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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
How does the vagus nerve decrease HR? In terms of ion movement t
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
26
Why does increased K+ cause Hr to decrease?
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
27
What does the membrane potential decrease by during vagal stimulation
Becomes 65 to -75 mV instead of - 55 to -60 mV
28
Does the parasympathetic NS extend or shorten duration of diastole and ventricular filling?
Extend
29
Does the sympathetic NS extend or shorten duration of diastole and ventricular filling?
Shorten
30
SV is intrinsically proportional to EDV t/f?
True
31
What is stroke volume?
The volume of blood pumped by ventricles during systole
32
How do you calculate Stroke volume?
EDV-ESV = SV
33
What is the Frank-Starling law?
The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
34
An increase in inotrophy is manifested as an increase in maximal dP/dt t/f?
True
35
What causes changes in ejection fraction?
Changes in inotrophy
36
What is ejection fraction?
The % of EDV ejected from the heart
37
Explain the frank-starling mechanism
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
How does stretching of myocytes increase contractility?
1. There is an optimum overlap of thick and thin filaments in sarcomeres 2. Troponin C has an increased affinity for calcium
39
What is the normal preload of the heart?
12mmHg
40
When can the cardiac sarcomeres be overstretched?
During heart failure when the ventricles fill with too much blood since they aren’t contracting and releasing blood into aorta/pul trunk
41
Explain how the frank-starling mechanism maintains normal cardiac output during bradycardia.
- 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
What can happen to stroke volume if blood pressure is raised?
- 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
How does the frank-starling mechanism maintain appropriate Stroke volume when someone has high blood pressure?
- 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
Can an increase in HR increase inotrophy?
Yes
45
What is the Bowditch Effect/Treppe Phenomenon
- 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
As HR increases, SV decreases, t/f? Why?
True. Reduced ventricular filling time
47
Explain the effect of increasing heart rate on cardiac output.
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
What is sick sinus syndrome?
When the pacemaker cells depolarise at a far slower rate than normal, decreasing HR
49
Why does CO fall in patients with very slow HR/bradycardia?
Because EDV is increased due to slow heart rate, ventricular sarcomeres become overstretched. Also the pericardium limits ventricular filling
50
What is atrioventricular block?
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
What are 2 defects of the pacemaker cells which cause excessively slow HR/bradycardia?
- slow sinus rhythm / sick sinus syndrome - atrioventricular block
52
How do you treat slow sinus rhythm / atrioventricular block?
Installing a pacemaker
53
How can the sympathetic NS increase contractility?
- 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
What are L -Type Ca++ channels?
Voltage gated Ca++ channels
55
How does increases influx of Ca++ into myocytes affect the fast response?
- prolongs the plateau phase of fast response - stronger contraction on sarcomeres in myocytes
56
What is isopreterenol?
A β adrenergic receptor agonist
57
How does vagal stimulation affect contractility?
- 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
What are more important in regulating ventricular myocytes contractility, parasympathetic or sympathetic effects?
Sympathetic
59
What is a positive inotrophy effect?
When contractility is increased
60
What is a negative inotrophic effect?
When contractility decreases
61
What factors increase inotrophy?
- sympathetic activation - circulating catecholamines - heart rate (bowditch effect) - afterload - parasympathetic NS inhibition
62
How do circulating catecholamis increase contractility?
Adrenaline can bind to B1 adrenergic receptors
63
What is the Fick’s principle equation ?
[O2]pul artery + [O2]alveoli = [O2]pul vein
64
What symbol is usually used to denote cardiac output?
Q
65
What is VO2?
O2 consumption per minute
66
How do you measure VO2?
Measure the volume and O2 context of expired air per minute.
67
How do you measure [O2]pul vein when measuring CO?
Measure it from an arterial blood sample, since O2 conc in pul vein is the same as in arteries
68
How do you measure [O2]pul artery when measuring CO?
Collect a blood sample from right ventricle/pulmonary artery via a catheter inserted up the brachial vein
69
What is the equation for calculating CO using Fick’s Law?
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
What is a method used to determine cardiac output in a non invasive way?
Doppler echocardiography
71
How does Doppler echocardiography work?
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
What are cardiac factors in relation to regulation of CO?
Factors which are intrinsic to the heart: - Heart rate - Myocardial contractility
73
What are coupling factors in relation to regulation of cardiac output?
Interactions of the heart with blood vessels: - preload - afterload

FM1020 (11 decks)

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