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
What length sarcomere is produced by a 10-12 mmHg filling pressure
2.2. um | this is the presystolic volume
26
What is a key difference in the regulation of tension between cardiac and skeletal myocyte
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
What is isotonic contraction
Where tension does not change but the length does change
28
What is isometric contraction
Length is unchanged but the tension does change
29
Describe the relationship of the muscle, pre load and the afteload
Muscle is streched by the preload which stimulates it to lift the afterload
30
What is the preload
Initial streching of the sarcomere length | The ventricular end diastolic volume
31
What is the afterload
The force which the ventricles have to act against in order to eject the blood -- essentially the arterial blood pressure and vascular tone
32
For an isotonic contraction what can be said about contraction for a heavier load
It will be slower
33
What is the relationship between shortening velocity and the afterload
There is an inverse relationship between shortening velocity and afterload
34
What are the 3 key results from a graph of initial velocity of shortening against the load
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
Describe 3 varying definitions of contractility
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
What is the effect of sympathetic stimulation by NAdr on contractility
Increases the Vmax (maximum initial velocity of shortening) | Increase the P0 (maximum force which can be produced)
37
What are the effects of sympathetic stimulation said to be ...
Positive chronotropic (time) and ionotropic (force)
38
What does the interbeat duration influence
The force of contraction
39
Why does an increased frequency of beats lead to a increase in contractility
With faster beats - less time for Ca to be resequestered | So Ca accululates with each beat