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Block 2 > Pressures & Flows In The Systemic & Pulmonary Circulation > Flashcards

Pressures & Flows In The Systemic & Pulmonary Circulation Flashcards

1
Q

Define Systolic Blood Pressure (SBP).

A

The pressure being exerted against the arterial wall during ventricular systole, measured at the point where the pulse sound is first heard when the sphygmomanometer pressure is reduced from a starting pressure of around 180mmHg.

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2
Q

Define Diastolic Blood Pressure (DBP).

A

The pressure being exerted against the arterial wall during ventricular diastole, measured at the pressure when the pulse sound disappears.

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3
Q

How is Blood Pressure (BP) written?

A

SBP/DBP

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4
Q

Define Mean Arterial Pressure (MAP).

A

The average arterial pressure during one cardiac cycle: 1/3 (SBP-DBP) + DBP.

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5
Q

What are baroreceptors?

A

Pressure sensors that detect stretch within blood vessels located throughout the vascular tree

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6
Q

What are the 2 types of baroreceptor?

A
  1. High pressure in arterial system

2. Low pressure in venous system + R heart

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7
Q

Where the most important arterial baroreceptors found?

A

Carotid sinus at the bifurcation of external + internal carotids

In the aortic arch

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8
Q

How do arterial baroreceptors carry out their function?

A
  1. Constantly fire with arterial wall stretch during systole
  2. Decreased BP causes decreased firing rate
  3. Signal carried via CN X + IX nerves to medulla
  4. Increase sympathetic activity + decrease vagal activity
  5. Increased CO + SVR
  6. Increased BP
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9
Q

What do arterial baroreceptors have a vital role in?

A

Compensation for sudden BP reduction

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10
Q

Why do we need low pressure venous baroreceptors as well as arterial baroreceptors?

A

Venous system unresponsive to arterial baroreceptors

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11
Q

Where are low pressure venous baroreceptors predominantly found?

A

Atria
Ventricles
Pulmonary arteries

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12
Q

What do low pressure venous baroreceptors do?

A

Mitigate BP changes in response to volume via:

  • Peripheral vasodilation
  • Reduced renal sympathetic outflow + inhibited release of ADH from posterior pituitary gland resulting in increased urine excretion
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13
Q

What are low pressure venous baroreceptors also called?

A

Atrial stretch receptors

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14
Q

What is the function of chemoreceptors?

A

Stimulated by a change in the chemical environment in which they are located primarily in the respiratory system (sometimes CVS)

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15
Q

How do chemoreceptors work?

A

Stimulated by hypoxia, hypercarbia + pH change

Increase sympathetic outflow to heart + peripheral vasculature via medullary centres causing increase CO + BP

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16
Q

Where is the pressure highest and lowest in the systemic circulation?

A

Highest in aorta

Lowest in vena cava

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17
Q

Where is the pressure highest and lowest in the pulmonary circulation?

A

Highest in pulmonary arteries

Lowest in pulmonary veins

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18
Q

Why is pressure low in capillaries?

A

Distensibility; stretch in response to increase volume rather than increasing pressure

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19
Q

If flow through the circulation is constant, what does this mean for volume?

A

Volume of pulmonary bed must significantly exceed that of systemic bed

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20
Q

Describe the arterial pressure curve.

A
  1. AV opens
  2. Systolic upstroke
  3. Systolic peak pressure
  4. Systolic decline
  5. Dicrotic notch as AV closes
  6. Diastolic runoff
  7. End-diastolic pressure
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21
Q

What does the dicrotic notch indicate?

A

That the pressure of the ventricle has decreased below that of the aorta as the AV closes

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22
Q

Why is there pulse pressure augmentation as you move peripherally along arteries?

A

Increased vessel wall rigidity/decreased wall elasticity

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23
Q

Explain the connection between Poiseuille’s equation and flow through a vessel.

A

Because of 4th power flow reduction, arterioles can influence blood flow with relatively minor radius changes

Each vessel running in parallel controls its own flow but vasoconstriction in one will increase combined resistance

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24
Q

What is the main function of veins?

A

Capacitance (storage) vessels

Regulate CO by modifying venous return

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25
Q

How can venous calibre be altered?

A

Increased sympathetic tone can sufficiently venoconstrict to maintain circulatory volume with 25% blood loss

Reduced tone + venodilation can accommodate rapid infusion of 500mls of blood

26
Q

How is blood flow in the venous system controlled?

A
  1. Valves: ensure one way flow of blood from tissue to heart; contract when muscles surrounding them contract
  2. Resistance via fixed obstructions e.g. rib 1 + neck as venous pressure < atmospheric
27
Q

What is lymph fluid?

A

The 10% of interstitial fluid drainage that is returned from tissues to the circulation

28
Q

How does lymph fluid flow around the body?

A

Flow passive + peristaltic

Valves ensure one way flow + contract with skeletal muscle contraction

Enter circulation via one way valves between endothelial cells in lymphatic capillary

29
Q

What is the main function of lymphatics?

A

Major route of nutrient transport from the bowel

30
Q

How is bacteria removed from lymphatics?

A

When lymph nodes are traversed

31
Q

What are the outcomes of control of local perfusion?

A
  • Delivery of O2 to tissues
  • Delivery of nutrients e.g. glucose, AAs + FAs
  • Removal of CO2 from tissues
  • Removal of H+ ions from tissues
  • Maintenance of proper [ion] in tissues
  • Transport of hormones + other regulatory substances to various tissues
32
Q

What are the 2 types of local perfusion control mechanisms?

A
  1. Acute: mins

2. Chronic: hrs-wks

33
Q

What is the main function of acute local perfusion control mechanisms?

A

Occurs through changes in diameter of valves in arterioles + capillaries

34
Q

What is local (organ) control of perfusion?

A

Causes dramatic differences of blood between + within organs keeping the baseline flow just above the minimum flow requirement

35
Q

Describe the 2 mechanisms used by acute local perfusion control mechanisms.

A
  1. Vasodilation: due to increased metabolic needs of tissue
  2. Other nutrient deficiencies e.g. glucose or B vitamins, as in Beri-Beri may exert individual control on individual tissue perfusion
36
Q

What are the 2 theories that may explain why vasodilation occurs?

A
  1. Oxygen demand theory: surrounding tissue hypoxia causes muscle relaxation
  2. Vasodilator substance theory: vasodilators e.g. ADP released from hypoxic tissue surrounding vessels
37
Q

What does Nitric Oxide (NO) do to blood vessels in acute local perfusion control mechanisms?

A

Sheer stress (e.g. high BP/volume) on small tissue arterioles cause release of NO in larger upstream arterioles to ensure adequate perfusion to match tissue metabolic demand via:

  1. NO released by endothelial cells
  2. Activation of cGMP-dependent protein kinase
  3. Vasodilation
38
Q

What does endothelin do to blood vessels in acute local perfusion control mechanisms?

A

Potent vasoconstrictor released from damaged endothelium acting locally to prevent excessive blood loss from traumatised blood vessels

39
Q

Why do you need chronic control mechanisms of local tissue perfusion?

A

Acute control mechanisms will increase blood flow to a level which falls short of meeting the increased tissue metabolic demands so chronic mechanisms complete the compensation process

40
Q

How do chronic local perfusion control mechanisms work?

A

Lack of O2/other nutrients in a tissue cause release of small peptides called angiogenic growth factors which stimulate increased tissue vascularity to a level determined by maximum tissue requirement

41
Q

What are the 3 ways in which systemic blood pressure is controlled by neural mechanisms?

A
  1. Afferents to the vasomotor centre in medulla
  2. Blood vessel innervation
  3. Cardiac innervation
42
Q

What directly stimulates afferents to the vasomotor centre in the medulla?

A

CO2

Hypoxia

43
Q

What are the excitatory and inhibitory inputs to the afferents to the vasomotor centre in the medulla?

A

Excitatory: from cortex via hypothalamus, from pain pathways + muscles, from carotid + aortic chemoreceptors

Inhibitory: from cortex via hypothalamus, from lungs + from carotid, aortic + cardiopulmonary baroreceptors

44
Q

What is the blood vessel innervation for neural perfusion control?

A

Noradrenergic nerve ends on vessels: vasoconstrictors - constant tone

Cholinergic fibres travel with sympathetic nerves: vasodilators - no constant tone

45
Q

What is the cardiac innervation for neural perfusion control?

A

Sympathetic stimulation to heart causes positive ionotropism + chronotropism

Constant opposition with vagal tone

46
Q

What hormones control blood pressure systemically?

A 
A + NA
Renin-angiotensin system
ADH
ANH
Local mediators
Kinins
47
Q

How do adrenaline and noradrenaline control blood pressure?

A

Secreted by sympathetic nerves which also stimulate their release from adrenal medulla

NA is a vasoconstrictor but A can also vasodilate (for e.g. in coronary arteries)

System provides dual control with local + systemic secretion of mediators

48
Q

How does the renin-angiotensin system control blood pressure?

A
  1. Decreased BP stimulates renin release from JGA
  2. Renin converts angiotensinogen to angiotensin I
  3. ACE converts angiotensin I to II
  4. Angiotensin II has various effects
  5. Aldosterone released from zona glomerulosa of adrenal cortex too
49
Q

What are the actions of angiotensin II?

A
  • Potent vasoconstrictor at arterial level
  • Increases TPR
  • Constricts renal afferent + efferent arterioles reducing renal blood flow + increasing Na + H2O retention
  • Increases thirst + H2O intake
  • Stimulates ADH secretion
  • Directly inhibits renin secretion via -ve feedback loop
50
Q

What are the actions of aldosterone?

A
  • Controls reabsorption of Na in renal CCD
  • Induces production of proteins in CD e.g. Na + K membrane channels
  • Increases Na reabsorption from gut, sweat + salivary glands
  • > increase blood volume + BP alike angiotensin II
51
Q

Where is antidiuretic hormone (ADH)/vasopressin produced?

A

Synthesized in hypothalamus + secreted from posterior pituitary in response to reduction in baroreceptor afferent stimulus e.g. BP drop

52
Q

What does antidiuretic hormone (ADH)/vasopressin do?

A
  • Potent vasoconstrictor
  • Reduces renal blood flow + GFR
  • Increases H2O permeability of CD luminal membrane by inserting protein channels for H2O reabsorption
  • > increase blood volume + BP
53
Q

Where are histamine and other ions released?

A

Produced within mast cells + released in response to allergic tissue inflammation

54
Q

What are the affects of histamine and other ions involved in blood pressure regulation?

A

Histamine: potent vasodilator, increases permeability (if severe can cause oedema)

Ca: vasoconstriction due to SMC action

Mg, H+ & CO2: vasodilation

55
Q

What are kinins?

A

Small polypeptides that are split away from α2-globulins in plasma or tissue fluids by proteolytic enzymes

E.G. kallikrein

56
Q

How do kinins work?

A
  1. Kallikrein activated by tissue maceration or inflammation
  2. Acts on α2-globulins to create kallidin
  3. Kallidin modified to form bradykinin by tissue enzymes
  4. Bradykinin causes arteriolar vasodilation + increases vascular permeability
57
Q

What enzymes inhibit bradykinin and kallikrein?

A

Carboxypeptidase inactivates bradykinin

Kallikrein inhibitor inhibits kallikrein

58
Q

What does Atrial Natriuretic Hormone (ANH) do?

A

Stimulation of stretch receptors in cardiac atrial cells stimulate ANP release which decreases BP via:

  • Increased renal excretion of Na + H2O
  • Increased GFR by dilating afferent + constricting efferent renal arterioles
  • Inhibition renin secretion + aldosterone release
59
Q

What cardiovascular changes occur in sepsis?

A
  • Hyperdynamic circulation
  • Local factor vasodilatation
  • Relative hypovolaemia
  • Increased tissue O2 demand
  • Decreased cardiovascular supply
60
Q

Describe the sepsis 6 in the management of sepsis.

A
  1. High flow O2
  2. Broad spectrum antibiotics
  3. IV fluid
  4. Blood cultures
  5. Measure serum lactate from bloods
  6. Measure hourly UO
61
Q

What are the 2 theories for why vasoconstriction may occur?

A
  1. Metabolic: increased BP increases flow which washes out vasodilator
  2. Myogenic: stretch placed on vessel walls induce constriction

Block 2 (45 decks)

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