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Cardiovascular and Respiratory > Cardiovascular Mechanics > Flashcards

Cardiovascular Mechanics Flashcards

1
Q

What can a healthy adult heart be viewed by?

A

nuclear magnetic resonance imaging (MRI)

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2
Q

What is calcium transient?

A

the rise and fall in calcium due to stimulation for contraction

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3
Q

when does calcium increase/decrease?

A

electrical event -> Ca2+ influx and release, then contractile event.
*graph
ca inc then decrease, same w contractile activity short after

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4
Q

Why is it called excitation-contraction coupling mechanism?

A

the electrical activity couples w the contractile activity

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5
Q

is sodium bicarbonate and potassium enough for heart contraction ?

A

no, need calcium for good contractility

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6
Q

importance of calcium for heartbeat?

A

influx of Ca2+ from outside cells to inside needed for contraction of cardiac muscle

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7
Q

does skeletal or cardiac muscle require calcium for stimulation?

A

skeletal no

cardiac yes, will not contract w out it

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8
Q

Ventricular cell structure

A

100 micrometres long and 15 micrometres wide.

cellsurface has T tubules (transverse tubules) invaginating into it. ( pushed deep into surface)

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9
Q

T tubules structure

A

Narrow - 200nm in diameter

spaced apart to lie alongside each z line of every myofibril = 2 micrometres apart

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10
Q

What do T tubules do?

A

carry surface depolarisation from action potential deep into the cell so you get synchronous activation of some proteins.

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11
Q

Where is the calcium stored in the muscle?

A

lacy structure called sarcoplasmic reticulum - lies above the myofilaments

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12
Q

What is the cardiac muscle cell made up of and any importance?

A

46% myofibrils
36% mitochondria - shows the high energy needs of heart and ventricular cells
4% sarcoplasmic reticulum - although only this much its vvv important in calcium regulation in cardiac muscle cell.
2% nuc
12% other

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13
Q

Where are ryanodine receptors found?

A

on the sarcoplasmic reticulum (hence also known as sr calcium release channels) in close proximity to the t tubule particularly the L type calcium channels * refer to the diagram

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14
Q

Mechanism of excitation - coupling reaction

A

The action potential travels down sarcolemma

Depolarisation deep into the cell through the t tubule system

Causes many L type Calcium channels to open by altering their conformation which permits calcium entry into cell (down its conc gradient)

Calcium influx can ‘feed’ myofilaments but main job is to bind to SR ca release channels.

Sr ca channels open up when calcium binds to them and calcium stored in sr is released into the cytosol.

Ca binds to troponin in myofilaments and causes contraction.

for relaxation, calcium pumped back into sr against conc grad by SR calcium ATPase = energy used

the amount of calcium that’s come into the cell needs to be effluxed from cell - done during the diastolic interval, decline and contraction by a protein called Na+/Ca2+ exchanger. uses downhill energy gradient of Na+ moving into cell to supply energy to expel calcium from it

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15
Q

What type of channels are ryanodine receptors?

A

Ligand operated - open when calcium binds to them

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16
Q

What happens at a steady state?

A

Cardiac muscle is in calcium balance ( same amount enters and removed)

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17
Q

When is calcium effluxed from the cell?

A

During the diastolic interval

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18
Q

What protein expels calcium and how?

A

Na+/ Ca2+ exchanger.

Uses energy from the movement of sodium into the cell

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19
Q

What is sympathetic stimulation?

A

Increasing phosphorylation of some proteins and increase calcium influx into the cell = change amount of calcium in the cytoplasm

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20
Q

What is the relationship between the amount of intracellular Ca2+ and force production?

A

sigmoidal

as calcium increases so does force

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21
Q

What is the active force production and what is it caused by?

A

when we increase muscle length we increase the force produced.

caused by cross bridge formation happening in response to calcium being released from the SR

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22
Q

What is passive force?

A

Cardiac muscle has elasticity, passive force is the recoiling of the cardiac muscle

23
Q

What is an isometric contraction?

A

Force is being produced without any shortening occurring.

muscle fibres do not change length but pressures increase in both ventricles

24
Q

Skeletal v cardiac

A

Similarities:
As muscle length increases so does force until muscle has reached an optimum length. after that it declines
Differences:
passive force in skeletal muscle is much less than cardiac
Cardiac muscle only works on ascending limb = cant overstretch cardiac muscle but can overstretch skeletal = pulling muscle

25
Q

Why does cardiac muscle produce more passive force than skeletal?

A

It is more resistant to stretch and less compliant than skeletal muscle which is due to the properties of the ecm and cytoskeleton

26
Q

What is the total force?

A

passive force + active force

27
Q

Why can’t cardiac muscle overstretch?

A

bc its retained in the pericardial sac

28
Q

What forms of contraction does the heart use?

A

isometric and isotonic

29
Q

What is isotonic contraction?

A

Shortening of the fibres and blood is ejected from the ventricles

30
Q

When do isometric and isotonic contraction occur?

A

Initially blood fills but doesnt go anywhere = isometric bc valves are closed. this builds up pressure in ventricle.

When pressure in ventricle > back pressure in aorta, blood expelled from vent and shortening occurs and blood expelled = isotonic

31
Q

What is preload?

A

Initial stretch on heart muscle, specifically resting ventricular walls, as blood fills the chambers during diastole.

stretch/filling determines preload before ejection

32
Q

What is afterload?

A

Pressure against which the heart muscle must eject blood during systole. (load against which eft ventricle ejects blood after opening aortic valve)

33
Q

As we increase preload we (X) force

A

increase

34
Q

As you increase the afterload, the amount of shortening the muscle undergoes is…

A

reduced.

velocity is also reduced

35
Q

small vs large preload leads to?

A
  1. small - shorter muscle lengths and less force produced.

2. large - longer muscle lengths and more force produced

36
Q

What are preload and afterload in the heart?

A 
pre = ventricular filling
after = back pressure in aorta
37
Q

What is preload dependent on?

A

Venous return

38
Q

What are the measures of preload?

A

end-diastolic volume, end diastolic pressure and right atrial pressure (edp indication)

39
Q

Measure of afterload?

A

diastolic blood pressure

40
Q

What did Frank and starling observe?

A

As the filling of the heart increases, the force of contraction also increases

41
Q

Definition of the Frank-Starling relationship?

A

intrisic law of heart:

increased diastolic fibre length increases ventricular contraction

42
Q

consequence of the FS relationship?

A

more venous return = more blood = greater stretch on ventricular muscles = more forceful contraction and vice versa.

ventricles pump greater stroke volume so that cardiac output exactly balances the venous return.

43
Q

What 2 factors cause the F-S relationship?

A

Changes in the number of myofilament cross bridges that interact (increased stretch increases length so no of cb increase)

Changes in the Ca2+ sensitivity of myofilaments

44
Q

Calcium in the FS relationship?

A

Precise mechanism still unclear.

hypothesis 1:
Troponin C
Hypoth 2:
Lattice spacing

45
Q

Troponin C role in fs?

A

at longer sarcomere lengths, the affinity of Troponin C for Ca2+ increased due to conformational change in the protein. Less Ca2+ required for the same amount of force
(troponin c regulates formation of cross-bridges)

46
Q

Lattice spacing

A

when we stretch, increase length but decrease space between actin and myosin (lattice spacing). the probability of forming strong binding cb increases. so more force for same amount of calcium

47
Q

What is stroke work?

A

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

48
Q

How to calculate stroke work?

A

SW= volume of blood ejected during each stroke (STROKE VOLUME) x The pressure at which the blood is ejected (PRESSURE)

SW=SV X P

49
Q

What will influence stroke work?

A

preload and afterload influence sv so will influence sw

cardiac structure affects pressure so sw affected too.

50
Q

What is the law of LaPlace?

A

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

wall tension = pressure in vessel x radius of the vessel
T=P X R.
If we incorporate wall thickness (h) then this can be amended to T=(PxR)/h

51
Q

What is the point of the law of LaPlace?

A

our goal is to have the same tension on both sides of the heart.
allows both sides of the hearts to work at different pressures. - by changing the radius

52
Q

left vs right ventricle wall radius?

A

Radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressures with similar wall stress. ( thick walls in left )

53
Q

What happens to failing hearts?

A

often become dilated which increase wall strength.

Cardiovascular and Respiratory (5 decks)

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