Control of circulation Flashcards

1
Q

Why do we need control?

A

In order to:
- Maintain blood flow
- Maintain arterial pressure
- Distribute blood flow
- Auto-regulate/homeostasis
- Function normally
- Prevent catastrophe! (maladapt in disease)

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2
Q

What are the components of circulation?

A
  • Anatomy
  • Blood
  • Pressure
  • Volume
  • Flow
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3
Q

Where is the majority of the blood volume in circulation?

A
  • small vessels then veins then large arteries
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4
Q

What are the three layers of blood vessels?

A

Tunica Intima : Innermost, Endothelial cells create slick surface for smooth blood flow , Only one cell thick

Tunica Media : Middle layer, smooth muscle cells, elastin protein sheets

Tunica Externa : Outermost, loosely woven fibres of collagen, elastic

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5
Q

Describe arteries?

A
  • Carry blood away at high pressure
  • Thick, strong walls containing muscles, elastic, fibrous (helps maintain high Bp)
  • Narrow lumen
  • No valves
  • Thick media compared to veins
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6
Q

Describe the arterioles?

A

Smallest arteries
Site of most resistance
Thick tunica media
Regulate blood flow to organs

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7
Q

What is TPR?

A
  • Total peripheral resistance
  • Basically arteriolar resistance
  • Vascular smooth muscle (VSM) determines radius
  • VSM Contracts = ↓Radius = ↑Resistance ↓Flow
  • VSM Relaxes = ↑Radius = ↓Resistance ↑Flow
  • Or Vasoconstriction and Vasodilatation
  • VSM never completely relaxed = myogenic tone
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8
Q

Describe the capillaries?

A
  • Supply all cells and take away waste
  • Very thin (one cell)
  • Very narrow
  • Allow diffusion of materials easily
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9
Q

Describe veins?

A
  • Return blood at low pressure
  • thin, fibrous, far less muscle and elastic tissue than arteries
  • valves for backflow
  • Wide lumen for less resistance
    Thicker externa than arteries
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10
Q

describe the lymphatics?

A
  • Fluid/protein excess filtered from capillaries
  • Return of this interstitial fluid to CV system: Thoracic duct; left subclavian vein
  • Uni-directional flow aided by:
    Smooth muscle in lymphatic vessels
    Skeletal muscle pump
    Respiratory pump
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11
Q

Cardiac output (CO) =

A

Heart rate (HR) x stroke volume (SV)

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12
Q

Blood pressure =

A

CO x TPR (like Ohms’ Law V=IR)

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13
Q

Pulse pressure =

A

systolic - diastolic pressure

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14
Q

Mean arterial pressure=

A

Diastolic pressure + 1/3 PP

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15
Q

Ohm’s Law =

A

V = IR
V: Voltage
I: Current
R: resistance

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16
Q

Poiseuille’s equation

A

Flow = radius to the power of 4
(Small difference in radius = big difference in flow)

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17
Q

What is the Frank- Starling Mechanism?

A
  • SV increases as End-Diastolic Volume increases
  • Due to Length-Tension (L-T) relationship of muscle
  • ↑EDV = ↑Stretch = ↑Force of contraction
  • Cardiac muscle at rest is NOT at its optimum length
  • ↑VR = ↑EDV = ↑SV = ↑CO (even if HR constant)
    Starlings law: Force of contrition is proportional to the end diastolic length of cardiac muscle fibre - the more ventricle fills the harder it contracts
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18
Q

What is the blood volume and its determinants?

A
  • Venous return important beat to beat (FS mechanism)
  • Blood volume is an important long term moderator
  • BV = Na+, H20
    Regulators:
  • Renin-Angiotensin-Aldosterone system
  • ADH
  • Adrenals and kidneys
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19
Q

What is the goal of control of circulation?

A

Maintain blood flow: CO= SV x HR
This needs pressure to push blood through the peripheral resisterance

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20
Q

What is blood pressure?

A

BP = Pressure of blood within and against the arteries

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21
Q

What is systolic BP?

A

Systolic = Highest, when ventricles contract (100-150mmHg)

22
Q

What is diastolic BP?

A

Diastolic = Lowest, when ventricles relax (not zero, due to aortic valve and aortic elasticity .. 60-90mmHg)

23
Q

What is the mean arterial pressure

A
  • Mean arterial pressure = D + 1/3(S-D)
  • Measured using a sphygmomanometer
  • Using brachial artery:
    Convenient to compress
    Level of heart
24
Q

How do we measure blood pressure?

A

Ingredients:
Arm, Sphygmomanometer, Stethoscope, 2 Ears

Directions:
Inflate cuff to above systolic BP (about 180) , until pulse
impalpable or Korotkoff sounds absent.

Serving suggestion:
Slowly deflate cuff, listening all the time.

25
Q

What sounds are we listening for when taking a blood pressure?

A

0) > Systolic Pressure = no flow, no sounds
1) Systolic pressure = high velocity = tap
2-4) Between S and D = thud
5) Diastolic pressure = sounds disappear

26
Q

What are some components of blood pressure control?

A
  • Local mediators
  • Humoral factors
  • Baroreceptors
27
Q

What is myogenic autoregulation?

A

Myogenic autoregulation: When blood flow is increased and stretches vascular smooth muscle the muscle automatically constricts until the diameter is normalised
or slightly reduced.
Furthermore when the smooth muscle isn’t getting stretched as much due to low blood pressure, the muscle relaxes and dilates in response.

28
Q

How does auto regulation vary?

A
  • Intrinsic ability of an organ
  • Constant flow despite perfusion pressure changes
    Renal/Cerebral/Coronary = Excellent
    Skeletal Muscle/Splanchnic = Moderate
    Cutaneous = Poor
29
Q

How does auto regulation vary?

A
  • Intrinsic ability of an organ
  • Constant flow despite perfusion pressure changes
  • Renal/Cerebral/Coronary = Excellent
  • Skeletal Muscle/Splanchnic = Moderate
  • Cutaneous = Poor
30
Q

How do we balance extrinsic and intrinsic control?

A

Brain & heart: intrinsic control dominates to maintain BF to vital organs
Skin: BF is important in general vasoconstrictor response and also in responses to temperature (extrinsic) via hypothalamus
Skeletal muscle: dual effects:- at rest, vasoconstrictor (extrinsic) tone is dominant; upon exercise, intrinsic mechanisms predominate

31
Q

Give an example of a vasoconstrictor?

A
  • Endothelin -1
32
Q

Give an example of a vasodilator?

A
  • Hypoxia
  • Adenosine
33
Q

What does the endothelium do in controlling functions?

A
  • Single layer or spindle/pavement cells with tight adhesions between adjacent cells
  • Little cytoplasm and intra-cellular organelles - but gap/adheren junctions are prominent
  • They may be fenestrated (have pores in them for rapid diffusion) in the liver, kidney glomeruli & endocrine tissues
  • In some areas they may be very thin (lung) to enable rapid fluid & gas transfer
  • Essential for control of the circulation
  • EDRF = Nitric Oxide (NO) = potent vasodilator
  • L-Arg is converted into NO by NO synthetase
  • Prostacyclin = potent vasodilator
  • Endothelin = potent vasoconstrictor
34
Q

What is the Furchgott’s Experiment?

A

He found that when the endothelium had been rubbed of a cell and acetyl choline was added the vessel constricted and the opposite for if it was in tact. Shows that endothelium has a vital role in dilation/constriction

35
Q

How does Nitric acid affect the vessels?

A

Nitric oxide: released by endothelial cells - triggers vasodilation [POTENT]

36
Q

How does Endothelin-1 affect the vessels?

A

Endothelin-1 (ET-1) - released by endothelium cells results in vasoconstriction [POTENT]

37
Q

How does Prostacyclin/ Prostaglandin I2 (PGI2)affect the vessels?

A
  • Prostacyclin/ Prostaglandin I2 (PGI2): released by endotheliaal cells - triggers vasodilation [POTENT]
38
Q

What is the response to hormones? (vasoconstrictors)

A
  • Vasoconstrictors: angiotensin II, vasopressin & adrenaline
39
Q

What is the response to hormones? (vasodilators)

A

Vasodilators: Atrial Natriuretic Peptide, adrenaline

40
Q

What are baroreceptors?

A

Cardiopulmonary baroreceptors:
- Located in the atria, ventricles & pulmonary artery
- When stimulated i.e high blood pressure leads to the inhibition of the pressor region/ vasoconstrictor centre in the medulla - leading to a fall in blood pressure
- Also inhibits the Renin-angiotensin & aldosterone system - since angiotensin II stimulates vasoconstriction which will increase blood pressure, also aldosterone stimulates more Na+ and thus H2O reabsorption thereby increasing blood volume and thus pressure
- Also inhibits vasopressin/ADH - since it too stimulates more water reabsorption
- Thus when stimulated the cardiopulmonary baroreceptors bring about a decrease in blood pressure by promoting vasodilation & fluid loss

41
Q

What are arterial baroreceptors?

A
  • Key role in short-term regulation of BP; minute to minute control, response to exercise, haemorrhage
  • If arterial pressure deviates from ‘norm’ for more than a few days they ‘adapt’/’reset’ to new baseline pressure eg. in hypertension
  • The major factor in long-term BP control is blood volume
  • stretch receptors that respond to pressure
42
Q

What are cardiopulmonary baroreceptors?

A
  • Cardiopulmonary baroreceptors (in atria, ventricles & pulmonary artery) control long term blood pressure
  • Stimulation = ↓vasoconstrictor centre in medulla, = ↓ BP
  • Also ↓release angiotensin, aldosterone & vasopressin (ADH), leading to fluid loss
  • Play an important role in blood volume regulation
43
Q

What is the medullary cardiovascular centre?

A
  • Located in the medulla, within this there is a region called the Pressor region (region responsible for raising blood pressure) - it is sympathetic 30 KP
  • The pressor region increases blood pressure by ↑ vasoconstriction, ↑ cardiac output (by ↑ heart rate and stroke volume (more forceful contraction)) and ↑ contractility
  • Pressor region > sympathetic route > medulla > spinal cord > synapses at T1-L2 > Heart
44
Q

What are the main neural influences on the medulla?

A
  • Baroreceptors
  • Chemoreceptors
  • Hypothalamus
  • Cerebral cortex
  • Skin
  • Changes in blood [O2] and [CO2]
45
Q

How does the hypothalamus respond to blood flow?

A
  • CV reflexes require hypothalamus and pons
  • Stimulation of anterior hypothalamus ↓ BP and HR; reverse with posterolateral hypothalamus
  • Hypothalamus also important in regulation of skin blood flow in response to temperature
46
Q

How does the cerebral cortex affect blood flow?

A

Cerebral cortex can affect blood flow & pressure. Stimulation usually ↑ vasoconstriction, but emotion can ↑ vasodilatation and depressor responses eg. blushing, fainting. Effects mediated via medulla but some directly

47
Q

What is the role of central chemoreceptors?

A

Central chemoreceptors in the medulla: respond mainly to a decrease in pH (due to CO2 diffusing across the blood brain barrier thereby reducing the pH of the CSF)
- Peripheral chemoreceptors:
* In the aortic arch & carotid sinus (base of internal carotid artery - at the division between the internal and external carotid), stimulated by a fall in PaO2 & a rise in PaCO2 & a fall in pH causing blood pressure to increase

48
Q

As a summary what is the short term response to an increased blood pressure?

A

Short term:
Baroreceptors
↑BP ⇒ ↑Firing ⇒ ↑PNS/↓SNS ⇒ ↓CO/TPR = ↓BP

49
Q

As a summary what is the long term response to an increased blood pressure?

A

Long term
Volume of blood
Na+, H20, Renin-Angiotensin-Aldosterone and ADH

50
Q

What is the pathological relevance?

A
  • Fainting
  • Orthostatic hypotension (standing quickly, too long, dehydration, hot room
    Fall in BP and Venous Pooling (X nerve). Failure to reflexly maintain BP and HR. Perfusion to brain reduced)
  • POTS (‘Postural orthostatic tachycardia syndrome’ - Standing
    Palpitation, dizzy, near syncope, sweating, debilitating
    Physiology = Excess tachycardia response
    Investigate = Tilt test
    HR↑ >40bpm; BP usually OK
  • Heart failure
51
Q

What is the physiological relevance?

A
  • Cold
  • Standing up
  • running
  • Injury
  • Blood loss (Eventually .. SHOCK (BP↓, Pulse↑, organ hypoperfusion and death - Treat: rapid volume replacement_
52
Q

What are the 3 layers of blood vessels?

A

Tunica Intima: Innermost, endothelial cells create smooth surface, only one cell thick

Tunica Media: Middle layer, smooth muscle cells, elastin

Tunica Externa: Outermost, loosely woven fibres of collagen, elastic