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FM1020 > PHYSIOLOGY - Cardiac Output > Flashcards

PHYSIOLOGY - Cardiac Output Flashcards

1
Q

Cardiac output definition

A

Volume of blood pumped per minute by each ventricle

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2
Q

Cardiac output equation

A

HR x SV = cardiac output

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3
Q

Normal cardiac output value

A

5 - 5.5 litre/min

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4
Q

How can heart rate and stroke volume be regulated ?

A

Autonomic nervous system

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5
Q

How does the ANS know when to stimulate the heart ?

A
  1. Sensory information relayed to hypothalamus
  2. Hypothalamus integrates this information and regulates the activity of the cardiac control centres
  3. Cardiac control centres alter HR, contractility and arterial pressure via ANS
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6
Q

Where are the cardiovascular control centres located?

A

Reticular regions of the Medulla oblongata and the pons

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7
Q

What is the parasympathetic nerve which stimulates the heart?

A

Vagus nerve / CN X

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8
Q

What do post-ganglionic sympathetic nerves innervate in the heart?

A

SA node
AV node
Contractile atrial and ventricular tissue

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9
Q

What do the postganglionic parasympathetic nerves innervate?

A

SA node
AV node
SOME contractile tissue in atria and ventricle

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10
Q

Does the parasympathetic or the sympathetic NS have more control over the atrial and ventricular contractile fibres?

A

Sympathetic

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11
Q

Is the ANS needed for generation of APs in slow response cardiac cells?

A

No

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12
Q

What neurotransmitter do sympathetic nerves release to the heart?

A

Noradrenaline

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13
Q

What neurotransmitter to parasympathetic nerves release to the heart?

A

ACh

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14
Q

What would happen to heart rate if you inhibited the sympathetic nerves?

A

It would decrease to about 30% below normal - at rest, sympathetic nerves discharge at a slow rate that maintains HR at 60-70 BPM

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15
Q

What would happen to heart rate with strong sympathetic stimulation?

A

HR would increase to about 180-200 BPM (In young adult humans)

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16
Q

What happens if you increase vagal activity?

A

HR will reduce

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17
Q

What would happen if you intensely stimulated the vagus nerve (e.g in an experiment)

A
  • The heartbeat would stop for a few seconds
  • The heart would usually restart and beat at about 20-40 BPM. This is vagal escape
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18
Q

Explain vagal escape.

A
  • if HR = 0, cardiac output = 0
  • reduction in CO triggers reflex stimulation of sympathetic nerves caused by baroreceptor reflex

-simultaneous sympathetic and vagal activity results in a HR of 20-40 BPM

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19
Q

What is physiologically more important, symp or parasymp stimulation?
Why?

A

Parasympathetic.
Because it exerts a more immediate response.

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20
Q

How does the sympathetic nervous system increase heart rate? Generally

A

It causes increased ion flow through HCN channels. This increases the rate of autorythmic depolarisation and hence the HR

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21
Q

What are the proper names for the HCN channals?

A

if Na+ channels

iCa Ca2+ channels

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22
Q

What does noradrenaline released from sympathetic nerves bind to on the heart?

A

B1 adrenergic receptors on pacemaker cells

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23
Q

What happens when norepinephrine binds to pacemaker cells?

A
  • cAMP levels rise
  • cAMP binds to if Na+ channels

-PKA activity increases
- PKA phosphorylates if Ca++ channels

  • HCN channels are more open
  • Spontatneous depolarisation rate in SA node increased
  • transmission of impulse through AV node also increased due to increased permeability of ion channels
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24
Q

Describe the adenyl-cyclise/cAMP intracellular signalling pathway.

A
  1. Noradrenaline binds to B1 adrenergic receptor
  2. Adenyl cyclase is stimulates
  3. Adenyl cyclase converts ATP to cAMP
  4. cAMP converts inactive PKA to active PKA
  5. PKA phosphorylates a protein which causes a cell response
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25
Q

How does the vagus nerve decrease HR? In terms of ion movement t

A
  1. Releases ACh
  2. ACh binds directly to and activates ACh gated K+ channels
  3. ACh binds to M2 muscarinic receptors which inhibits cAMP production.
  4. Opening of HCN channels is decreased
  5. Hyperpolarisation happens in AV node as well, resulting in slowed transmission of impulse to ventricles
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26
Q

Why does increased K+ cause Hr to decrease?

A

The membrane potential becomes more negative, so more + ions are needed to depolarise the cells

Also because HCN channels are more closed than normal during vagal stimulation, rate of + ions influx is slower

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27
Q

What does the membrane potential decrease by during vagal stimulation

A

Becomes 65 to -75 mV instead of - 55 to -60 mV

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28
Q

Does the parasympathetic NS extend or shorten duration of diastole and ventricular filling?

A

Extend

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29
Q

Does the sympathetic NS extend or shorten duration of diastole and ventricular filling?

A

Shorten

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30
Q

SV is intrinsically proportional to EDV t/f?

A

True

31
Q

What is stroke volume?

A

The volume of blood pumped by ventricles during systole

32
Q

How do you calculate Stroke volume?

A

EDV-ESV = SV

33
Q

What is the Frank-Starling law?

A

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

34
Q

An increase in inotrophy is manifested as an increase in maximal dP/dt t/f?

A

True

35
Q

What causes changes in ejection fraction?

A

Changes in inotrophy

36
Q

What is ejection fraction?

A

The % of EDV ejected from the heart

37
Q

Explain the frank-starling mechanism

A
  1. Increase in EDV results in increased stroke volume
  2. Increase in EDV increases ventricular pressure, which stretches ventricular myocytes
  3. Increased stretch on myocytes causes increased contractility
  4. Increased contractility means a higher SV
38
Q

How does stretching of myocytes increase contractility?

A
  1. There is an optimum overlap of thick and thin filaments in sarcomeres
  2. Troponin C has an increased affinity for calcium
39
Q

What is the normal preload of the heart?

A

12mmHg

40
Q

When can the cardiac sarcomeres be overstretched?

A

During heart failure when the ventricles fill with too much blood since they aren’t contracting and releasing blood into aorta/pul trunk

41
Q

Explain how the frank-starling mechanism maintains normal cardiac output during bradycardia.

A
  • during bradycardia there is an increased duration of ventricular filling
  • this means there is an increased EDV
  • increased stretch = increased contractility = increased SV
  • reduction in HR is compensated by increased SV and Cardiac output remains constant
42
Q

What can happen to stroke volume if blood pressure is raised?

A
  • if bp is raised there is an increased afterload
  • this delays opening of semilunar valves and ventricular ejection
  • ventricles have to contract for longer to open semilunar valves
  • this causes a reduction in SV and an increase in ESV
43
Q

How does the frank-starling mechanism maintain appropriate Stroke volume when someone has high blood pressure?

A
  • increased ESV means that there will be an increased EDV during the following cycle due to constant venous return
  • increased contractility on the heart restores SV
44
Q

Can an increase in HR increase inotrophy?

A

Yes

45
Q

What is the Bowditch Effect/Treppe Phenomenon

A
  • Increase in HR causes increase in intracellular Ca++
  • Ca++ enters the cell during the plateau phase, so if there are more APs, there are more plateau phases
  • also increased no. Of depolarisations causes more voltage gated Ca++ channels to open
46
Q

As HR increases, SV decreases, t/f? Why?

A

True.
Reduced ventricular filling time

47
Q

Explain the effect of increasing heart rate on cardiac output.

A
  1. Initial increases will elevate CO, because the increase in HR overcomes any effect of a reduction in SV
  2. At about 100-200bpm, CO will remain constant, the effect of reduction of SV is balancing the effect of increased HR
  3. At greater than 200bpm CO will decrease as ventricular filling time is severely restricted and SV becomes very low
48
Q

What is sick sinus syndrome?

A

When the pacemaker cells depolarise at a far slower rate than normal, decreasing HR

49
Q

Why does CO fall in patients with very slow HR/bradycardia?

A

Because EDV is increased due to slow heart rate, ventricular sarcomeres become overstretched.
Also the pericardium limits ventricular filling

50
Q

What is atrioventricular block?

A

When the impulse cannot spread from atria to ventricles.
The AV node then generates it’s own AP but they take longer to generate

51
Q

What are 2 defects of the pacemaker cells which cause excessively slow HR/bradycardia?

A
  • slow sinus rhythm / sick sinus syndrome
  • atrioventricular block
52
Q

How do you treat slow sinus rhythm / atrioventricular block?

A

Installing a pacemaker

53
Q

How can the sympathetic NS increase contractility?

A
  • symp nerves release noradrenaline which binds to B1 adrenergic receptors on myocytes.
  • cAMP levels increase, PKA increased
  • L-type Ca++ channels are opened for a longer time when phosphorylated by PKA
  • contractile strength increases
54
Q

What are L -Type Ca++ channels?

A

Voltage gated Ca++ channels

55
Q

How does increases influx of Ca++ into myocytes affect the fast response?

A
  • prolongs the plateau phase of fast response
  • stronger contraction on sarcomeres in myocytes
56
Q

What is isopreterenol?

A

A β adrenergic receptor agonist

57
Q

How does vagal stimulation affect contractility?

A
  • ACh released from vagus nerve
  • promotes closure of L type Ca++ channels by :
    -BInding to M2 muscarinic receptors and inhibiting cAMP production
    -inhibiting release or noradrenaline from neighbouring sympathetic nerves
58
Q

What are more important in regulating ventricular myocytes contractility, parasympathetic or sympathetic effects?

A

Sympathetic

59
Q

What is a positive inotrophy effect?

A

When contractility is increased

60
Q

What is a negative inotrophic effect?

A

When contractility decreases

61
Q

What factors increase inotrophy?

A
  • sympathetic activation
  • circulating catecholamines
  • heart rate (bowditch effect)
  • afterload
  • parasympathetic NS inhibition
62
Q

How do circulating catecholamis increase contractility?

A

Adrenaline can bind to B1 adrenergic receptors

63
Q

What is the Fick’s principle equation ?

A

[O2]pul artery + [O2]alveoli = [O2]pul vein

64
Q

What symbol is usually used to denote cardiac output?

A

Q

65
Q

What is VO2?

A

O2 consumption per minute

66
Q

How do you measure VO2?

A

Measure the volume and O2 context of expired air per minute.

67
Q

How do you measure [O2]pul vein when measuring CO?

A

Measure it from an arterial blood sample, since O2 conc in pul vein is the same as in arteries

68
Q

How do you measure [O2]pul artery when measuring CO?

A

Collect a blood sample from right ventricle/pulmonary artery via a catheter inserted up the brachial vein

69
Q

What is the equation for calculating CO using Fick’s Law?

A

Q = q2 / ( [O2]pul vein - [O2]pul artery )

Co = O2 absorbed per minute by the lungs (ml/min) \ arteriovenous O2 difference (ml/L of blood)

70
Q

What is a method used to determine cardiac output in a non invasive way?

A

Doppler echocardiography

71
Q

How does Doppler echocardiography work?

A

Ultrasound technology uses the Doppler effect to determine the direction and velocity of blood flow

SV and thus CO is calculated from the velocity of blood and the area of the aorta

72
Q

What are cardiac factors in relation to regulation of CO?

A

Factors which are intrinsic to the heart:
- Heart rate
- Myocardial contractility

73
Q

What are coupling factors in relation to regulation of cardiac output?

A

Interactions of the heart with blood vessels:
- preload
- afterload

FM1020 (11 decks)

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