Cardiac Output: Lecture 7 Flashcards

1
Q

How is the heart rate regulated?

A

PNS and SNS

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2
Q

What are the 3 factors regulating the stroke volume?

A
  1. Cardiomyocyte length-tension relationship
  2. Frank-Starling mechanism
  3. SNS
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3
Q

What is the default pacemaker heart rate?

A

100

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4
Q

What is the resting heartbeat?

A

70

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5
Q

What is the cardiac output formula?

A

Q = HR x SV

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6
Q

How do we calculate stroke volume?

A

end of diastole - end of systole

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7
Q

What are the units of stroke volume?

A

ml/beat

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8
Q

Does our cardiac output increase when exercising?

A

yessir both HR and SV will increase

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9
Q

What is the negative regulator of the heart rate?

A

PNS

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10
Q

What is a positive regulator of the heart rate?

A

SNS

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11
Q

What are the 2 positive regulators of stroke volume

A
  1. Extrinsic control
    - SNS
  2. Intrinsic control
    - end-diasolic volume
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12
Q

True or False
If we increase SNS activity that will increase venous return which will increase end-diastolic volume

*What kind of feedback loop is this?

A

true, positive feedback loop

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13
Q

Which kind of cells have autorhythmic potential?

A

SA and AV node cells

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14
Q

Which kind of cells are non-autorhythmic cells?

A

cardiac muscle cells

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15
Q

Which kind of cells are non-contractile?

A

SA and AV node cells

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16
Q

Which cells are contractile?

A

Cardiac muscle cells

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17
Q

Which cells regulate stroke volume?

A

cardiac muscle cells

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18
Q

Which cells regulate heart rate?

A

SA and AV node cells

19
Q

Is stroke volume dictated by changes in action potential?

A

no, it is dictated by changes in the excitation-contraction coupling (specifically changes in calcium)

20
Q

To slow or increase the heart rate we need to change what?

A

pacemaker activity

21
Q

If we slow down the pacemaker potential what happens to the heart rate?

A

slower heart rate

22
Q

If we speed up/increase the pacemaker potential what happens to the heart rate?

A

increase the heart rate

23
Q

How does the PNS slow down the heart rate using ions?

A
  • increase the amount of K+ efflux (pushing K+ outside of the cell), which will drive the membrane potential negative

ie. making it further away from the threshold potential

  • decrease the amount of Na+ influx into the cell (keeping sodium ions outside of the cell), making it more negative
  • decrease the amount of Ca2+ entering the cell
24
Q

With PNS does the threshold potential change?

24
Q

How does the PNS slow the heart rate down? what does it use?

A

increased acetylcholine

25
Q

How does the SNS speed up the heart rate? what does it use?

A

increased norepinephrine and increased epinephrine

26
Q

How does the SNS speed up the heart rate using ions?

A
  • increase the influx of Na+ and Ca2+
    more sodium from outside the cell is going into the (negative) inside the cell, more Ca goes through the T-type calcium channel
  • much faster rise in the resting membrane potential towards the threshold potential
27
Q

True or False
PNS and SNS are only changing the pacemaker potential

28
Q

What is the difference between the PNS and SNS when it comes to speeding and slowing down the heart rate?

A
  • PNS affects K+ as it increases the efflux of K+
29
Q

Can we have both PNS and SNS β€œon” at the same time about affecting the heart rate?

A
  • yes they can both be on however one will be more dominant at any given time
30
Q

What is the key regulator of stroke volume?

A
  • cardiac muscle cell, ventricular contraction
    how much blood is being pumped out of the heart
31
Q

What is the intrinsic control that regulates stroke volume?

A

end-diastolic volume

32
Q

True or False
Stroke volume is determined mainly by end-diastolic volume + venous return

33
Q

When measuring the length-tension curve for skeletal muscle what is on the x and y axis?

A

x-axis: length of sarcomere in percentage
y-axis: tension/force

34
Q

How do we generate a maximum amount of force in skeletal muscle?

A

if each myosin head is binging with an active site on actin, the most number of cross-bridges formed

35
Q

When our muscles are stretched are we going to have lots of cross-bridges forming? why or why not?

A
  • NO
  • actin and myosin are stretched apart and therefore there is not much overlapping of the two
36
Q

What does the Frank-Straling Mechanism represent?

A

length-tension relationship of cardiac muscle

36
Q

When our muscles are shortened are we going to have lots of cross-bridges forming? why or why not?

A
  • NO
  • now the actin filaments are overlapping with fellow actin and therefore hide the active sites for the myosin to interact
37
Q

What is on the x and y axis for the length-tension relationship of cardiac muscle?

A

x-axis: End-diastolic volume
y-axis: Stroke volume

38
Q

Can we ever overly stretch the heart?

A

No, not possible

39
Q

What is the extrinsic control of stroke volume?

40
Q

If we use the SNS to increase the Calsium release in every cardiac muscle cell what happens to the stroke volume?

A
  • increase the amount of Ca2+ entering the cell via the L-type calcium channel which releases more calcium to bind the the Ryanoide receptor, thus increasing more calcium causing the stork volume to increase
41
Q

When the stroke volume increases due to SNS, is the end-diastolic volume also increasing?

42
Q

The contraction time in the heart goes from ________ to _______ with stimulation of the SNS

A

300ms to 250ms