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CVS > CVS 10 - Regulation of CVS > Flashcards

CVS 10 - Regulation of CVS Flashcards

1
Q

Veins store blood volume (they have capacitance). What 4 factors affect venous volume distribution?

A
  1. Peripheral venous tone
  2. Gravity
  3. Skeletal muscle pump
  4. Breathing
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2
Q

What does central venous pressure determine?

A

Amount of blood flowing back to the heart, which determines stroke volume

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3
Q

What are the 3 ways of regulating flow?

A
  1. Local mechanisms
  2. Hormonal mechanisms
  3. Autonomic nervous system
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4
Q

Compare and contrast myogenic theory and metabolic theory.

A

Both theories try to explain why there is a decrease in R when P drops, which increases F.

Myogenic: VSMC respond to stretch. As P increases, muscle fibres contract to keep flow constant

Metabolic: If vessels supplying a vascular bed contract, F decreases and so the vascular bed produces more metabolites that cause vasodilation. This allows greater flow to the vascular bed.

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5
Q

How can autoregulation be changed?

A

If a vessel becomes injured. Platelets aggregate around injured vessels and release serotonin (a powerful vasoconstrictor)

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6
Q

Give 3 ways in which systemic blood flow is regulated.

A
  1. Kinins - interact with RAS and relax VSMC
  2. ANP (Atrial Natriuretic Peptide) -peptides secreted from atria. Atria stretching causes more ANP release causing vasodilation.
  3. Circulating vasoconstrictors - vasopressin/Ang 2/NA
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7
Q

Difference in structure between sympathetic and parasympathetic neurone?

A

Parasympathetic Neurone = long preganglionic neurone, short post ganglionic neurone.

(sympathetic is the other way round)

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8
Q

In the autonomic NS, which aspect of heart does sympathetic control? Which part does parasympathetic control?

A
  1. Sympathetic = controls flow

2. Parasympathetic = regulates HR

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9
Q

Which vessels do sympathetic nerve fibres innervate?

A

All vessels except capillaries.

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10
Q

Describe the distribution of sympathetic nerve fibres. Why is this important?

A

More sympathetic innervation to vessels supplying Kidneys, Gut, Spleen, Skin.

That way, NA (which binds more preferentially to a1-receptors) cause SM contraction and vasoconstriction.

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11
Q

Describe the concentration dependent nature of adrenaline.

A

Adrenaline binds with high affinity to b2-adrenoreceptors and cause vasodilation.

At high concentrations however, adrenaline can bind to a-adrenoreceptors and cause vasoconstriction (overriding the vasodilatory effects of b2-adrenoreceptor stimulation).

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12
Q

Which receptor is activated when blood vessels constrict?

A

a1-adrenoreceptor

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13
Q

Where is the Vasomotor Centre (VMC) located?

A

Located bilaterally in the medulla and pons.

It transmits impulses via the spinal cord to almost all blood vessels

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14
Q

What are the 3 parts of the VMC.

A
  1. Vasoconstrictor Area (pressor)
  2. Vasodilator (depressor)
  3. Cardioregulatory Inhibitory Area
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15
Q

What can higher centres in the brain do?

A

They can exert excitatory/inhibitory effects on VMC.

They allow an anticipatory response to exercise - HR and VR increases slightly before exercise due to this

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16
Q

What do the lateral portions of the VMC generally control?

A

Controls HR and Contractility

17
Q

What do the medial portions of the VMC control?

A

They transmit signals via Vagus nerve to the heart - tends to decrease HR.

18
Q

How is blood vessel diameter nervously controlled?

A
  1. Blood vessels receive sympathetic postganglionic innervation (through NA)
  2. Baseline frequency of impulses maintains Vasomotor tone.
  3. Increasing nerve traffic = vasoconstriction
  4. Decreasing nerve traffic = vasodilation
  5. Very little parasympathetic innervation of vascular system.
19
Q

Which 3 areas allow control of blood vessel radius?

A
  1. Local controls (auto regulation)
  2. Circulating hormones
  3. Sympathetic vasoconstrictor nerves
20
Q

Heart rate (cardiac innervation) is influenced by dual innervation - sympathetic and parasympathetic. How does parasympathetic work? How does Ach work?

A

Parasympathetic slows HR down - Ach decreases gradient of pacemaker potential, meaning potential takes longer to reach threshold and fire.

Sympathetic increases HR - A and NA increases gradient of pacemaker potential.

21
Q

How is force of contraction controlled (other than Starlings Law).

(CONTRACTILITY CANNOT BE CHANGED BY PARASYMPATHETIC ACTIVITY)

A
  1. NA binds to b1-adrenoreceptors.
  2. cAMP levels increased. cAMP activated PKA, which phosphorylates L-type Ca channels and SR Ca release Channel and SERCA.
  3. Therefore, more Ca influx , and more Ca uptake into stores.
  4. Overall, force of contraction increased.
22
Q

How can SV be increased?

A
  1. Increase sympathetic activity (extrinsic)
  2. Increase plasma adrenaline
  3. Increase EDV - by increasing venous return, increase atrial pressure and decreasing intrathoracic pressure (e.g. increasing respiratory movements)
23
Q

What does the fight or flight response affect?

A
  1. Respiratory movement
  2. Plasma adrenaline
  3. Increased sympathetic activity
24
Q

How do the Aortic Arch baroreceptor and the Carotid sinus baroreceptor feed back to the VMC?

A

Aortic Arch Baroreceptor = Vagus Nerve

Carotid Sinus Baroreceptor = Glossopharyngeal nerve

25
Q

What do baroreceptors do?

At what pressures are the baroreceptor reflexes most sensitive?

A

They respond to changes in pressure

Baroreceptor reflex most sensitive around 90-100mmHg.

26
Q

Explain how baroreceptors can cause a decrease in HR if pressure increases.

A
  1. Receptor fires more via afferent (vagus) nerve. Increases parasympathetic activity.

INCREASE BARORECEPTOR FIRING = INCREASED PARASYMPATHETIC ACTIVITY

  1. Simultaneously, inhibitory interneurones are activated which slow down sympathetic activity. (This also causes vasodilation)

Increased baroreceptor firing = decreased sympathetic activity

27
Q

Where does parasympathetic stimulation of the heart come from?

A

Vagus nerve

28
Q

MAP =?

A

MAP = CO x TPR

CVS (16 decks)

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