Cardiovascular Mechanics Flashcards

1
Q

What does a ventricular cell require for contraction?

A

Calcium and excitation of cell

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2
Q

Outline the basic process leading up to the contraction of a ventricular cell

A

Excitatory event (AP) at myocyte leads to influx of Ca2+ and then Ca2+ release which causes contraction

The contraction is very dependent on the influx of external Ca2+ → heart cell won’t contract unless this happens

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3
Q

What is the length and width of myocytes?

A

100μm long and 15μm wide

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4
Q

T tubules

A

Invaginations of sarcolemma

Are 200nm
Carry depolarization deep into cell

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5
Q

What are myocytes made of

A

46% myofibrils, 36% mitochondria (high energy requirement), 4% sarcoplasmic reticulum, 2% nucleus and 12% other

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6
Q

Describe the mechanism of excitation-contraction coupling/calcium induced calcium release, starting from an AP (remember to detail how the myocyte relaxes/stops contraction)

A

1) AP produced along cell surface membrane (sarcolemma)

2) Depolarisation carried deep into cell down T-tubule and sensed by L-type Ca2+ channels in T-tubules

3) LTCC opens so extracellular Ca2+ flows down its conc. grad into cytosol

4) This Ca2+ binds to ryanodine receptors on sarcoplasmic reticulum, (which are Ca2+ release channels on SR), that then open

5) Ca2+ stored in SR released into cytosol- this Ca2+ binds to troponin C in myofilaments and activates contraction

6) To relax, Ca2+ is actively pumped against conc grad by SR Ca2+ ATPase into SR where it’s ready to be released by next wave of depolarisation

7) The Ca2+ that came into cell to trigger release of Ca2+ is removed from cell during diastolic interval by Na+/Ca2+ exchanger in T-tubule which uses downhill movement energy of Na+ into cell to pump Ca2+ out of cell

8) Myocyte now in Ca2+ balance

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7
Q
  • Can the hearts contractility be sustained by saline solution with bicarbonate of soda and potassium chloride?
A

No; the addition of lime or a calcium salt will restore good contractility.

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8
Q

Does skeletal muscle need external calcium for contraction?

A

No

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9
Q

Explain the length-tension relation (LTR) in muscle

A
  • As you increase muscle length and stimulate it, active force production increases due to cross bridge formation happening in response to Ca2+ being released from SR
  • Cardiac cells also have some elasticity so have a tendency to recoil as they are stretched- meaning as you increase muscle length, base force produced increases too (called passive force)
    • Passive force increases continuously
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10
Q

What are active and passive force due to?

A

Active - Dependent on sarcomere shortening, forces act in the direction of point of muscular attachment towards centre

Passive - Based on the resistance to stretch of the muscle

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11
Q

Total force

A

Passive force +active force

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12
Q

Why does cardiac muscle produce more passive force than skeletal muscle?

A

Cardiac muscle is more resistant to stretch and less compliant than skeletal muscle

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13
Q

What does it mean that the cardiac muscle only works on the ascending limb of the length-tension relationship?

A

You can’t overstretch cardiac muscle- you can with skeletal muscle (where you pull a muscle)

Heart is contained in pericardial sac so can only stretch a certain amount

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14
Q

Why is there a descending limb

A

force increases with length, but after a certain length force decreases in both
In actzive force when the distance is so long that the myosin and actin filaments are far they can’t form cross bridge so no sarcomere shortening

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15
Q

Isometric contraction

A

Muscle fibres don’t change length but pressure increases in both ventricles

When ventricles fill with blood we get isometric contraction and valves are closed so blood doesn’t go anywhere- builds up ventricular pressure

e.g. plank

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16
Q

What is isotonic contraction of the heart?

A

Shortening of fibres and blood is ejected from ventricles

When pressure in ventricles from isometric contraction overcomes backpressure in aorta, blood is expelled from ventricle, ventricular cells shorten and blood pushed out

E.g. Bicep curls, bench press etc.

17
Q

Preload

A

Degree to which cardiac muscle cells are stretched from filling of the ventricles, prior to contraction (during diastole)

18
Q

What is preload dependent on

A

Venous return

19
Q

What are the (3) measures of preload?

A

End-diastolic volume (EDV)

End-diastolic pressure (EDP)

Right atrial pressure

20
Q

What is afterload

A

Pressure (in the aorta) that ventricles must overcome, to pump blood out of heart

Afterload is the load against which the left ventricle ejects after opening of aortic valve

As afterload increases, the amount of muscle shortening decreases and the velocity of shortening decreases

21
Q

How do we measure after load

A

Diastolic blood pressure (the one in the aorta)

aortic pressure

22
Q

Define the Frank-Starling relationship and what the consequence is in terms of cardiac output

A

Definition - Increased diastolic fibre length increases ventricular contraction

(As filling of the heart increased, force of contraction of ventricular muscle also increased)

Consequence - Ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return

Diastolic fibre length^ → Ventricular stretching^ → Greater SV → Increased cardiac output

23
Q

What are the 2 factors that are thought to cause the Frank-Starling relationship and then explain each one?

A
  • Change in number of myofilament cross bridges that interact- what does this mean?As you stretch muscle, you increase number of myofilament cross bridges so more myosin and actin interactionsAt shorter lengths than optimal the actin filaments overlap on themselves so reducing the number of myosin cross bridges that can be made!https://s3-us-west-2.amazonaws.com/secure.notion-static.com/46123b47-7266-47f6-a72b-1af39d732e4a/Untitled.png
  • Changes in Ca2+ sensitivity of myofilaments- meaning?
    Calcium is needed for myofilament activation
    At longer sarcomere lengths the affinity for troponin c for calcium increases due to conformational change in protein so less calcium is needed for same amount of force
24
Q

Stroke work

A

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

Stroke work = volume of blood ejected during each stroke (SV) x pressure at which blood is ejected (P)

Stroke work = Stroke Volume x Pressure

Affected by preload and afterload

25
Q

What is the law of LaPlace

A

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

Wall tension = pressure in vessel x radius of vessel

T = P x R

Incorporating wall thickness (h) amends this to: T = (P x R)/h

26
Q

Which ventricle of the heart generates greater pressure and why?

A

Radius of walls of left ventricle lower than that of right ventricle hence it can generate higher pressures but the tension/stress in the walls remains roughly the same.

LV: Lower R therefore greater P; T is constant.

27
Q
  • What happens to the structure a failing heart?
A

Becomes dilated and spherical which increases wall stress