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Cardiovascular physiology > Control of blood flow > Flashcards

Control of blood flow Flashcards

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1
Q

What is perfusion pressure?

A

Arterial bp - venous bp

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2
Q

What is equation for tissue blood flow?

A

Perfusion pressure/resistance

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3
Q

What is equation for resistance?

A

Poiseuille’s law

8 x viscosity x l / pi x r^4

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4
Q

What are the two ways that blood flow can be controlled?

A

Change blood pressure

Change resistance

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5
Q

3 ways of changing pressure?

A

Cardiac contraction (i.e. hormones, nerve, Starling)

Water/salt balance (i.e. blood volume through kidney, sweating)

Vessel compliance and tension

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6
Q

Why does increasing volume increase pressure?

A

Blood virtually incompressible unlike air

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7
Q

Normally increasing blood volume increases pressure, Why is increase in blood volume dampened in circulatory system?

A

Arteries are compliant and stretch to accommodate more fluid without proportional increase in pressure

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8
Q

Why does bp increase with age (how do arteries change)?

A

Vessels more stiff and less compliant e.g. atherosclerosis

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9
Q

What is problem with controlling blood flow by changing blood pressure?

A

Changes in bp often associated with pathology, and doesn’t allow local regulation to be achieved.

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10
Q

What is after-load?

A

The resistance against which heart has to work to pump blood into arteries

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11
Q

What is resistance to blood flow determined by (i.e. afterload)?

A

Diameter, total cross sectional area and blood viscosity

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12
Q

Why are arterioles resistance vessels?

A

Greatest drop in blood pressure as blood flows through arterioles.

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13
Q

Which vessel is mainly responsible for resistance to flow?

A

Arterioles

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14
Q

How does blood flow change going from arteries through to veins?

A

Stays the same, from artery, arterioles, capillary etc

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15
Q

How do pressure and resistance change as you go from artery to venules?

A

In arterioles, large rise in resistance and thus drop in pressure (to maintain constant flow)

Resistance then drops by the time you’ve reached capillaries and remains low, as does pressure.

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16
Q

How can large arteries change to increase bp?

A

Large artery contraction reduces their compliance and increases bp

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17
Q

Describe the state of the muscles of arterioles?

A

Most in tonic constriction due to symp stimulation

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18
Q

How does increase in diameter by factor 2 change bp?

A

By factor 16

2^4

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19
Q

Same flow throughout given vascular bed so greatest fall in pressure in region…

A

Of greatest resistance

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20
Q

How can arteriole resistance be altered?

A

Modulate vascular tone

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21
Q

Describe how control of vascular tone of arteries and arterioles differ

A

Artery under extrinsic control only, arterioles both intrinsic and extrinsic

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22
Q

High basal tone of arterioles in areas where….

A

Blood flow needs to be changed to greater degree e.g. skeletal muscle

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23
Q

What happens when you vasoconstrict arterioles (to larger vessels and capillaries)?

A

Pressure upstream increases (hence hypertension in large vessels)

Also decrease capillary perfusion downstream

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24
Q

What happens to capillaries as you vasodilate?

A

Increased capillary recruitment and increase capillary perfusion

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25
How do arterial and capillary bp change with vasoconstriction of arterioles?
Arterial bp increases | Capillary pressure decreases
26
How does capillary recruitment occur, which tissue is it important for?
Some capillaries only recruited at higher perfusion pressures important in skeletal muscle
27
Describe relationship between arterial bp and blood flow
Directly proportional
28
Where is high basal flow needed (which organs), what's the consequence?
Vascular beds of kidneys and brain (otherwise renal failure, coma)
29
What does perfusion normally match?
Metabolic rate
30
Which organs are overperfused (greater than metabolic need, why?
Other/non-metabolic need for high blood flow Kidney: blood needed to be filtered Skin: blood to lose heat
31
Which organs are usually underperfused?
Brain and heart
32
What are some extrinsically triggered factors that can affect local flow?
Sympathetic: Adrenaline, noradrenaline Parasympathetic: Acetylcholine Angiotensin
33
What are some local autocoids that control blood flow locally?
``` Histamine Bradykinin Prostaglandis Leukotrienes Endothelins NO ```
34
What are metabolic factors that control blood flow locally?
``` High extracellular K+ Acidity Adenosine Temp Hypoxia ```
35
Where do we not see autoregulation?
Pulmonary, cutaneous
36
What does autoregulation allow?
Tissues to control/stabilise perfusion independent of arterial bp
37
What is the Bayliss effect?
Myogenic autoregulation keeps blood flow constant. as blood pressure distends vessels, they undergo sustained contraction (maintains basal tone)
38
What is the mechanism behind the Bayliss effect?
Stretch creates tension, opens non-specific cation channels, opens voltage gated Ca2+ channels, raised concentration of Ca2+ leads to contraction of the vessel.
39
What can override autoregulation?
Local metabolic control
40
How can high perfusion pressure contribute to autoregulation?
Increased perfusion pressure increases blood flow, flushing away vasodilators so vascular tone increases
41
How can local metabolic control allow flow to a individual vascular bed to be controlled?
Flow altered based on tissue's metabolic demand. Arterioles sensitive to metabolic demands of tissue
42
What can trigger increase in local factors?
Increased metabolites, ischaemia, increased sheer stress to elevated blood flow
43
What do metabolic byproducts cause, why is this important?
Vasodilation, increased blood flow through vascular bed for increased oxygen supply and waste removal
44
What is metabolic hyperaemia?
Increase in blood flow to a more metabolically active tissue
45
Where is adenosine release important?
Coronary circulation, less so skeletal
46
How does adenosine cause vasodilation?
Increased ATP demand in coronary vessels as oxygen consumption increases Less ATP available as it's used up, AMP builds up released from cells Forms adenosine (primary product of ATP breakdown) Stimulates A2A receptors on smooth muscle Increases cAMP Decreased MLCK activity (PKA phosphorylates) vasodilation
47
What does adenosine do to kidney circulation?
Vasoconstriction (A1 adenosine receptor)
48
Where is acidity an important local factor?
The brain
49
How does acidity lead to increased cerebral circulation?
Increased rate of metabolism/respiration/oxidative phosphorylation Increased pCO2 Increased carbonic acid concentration Increased acidity decreases open probability of ion channels in membrane and inhibits MLCK Vasodilation
50
What does low pCO2 cause to vessels in brain, what are the symptoms?
Vasoconstrict, so dizziness
51
Where is accumulation of K+ important metabolic factor?
Skeletal muscle and brain
52
What is the mechanism for increased K+ extracellularly and blood flow?
K+ release by action potentials in active muscle fibres In intense exercise, high frequency of AP fired, not all of K+ can go back into cell Small increase in extracellular potassium conc Leads to Increased potassium permeability Hyperpolarisation as Ek is neared Vasodilation
53
Where does reactive hyperaemia occur?
Skeletal muscle
54
What is reactive hyperaemia?
If you contract muscle, muscle compresses arterioles and capillaries, TPR increases, leading to ischaemic tissue then you accumulate metabolites, When you release compression, leads to massive increase in blood flow as these vasodilator metabolites cause vasodilation
55
How can metabolic demand be coupled to blood flow given arterioles are upstream of capillary beds?
Arteriole can affect capillary perfusion Intracellular signal in response to vasoactive substance propagating through gap junctions. Paracrine signalling, e.g. in nephron, cells of macula densa which sense metabolic demand and are stuck on top of afferent arteriole.
56
Why is local control systems better than sympathetic stimulation to control vascular tone?
Sympathetic system can't be used as well to respond to needs of a particular tissue/organ
57
How is endothelium important in control of blood flow, what does it respond to?
Produce modulators of local vessel tone in response to changes in local environment
58
What does endothelium produce (gas) and when?
NO produced in response to hypoxia, shear stress, circulating neuroendocrine factors (e.g. Ach, bradykinin)
59
How is NO made?
Stimuli increases intracellular calcium, binds calmodulin and activates eNOS (produces NO)
60
What happens to NO after it's made?
Diffuses into vessel wall, activation of guanylyl cyclase, cGMP made, activates PKG
61
What does PKG phosphorylate?
MLCP which is activated to inhibit MLCK K+ channels (which open) so reduced Ca2+ influx through VGCC SERCA - so Ca2+ removal from cytosol Ca2+ channels so they open less
62
What else apart from NO does endothelium produce?
Prostacyclin 2 PGE2 Endothelium derived hyperpolarising factor
63
What are some vasoconstrictors?
Thromboxane AE, endothelins
64
What are some autacoids that are vasodilators?
``` Prostaglandis Leukotreienes Histamine Bradykinin NO ```
65
What produces Thromboxane A2?
Platelets
66
Why is extrinsic control of blood flow important?
Fulfil wider CV functions and anticipate future demand (e.g. coordinated response to exercise)
67
How does SNS lead to vasoconstrition?
NA acts on alpha 1 on vascular smooth muscle. Also ATP and neuropeptide Y often cotransmitters with NA which cause rapid and long lasting vasoconstriction respectively
68
What underpins resting tone of most arteries and arterioles?
Tonic activity of sympathetic vasoconstrictor fibres
69
How does stimulation of beta receptors in kidney lead to vasoconstriction?
Activate renin angiotestin aldosterone system (RAAS) Angiotensin 2 production and vasoconstriction through stimulation of AT1 receptors on smooth muscle
70
How can sympathetic stimulation cause vasodilation?
Beta 2 receptors in arterioles (and some veins) supplying skeletal muscle. activated by NA
71
How can parasympathetic fibres cause vasodilation?
In cerebral and coronary arteries, ACh released acting on M2 receptors on VSM. Hyperpolarisation and vasodilation
72
What does ADH get produced in response to?
Fall in blood volume
73
What releases ADH?
Posterior pituitary
74
What does vasopressin do to blood vessels?
Vasoconstriction in most tissues but vasodilation in cerebral and coronary tissue (redistribute blood)
75
When is renin secreted?
Fall in blood pressure and fall in Na+ in distal tubule
76
What does renin do help to maintain bp and thus blood flow?
Converts angiotensinogen to angiotensin 1, which is converted to angiogensin 2 in lungs (by ACE). Angiotensin 2 causes vasoconstriction. Also causes increased aldosterone secretion leading to greater salt and water reabsorption from distal tubule so increased blood volume
77
What is ANP, where is it made?
Atrial natriueretic peptide made by atrial myocytes
78
When is ANP made?
In response to high cardiac filling pressures. Triggers excretion of salt and water by renal tubules and weakly vasodilates resistance vessels
79
How is coronary circulation mainly controlled?
Metabolic hyperaemia (adenosine) Sympathetic stimulation and circulating adrenaline (beta 2 receptors on VSM causes vasodilation)
80
Why does oxygen extraction for heart need to be very high?
During periods of high cardiac work as contraction more forceful and frequent. High pressure in ventricular wall in systole shuts off coronary circulation
81
What are the 2 resistance vessels in cutaneous circulation, what controls them?
Arterioles (sympathetic and local metabolic control) Arteriovenous anastomoses AVAs (sympathetic vasoconstrictors control only)
82
How does fall in temp affect cutaneous circulation?
Receptors in hypothalamus detect it. Sympathetic signalling increases so AVA constrict so high resistance shunt created and reduced cutaneous flow. Directs blood away from surface of skin
83
What is the effect of dilating AVAs?
Increased heat loss
84
What are the different ways skeletal muscle circulation can be altered?
Metabolic hyperaemia (esp K+, some adenosine) Capillary recruitment Reactive hyperaemia (autoregulation affects flow too)
85
How does TPR fall in exercise, what stops it completely falling in exercise?
Metabolic hyperaemia (e.g. K+) causes vasodilation, TPR decreases. Fall in bp detected by baroreceptors which trigger sympathetic activation to further increase perfusion of active muscle and prevent excessive fall in TPR.
86
How is renal circulation controlled?
Autoregulation keeps flow constant Angiotensin 2 and ADH (vasoconstrictors regulate renal blood flow) Sympathetic stimulation: vasoconstriction
87
What alters pulmonary circulation?
Hypoxia/hypercapnia arterioles constrict, diverting blood to well oxygenated areas (better V/Q mismatch). Pulmonary hypoxic vasoconstriction
88
Why is there no autoregulation in pulmonary circulation?
If excessive vasoconstriction occurred in pulmonary regulation, blood from RHS of heart would not be able to bypass lungs to reach LHS and also lungs vulnerable to hypertension (oedema)
89
What does 5HT do?
Vasodilator via NO production
90
What does vagus stimulation to coronary resistance vessels do?
Dilates them
91
True of false, lowered pH, and hypoxia causes relaxation of coronary vessels?
False, adenosine is the only real coronary vasodilator
92
How do you calculate mean arterial blood pressure?
Estimated using a formula in which the lower (diastolic) blood pressure is doubled and added to the higher (systolic) blood pressure and that composite sum then is divided by 3
93
Is MAP calculated by arithmetic average of diastolic and systolic pressure?
No
94
When do the heart sounds come relative to the ECG?
1st: After QRS 2nd: After T wave
95
Describe ECG for 3rd degree heart block
Third-degree AV block exists when more P waves than QRS complexes exist and no relationship (no conduction) exists between them.
96
What vessels have the greatest compliance?
Veins

Cardiovascular physiology (11 decks)

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