Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS 242 - CVS respiratory > Myocardial mechanics > Flashcards

Myocardial mechanics Flashcards

1
Q

What is the process of excitation-contraction coupling?

A

1) Electrical excitation from ALPHA motor neuron
2) Series of events including Ca2+ - delay in muscle contraction
3) T-tubules and intercalated discs rapidly transmit action potentials to the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are intercalated discs present?

A

In cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the sarcolemma?

A

The myocyte plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are t-tubules?

What do they allow?

A

Invaginations of the sarcolemma that dive deep into the myocyte

Allows action potentials to stimulate ALL parts of the muscle SIMULANEOUSLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the action potential down the t tubules activate?

A

Sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the sarcoplasmic reticulum?

What does it store?

A

Specialised type of SER

Fluid-filled membranous sac that surrounds each myofibril

Stores Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the structure of the SR?

A
  • Voltage gated ion channels

- Cisterns - store the water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are the cisterns of the SR?

A

At the END of the myofibrils

In a triad:

  • 2 cisternes
  • 1 central T-tubule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What occurs in a relaxed muscle with Ca2+?

A
  • Sarcoplasmic [Ca2+]
  • Ca2+ pumps MOP UP calcium from the sarcoplasm and stores it in the sarcoplasmic reticulum
  • Sarcoplasmic reticulum [Ca2+] ~10nm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is CALSEQUESTIN present?

What does it do?

Why is this advantageous?

A

Present in the SR

Binds to FREE Ca2+ - lowering [Ca2+]

Advantageous:
1) Makes it seem like low Ca2+ in SR

2) Pumps work more efficiently and quickly
3) More Ca2+ stored in the SR
4) More Ca2+ can be released during contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the additional proteins involved in muscle contraction?

A

1) Tropomyosin
2) Myosin and actin
3) Titin
4) Troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does tropomyosin do?

A
  • Covers the actin/myosin binding site
  • Preventing the myosin head from sticking to the actin molecule
  • Muscle remains relaxed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does titin do?

A

Tethers myosin

  • Prevents the muscles from pulling apart completely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does troponin do?

A

Connects to tropomyosin

  • Pulls tropomyosin away from the actin/myosin binding site when bound to Ca+
  • Myosin head can bind to actin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why can troponin not work in relaxed muscle?

A

No Ca2+ to bind to the troponin for it to pull the tropomyosin away and reveal actin/myosin binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What occurs during muscle contraction?

A

EXCITATION-CONTRACTION COUPLING:

1) Action potential arrives - depolarisation of the membrane
2) Action potential propagates down down the T-tubules - activates VG Ca2+ ion channels in the sarcoplasmic
3) Voltage gated Ca2+ channels open
4) Ca2+ rapidly diffuses out of the SR down the concentration gradient into the SARCOPLASM
5) Ca2+ binds to toponin - conformational change
6) Troponin pulls tropomyosin from the myosin/actin binding
7) Myosin head sticks to the binding site on actin
8) If ATP/ADP available - cross bridge cyclic occurs and muscle actively shortens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is there a delay in the activation of the sarcolemma and muscle contraction?

A

Ca2+ channels needing to be open etc. (cascade)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the consequences of the sliding filaments?

A

Muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is muscle tension that the myocytes can develop?

A

Proportional to the no. of cross bridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the no. of cross bridges that can form?

What does this mean?

A

Proportional to the sarcomere length

Means there is an OPTIMUM resting length for the maximum tension generation (as there is a point were there will be maximum no. of cross bridges forming)

21
Q

What is the frank-stalin relationship?

A

The length-tension relationship

22
Q

Describe the frank-stalin relationship graph

A

Short sarcomeres:

  • Overlapping thin filaments
  • LESS tension generated
  • Action interfere with binding sites
  • No actin-myosin binding

Optimum length:
- Absolute maximum no. of actin-myosin binding sites

Increase length past optimum:

  • Actin and myosin are pulled apart
  • Reduced area for cross bridge formation

Increase length too much:
- No binding at all

23
Q

What is the optimum length of the sarcomere?

A

Where the MAXIMUM no. of binding sites

Where the MAXIMUM tension is generated

24
Q

How do muscles constantly work at the optimum range?

A

Tendons and bones and angle of the joints

25
Q

How can the frank-stalin relationship occur in heart muscle when the heart isn’t joined to any bones?

A
  • If increase the venous return –> heart keeps expanding
  • Sarcomere length increase
  • Forced produced is less (more than optimum sarcomere length)
  • More blood left in the heart (can’t expel blood properly)
  • Heart is stretched more
  • Go onto the descending part of the frank-stalin curve
26
Q

What can happen if go on the descending curve of the frank-stalin in the cardiac muscle?

A

Heart faliure

27
Q

As well as sarcomeres, what else contributes to tension curve?

A

Passive elastic structures

28
Q

What is the ACTIVE force in the heart?

PASSIVE force?

A

Active force - contraction of the myocytes

Passive force - Elastic recoil

29
Q

What happens when add the active force and passive force together?

A

Graph that keeps on INCREASING

30
Q

What length is the sarcomere at maximum tension?

At maximum cross-bridges?

A
  1. 2 micro metres

2. 2 micro metres

31
Q

How should the heart fill be to create a heart to generate sarcomeres in 2.2 micro metres?

What is this pressure called?

A

10-12mmHg filling pressure

Called the pre-systolic pressure

32
Q

What is the presystolic pressure?

A

The pressure at rest when the blood fills the left ventricle

33
Q

How is muscle contraction strength increase in skeletal muscle?

A

Recruit more motor units to increase muscle contraction

34
Q

How is muscle contraction strength increase in cardiac muscle?

A

DON’T RECRUIT more muscle fibres

Instead, just CHANGE THE FORCE that each myocyte is able to produce

35
Q

What is the force-velocity relationship?

A

Heavier the weight/load - the slower the rate of contraction

36
Q

What is isotonic contraction?

A

Contraction of the muscle where the tension remains the SAME throughout contraction

37
Q

What is the muscle in the vessels stretched by?

A

The pre-load (end diastolic volume)

38
Q

What is the afterload?

A

Force at which the cardiac myocytes have to push against to eject blood:

  • Arterial blood pressure
  • Vascular tone
39
Q

What is the relationship between shortening velocity and afterload?

A

Inverse relationship:

Increase afterload - decrease shortening velocity

40
Q

What happens to the contraction strength if increase the pre-load?

A

STRONGER contraction (providing stay in the optimum range of the sarcomere)

41
Q

When is a change in contractility shown?

A

When the output of the heart changes but the diastolic volume remains the same

42
Q

When does contractility in the heart increase?

A

When more cross bridges from per stimulus (due to increase in Ca2+ per stimulus)

43
Q

What does the contractility reflect?

A

The QUALATIVE state of the actin/myosin cross-bridges

44
Q

What are changes in contractility called?

A

Positive (increase) or negative (decrease) IONOTROPIC effects

45
Q

What are the changes in speed/rate of contraction called?

A

Chronotropic effects

46
Q

What does noradrenaline release from the sympathetic nervous system cause?

A

Increase in MAXIMAL FORCE (ionotropic) and in Vmax (chronotropic - rate)

47
Q

What increases the initial velocity of shortening?

A

Amount of noreadrenaline

48
Q

Describe the frequency-force relationship?

A

Inter-beat duration (between beats) influences the FORCE of contraction:

  • Positive ionotropic/chronotropic
  • If increase the FREQUENCY (chronotropic) of stimulation (reduce inter-beat duration) INCREASE contractility (ionotropic)
49
Q

Why does the increase in frequency of beats increase the force contraction?

A

Changs the Ca2+ availability within the sarcoplasm:

  • Pumps in the SR have MAXIMUM RATE of which they work to remove Ca2+ from the sarcoplasm
  • When they reach this rate - can’t increase any further
  • If stimulate the muscle quickly - amount of Ca2+ in the sarcoplasm increase very quickly
  • Accumulation of Ca2+ with each beat
  • Ca+ bind to troponin - uncovering the actin/myosin binding site

BMS 242 - CVS respiratory (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions