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Cardio > Force Generation by the Heart > Flashcards

Force Generation by the Heart Flashcards

1
Q

Describe cardiac muscle?

A 
Striated 
No neuromuscular junctions
Protein channels which form low resistance electrical communication pathways between neighboring myocytes 
Intercalated discs - desmosomes 
Contains gap junctions
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2
Q

What causes striations?

A

Regular arrangement of contractile proteins

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3
Q

Why are there no neuromuscular junctions in the heart?

A

Because cardiac muscle does not require nervous stimulation- it is myogenic

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4
Q

What do protein channels in cardiac muscle ensure?

A

Ensure that each electrical excitation reaches all of the cardiac myocytes (All or none law of the heart)

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5
Q

What do the desmosomes between intercalated provide?

A

Provide mechanical tension between adjacent cardiac cells

they ensure the tension developed by one cell is transferred to the next cell

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6
Q

What does each muscle contain?

A

Myofibrils - contractile units of muscle

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7
Q

What do myofibrils have?

A

Alternating segments of thick and thin protein filaments (actin and myosin) actin is lighter appearance, myosin is darker

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8
Q

How are actin and myosin arranged in a myofibril?

A

Into sarcomeres (smallest functional unit of a muscle)

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9
Q

How is muscle tension produced?

A

Sliding of actin filaments on myocin filaments

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10
Q

What is the sliding filament theory?

A

Explanation of how muscle shortens and produces force

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11
Q

What does force generation depend on?

A

ATP dependant interaction between actin and myocin filaments

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12
Q

ATP is required for both contraction and relaxation. True or false?

A

True

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13
Q

What is Ca2+ required for?

A

Switching on cross bridge formation

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14
Q

Where is Ca2+ released from?

A

Sarcoplasmic reticulum

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15
Q

What is the release of Ca2+ from SR dependent on in cardiac muscle?

A

Presence of extracellular Ca2+

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16
Q

Systole- what happens with calcium?

A

Ca2+ influx during plateau phase
Ca2+ induced Ca2+ release from sarcoplasmic
reticulum
Ca2+ influx activates contractile machinery

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17
Q

What happens when an AP has passed after systole?

A

Ca++ influx ceases
Ca++ is re-sequestered in sarcoplasmic reticulum by Ca++ ATPase
Heart muscle relaxes

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18
Q

Describe the muscle fibre when relaxed?

A

No cross-bridge binding site because the cross-bridge binding site on actin is physically covered by the troponin-tropomyosin complex

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19
Q

What does the bindning of actin and myosin cross-bridge trigger?

A

Power stroke that pulls actin in during contraction

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20
Q

Describe the muscle fibre when excited?

A

Ca++ binds with troponin
Pulling troponin-tropomyosin complex aside to expose cross-bridge binding site
Cross-bridge binding occurs

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21
Q

What is the importance of a refractory period in the cardiac cycle?

A

The long refractory period is protective for the heart preventing generation of tetanic contractions in the cardiac muscle

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22
Q

What triggers contraction?

A

The ventricular muscle AP

23
Q

What is a refractory period?

A

Period following an AP in which it is not possible to produce another AP

24
Q

Theory of a refractory period?

A

During plateau phase of a ventricular AP: The Na+ channels are in the depolarised closed state- not available for opening
During the descending phase of AP- The K+ channels are open and membrane cannot be depolarized

25
Q

Define Stroke volume?

A

Volume of blood ejected from each ventricle per heart beat

26
Q

Stroke volume equation?

A

SV= End diastolic volume - end systolic volume

27
Q

What is SV regulated by?

A

Intrinsic and extrinsic mechanisms
Intrinsic= within the heart itself
Extrinsic= Nervous and hormonal control

28
Q

What are changes in stroke volume brought about by?

A

Changes in the diastolic length/diastolic stretch of myocardial fibers

29
Q

What is the diastolic length/stretch (CARDIAC PRELOAD) determined by?

A

The volume of blood within each ventricle at the end of diastole - The END DIASTOLIC VOLUME

30
Q

What is the end diastolic volume determined by?

A

Venous return to the heart

31
Q

Another name for the Frank-starling mechanism ?

A

Starling’s law of the heart

32
Q

What does the Frank starling mechanism 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)

33
Q

What relationships does Starling’s law of the heart outline?

A

Relationship between venous return, end diastolic volume and stroke volume

34
Q

What does diastolic stretch increase?

A

Affinity of troponin for Ca++

35
Q

How is optimal length achieved in cardiac muscle?

A

Stretching the muscle. In skeletal muscle it is achieved at resting muscle length

36
Q

What happens if venous return to right atrium increases?

A

EDV of right ventricle increases which leads to increased SV into pulmonary artery

37
Q

Venous return to left atrium from pulmonary vein increases?

A

EDV of left ventricle increases= larger SV into aorta

38
Q

Define afterload?

A

The resistance into which the heart is pumping

39
Q

When is the afterload imposed?

A

After the heart has contracted

40
Q

What happens if the afterload increases?

A

-At first the heart is unable to eject full SV so the end diastolic volume increases
If it continues-Eventually the ventricular muscle mass increases to overcome resistance

41
Q

What is an increase in ventricular muscle mass called?

A

Ventricular hypertrophy

42
Q

What do you call increased afterload existing continuously?

A

Hypertension

43
Q

What type of nerves is the ventricular muscle supplied by

A

Sympathetic nerve fibers

44
Q

What is extrinsic neurotransmitter?

A

Noradrenaline

45
Q

What does stimulation of sympathetic nerves do to the heart?

A

Increases the force of contraction - positive inotropic effect
Positive chronotropic effect- - increases the HR

46
Q

What does extrinsic control involve?

A

Nerves and hormones

47
Q

What does heart failure do to Frank-Starling curve?

A

Shifts it to the right

48
Q

What does sympathetic nerve stimulation do to Frank-Starling curve?

A

Shifts it to the left

49
Q

Effect of parasympathetic nerves on ventricular contraction ?

A

Very little innervation of ventricles by vagus in man- little/no effect on SV
Vagal stimulation has influence on rate not force of contraction

50
Q

Hormones that control stroke volume?

A

Adrenaline and noradrenaline
These are released from adrenal medulla and have inotropic and chronotropic effects
The effects are normally minor compared to effects of noradrenaline from sympathetic nerves

51
Q

Define cardiac output?

A

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

52
Q

CO equation?

A

CO= SV x HR

53
Q

What is the resting CO in a healthy adult?

A

5 litres per minute

Cardio (36 decks)

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