate of ventricular relaxation increases (increased rate of Ca pumping. This reduced he duration of diastole.

51
Q

what is the effect of sympathetic nerve stimulation on ventricular contraction in the starling curve ?

A

the curve is shifted to the left

52
Q

what shifts the curve to the right/

A

hear failure

53
Q

what is the effect of parasympathetic nerves on ventricular contraction?

A

vey little innervation of ventricles.

vagal stimulation has a major influence on rate, not force, of contraction

54
Q

which hormones have an effect on the control of SV?§

A

adrenaline and noradrenaline have an inotropic and chronotropic effect

Cardiovascular: physiology (11 decks)

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