Pressures and Flows in the Systemic Circulation Flashcards Preview

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Flashcards in Pressures and Flows in the Systemic Circulation Deck (26)
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1

Define systolic blood pressure

The pressure exerted against the arterial wall during ventricular systole

Measured at the point where the pulse sound is first heard where the sphygmomanometer pressure is reduced from starting pressure (usually around 180mmHg)

2

Define diastolic blood pressure 

The pressure being exerted against the arterial wall during ventricular diastole

Measured at the point at which the pulse disappears

 

3

Define mean arterial pressure 

How is it calculated?

The average arterial pressure during one cardiac cycle

Calculated by:

  • MAP = SBP + 2(DBP) / 3 

4

What are baroreceptors?

What are the different types?

Where are the most important ones located?

Receptors that detect stretch within blood vessels

Located throughout vascular tree

2 types:

  • High pressure= arterial
  • Low pressure= venous and right side of heart

Most important ones located in the carotid sinus and the aortic arch 

5

Describe the mechanism of action of arterial baroreceptors

What is their role?

Continuous feedback loop

Continuously fire with arterial stretch during ventricular systole

Vital role to compensate in sudden reduction in blood pressure:

  • Decreased BP causes decreased firing rate
  • Reflex via medulla acts to increase BP by:
    • Increased sympathetic activity:
      • Increases cardiac output and systemic vascular resistance
    • Decrease vagal activity:
      • Increases cardiac output 

 

6

Describe the mechanism of action of venous baroreceptors

Where are they found?

Unresponsive to arterial baroreceptors

Predominantly in atria, ventricles and pulmonary arteries

Respond to volume changes and cause either vasoconstriction or vasodilation 

  • Increased volume = vasodilation
    • Causes increased renal excretion by inhibiting release of ADH from posterior pituitary and reduces renal sympathetic outflow 

7

What are chemoreceptors?

Receptors stimulated by a change in their immediate environment. Stimulated by:

  • Hypoxia
  • Hypercapnia
  • pH change 

Causes increased sympathetic stimulation of heart and peripheral vasculature via medullary centres to increase cardiac output and blood pressure. 

Affect the respiratory and cardiovascular system 

8

Why does pulse pressure increase moving peripherally from the aorta to the arteries?

Increasing vessel wall rigidity

Aorta has high elasticity so can absorb some of the pressure frm ventricular systole without increasing aortic pressure. 

9

How can veins respond to rapid alterations in blood volume?

How do they alter cardiac output?

Can accommodate up to 25% blood loss by venoconstriction

Can accommodate up to 500ml rapid infusion by venodilation

Modify cardiac output by modifying venous return 

10

What provides resistance to venous flow?

Fixed structures such as first rib, the neck (subject to atmospheric pressure which is higher than venous)

11

What does local perfusion control?

Delivery of oxygen to tissues

Delivery of nutrients, e.g. glucose, amino acids, fatty acids

Removal of CO2 from tissues

Removal of H+ from tissues

Maintenance of appropriate ion concentrations in tissues 

Transport of hormones e.t.c to tissues 

12

Which acute mechanisms control local perfusion?

Vasodilation: from either hypoxia or vasodilators released. 

Nutrient deficiencies

Vasoconstriction: from either myogenic mechanism (stretch placed on vessel wall induces constriction) or metabolic theory (high blood pressure washes away vasodilator substances) 

Nitric Oxide: released by endothelial cells in response to stress of extra blood flow. Activates cGMP-dependent protein kinase which causes vasodilation.

  • Stress on small arterioles initiates release of NO from larger vessels upstream to ensure adequate perfusion to match increased demand. 

Endothelin: causes local vasoconstriction, released from damaged endothelium. Prevents blood loss

 

13

What is chronic local control?

Control of the amount of blood vessels supplying a tissue 

14

Which mechanisms control chronic local perfusion?

Lack of oxygen in tissues causes release of angiogenic growth factors which stimulate increased vascularity to a level which is adequate for tissue requirement. 

 

15

Describe neural blood pressure control 

Afferents to vasomotor centres in medulla:

  • Direct stimulation: CO2, hypoxia
  • Excitatory inputs: 
    • Pain pathways and muscles
    • Carotid and aortic chemoreceptors
    • Cortex via hypothalamus
  • Inhibitory inputs:
    • Lungs
    • Carotid, aortic and cardiopulmonary chemoreceptors
    • Cortex via hypothalamus

 

16

What type of nerves innervate blood vessels?

Cholinergic: fibres travel with sympathetic nerves

  • Vasodilators: no constant tone 

Noradrenergic: on all vessels 

  • Vasoconstrictors: constant tone

 

17

What does sympathetic innervation to the cardiac muscle cause?

Positive ionotropy and postitive chronotropy 

(Increases speed and force of contraction of the heart muscle)

(In constant opposition with vagal innervation)

 

18

How do sympathetic and parasympathetic nerves control BP?

  • Adrenalin and noradrenalin
    • Secreted by sympathetic nerves which also stimulate their release from the adrenal medulla (control with both local and systemic secretion)
    • Noradrenaline= vasoconstriction
    • Adrenaline= vasoconstriction and can also vasodilate, e.g. coronary arteries. 

19

Which hormones are involved in the control of blood pressure?

  • Atrial natriuretic peptide
  • Anti-diuretic hormone
  • Adrenalin and noradrenalin
  • Kinins
  • Renin-angiotensin system

 

20

How does the renin-angiotensin system affect BP?

  • Renin-angiotensin system
    • ​Potent vasoconstrictor at arterial level
    • Increases total peripheral resistance
    • Constricts renal afferent and efferent arterioles reducing renal blood flow and increasing sodium and water retention
    • Stimulates ADH secretion
    • Increases thirst

21

How does anti-diuretic hormone (vasopressin) affect BP?

  • Synthesised in hypothalamus and released from posterior pituitary in response to afferent baroreceptor stimulus. 
  • Potent vasoconstrictor
  • Can reduce renal blood flow and GFR
  • Increases water permeability of the collecting duct luminal membrane by inserting protein channels for water reabsorption. 

22

How does histamine affect BP?

Released from mast cells 

Potent vasodilator

Can cause oedema

 

23

How do kinins affect blood pressure?

What are they activated and inactivated by?

 

Kallikrien: activated by tissue inflammation or maceration. Acts on alpha2 globulins to produce Kallidin which is modified to produce bradykinin.

  • Inhibited by kallikrien inhibitor

Bradykinin is a vasodilator and increases vascular permeability

  • Inactivated by carboxypeptidase

 

24

How does atrial natriuretic hormone affect blood pressure?

Activation of stretch receptors in cardiac muscle cells causes release of ANP.

Causes renal excretion of sodium and water

Increases GFR by dilating afferent and constricting efferent arterioles

Inhibits renin secretion and aldosterone release. 

25

Which factors cause vasoconstriction?

  • Local factors:
    • Low temperature
    • Autoregulation
  • Local hormones:
    • Endothelin
    • Serotonin
  • Circulating hormones:
    • Noradrenaline
    • Adrenaline
    • Angotensin II
    • Neuropeptide Y
    • Vasopressin
  • Neural control:
    • Increased noradrenergic vasomotor stimulation

26

Which factors cause vasodilation?

  • Local factors:
    • CO2
    • Hypoxia
    • Potassium
    • Adenosine
    • Lactate
    • Increased temp
    • Decreased pH
  • Local hormones:
    • Nitric oxide
    • Kinins
  • Circulating hormones:
    • Atrial natriuretic peptide
    • Substance P
    • Histamine
    • VIP
    • Adrenaline in skeletal muscle and liver
  • Neural factors:
    • Decreased noradrenergic vasomotor stimulation
    • Activation of cholinergic discharge dilator fibres to skeletal muscle