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Flashcards in cardiac control 2 Deck (45)
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1
Q

stroke volume =

A

EDV - ESV

2
Q

cardiac output =

A

SV x HR

3
Q

blood pressure =

A

Q(cardiac output) x TPR(total peripheral resistance)

4
Q

venous volume distribution is affected by?

A

peripheral venous tone, gravity, skeletal muscle pump and breathing

5
Q

what does central venous pressure determine?

A

determines the amount of blood flowing back to the heart

this in turn determines stroke volume

6
Q

flow is primarily changed by?

A

altering vessel radius

since constriction reduces compliance and venous return

7
Q

F = (Poiseuille’s equation)

R inversely proportional to?

A

§ Remember the two important equations and relationships:
𝐹= Δ𝑃/𝑅
𝑅 ∝ 1/𝑟^4

8
Q

Autoregulation =

A

Autoregulation = the intrinsic capacity to compensate changes in perfusion pressure by changing vascular resistance.

9
Q

Myogenic Theory –

A

Smooth muscle responds directly to tension changes in the vessel wall e.g. stretch sensitive receptors.

10
Q

Metabolic Theory –

A

As blood flow decreases, metabolites accumulate and vessels dilate in response.

11
Q

Injury Theory –

A

Serotonin release from platelets causes vasoconstriction.

12
Q

examples of local mechanisms regulating blood flow

A

autoregulation
myogenic theory
metabolic theory
injury

13
Q

local endothelium derived hormones

A
  1. Nitric Oxide (NO) – vasodilation, produced from arginine, NO diffuses into vascular smooth muscle cells
  2. Prostacyclin- vasodilator, synthesised from prostacyclin precursor, also has an antiplatelet and anticoagulant effects
  3. Thromboxane A2 – vasoconstrictor, synthesised from prostacyclin precursor, also heavily synthesised in platelets
  4. Endothelins – POTENT vasoconstrictors. generated from the nucleus of endothelial cells- has minor vasodilator effects but principally a vasoconstrictor
14
Q

circulating non-endothelium derived hormones

A
  1. Kinins: binds to receptors on endothelial cells and stimulate NO synthesis- vasodilator effects
  2. ANP (arterial natriuretic peptide): Secreted from the atria in response to stretch. Vasodilator effects to reduce BP.
  3. Circulating Vasoconstrictors: ADH/Vasopressin from posterior pituitary in response to high blood osmolality. binds to V1 receptors on smooth muscles and causes vasoconstriction.
    Angiotensin II from renin secretion: potent vasoconstrictor product from the renin-angiotensin-aldosterone axis. Also stimulates SNS activity and ADH secretion.
15
Q

Autonomic nervous system includes 2 branches

A

parasympathetic and sympathetic

16
Q

SNS is important in?

A

SNS is important in controlling the circulation.

17
Q

PNS is important in?

A

§ PNS is important in regulating heart rate.

18
Q

Sympathetic innervation to blood vessels:

A

Sympathetic innervation to blood vessels:
§ SNS nerve fibres innervate ALL vessels except capillaries, pre-capillary sphincters and some metarterioles.
§ Distribution of fibres is variable, more fibres innervate vessels to kidney, gut spleen and skin and less innervate skeletal muscle and the brain.

19
Q

pre-ganglionic fibres use what as their neurotransmitter?

A

ACh

20
Q

PNS post ganglionic NT

A

ACh

21
Q

SNS post ganglionic NT

A

NA

22
Q

noradrenaline prefers to bind to what receptors?

A

preferentially binds to alpha-1 adrenoceptors to cause smooth muscle contraction/vasoconstriction.

Circulating adrenaline binds with high affinity to smooth muscle beta-2-adrenoreceptors to cause vasodilation in some organs, however the effect is very concentration-dependent

At high concentrations, adrenaline can bind to ALPHA adrenoreceptors which can override the vasodilatory effects of the beta-2-adrenoreceptor stimulation and produce vasoconstriction

The constriction you see in blood vessels is an alpha-1-adrenoreceptor effect

23
Q

vasomotor centre location

A

VMC is located bilaterally in the reticular substance of the medulla and the lower third of the pons

24
Q

The VMC consists of a:

A

Vasoconstrictor Area (Pressor)

Vasodilator Area (Depressor)

Cardioregulatory Inhibitory Area

25
Q

what do each of the different parts do?

  • higher centres of the brain
  • lateral portions of the VMC
  • medial portion of the VMC
A

Higher centres in the brain (such as the hypothalamus) can exert excitatory and inhibitory effects on the VMC

Lateral Portions of the VMC controls heart activity by influencing heart rate and contractility

Medial Portions of the VMC transmits signals via the vagus nerve to the heart that tends to decrease heart rate

The VMC allows an anticipatory response to exercise - your heart rate and ventilation rate will go up slightly before exercise because of these higher sensors in the brain

26
Q

nervous control of vessel diameter- how does it work?

A

Blood vessels receive sympathetic postganglionic innervation
The neurotransmitter involved is NORADRENALINE
There is ALWAYS some tonic activity

At baseline, there is a certain frequency of the impulses which maintains vasomotor tone

If you increase the nerve traffic then you can constrict the vessel

If you decrease the nerve traffic then you can dilate the vessel

So by altering this activity you can make the vessel either dilate or constrict

There is NOT much parasympathetic innervation of the vascular system

27
Q

Control of Blood Vessel Radius

THREE areas allow control of vessel radius:

A

Local Controls (Autoregulation)

Circulating Hormones

Sympathetic Vasoconstrictor Nerves

28
Q

cardiac innervation by dual innervation

what are they and how do they work?

A

dual innervation - sympathetic and parasympathetic

The sinoatrial nodal cells receive sympathetic and parasympathetic innervation

Normal resting heart rate is around 70 bpm

Parasympathetic slows heart rate down because acetylcholine decreases the gradient of the pacemaker potential - this means that the potential takes longer to reach threshold and fire

Sympathetic increases heart rate because adrenaline and noradrenaline increases the gradient of the pacemaker potential so threshold is reached more quickly

If we cut the sympathetic nerves we lose the ability to increase heart rate so heart rate falls

29
Q

with no cardiac innervation what is the normal activity?

A

100bpm

30
Q

controlling force of contraction can be increased using which law?

A

Force of contraction can be increased by Starling’s Law

31
Q

how does controlling force of contraction work using sympathetic activity?

A

Sympathetic activity will also increase the force of contraction

Noradrenaline binds to Adrenoreceptors which increases the amount of cAMP which activates PKA which phosphorylates the L-type calcium channels and the SR calcium release channel and SERCA

So you get MORE CALCIUM INFLUX and more calcium taken back up into the stores

Action of noradrenaline on beta-1-receptors in the heart will increase contraction

So we can alter heart rate and strength of contraction by sympathetic activity

Strength of contraction CAN NOT be changed by parasympathetic activity

32
Q

controlling stroke volume by two methods

A

Increased Sympathetic Activity

Plasma Adrenaline

since:
Intrinsic control of stroke volume: venous return which sets the end-diastolic volume (stretch) which increases the force of contraction

We can get more blood back to the heart (increase venous return) if we increase respiratory movements - decreasing intrathoracic pressure helps the filling of the heart

33
Q

what occurs as part of the flight or flight response?

A

We can get rapid changes in RESPIRATORY MOVEMENT, PLASMA ADRENALINE and INCREASE SYMPATHETIC ACTIVITY as part of the fight or flight response

34
Q

where are baroreceptors located?

A

aortic arch and in the carotid sinus (carotid bodies)

35
Q

Baroreceptors in the carotid bodies feedback to

A

Baroreceptors in the carotid bodies feedback to the vasomotor centre via the glossopharyngeal nerve

36
Q

The aortic arch baroreceptors feedback to

A

The aortic arch baroreceptors feedback to the vasomotor centre via the vagus nerve

37
Q

how do baroreceptors work?

A

change firing in response to arterial pressure

38
Q

Carotid sinus baroreceptors respond to pressure between

A

Carotid sinus baroreceptors respond to pressure between 60 and 80 mmHg

39
Q

Baroreceptor reflex is most sensitive around

A

Baroreceptor reflex is most sensitive around 90-100 mmHg

40
Q

Increase in baroreceptor firing =

A

Increase in in parasympathetic activity as
When the receptor sees an increase in pressure it fires more - the nerve activity is increased

The sympathetic nerves are connected via a series of inhibitory interneurones which slows down the tonic activity
Increase in baroreceptor firing = DECREASE in sympathetic activity to heart, arterioles and veins

41
Q

increased parasympathetic stimulation of the heart

A

decreases heart rate

42
Q

where are cardioregulatory and vasomotor centres located

A

medulla oblongata

43
Q

Increased Blood Pressure =

mechanics

A

huge increase in firing activity throughout from the baroreceptor

The increase in baroreceptor firing is fed back to the vasomotor centre which triggers increased traffic in the vagus nerve

REMEMBER: parasympathetic activity reflects exactly what happens in terms of baroreceptor activity

Increase in parasympathetic activity causes an increase in acetylcholine production in the SAN which decreases the gradient of the pacemaker potential and causes a decrease in heart rate

Increase in baroreceptor activity also decreases the sympathetic nerve traffic which also brings about a decrease in heart rate

Sympathetic cardiac nerves also have an effect on the force of contraction - so less innervation from sympathetic nerves leads to a decrease in the force of contraction

Decrease in sympathetic activity also leads to an increase in vessel radius

These changes in heart rate, contraction and dilation leads to a DECREASE IN BLOOD PRESSURE

44
Q

which nerves are involved in control of venous return

A

sympathetic vasoconstrictor nerves

45
Q

Mean Systemic Arterial Pressure =

A

Cardiac Output x Total Peripheral Resistance