Control of BP Flashcards

1
Q

Why do we aim to maintain a constant arterial blood pressure ?

A

Because if too low, blood flow to organs would fail. If too high, damage to vessels and organs (auto-regulation helps protect capillary from high BPs)

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2
Q

To what extent is 5L/min enough blood to perfuse the entire body ?

A

5L/min not sufficient to perfuse entire body (allocated based on tissue demands)

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3
Q

How quick of nervous control of arterial BP?

A

Very:

  • Can increase arterial pressure to 2x normal within 5-10s
  • Can decrease arterial pressure to 50% normal within 10-40s
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4
Q

What are the fundamental components of a reflex control system ?

A

1) Internal variable to be maintained
2) Receptors sensitive to change in the variable
3) Afferent pathways from the receptors
4) An integrating center for the afferent inputs
5) Efferent pathways from the integrating center
6) Target effectors that alter their activities

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5
Q

Identify the internal variable and receptors of the BP reflex control system. What is the end goal of this control system ?

A

1) Internal variable to be maintained: MABP
2) Receptors: Baroreceptors

End goal is to reduce the minute-to- minute variations of arterial pulse.

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6
Q

Identify the main formula used to calculate MABP.

A

MABP = CO x Total Peripheral Resistance

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7
Q

Where are baroreceptors located ?

A

In the arterial side:

  • In carotid sinus
  • In aortic arch

In veinous side:
widesperad

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8
Q

What do arterial baroreceptors sense ? How do they work ?

A
  • Pressure
  • Activated in response to stretch (which is generated by pressure of blood). They are constantly firing (not muted) but the rate of impulses can be varied depending on degree of stretch around a set-point (as BP ↑, get stretch of baroreceptors, ↑ firing rate and vice versa)
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9
Q

What is the most significant different between carotid and aortic baroreceptors ?

A

Carotid baroreceptors operate at pressure ranges which are much more sensitive to
the ranges that we want to maintain (Finer control)

Aortic ones are less sensitive to drops in BP
but much more sensitive in massive increases in BP

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10
Q

Identify the afferent fibers from the different baroreceptors.

A

From the aortic baroreceptor: Afferent fibers follow vagus (Xth cranial) nerve

From the carotid baroreceptor: Afferent fibers follow (IXth cranial) glossopharyngeal nerve

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11
Q

What is a normal set point for MABP (around which baroreceptors are sensitive to changes in pressure) ?

A

Between 70 and 100 mmHg.

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12
Q

Give an example of situation where the set point for MABP can change over time.

A

Hypotension, a pathological reason causing you not to achieve the normal variable. Consequently, overtime, the receptor can desensitise and cause the normal set point to increase (to about 100 mmHg).

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13
Q

What is the effect of exercise on MABP ?

A

Increase it a little (approximately 95 mmHg in a healthy individual)

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14
Q

Graph the rate of baroreceptor firing in response to changing arterial pressure. Explain the shape of the graph.

A

Refer to middle slide on page 3 in lecture on “Control of BP”.

Below 40 mmHg, no real firing occurs. As arterial pressure increases, rate of firing increases.
Midpoint around 90 mmHg arterial pressure.
Around 160 mmHg, get saturated (rate of firing does not increase anymore, plateau).

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15
Q

Does the blood still have oscillating pressure by the time it gets to the carotid baroreceptors ?

A

Yes, it does (not yet fully flattened, but still well controlled).

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16
Q

What would be the consequence if we were denervate baroreceptors (stop afferent fibers from aortic and carotid bodies from going to the CNS) ?

A

Lose fine regulation control (variation of BP oscillates hugely, poorly controlled).

17
Q

Distinguish between the effects of the following three scenarios:
In all three cases, 8% of blood has been lost.
1) The carotid sinus baroreceptor reflexes were intact and the aortic reflexes were interrupted.
2) The aortic reflexes were intact and the carotid sinus reflexes were interrupted
3) All sinoaortic reflexes were abrogated.

A

In all cases, decreased veinous return (due to blood loss) leads to some loss in arterial pressure.

1) Small reduction in arterial pressure (carotid baroreceptors sensitive to small increases and drops in arterial pressure, so they are able to instigate a response)
2) Intermediate reduction in arterial pressure (aortic baroreceptors insensitive to drops in pressure, so they don’t contribute hugely to this reflex)
3) Large reduction in arterial pressure (due to loss of system which can detect and instigate responses)

18
Q

Where are cardiopulmonary baroreceptors located ?

A

Atria, ventricles, veins and pulmonary vessels

19
Q

What is the most significant difference between cardiopulmonary and arterial baroreceptors ?

A

Cardiopulmonary baroreceptors sense central blood volume whereas arterial baroreceptors sense changes in pressure.

20
Q

What does the rate of firing of cardiopulmonary baroreceptors depend on ?

A

The rate of firing of cardiopulmonary baroreceptors depends on blood volume (lower rate of firing with lower blood volume and vice versa).

21
Q

What are the consequences of lower firing rate of cardiopulmonary baroreceptors (following a decrease in blood volume) ?

A
  • Sympathetic nerve activity to the heart and blood vessels ↑
  • Parasympathetic nerve activity to the heart ↓
22
Q

Following a haemorrage, which type of baroreceptor senses the loss of blood first ?

A

Cardiopulmonary baroreceptors

23
Q

Describe the Atrial reflex control of BP (Bainbridge Reflex).

A

Sympathetic-mediated reflex in response to increased blood in atria
–↑HR and ↑contrac tility
– prevents damming of blood in veins etc

24
Q

What happens if aortic/carotid baroreceptors sense high pressure at the same time as the atrial reflex control of BP (Bainbridge Reflex) ?

A

Bainbridge Reflex can override aortic/carotid baroreceptors response, which would result in increase total peripheral resistance (and cause BP to skyrocket).
As a result of the reflex, peripheral resistance is dropped to allow blood to be pumped out without an unnecessary increase in BP.

25
Q

Where is the integrating center for the afferent inputs ? Describe the main features of this center.

A

Medullary cardiovascular control (MCVC) “vasomotor” centre

1) Sensory area (Input from baroreceptors)
2) Lateral portion (Efferent sympathetic nerves)
3) Medial portion (Efferent parasympathetic (vagal) nerves)

26
Q

Identify the main target effectors in reflex control of blood pressure. How do they relate to MABP ?

A

1) Heart
2) Blood vessels

MABP = CO (heart) x Total Peripheral Resistance (blood vessels)

27
Q

Describe the main sympathetic and parasympathetic effects on the heart.

A
  • Both control heart rate but sympathetic can also significantly effect stroke volume.
  • Work simultaneously but at rest parasympathetic = predominate tone
28
Q

How can we increase heart rate without even using sympathetic innervation ?

A

By relieving parasympathetic innervation (thus allowing intrinsic rate of SAN to increase HR)

29
Q

Describe the main sympathetic and parasympathetic effects on the blood vessels.

A

Parasympathetic NS has no effect on blood vessels.

Sympathetic effects on blood vessels:

1) Continuous low-level tone affects total peripheral resistance
- “sympathetic vasoconstrictor tone” exerts “vasomotor tone” on vessels
- kept partially constricted (contributes to total peripheral resistance)
- Can dilate vessels by reducing sympathetic outflow

2) Veins also innervated by sympathetic
- ↓ capacitance ↑ venous return ↑ stroke vol ↑ cardiac output

30
Q

How can we cause vessels to dilate, given that parasympathetic system does not control blood vessels ?

A

By reducing sympathetic outflow

31
Q

Define CNS ischaemic response.

A

Emergency pressure reflex control system when blood flow to the medullary CVCC is ↓↓↓ (sensed through chemoreceptors) through:

– ↑ peripheral vasoconstriction (almost completely occludes some peripheral vessels)
–↑sympathe tic s timula tion of heart
– ↑↑ systemic arterial pressure (as high as 250 mmHg for 10 min)

ONLY FOR THE SHORT TERM

32
Q

Summarize the main ways in which cardiac output may be altered.
Draw this.

A

Three main things:

  1. Increase EDV (intrinsic control, through preload) results in increased force of contraction, and hence stroke volume (via Frank Starling mechanism)
    -EDV itself can be increased through:
    Increased Venous Pressure –> Increased Venous Return –> Increased Atrial Pressure –> Increased EDV
    -Venous Pressure itself can be increased through 1) Sympathetic Innervation of Veins (affecting their tone),
    2) Skeletal Muscle Pump 3) Respiratory Pump
    (frequency and depth) 4) Blood Volume)
  2. Increase Sympathetic activity (as well as increase in adrenaline) increase force of contraction and hence stroke volume + increase heart rate (via SAN)
  3. Decrease parasympathetic activity increases HR (chronotropic effect)

Anything that changes either stroke V or heart rate will change cardiac output since
CO = HR x SV

REFER TO FIRST SLIDE ON PAGE 7 OF LECTURE ON “CONTROL OF BP”

33
Q

How may we influence total peripheral resistance ? Draw this.

A

Through 1) Arteriolar Radius 2) Viscosity

  • Arteriolar radius can be influenced by Neural, Hormonal, and Local control (latter will influence whether a capillary bed is being perfused or not, but will not have a huge effect on peripheral resistance)
  • Viscosity depends on Hematrocrit

REFER TO SECOND SLIDE ON PAGE 7 OF LECTURE ON “CONTROL OF BP”

34
Q

How does long term regulation of BP occur ? In the short/intermediate term ?

A

Via blood volume.

Via neuronal reflex mechanisms.

35
Q

Draw a diagram illustrating how neuronal reflex mechanisms influence MABP.

A

Refer to first slide on page 6 of lecture on “Control of BP”

36
Q

What steps would be taken by the CVS if BP was to drop ?

A

If pressure drops, decrease PSNS output to increase Heart Rate (that will not gonna solve the entire problem, because MABP won’t be maintained unless we also get a consummate return of blood to pump out with increased HR)

Increase sympathetic output can cause increase in HR, in stroke V via contractility, and independently increase in stroke V by decreasing capacity of veins, therefore forcing more blood back in heart, causing greater stretch in ventricles, resulting in greater force of contraction (Frank Starling mechanism)