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
How does the PNS slow the heart rate down? what does it use?
increased acetylcholine
25
How does the SNS speed up the heart rate? what does it use?
increased norepinephrine and increased epinephrine
26
How does the SNS speed up the heart rate using ions?
- 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
True or False PNS and SNS are only changing the pacemaker potential
True
28
What is the difference between the PNS and SNS when it comes to speeding and slowing down the heart rate?
- PNS affects K+ as it increases the efflux of K+
29
Can we have both PNS and SNS "on" at the same time about affecting the heart rate?
- yes they can both be on however one will be more dominant at any given time
30
What is the key regulator of stroke volume?
- cardiac muscle cell, ventricular contraction how much blood is being pumped out of the heart
31
What is the intrinsic control that regulates stroke volume?
end-diastolic volume
32
True or False Stroke volume is determined mainly by end-diastolic volume + venous return
True
33
When measuring the length-tension curve for skeletal muscle what is on the x and y axis?
x-axis: length of sarcomere in percentage y-axis: tension/force
34
How do we generate a maximum amount of force in skeletal muscle?
if each myosin head is binging with an active site on actin, the most number of cross-bridges formed
35
When our muscles are stretched are we going to have lots of cross-bridges forming? why or why not?
- NO - actin and myosin are stretched apart and therefore there is not much overlapping of the two
36
What does the Frank-Straling Mechanism represent?
length-tension relationship of cardiac muscle
36
When our muscles are shortened are we going to have lots of cross-bridges forming? why or why not?
- NO - now the actin filaments are overlapping with fellow actin and therefore hide the active sites for the myosin to interact
37
What is on the x and y axis for the length-tension relationship of cardiac muscle?
x-axis: End-diastolic volume y-axis: Stroke volume
38
Can we ever overly stretch the heart?
No, not possible
39
What is the extrinsic control of stroke volume?
SNS
40
If we use the SNS to increase the Calsium release in every cardiac muscle cell what happens to the stroke volume?
- 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
When the stroke volume increases due to SNS, is the end-diastolic volume also increasing?
Naurr
42
The contraction time in the heart goes from ________ to _______ with stimulation of the SNS
300ms to 250ms