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Flashcards in Regulation of Blood Pressure Deck (26)
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1
Q

Why is it important to maintain tissue perfusion across the whole body?

A
  • To keep a relatively constant arterial blood pressure.
    • When too low, blood flow to organs fails.
    • When too high, there can be damage to vessels and organs.
  • To control distribution of the total cardiac output.
    • 5L/minute is not sufficient to perfuse the entire body.
    • Needs to respond to tisue demands.
    • Satisfied by local control mechanisms.
2
Q

Describe the nervous control of arterial pressure.

A
  • Nervous control of arterial pressure is rapid.
  • It can increase arterial pressre to 2x normal within 5-10s.
  • It can decrease arterial pressure to 50% normal within 10-40s.
3
Q

What are the fundamental components of a reflex control system?

A
  • Internal variable to be maintained.
  • Receptors sensitive to change in the variable.
  • Afferent pathways from the receptors.
  • An integrating centre for the afferent inputs.
  • Efferent pathways from the integrating centre.
  • Target effectors that alter their activities.
4
Q

How is mean arterial blood pressure calculated?

A
  • Total peripheral resistance is the factor which varies most in maintaining mean arterial blood pressure.
5
Q

Describe the feedback control of mean arterial pressure.

A
  • Main baroreceptor locations:
    • Walls of the aorta
      • Afferent fibres follow the vagus nerve (CNX).
    • Carotid artery
      • Afferent fibres follow glossopharyngeal nerve (CNIX).
  • Baroreceptor activity:
    • Stretch receptors
    • Firing rate increases when BP increases.
    • Firing rate decreases when Bp decreases.
    • Sensitive around a ‘set-point’.
      • Set point can change (e.g. hypertension).
6
Q

Describe the rate of baroreceptor firing and the relationship this has with phasic aortic pressure.

A
7
Q

What is the primary purpose of baroreceptor control of blood pressure?

A
  • To reduce the minute-to-minute variations of arterial pressure
8
Q

What is the role of cardiopulmonary baroreceptors?

A
  • Cardiopulmonary baroreceptors are ‘low-pressure’ receptors which sense central blood volume.
    • Atria, ventricles, veins and pulmonary vessels.
  • If the rate of cardiopulmonary baroreceptors firing decreases, (signalling decreased blood volume), then:
    • Sympathetic nerve activity to the heart and blood vessels increases.
    • Parasympathetic nerve activity to the heart decreases.
9
Q

Describe the integrated control of BP (medullary cardiovascular control (MCVC) ‘vasomotor’ centre).

A
  • Medullary cardiovascular control (MCVC) ‘vasomotor’ centre:
    • Sensory area
      • Input from baroreceptors
    • Lateral portion
      • Efferent sympathetic nerves
    • Medial portion
      • Efferent parasympathetic (vagal) nerves
10
Q

What are the sympathetic and parasympathetic effects on the heart?

A
  • Both control heart rate and normally function simultaneously.
    • At rest, parasympathetic - predominate tone.
    • Sympathetic can significantly affect stroke volume and rate.
11
Q

What are the sympathetic and parasympathetic effects on blood vessels?

A
  • Sympathetic effects on blood vessels:
    • Continuous low-level tone affects total peripheral resistance.
      • ‘Sympathetic vasoconstrictor tone’ exerts ‘vasomotor tone’ on vessels.
      • Therefore, vessels are kept partially constricted.
    • Remember veins are also innervated by the sympathetic NS.
      • Decreased capacitance, therefore increased venous return, therefore increased stroke volume, therefore increased cardiac output.
12
Q

Describe the CNS ischaemic response.

A
  • Emergency pressure control system
    • ‘Last ditch stand’
  • When blood flow to the medullary CVCC is massively decreased:
    • Increased peripheral vasoconstriction
      • Almost completely occludes some peripheral vessels.
    • Increased sympathetic stimulation of the heart.
    • Greatly increased systemic arterial pressure.
      • As high as 250mmHg for 10 minutes.
13
Q

Describe the fine control of blood flow.

A
  • Local control superimposed on organ dist. of CO
    • Tissues auto-regulate blood flow.
      • Build-up of local factors (e.g. adenosine)
      • Independent of innervation / hormonal control
  • Intrinsic ability to maintain blood flow safely across capillaries if BP is raised.
    • Myogenic theory (acute auto-regulation)
      • Stretch-induced vascular depolarisation of smooth muscle due to increased arterial pressure.
  • Remember not all capillaries in an organ are perfused simultaneously.
14
Q

Summarise cardiac output.

A
15
Q

Summarise total peripheral resistance.

A
16
Q

How is blood pressure regulated long-term?

A
  • Control of body fluid volume by the kidneys - renal body fluid feedback system.
  • When arterial pressure increases, urine production increases.
  • When arterial pressure decreases, urine production decreases.
17
Q

Describe the long-term regulation of blood pressure.

A
  • 2 primary determinants:
    • The renal output curve for salt and water
    • The level of salt and water intake
  • It is impossible to change long-term mean arterial blood pressure without changing one or both of these.
18
Q

Describe the effects of anti-diuretic hormone (ADH).

A
  • A.K.A. arginine vasopressin.
  • Released by the pituitary gland in response to:
    • Increased osmotic pressure
      • Sensed by hypothalamic osmoreceptors.
    • Hypovolemia (10% loss of greater)
      • Atrial baroreceptors normally inhibit ADH release.
      • Decreased volume leads to decreased firing rate, therefore increased ADH release.
    • Hypotension
      • Decreased arterial baroreceptor firing.
      • Increased sympathetic activity and increased ADH release.
    • Angiotensin II
19
Q

What is the effect of ADH on blood volume?

Describe the mechanism.

A
  • ADH increases blood volume by:
    • Causing increased water permeability in renal collecting ducts.
      • Therefore decreased urine production.
20
Q

What is the effect of ADH in severe hypovolemic shock?

A
  • ADH release is high
  • Causes vasoconstriction
    • Therefore increased total peripheral resistance
21
Q

Summarise the regulation of blood osmolarity.

A
22
Q

Describe Renin.

A
  • Proteolytic enzyme released from the kidneys in response to:
    • Sympathetic nerve activation
      • Mediated by baroreceptor feedback
    • Renal artery hypotension
      • Independent of baroreceptor feedback
    • Decreased sodium in kidney distal tubules
23
Q

Summarise the renin-angiotensin-aldodterone system (RAAS).

A
24
Q

Describe the action of the RAAS.

A
  • Renin released from kidney juxtaglomerular cells.
  • Angiotensin II acts on resistance vessels.
    • Therefore increased total peripheral resistance.
  • Angiotensin II acts directly on the kidneys.
    • Constricts renal arteries, therefore decreased blood flow via kidneys.
  • Angiotensin II causes release of aldosterone from the adrenal glands.
    • This causes increased Na+ and water reabsorption.
  • Angiotensin II stimulates release of ADH from the pituitary.
25
Q

What is atrial-natriuretic hormone?

Describe its mechanism of action.

A
  • 28 amino acid peptide synthesised and stored in muscle cells of the atria.
    • Released in response to stretch of the atria.
    • Helps oppose the effects of the RAAS.
  • May help counteract volume overload.
26
Q

What are the other factors which affect blood pressure control?

A
  • Cortex
    • Conscious effects of emotions
      • Nerves from cortex to medullary CVC centre.
  • Time of day
    • Diurnal variations due to hormones and cortical input.
  • Respiration
    • Via mechanical movements
    • Via chemoreceptors
      • Aortic and carotid bodies detect changes in pO2
      • If pO2 is decreased, rate of firing is increased