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Cardiovascular system > Crdiovascular control 2 > Flashcards

Crdiovascular control 2 Flashcards

1
Q

Define stroke volume

A

The volume of blood pumped out of the heart in each beat.

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2
Q

What is venous volume distribution affected by

A

Venous volume distribution affected by peripheral venous tone, gravity, skeletal muscle pump & breathing

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3
Q

Describe central venous pressure (pressure in the right atrium)

A

Central venous pressure (mean pressure in the right atrium) determines the amount of blood flowing back to the heart.

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4
Q

What does the amount of blood flowing back to the heart determine

A

The amount of blood flowing back to the heart determines stroke volume (using Starling’s Law of the Heart)

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5
Q

What is meant by the tone of a blood vessel

A

How constricted they are

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6
Q

What are the consequences of venous constriction

A

In veins, constriction reduces compliance and venous return

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7
Q

What does constriction determine in the arterioles

A

In arterioles, constriction determines:
Blood flow to downstream organs
Mean arterial blood pressure
The pattern of blood flow to organs

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8
Q

What is flow primarily altered by

A

Changes in the radius of the blood vessel.

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9
Q

Describe the suck-pump analogy of the heart

A

The heart pumps out how much blood returns (Frank-Starling relationship).

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10
Q

Describe the two different methods of regulating blood flow

A

Local mechanisms are intrinsic to the smooth muscle (or closely associated)- Important for reflex local blood flow regulation within an organ.
Systemic mechanisms are extrinsic to the smooth muscle- circulating hormones and the autonomic nervous system.

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11
Q

What happens in the systemic mechanisms

A

It affects the constriction or distension of the blood vessels all over the body.

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12
Q

Without any compensatory mechanisms, what would you expect to happen if perfusion pressure decreased

A

Resistance to increase (passive constriction as the intravascular pressure falls)
Flow to decrease

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13
Q

What is meant by autoregulation

A

Autoregulation is the intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance)
Flow increases and resistance decreases in response to a decrease in perfusion pressure.

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14
Q

Describe the myogenic theory for autoregulation

A

Myogenic theory states that smooth muscle fibres respond to tension in the vessel wall (e.g. as pressure rises, fibres contract; stretch sensitive channels involved)
Hence low pressure, less constriction, dilation

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15
Q

Describe the metabolic theory for autoregulation

A 
Metabolic theory (as blood flow decreases, metabolites accumulate and and vessels dilate; subsequent increased flow ‘washes’ metabolites away)
Feedback mechanism.
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16
Q

How can injury influence blood flow

A

serotonin release from platelets causes constriction, hence reducing the volume of blood lost.

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17
Q

List the local (endothelial derived hormones) involved in the regulation of blood flow

A

Nitric Oxide
Prostacyclin
Thromboxane A
Endothelins

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18
Q

List the circulating (non-endothelial derived hormones) involved in the regulation of blood flow

A 
Kinins
Atrial natriuretic peptide (ANP)
Vasopressin
Noradrenaline/Adrenaline 
Angiotensin 2
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19
Q

Describe nitric oxide

A

potent vasodilator produced from arginine. NO diffuses into vascular smooth muscle cells.

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20
Q

Describe prostacyclin

A

cardioprotective vasodilator synthesised from prostaglandin precursor (PGH2) – also has antiplatelet and anticoagulant effects

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21
Q

Describe thromboxane A

A

vasoconstrictor synthesised from prostaglandin precursor (PGH2) – also heavily synthesized in platelets (amplify platelet activation)

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22
Q

Describe endothelin

A

vasoconstrictors generated from the nucleus of endothelial cells – has minor vasodilator effects but principally a vasoconstrictor

23
Q

Describe Kinins

A

hormones that bind to receptors on endothelial cells and stimulate NO synthesis – vasodilator effects

24
Q

Describe Atrial natriuretic peptide

A

secreted from the atria in response to stretch – vasodilator effects to reduce BP

25
Q

Describe Vasopressin

A

secreted from posterior pituitary in response to high blood osmolality. Binds to V1 receptors on smooth muscle to cause vasoconstriction

26
Q

Describe adrenaline/noradrenaline

A

secreted from adrenal gland and causes vasoconstriction

27
Q

Describe angiotensin 2

A

potent vasoconstrictor product from the renin-angiotensin-aldosterone axis. Also stimulates SNS activity and ADH secretion.

28
Q

Describe the use of ACE inhibitors as an anti-hypertensive treatment

A

Reduces the production of angiotensin 2, thus the vessels are constricted less, reducing BP.

29
Q

What is the SNS important in controlling

A

SNS is important for controlling the circulation

30
Q

What is the PNS important in controlling

A

PNS is important for controlling the heart rate

31
Q

Describe the neurotransmitters used in the pre-ganglionic neurons and the post-ganglionic neurones

A

Pre-ganglionic fibres use ACh as their neurotransmitter
PNS post ganglionic NT = ACh
SNS post ganglionic NT = NA

32
Q

Where do the sympathetic pre-ganglionic neurons synapse

A

In the paravertebral ganglion.

33
Q

What do the SNS fibres innervate

A

SNS fibers innervate the heart and ALL VESSELS except capillaries and precapillary sphincters and some metarterioles

34
Q

Why is it difficult to predict the effects of the SNS on a specific vascular bed

A

SNS innervation elsewhere is variable:
Heavily innervated: kidneys, gut, spleen and skin
Poorly innervated: skeletal muscle and brain

35
Q

How does noradrenaline cause vasoconstriction

A

Noradrenaline preferentially binds to α1 adrenoceptors to cause smooth muscle contraction and vasoconstriction.

36
Q

Where is the vasomotor centre located

A

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

37
Q

What is the vasomotor cortex composed of

A

The VMC is composed of a vasoconstrictor (pressor) area, a vasodilator (depressor) area and a cardioregulatory inhibitory area

38
Q

How does the vasomotor transmit impulses

A

The VMC transmits impulses distally through the spinal cord to almost all blood vessels
Lateral portions of VMC controls heart activity by influencing heart rate and contractility
Medial portion of VMC transmits signals via vagus nerve to heart that tend to decrease heart rate

39
Q

Explain how the vasomotor centre can take into account thinking about events

A

Many higher centers of the brain such as the hypothalamus can exert powerful excitatory or inhibitory effects on the VMC
Anticipatory response- adrenaline is released when preparing for exercise or a stressful event.

40
Q

Describe the nervous control of vessel diameter

A

Blood vessels receive SNS post-ganglionic innervation Neurotransmitter = noradrenaline (NA)
Always some level of tonic activity which can be:
Increased – causing vasoconstriction
Decreased – causing vasodilation
Generally no PNS innervation to vasculature

41
Q

What can increase heart rate

A

SNS stimulation

Increased plasma adrenaline

42
Q

What can decrease heart rate

A

PNS stimulation

43
Q

What does the fact that heart rate increases when both the sympathetic nerves and parasympathetic nerves are cut indicate

A

That PNS activity is always lowering activity- and has a more dominant effect at rest.

44
Q

Describe how the SNS can control the force of contraction

A

Noradrenaline binds to B1 receptors on heart
Increased cAMP and protein kinase A
PKA phosphorylates L-Type calcium channel, SR Ca2+ release channel and Ca2+ ATPase
Ca2+ influx increased
Ca2+ uptake into intracellular stores increased
Ca2+ release from intracellular stores increased
More calcium binding to troponin- greater force of contraction

45
Q

What are the intrinsic factors that can increase stroke volume

A

Increased venous return — increased atrial pressure – increased EDV
Increased respiratory movements — decreases intrathoracic pressure — increased EDV.

46
Q

What are the extrinsic factors that can increase stroke volume

A

Plasma adrenaline

SNS efferent to heart

47
Q

Describe the baroreceptors

A

Mechanoreceptors in carotid sinus change their firing rate in response to changes in pressure
Mechanoreceptors in aortic arch change their firing rate in response to changes in pressure
Aortic arch- vagus nerve afferents
Carotid sinus- Glossopharyngeal nerve efferents

48
Q

What do baroreceptors respond to

A

Stretch, the more they stretch (higher BP) the more they fire

49
Q

Describe baroreceptor activity

A

Carotid sinus baroreceptors respond to pressures between 60 and 180 mmHg.
Baroreceptors respond to changes in arterial pressure
Baroreceptors reflex is most sensitive at pressures around 90-100 mmHg- physiological BP
- Greatest change in impulse rate per unit change in pressure occurs about this point

50
Q

Describe reciprocal innervation

A

Afferent nerves bifurcate- PNS branch and SNS branch
PNS branch linked to heart
Bifurcation -series of inhibitory interneurons
Tonic activity from SNS to blood vessels and heart

51
Q

Explain how increased baroreceptor firing decreases blood pressure

A

Increased afferent input from increased baroreceptor activity stimulates parasympathetic nerves to heart
It also simultaneously inhibits sympathetic innervation to heart, arterioles and veins
Decreasing HR and causing vasodilation of the blood vessels.

52
Q

Describe how the BP reflex activity is controlled by carotid sinus activity

A

Increase blood pressure – increases baroreceptor stretch – increased firing of carotid sinus nerve
Increased firing of vagus nerve
Decrease firing of sympathetic cardiac and vasoconstrictor nerves(resistance and capacitance vessels).

53
Q

What are the consequences of a haemorrhage

A 
Decreased blood volume
Decreased venous pressure
Decreased venous return 
Decreased arterial pressure
Decreased EDV
Decreased SV
Decreased Cardiac Ouput
Decreased BP
54
Q

How does the body respond to a haemorrhage

A

Reduced baroreceptor firing
Increased SNS discharge to heart, reduced PNS discharge
Increase in contractility- increased stroke volume- increased cardiac output- increased mean arterial pressure

Increased SNS discharge to veins
Increased venous tone
Increased venous pressure
Increased venous return
Increased EDV
Increased cardiac output- increased MAP

Increased SNS discharge to arterioles
Arteriolar constriction
Increased Total Peripheral Resistance — Increased MAP

Cardiovascular system (19 decks)

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