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Feedback control & physiology > Force generation by the heart > Flashcards

Force generation by the heart Flashcards

1
Q

what are striations caused by?

A

regular arrangements of contractile protein

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2
Q

what are cardiac myocytes electrically coupled with?

A

gap junctions

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3
Q

what are gap junctions?

A

protein channels which form low resistance electrical communication pathways between neighbouring myocytes
- they ensure that each electrical excitation reaches all the cardiac myocytes

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4
Q

where are desmosomes found?

A

within intercalated discs

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5
Q

what is purpose of desmosomes?

A

provide mechanical adhesion between adjacent cardiac cells
- They ensure that the tension developed by one cell is transmitted to the next

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6
Q

simply what is purpose of gap junctions & desmosomes?

A

gap junctions = allow spread of action potential
desmosomes = allow adhesion

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7
Q

what is actin?

A

(thin filaments) causes the lighter appearance in myofibrils & fibers

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8
Q

what is myocyin?

A

(thick filaments) cause the darker appearance

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9
Q

what are myofibrils?

A
  • they are found inside cardiac muscle cells (like lots of tubes in a muscle fibre)
  • contain alternating segments of thick & thin protein filaments
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10
Q

what are sarcomeres?

A

each myofibril = has several sarcomeres

sarcomere is the area between actin (between light & dark on myofibril)

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11
Q

what is the sliding filament theory?

A

explanation of how muscle shortens and produces force
= overlap of actin and myosin filaments, shortening the sarcomere

  • calcium needs to bind to troponin to change conformation so exposed binding site on actin for myocyin
  • myocyin heads cross-bridge and bind to actin which then makes conformational change resulting in the overlap - thin filament pulled inward during contraction
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12
Q

what are the 2 requirements for cross bridging in muscle contraction?

A
  • ATP
  • calcium
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13
Q

what is tropomyosin and troponin?

A

they physically cover myocyin binding site on actin
- when muscle relaxed tropomyosin and troponin cover binding site
(Ca2+ binds to change conformation and uncover)

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14
Q

where does calcium get released from in action potential - so it can bind to troponin and tropomyosin?

A
  • released from sarcoplasmic reticulum
  • the release of Ca2+ from SR is dependent on the presence of extra-cellular Ca2+
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15
Q

what happens with calcium once action potential passed?

A
  • Ca2+ influx ceases
  • Ca2+ re-sequestered in SR by Ca2+ ATPase & heart muscle relaxes
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16
Q

what is the importance of the long refractory period?

A

so muscle can’t contract before other contraction finished so not sustained contraction as sustained contraction bad for heart (tetanic contraction)
→because if you could produce another action potential then loop would just keep going and sustained contraction

= by the time it’s ready to produce another action potential - contraction already over so it’s all good to contract again

17
Q

what is a refractory period?

A

period following action potential where it isn’t possible to produce another action potential

18
Q

what is stroke volume?

A

the volume of blood ejected by each ventricle per heart beat

19
Q

how to calculate stroke volume?

A

SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV)

20
Q

what is stroke volume regulated by?

A

INTRINSIC and EXTRINSIC mechanisms

21
Q

what is diastolic length/stretch of myocardial fibers determined by?

A

the end diastolic volume = the volume of blood within each ventricle at the end of diastole

22
Q

what determines the cardiac preload?

A

= end diastolic volume

23
Q

what is the cardiac preload?

A

the diastolic length/diastolic stretch of myocardial fibers
= the force that stretches the cardiac muscle prior to contraction

24
Q

what is relationship between end diastolic volume and venous return?

A

end diastolic volume is determined by the venous return to the heart (larger EDV means larger cardiac preload)

25
Q

what is Frank-Starling relationship?

A

describes the relationship between end diastolic volume and stroke volume (directly proportional)

26
Q

what does the Frank-Starling mechanism and Starlings law state?

A

the more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)

27
Q

what are 2 factors increased by stretch muscle?

A
  • move toward optimum length (stretch muscle in heart always moves towards optimal length unlike skeletal muscle where there is overstretch)
  • increase affinity of troponin for Ca2+
28
Q

what does starlings law say about stroke volume of RV and LV?

A
  • If venous return to right atrium increases, EDV of right ventricle increases
  • Starling’s Law leads to increased SV into pulmonary artery
  • Venous return to left atrium from pulmonary vein increases, EDV of left ventricle increases
  • Starling’s Law leads to increased SV into aorta

*so saying that increase in right →increase in left too

29
Q

what is afterload?

A

the resistance into which heart is pumping

30
Q

what is the extra load?

A

imposed AFTER the heart has contracted

31
Q

what is affect of increased afterload?

A
  • at first, heart unable to eject full SV, so EDV increases
  • If increased AFTERLOAD continue to exist (e.g. untreated hypertension), eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
32
Q

what is positive inotropic effect?

A

stimulation of sympathetic = increase force of contraction

33
Q

what is the inotropic effect of noradrenaline on ventricular contraction?

A
  • force of contraction increases (activation of calcium channels = calcium influx)
  • effect is mediated by cAMP
  • The peak ventricular pressure rises
  • Rate of pressure change (dP/dt) during systole increases
  • This reduces the duration of systole
  • Rate of ventricular relaxation increases (increased rate of Ca2+ pumping)
  • this reduced duration of diastole
34
Q

what is cardiac output?

A

The volume of blood pumped by each ventricle per minute is known as the Cardiac Output (CO)

35
Q

what is resting CO in a healthy adult?

A

approximately 5 litres per minute (70 ml SV x 70 beats per minute = 4900 ml CO)

36
Q

how do you calculate CO?

A

CO = SV x HR

37
Q

does vagal stimulation influence contraction?

A

NO - influences rate not force of conraction

38
Q

where are adrenaline & noradrenaline released from?

A

adrenal medulla - they have inotropic & chronotropic effect

39
Q

what is inotropic?

A

modifying the force or speed of contraction of muscles

Feedback control & physiology (13 decks)

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