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Bioregulatory systems 3 > cardiovascular mechanisms > Flashcards

cardiovascular mechanisms Flashcards

1
Q

What is the size of ventricular cells?

A

100micrometres long

15 micrometres

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2
Q

How wide are t tubules openings

A

200nm in diameter

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3
Q

how are t -tubules spaced?

A

so that a t-tubule lies alongside each z-line of every myofibril

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4
Q

What is the structure of the sarcoplasmic reticulum like?

A
  • lace like
  • stores Ca2+
  • wraps itself round T-tubules
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5
Q

What do t-tubules do?

A

carry surface deep polarisation deep into the cell

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6
Q

What is the make up of a cardiac cell?

A

Myofibrils-46%

Mitochondria-36%

Sarcoplasmic reticulum-4%

Nucleus-2%

Other-12%

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7
Q

How much calcium is needed for the heart to contract?

A

a milimol

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8
Q

describe calcium induced calcium release?

A
  • upon excitation the depolarisation of the t-tubule is sensed by the L-type calcium channel causing it to open
  • calcium moves down its concentration gradient into the cell
  • most of the calcium then goes to bind to the SR CALCIUM RELEASE CHANNEL(Ryanadine) causing a conformational change in the channel causing it to open
  • different calcium stored in the SR can then flow out, and bind to myofilament to produce muscle contraction
  • calcium is pumped back up in the the SR to be stored by the SR CALCIUM ATPASE or pumped out of the cell by Na+/Ca+ exchanger
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9
Q

How is calcium prevented from building up in the cell?

A

-Na+/Ca+ exchanger on the t- tubule membrane take calcium out of the cell during relaxation -it uses the downhill energy gradient of sodium to provide the neccesary energy to expel calcium from the cell

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10
Q

What is the relationship between calcium in the cytoplasm of a muscle cell and force production?

A

Sigmoidal

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11
Q

What happens as muscle length increases?

A
  • More ACTIVE force produced
  • elastic components of the muscle also stretches to produce a passive force
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12
Q

What is the length-tension/force relationship?

A

The more you stretch the muscle up to a certain value the more active and passive force is produced and therefore the more total force excibited by the muscle (active +passive= total)

However if you stretch it too much the ACTIVE force decreases again as the mysin head(on myosin filaments) do not overlap with the actin strands so cant bind =no contractive force

The PASSIVE force will continue to increase as the muscel length increases

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13
Q

Which one out of skeletal and cardiac muscle produces the least passive force and why?

A

Cardiac muscle is MORE RESISTANT to stretch so is LESS COMPLIANT than skeletal muscle. This is due to the properties of the extracellular matrix and cytoskeleton and because the heart is in the PERICARDIUM sac preventing it from overstretching.

-Therefore it releases the least passive force as passive force increases with more stretch and skeletal muscels can keep stretching whereas cardiac can’t

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14
Q

What are the two forms of contraction used by the heart?

A

ISOTONIC-produces force by changing the length of the muscle(mostly shotening in the heart) e.g. blood is ejected for the ventricles

ISOMETRIC-produces force when muscle fibres are not changing length as no contraction happening yet. Increase in pressure but not volume

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15
Q

what is Preload?

A

weight(blood) that STETCHES the muscle before it is stimulated to contract

Initial stretching of the heart during diastolic filling

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16
Q

What is the afterload?

A

PRESSURE the heart must work against to eject blood during systole

RESISTANCE the left ventricle must overcome to circulate the blood

17
Q

Describe the relationship between afterload and shortening in isotonic contraction?

A

The more afterload you have to lift the less shortening the muscle can do

18
Q

What happens to the afterload and shortening relationship if there is more preload?

A

-more preload=longer muscle lengths =more shortening/ contraction for the same amount of afterload(look at diagrams)

19
Q

What is the relationship between preload and afterload?

A

more preload =more stretch/length of muscle =more force of muscle =more shortening/contraction of muscle for the same amount of afterload (therefore meaning you can lift a larger weight more if you have more pre stretch)

20
Q

What determines the preload of the heart?

A

VENOUS RETURN -ventricular filling during diastole(ventricles relaxed) -this filling with blood caused the ventricular walls to stretch(preload)

21
Q

What are measures of preload?

A
  • end-diastolic volume(the amount of volume of blood in the heart before it starts to contract)
  • end diastolic pressure
  • right atrial pressure
22
Q

What is meant by the in vivo correlates of preload?

A

volume of blood in the heart just before ventricles contracts

23
Q

What is the in vivo correlates of afterload?

A

the load/pressure the heart will experience against which the LEFT VENTRICLE ejects blood after opening of the aortic valve(this is essentially the diastolic blood pressure)

24
Q

What happens if the afterload of the heart increases?

A

decreases the amount of isotonic shortening that occurs

decreases the velocity of shortening

25
Q

How can you measure afterload of the heart?

A

diastolic blood presssure

26
Q

What factors affect the contraction of the heart?

A

ISOMETRIC CONTRACTION: Ventricular filling- because this effects the preload

ISOTONIC CONTRACTION: Pressure in the aorta-this effects the afterload and therefore effects the shortening of the muscle fibres and the velocity of the shortening

27
Q

What is the Frank Starling relationship?

A

Increase ventricular filling=increased DIASTOLIC FIBRE LENGTH (due to filling of heart) =INCREASES VENTRICULAR CONTRACTION

consequence: ventricles pump greater stroke volume so that cardiac output exactly balances the GREATER VENOUS RETURN

28
Q

What 2 factors cause the Frank Starling relationship?

A

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

29
Q

What is the stroke work?

A

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

30
Q

How do you calculate stroke work?

A

volumE of blood ejected during each stroke(SV) x the pressure at which the blood is ejected

31
Q

What affects the stroke volume and the pressure at which the blood is ejected?

A

SV- preload and afterload greatly influence stroke volume

P- effected by cardiac structure

32
Q

What is the law of LaPlace?

A

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

33
Q

How do you calculate wall tension

A

Wall tension= pressure in the vessel x radius of vessle T=PxR you can also incorporate wall thickness(h) into this t=(PxR)/h

34
Q

As the muscle length increases what happens?

A

Passive forces increase CONTINUOUSLY but the active forces increase up to a point and then decrease

35
Q

Describe how muscle fibres shorten starting from depolarisation?

A

1-The sinoatrial node depolarises

2-Action potential travels down the t-tubules

3-Ca2+ enters cell

4-Ca2+ binds to the RYANODINE receptor on the SR

5-Ca2+ enters the cytoplasm from the sarcoplasmic reticulum

6-Ca2+binds to Troponin C=this unbind from actin

7-Myosin head can now bind to the actin

8-Muscle fibres shorten

36
Q

Why doesn’t the heart rip given the high internal pressure?

A

dependent on wall stress

Radius of curvature of the walls in the Left Ventricle is less than that of the right ventricle allowing the Left ventricle to generate higher pressure with similar WALL STRESS

37
Q

How is wall stress kept in giraffe?

A

giraffe las long narrow thick walled ventricle

38
Q

What is the difference between active and passive force of the muscles?

A

Active tension

  • generated by sarcomeres
  • As muscle length increases so does this but only upto a certain point and then it decreases

Passive tension:

-arises from elastic elements in muscle fibres when they are stretched beyond there normal resting length

as muscle length increases passive tension continuosly increases

39
Q

How does an increase in afterload effect the stroke volume?

How does preload change secoondarily due to this ?

A

Increase afterload reduces stroke volume (because increased left ventricular diastolic pressure and resistance for ventricles to act against to eject blood =less blood ejected)

This means that the preload increases =increased stretch of the heart=increase contraction(Frank sterling law)=increased heart rate

The increase in heart rate compensates for the decrease in stroke volume to maintain the same cardiac output (cardiac output =heart ratex stroke volume)

Bioregulatory systems 3 (11 decks)

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