Force generation by the heart Flashcards

1
Q

What causes the striation of cardiac muscle?

A

regular arrangement of contractile protein within the cardiac muscle cells

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2
Q

What ensures that the electrical excitation reaches all of the cardiac myocytes?

A

Gap junctions

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3
Q

What are desmosomes?

A

structures within the intercalated discs 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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4
Q

what are myofibrils?

A

Intracellular organelles in the muscle fibres. They are the contractile units of the muscle

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5
Q

What is a sarcomere?

A

it is the functional unit of the muscle. Actin and myosin are arranged into sarcomeres within each myofibril

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6
Q

What is the functional unit of a cell?

A

The smallest unit that can do all the functions of the tissue

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7
Q

How do muscles contract?

A

Sliding of the actin filaments on the myosin filaments.

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8
Q

What has to be present for cross bridges to generate?

A

ATP

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9
Q

What two molecules must be present for contraction and relaxation of muscle?

A

ATP and Ca++

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10
Q

How does calcium switch on cross bridge formation?

A
  • myosin binding sites on actin are covered by regulatory proteins (troponin and tropomyosin)
  • when calcium binds to these regulatory proteins, it causes a conformational change causing the proteins to release from the myosin binding site on actin.
  • Thereby allowing myosin to form a cross bridge
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11
Q

Where is calcium stored in cardiac muscle cells?

A

in the lateral sacs of the sarcoplasmic reticulum

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12
Q

What is required for SR to release calcium?

A

The presence of extra cellular Ca++

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13
Q

What happens when there is not enough intracellular calcium?

A

Muscles relax

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14
Q

What happens during the plateau phase of action potential?

A

Calcium will flow through the L type Ca++ channels into the cardiac myocytes. This will then cause SR to release calcium

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15
Q

What happens when the action potential has passed?

A

, Ca++ influx ceases, Ca++ re-sequestered in SR by Ca++-ATPase, heart muscle relaxes

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16
Q

True/ False. During the plateau phase of ventricular action potential, the Na+ channels are in the hyperpolarised, open state

A

False,
During the plateau phase of ventricular action potential the Na+ channels are in the depolarised closed state i.e. they are not available for opening

17
Q

What is the benefit of the long refractory period?

A

To protect the heart muscle via preventing generation of tetanic contractions.

18
Q

What is the long refractory period?

A

is a period following an action potential in which it is not possible to produce another action potential

19
Q

True/False. During the descending phase of action potential the K+ channels are open and the membrane can not be depolarised

A

True

20
Q

What is stroke volume?

A

This is defined as “the volume of blood ejected by each ventricle per heart beat”

21
Q

What is the equation for Stroke volume?

A

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

22
Q

What is the stroke volume regulated by>

A

Intrinsic and extrinsic mechanisms.

  • intrinsic- within the heart muscle itself
  • extrinsic- nervous, hormonal control
23
Q

What causes changes in stroke volume?

A

changes in the DIASTOLIC LENGTH of MYOCARDIAL FIBERS

24
Q

What is the end diastolic volume?

A

the volume of blood within each ventricle at the end of diastole.
-It is determined by the venous return to the heart

25
Q

What is the cardiac preload?

A

How much the heart is loaded with blood before it contracts

26
Q

What is the Starling’s law of the heart?

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 does Afterload mean?

A

Resistance into which the heart is pumping

28
Q

How does the body respond to increased afterload?

A
  • increased afterload leads to decreased stroke volume and therefore EDV increases to compensate
  • hypertrophy is afterload increases over time.
29
Q

What is a positive inotropic effect?

A

Increase in the force of contraction

30
Q

What are the effects of noradrenaline on ventricular contraction?

A

Leads to a stronger and faster contraction.

  • force of contraction increases by activation of Ca channels
  • peak ventricular pressure rises
  • rate of pressure change during systole increases
  • reducing the duration of systole
  • rate of ventricular relaxation increases
  • this reduces the duration of diastole
31
Q

Any end diastolic value will lead to an increased stroke volume if sympathetic stimulation occurs. T/F?

A

True

32
Q

What is the extrinsic control of stroke volume?

A

Hormones adrenaline and noradrenaline are released from adrenal medulla and have inotropic and chronotropic effects

33
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute

34
Q

What is the equation for cardiac output?

A

CO=SV x HR