CVS 2 - Mechanical Properties of the Heart 1 Flashcards Preview

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Flashcards in CVS 2 - Mechanical Properties of the Heart 1 Deck (30)
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1
Q

Describe the process of cardiac contraction for a single ventricular cell.

A
  1. Electrical event
  2. Ca transient (increase in Ca conc in sarcoplasm temporarily)
  3. Contractile event
2
Q

Describe a single ventricular cell.

A
  1. T-tubules roughly 200nm

2. Spread about 2 um apart- each T-tubule lies alongside Z-line of every myofibril

3
Q

What is different about cardiac contraction and skeletal muscle contraction?

A

Heart won’t beat without extracellular calcium whereas skeletal muscle can contract without external calcium

4
Q

Describe excitation-contraction coupling in the heart.

A
  1. L-type calcium channel senses depolarisation; external calcium enters the cell.
  2. Some Ca directly causes contraction
  3. The rest of the Ca binds to Ryanodine receptors (aka SRCRC). Causes release of Ca from SR.
  4. After Ca has had its effect, some Ca taken up into SR b Ca ATPase channels (aka SERCA).
  5. Same amount of Ca that entered the cell is effluxed by a Sodium/Calcium Exchanger - THIS PROCESS DOES NOT REQUIRE ENERGY
5
Q

What kind of relationship is the Force-Ca conc relationship?

A

Sigmoidal

6
Q

Describe Length-Tension relationship in cardiac muscle in isometric contraction.

A

Isometric - muscle doesn’t shorten, it just pulls on force transducer

Increase in muscle length causes an increase in force, UPTO A POINT.

AFTER THIS POINT, FURTHER STRETCHING DOESNT GENERATE MORE FORCE - because not enough overlap between filaments to produce force.

7
Q

What does overstretching the muscle lead to?

A

Decrease in force.

This is what happens in skeletal muscle when you pull a muscle

8
Q

What is passive force?

Does skeletal muscle or cardiac muscle exert more passive force?

A

Passive force = based on resistance to stretch of the muscle

Cardiac muscle more resilient to stretch so exerts more passive force.

9
Q

Why is cardiac muscle more resistant to stretch?

A

Due to properties of the ECM and Cytoskeleton

10
Q

Why is cardiac muscle very unlikely to be overstretched?

A

Due to the pericardium, which restricts stretching.

Therefore, only the ascending limb of the length-tension graph is important

11
Q

Which 2 forms of contraction does the heart use?

A
  1. Isometric - resists high pressure, no change in length but change in tone.
  2. Isotonic - fibres shorten when blood ejected from ventricles.
12
Q

What is preload?

A

Weight that stretched the muscle before it is stimulated to contract (i.e. filling of ventricles)

It is dependent on venous return

13
Q

What is after load?

A

Weight that is not apparent to muscle in resting state - encountered only once muscle has started to contract.

“The load against which the LV ejects blood after opening of the aortic valve”

Basically BP

14
Q

What does more after load mean?

A

More Afterload = Less shortening

More after load = less velocity of shortening

15
Q

What does preload govern?

A

Amount of force muscle is capable of producing

16
Q

What are measures of preload?

A
  1. End diastolic volume
  2. End diastolic pressure
  3. Right atrial pressure

(Preload is the stretching of the ventricular walls as blood fills)

17
Q

How can afterload be measured?

A

Diastolic arterial blood pressure

18
Q

2 results of increased after load.

A

Decreased shortening + decreased velocity of shortening

19
Q

Describe 2 features of increased aortic pressure (increased afterload)

A
  1. Increase in aortic pressure = decrease in shortening

2. At the same aortic pressure, more ventricular filling (more preload) means increased shortening

20
Q

Describe Starling’s Law.

A

Increased diastolic fibre length increases ventricular contraction.

aka - increased preload leads to increased shortening and speed of shortening

Consequence: Increased diastolic fibre length causes ventricles to pump an increased stroke volume so that cardiac output exactly balances increased venous return (at eqm)

aka - amount of blood coming into ventricles determines strength of ventricular contraction and so determines amount of blood leaving ventricles.

21
Q

Which 2 factors cause the Frank-Starling relationship (Starlings Law).

A
  1. Changes in number of myofilament cross bridges that interact
  2. Changes in Ca sensitivity of myofilaments
22
Q

Describe how changes in the number of cross bridges affects Frank-Starling relationship.

A
  1. At sub-optimal lengths, actin filaments overlap which reduces the number of myosin cross bridges that can form.
  2. Increased stretching of muscle allows more optimum interdigitation of actin and myosin filaments.
23
Q

What happens when myofilaments are stretched?

A

Ca sensitivity increases

24
Q

Explain the 2 possibilities for increased Ca sensitivity with stretched myofilaments.

A
  1. Increased Troponin C affinity for calcium due to conformation change in protein (at increased sarcomere lengths) - less Ca needed for same amount of force
  2. Stretching causes space between myosin and actin filaments to decrease. This increases the probability of forming strong cross bridges - more force for same Ca
25
Q

What is stroke work?

A

Work done by the heart to eject blood under pressure into the aorta and pulmonary artery

SW = SV x P

26
Q

What factors greatly affect stroke volume?

A

Preload and afterload

27
Q

What greatly affects pressure?

A

Structure of the heart

28
Q

What is the Law of Laplace?

A

When the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius.

Increased radius = increased tension (increased force around the sides)

Force around sides (T) = P x r

29
Q

What is the physiological relevance of the Law of Laplace?

A
  1. Same wall tension must be maintained.
  2. T =P x r
  3. Tension must be same, but LV requires much higher pressure, meaning that it has a lower radius of curvature.

IT ALLOWS LV TO GENERATE HIGH PRESSURES WITH SAME WALL TENSION

30
Q

What happens as muscle length increases?

A

Passive force increases continuously