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BMS242 CVS Phys > L12 - Myocardial Mechanics > Flashcards

L12 - Myocardial Mechanics Flashcards

1
Q

What describes the electrical excitation leading to contraction

A

Excitation - contraction - coupling

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2
Q

What does excitation contraction coupling describe

A

The electrical excitation leading to the contraction

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3
Q

What is the role of the T-tubules

A

Cause activation of many sarcomeres at one time

Leads to a faster contraction

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4
Q

What is the structure of the T-tubules - how does this relate to their function

A

Invaginations of the sarcolemma

They allow the depolarisation to spread deep into the cell

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5
Q

What do intercalated discs contain

A

Ion channels

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6
Q

What is the role of the intercalated discs

What does this form?

A

Between the ion channels - this ionically links the myofibrils forming a functional syncitium

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7
Q

Describe the sarcoplasmic reticulum

A

Fluid filled membranous sac - acts a as Ca store

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8
Q

Where are the cisterns found

A

At the end of the SR

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9
Q

What do T-tubules and cisterns form

A

Triads

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10
Q

Describe the sliding filament theory / state for a relaxed muscle

A

Ca in sarcoplasm low
Ca pumps sequester Ca in SR
Tropomyosin obscures the actin-myosin binding site preventing cross bridge formation

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11
Q

What is the role of calsequesterin

A

Binds to free Ca in the SR - gives impression that Ca is SR is low so pumps can work faster

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12
Q

Describe sliding filament theory when muscle is contraction

A

Propagation of AP along T-tub activation of VGCC
CA SR rises
Ca binds to Tn-C
Conf change in tropomysosin - actin mysoing binding site exposed
Cross bridge can form and cycling can occur if ATp/ADP/Pi available

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13
Q

What is muscle tension proportional to

A

The number of cross bridges

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14
Q

What is the number of cross bridges proportional to

A

The length of the sarcomere

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15
Q

What produces a maximum tension generation

A

An optimum resting length

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16
Q

Why isnt max tension gen. with short sarcomeres

A

Because of overlapping thin filaments

17
Q

What isnt max tension gen. with long sarcomeres

A

Reduced area for cross bridge formation so less tension is generated

18
Q

What differs between the heart and other muscles - what are the implications of this

A

Heart is not bound by any joints so it is possible for it to go beyond the optimum length
This leads to less force ==> so more blood left in with each contraction and can lead to heart failure

19
Q

What is the optimum sarcomere length for cardiomyocytes

A

2.2 - 2.6 um

20
Q

Describe the process that would be undertaken to measure length-tension

A

Clamped muscle held fixed at one end - other end attached to a force transducer
Electrical stimulation via electrode
Record l of muscle and force gen by the contraction
Lengthen muscle and repeat over a range of muscle lengths

21
Q

What happens to the active force as sarcomere length increases

A

Starts increasing to a maximum and then decrease

22
Q

What happens to passive force as sarcomere length increases

A

At 0 until high sarcomere length then increases

23
Q

What happens to total force as sarcomere length increases

A

Increases - peaks - begins to decrease as active force decreases BUT passive force increases so total froce begins to increase

24
Q

Describe how an engineer would model a cardiomyocyte

A

One contractile element with a critcal damper to prevent oscilations
One spring in parallel - representing the neck of the cross bridge
One spring in series - representing the accessory protein of the sarcomere (titin)

25
Q

What length sarcomere is produced by a 10-12 mmHg filling pressure

A

2.2. um

this is the presystolic volume

26
Q

What is a key difference in the regulation of tension between cardiac and skeletal myocyte

A

In cardiac greater regulation at the cellular level
In skeletal muscle to cause greater tension more fibres are recruited
In caridac the force produced by each myocyte is changed

27
Q

What is isotonic contraction

A

Where tension does not change but the length does change

28
Q

What is isometric contraction

A

Length is unchanged but the tension does change

29
Q

Describe the relationship of the muscle, pre load and the afteload

A

Muscle is streched by the preload which stimulates it to lift the afterload

30
Q

What is the preload

A

Initial streching of the sarcomere length

The ventricular end diastolic volume

31
Q

What is the afterload

A

The force which the ventricles have to act against in order to eject the blood – essentially the arterial blood pressure and vascular tone

32
Q

For an isotonic contraction what can be said about contraction for a heavier load

A

It will be slower

33
Q

What is the relationship between shortening velocity and the afterload

A

There is an inverse relationship between shortening velocity and afterload

34
Q

What are the 3 key results from a graph of initial velocity of shortening against the load

A

A high preload gives a high maximal force (high preload = high P0)
For any given afterload a high preload gives a high velocity of shortening
Maximum initial velocity of shortening is constant

35
Q

Describe 3 varying definitions of contractility

A

Change occurs when a heart changes its output per beat with the EDV remaining constant
Changes can occur when more crossbridges form per stimulus
May reflect the qualitative state of the actin/myosin cross bridges

36
Q

What is the effect of sympathetic stimulation by NAdr on contractility

A

Increases the Vmax (maximum initial velocity of shortening)

Increase the P0 (maximum force which can be produced)

37
Q

What are the effects of sympathetic stimulation said to be …

A

Positive chronotropic (time) and ionotropic (force)

38
Q

What does the interbeat duration influence

A

The force of contraction

39
Q

Why does an increased frequency of beats lead to a increase in contractility

A

With faster beats - less time for Ca to be resequestered

So Ca accululates with each beat

BMS242 CVS Phys (12 decks)

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