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Y1 BRS > Cardiovascular mechanics > Flashcards

Cardiovascular mechanics Flashcards

1
Q

Which ion do ventricular cells require for contraction?

A

Calcium

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2
Q

What is the shape of ventricular cells?

A

Rod shaped

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3
Q

What is the distinctive difference regarding the heart v skeletal muscle for contraction?

A

The heart will not beat without external calcium difference to skeletal muscle which is independent

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4
Q

What is the 3 stages for ventricular contraction?

A 
Electrical event (action potential)
Calcium transient (Amount of calcium  in sarcoplasm has increased for short period of time)
Contractile
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5
Q

What is the length and width of a ventricular cell?

A

100microm,

15 Microm

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6
Q

Describe the position of T-tubules respect to the Z-discs of a sarcomere?

A

The t-tubules is intermediate between each z-line of Myofibrils, transmitting surface depolarisation deep into the cell

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7
Q

SAQ: What organelle is prevalent in ventricular cells?

A

Mitochondria

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8
Q

SAQ: Why is there a high prevalence of mitochondria within ventricular cells? (2 marks)

A

Supply adequate amount of ATP (1)

To supply the sliding filament theory (2), myosin globular heads require ATP binding to reconfigure in high energy state.

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9
Q

Which type of channel opens in response to the action potential within the cardiomyocyte?

A

L-type calcium channel

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10
Q

Why do L-type calcium channels open?

A

Upon excitation, the depolarisation is sensed by the ion channel within the cardiomyocyte, opening in response

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11
Q

How does extracellular calcium enter into the cardiac cell?

A

Passive diffusion across concentration gradient

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12
Q

What is the fate of the diffused intracellular calcium?

A

Minor proportion directly activates the contraction of sarcomere, binding onto TnC of actin filaments, causing contraction

Majority bind to ryanodine receptors on SR to cause Ca efflux from SR.

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13
Q

Which receptor does Calcium ions bind onto within the sarcoplasmic reticulum?

A

Ryanodine receptor

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14
Q

Upon ligand calcium activation of ryanodine receptor, what occurs?

A

Receptor undergores conformation change, opening the ryanodine receptor, thus enabling calcium efflux from sarcoplasmic reticulum

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15
Q

Which complex does calcium bind to on the actin filaments?

A

Troponin-C.

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16
Q

Upon TnC-Ca binding, what occurs to the actin filaments?

A

Myosin-binding site becomes exposed, through withdraw of tropomyosin complex, enables myosin head to bind, and undergo power stroke, sarcomere shortening is activated

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17
Q

How is ionic balance achieved within ventricular cells upon relaxation phase?

A

Calcium is actively pumped out into stored position by Ca2+ ATPase channels of sarcoplasmic reticulum.
Same
Calcium-induced calcium release via sodium-calcium exchanger

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18
Q

How much calcium is effluxed from the sodium-calcium exchanger?

A

Same amount of calcium that came in = same amount effluxed

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19
Q

Is calcium-induced released passive or active?

A

Passive

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20
Q

Why is calcium-induced release passive?

A

Does not require energy, since energy is transferred through the passive diffusion of sodium ions into the cell to expel calcium

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21
Q

What is the relationship between contractile force and cytoplasmic calcium concentration?

A

Sigmoidal relationship

As intracellular cytoplasmic calcium increases, the force exerted by muscles increases

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22
Q

What is the optimum cytoplasms calcium concentration sufficient to produce maximum force?

A

10micrometers

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23
Q

What is the relationship between muscle length and baseline force?

A

Direct proportionality

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24
Q

What is the relationship shown by the active force production line?

A

Cardiac preparation increases, muscular force increases

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25
Q

What is the relationship with muscle length and passive force?

A

Direct proportionality

26
Q

Why does passive force increase as muscle length increases?

A

Elastic components (elating) stretch, passive tension is produced; cytoskeletal components of cells stretch, elastic potential energy is stored, during no sarcomere shortening of the muscle isometric contraction

27
Q

What is an isometric contraction?

A

Tension provided does not cause muscular shortening, exerts pulling force

28
Q

Why is there a limit of proportionality for active force line?

A

Stretching point
Further stretching cannot occur to generate force, insufficient overlap between actin and myosin filament within the A band

29
Q

Why is passive force greater in cardiomyocytes than myocytes?

A

Cardiac is less compliant, and resilient to stretch, thereby can withstand greater isometric contractions before sarcomere shortening proceeds.

30
Q

Why are cardiac muscles less compliant?

A

Due to its extracellular matrix and cytoskeleton

31
Q

Why is there a descending limb in the muscle force relationship?

A

Overstretch of muscle beyond the actin and myosin filament overlap will result in a decrease in force, behaviour is exhibited in skeletal muscle.

32
Q

What is passive force?

A

based on resistance to stretch of the muscle

33
Q

What is the total force produced?

A

Active force + Passive force

34
Q

Why is there not an descending limb of length-tension curve?

A

Important in physiological circumstance in cardiac muscle; the descending limb does not occur in physiological condition because pericardium restricts stretching

35
Q

What is an isometric contraction?

A

Sarcomeres and muscle fibres do not change length, however pressures increase in both ventricles, attributed to the passive force of cytoskeleton stretch.

36
Q

What is an isotonic contraction?

A

Shortening of fibres, and blood is subsequently ejected from ventricles.

37
Q

What is preload?

A

Degree to which cardiomyocytes are stretched from filling of the ventricles prior to contraction. Therefore, preload is a way of expressing end-diastolic volume. Increasing ventricular filling, increases EDV, and cardiac muscle is stretched to a greater degree.

38
Q

What influences preload directly?

A

Venous return and end diastolic volume

39
Q

What is end-diastolic volume?

A

The volume of blood resident within the ventricles before ventricular systole

40
Q

How does tachycardia affect preload?

A

Decreases, reduced duration of ventricular diastole, thus diastolic volume decreases, shorter filling, lowering preload

41
Q

How does a reduced preload due to tachycardia overcome?

A

Increased contractility, raises the stroke volume

42
Q

What is the Frank-Starling relationship?

A

Ventricular stretch and contraction. Within physiological limits, the force of heart contraction is directly proportional to initial length.
Greater stretch = more preload = contractility increased = greater stroke volume

43
Q

What is cardiac contractility?

A

Cardiac contractility: Tension developed and velocity of shortening (Strength of contraction) of myocardial fibres at a given preload, and afterload.

44
Q

How does sympathetic activity influence preload?

A

Increased venous return to heart, contributes to ventricular filling, EDV + preload.

45
Q

What is afterload?

A

The load against which the left ventricle ejects blood after opening the aortic valve.

Refers to the tension/force that the ventricle must develop to pump blood effectively against the resistance in the vascular system.

46
Q

Which conditions increase afterload?

A

Vasoconstriction, stenosis, atherosclerosis

HYPERTENSION

47
Q

Why does vasoconstriction, stenosis and hypertension cause greater afterload?

A

Greater backforce on aortic valves, thus greater pressure is required to open the aortic semi-lunar valves for ventricular systole to occur (Magnitude of isotonic contraction must increase)

48
Q

What effect does an increased afterload have on isotonic shortening?

A

Decreases isotonic shortening, and contractility (velocity of shortening)

49
Q

Which factors decrease vascular resistance?

A

Vasodilation (Increased radius)

50
Q

What are the measure of afterload?

A

Diastolic arterial blood pressure

Afterload is blood pressure

51
Q

Why do shorter muscle lengths produce less tension?

A

Reduces actin-myosin filament overlap, fewer cross-bridges can be made.

52
Q

Which two factors influence cardiac contractility?

A

Changes in the number of myofilament cross-bridges that interact
Changes in calcium sensitivity of the myofilaments

53
Q

How does ventricular stretching influence contractility in respect to calcium?

A

Ventricular stretching subsequently increases the contact between the myosin heads with the myosin binding sites presented by the thin actin filaments, lattice-spacing decreases.
Decreasing myofilament lattice spacing increases the probability of forming strong-binding cross-bridges; providing more force for the same amount of activating calcium.

54
Q

How does calcium sensitive influence contractility?

A

Ca2+ required for myofilament activation, troponin C (TnC), is thin filament protein that binds Ca2+, subsequently causing tropomyosin to expose the myosin binding sites, regulating the formation of cross-bridges between actin and myosin.
At longer sarcomere lengths, the affinity of TnC for Ca2+ is increased due to conformational change in protein; thereby less Ca2+ is required for equivalent amount of force.

55
Q

What is stroke work?

A

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

56
Q

What is stroke work?

A

Area beneath pressure volume loop

Stroke volume x pressure

57
Q

What is stroke volume?

A

End diastolic volume - end systolic volume

58
Q

Which factors affect stroke work?

A

Preload
Contractility
Afterload

59
Q

What is Law of Laplace?

A

Assuming pressure within a cylinder is held constant, the tension exerted onto the walls increases with increasing radius. (h=Wall thickness)
Increase radius = Increase tension
𝑾𝒂𝒍𝒍 π‘»π’†π’π’”π’Šπ’π’=𝑷 𝒙 𝑹
𝑻=𝑷𝑹/𝒉

60
Q

How is the left ventricular adapted to cope with systemic circulation (afterload increased) in regards to Law of Laplace?

A

Radius of curvature is comparatively less than RV, allowing LV to generate higher pressures with equivalent wall stress

Y1 BRS (39 decks)

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