Cardiac Function 2 Flashcards

1
Q

What is CO (or Q)?

A
  • cardiac output

- volume of blood pumped out by each ventricle per minute

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2
Q

CO =

A

SV (stroke volume) x HR

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3
Q

Average CO =

A

~5 L/min at rest

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4
Q

Average blood volume in body =

A

~5.5 L

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5
Q

How is CO controlled?

A
  • through regulation of HR and SV

- extrinsic and intrinsic regulation

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6
Q

What are extrinsic mechanisms? Give an example.

A
  • from external

- neural and hormonal

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7
Q

What are intrinsic mechanisms?Give an example.

A
  • from within

- autoregulation

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8
Q

How is HR determined?

A

by SA node firing frequency

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9
Q

SA node intrinsic firing rate = . This means that HR =

A
  • 100/min

- no extrinsic control on heart; HR = 100

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10
Q

SA node is under control of ____ and ______.

A
  • ANS

- hormones

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11
Q

What system dominates HR changes at rest?

A
  • parasympathetic system

- HR = 75

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12
Q

What system dominates HR changes during excitement/exercise?

A
  • sympathetic system

- HR increases

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13
Q

Describe how increased sympathetic activity leads to increased heart rate.

A
  • increased sympathetic activity (nerves or epinephrine)
  • targets SA node
  • opens funny & Ca 2+ channels
  • increase rate of AP firing
  • increase heart rate
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14
Q

In looking at the effects of the autonomic nervous system on SA nodal cell potentials, the slope of the depolarization period to threshold is…

A

steep

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15
Q

In looking at the effects of the autonomic nervous system on SA nodal cell potentials, how does is slowly turn into parasympathetic?

A
  • slope slowly decreases

- membrane potential slowly decreases

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16
Q

Describe how increased parasympathetic activity leads to decreased heart rate.

A
  • increased parasympathetic activity
  • targets SA node
  • K+ channels open; Ca 2+ channels close
  • decrease rate of AP firing and hyperpolarize cell
  • decrease heart rate
17
Q

How does epinephrine effect HR?

A
  • same effect as sympathetic nervous system
  • increases action potential frequency at SA node
  • increases velocity of action potential conduction in muscle fibres
18
Q

How do thyroid hormones, glucagon, and insulin have an effect on HR?

A

contraction

19
Q

Activity of sympathetic neurons projecting to SA node does what to HR?

A

raises HR

20
Q

Activity of parasympathetic neurons projecting to SA node does what to HR?

A

lowers HR

21
Q

Levels of circulating epinephrine does what to HR?

A

raises HR

22
Q

What are the 3 primary factors affecting stroke volume?

A
  • ventricular contractility
  • end-diastolic volume
  • afterload
23
Q

Describe the influence of ventricular contractility.

A
  • more forceful contraction will expel more blood

- sympathetic control of ventricular contraction

24
Q

Describe the sympathetic control of ventricular contraction.

A
  • sympathetic innervation of muscle cells

- Norepinephrine → β1 adrenergic receptors → cAMP

25
Q

Describe the second-messenger system.

A
  • augment open Ca 2+ channels
  • increase Ca 2+ release from sarcoplasmic reticulum (SR)
  • increase myosin ATPase rate
  • enhance rate of Ca 2+ - ATPase activity on SR
26
Q

With changes in ventricular contractility induced by sympathetic activity, what goes up?

A

tension

27
Q

Describe how parasympathetic innervation of contractile cells effects stroke volume.

A

not significant

28
Q

Describe how hormones affect stroke volume.

A
  • epinephrine binds to adrenergic receptors

- thyroid hormones, insulin, and glucagon increase force of contraction

29
Q

What is Starling’s law (Frank Starling law)?

A
  • influence of end-diastolic volume on stroke volume

- output (SV) = input (VR)

30
Q

Describe how according to Starling’s law, increased EDV leads to increased SV.

A
  • increased EDV (VR) stretches muscle fibres
  • fibres closer to optimal length
  • optimal length = greater strength of contraction
  • result = increased SV
31
Q

Name 2 factors affecting EDV.

A
  • end diastolic pressure = preload

- afterload

32
Q

What makes up end diastolic pressure (preload)?

A
  • filling time
  • atrial pressure
  • central venous pressure
33
Q

What is afterload?

A

pressure in aorta during ejection

34
Q

Increased venous return results in…

A
  • increased EDV

- increased SV

35
Q

Increased sympathetic activity or epinephrine results in…

A
  • increased contractility

- increased SV

36
Q

Decreased arterial pressure (afterload) results in …

A

increased SV