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Unit 12 Week 1 (Sam) > Control of blood flow > Flashcards

Control of blood flow Flashcards

1
Q

Blood flow is driven by

A

pressure gradients (created by the pumping of the heatrt)

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2
Q

arterial blood pressure is kept constant moment to moment by the baroreceptor reflex

A
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3
Q

if you want to alter the blood flow to structures downstream you need to alter

A

upstream resistance

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4
Q

Darcy’s law of flow

A

change in BP= BF x Resistance

Therefore

BF= change in blood pressure (perfusion pressure) / R

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5
Q

Poisevilles law

A

small changes in the radius of the lumen of the blood vessels can have significant effects on the resistance of vessels

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6
Q

what are the 4 general blood flow control mechanisms

A
  1. local
  2. endothelial
  3. hormonal
  4. neural
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7
Q

body’s blood flow response to exercise

A
  • central command- triggers increase HR prior to exercise, feedback mechanisms, reset arterial baroreceptor
  • haemodynamics- redistribute blood flow away from non-essential organs -e.g., functional metabolic hyperaemia and inactive symp vasoconstriction
  • increased venous return- sympathetic venoconstriction, skeletal muscle pump, respiratory muscle pump
  • Recruitment and distension of previously closed capillaries in lungs
  • Trade off between cutaneous vasoconstriction and thermoregulation- constrict to maintain MAP, offsetting sk muscle dilation
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8
Q

local mechanism for controlling blood flow

A

metabolic + myogenic

used to autoregulate blood flow when BP changes

used to increase BF in response to an increased demand (e.g., exercise): active hyperaemia

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9
Q

Endothelial mechansim for controlling BF

A

nitric oxide- vasodilator

prostaglandins- vasodilator

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10
Q

hormonal (endocrine) mechanism for BF control

A

ADH- decreses water excretion and directly causes vasoconstriction

adrenaline- incresae contractility and heart rate- increased CO- increaed BP

Ang II- causes vasoconstriction and sodium and water retention

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11
Q

neural (central) mechnism for controlling BF

A

increase to sym outflow to arterioles causes vasoconstriction

Postganglionic symp neurones release NA onto arteriolar sm. muscle cells

stimulation of a1-adrenoreceptors cause a rapid increase in [Ca2+]cyt in arteriolar sm. muscle cells

contraction

at the same time epinephrine acts on B2 receptors in coronary arteries causing vasodilation

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12
Q

Intrinsic mechanisms to control BP

A

“regulation of BF to an organ by factors originating from within the organ”

a) autoregulation- metabolic, myogenic, endothelial
b) paracrine

C) Endothelial

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13
Q

active hyperaemia

A

example of intrinsic metabolic control of BF

increase in organ BF is associated with increased metabolic activitity of the tissue

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14
Q

functional hyperaemia

A

example of intrinsic metabolic control of BF

due to presence of metabolites and a change in general conditions

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15
Q

paracrine mechnosm for BF control

A

example of intrinsic control of BF

vasodilator and increases myocardial contractility

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16
Q

endothelial secretions mechnism of controlling BF

A

example of intrinsic control of BF

NO- vasodilator

endothelin- vasoconstrictor

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17
Q

myogenic response to stretch

A

stretching of afferent arterioles causes ion channels to open

increased presence of cations causes pacemaker cells to depolarise quicker

autoregulation especially in the afferent arteriole

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18
Q

extrinsinc factors for comntrolling blood flow

A

“regulation of BF to an organ by factors originating from outside the organ”

A) neural

b) endocrine

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19
Q

neural factors for controlling BF

A

example of an extrinsic factor

sympathetic vasoconstrictor fibres

parasympathtic vasodilators

nociceptive C-fibres

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20
Q

endocrine factors for controlling BF

A

examples of extrinsic factors for controlling BF

catecholamines- e.g., adrenaline casues vasodilation in muscle and liver vasculature at low levels B2-adrenergic and vasoconstriction at high levels a-adrenoreceptors

oestrogen- vasodilator and hypotensive

ADH and AngII hypertensive

ANP hypostensive

21
Q

intrinsic and extrinsic factors work together to shape a

A

co ordinated and whole body response

22
Q

with the onset of exercise the CV system has to:

A

increase BF to active muscles

increase BF through pulmonary circulation

increase heat loss via BF to skin

maintain ABP

23
Q

central command

A

“feedforward response that triggers an increase in HR prior to exercise onset”

motor cortex + other motor areas are responsible for triggering activation of the medullary cardiovascular control centres

this leads to increase HR prior to exercise

triggers central resetting

24
Q

central resetting

A

triggered by central command, arterial baroreflex is reset, allowing for greater hypertension during exercise

25
Q

what are the feedback mechanisms during the onset of exercise

A

increase in sympathetic efferent outflow to the CNS (e.g., by carotid body baroreceptors)

supported by additional feedback from the medullary control centres from:

a) skeletal muscle mechanoreceptors and metaboreceptors
b) arterial baroreceptors

26
Q

metaboreceptor

A

kind of chemorecepotr in sk muscle that responds to an increase in the production of metabolic products

stimulates increase in BF to area

27
Q

haemodynamics are due to

A

LOCAL not central (neural) mechanisms

28
Q

haemodynamics are

A

distribution of blood flow

29
Q

By which 3 mechanisms does venous return increase during exercise

A
  1. Symp venoconstriction
  2. skeletal muscle pump
  3. respiratory muscle pump
30
Q

symp venoconstriction affecting venous return

A
  • venous system capacity is reduced and blood is squeezed out
  • valves ensure blood is forced forward and not backwards
  • decrease in venous capacity — increased pre diastolic filling — starlings law of th heart —- increased contractility —- increased cardiac output
31
Q

skeletal muscle pump and venous return

A

surrounding muscles external to the vessels contract, compressing the veins

veins are distensible and this increases BP

this increases the rate of venous return

32
Q

respiratpry muscle pump and venous return

A
  • inspiration triggers a drop in intrapleural pressure in the thoracic cavity
  • this decreaes venous pressure in the vena cava
  • enhances pressure gradient to drive venous retur

negative pressure pulls open extra alveolar vessels

Expiration causes the converse changes- compressing the vena cava

Hyperventilation increases the rate with which blood is returned to the heart

33
Q

pulmnonary circulation overview

A
  • low pressure- prevents oedema and limits afterload for RV
  • high flow- low resistance system receives entire CO
  • there are regional variations in BF
  • passive adaptations in pulmonary vascular resistance- to large changes in CO and lung volume
  • active local control of blood vessel radius- response to change in PO2
34
Q

how does alveolar interdependance at different lung volumes affect BF

A

low lung volumes- capillaries (alveolar blood vessels) are less squashed so less resistance. However high arterial R as there is little interdependance (less elastic recoil)

high volumes- opposite is true

caps contribute to ~40% of TR of pulmonary resistance and a lot to systemic

emphysema patients breathe at higher volumes to reduce airway resistance, this increases TPR, PBP causing right ventricular hypertrophy — taller R wave lead III ECG

35
Q

perfusion differnces in the lung

A

due to gravity, perfusion is greater at the base

low pressure nad high distensibility of the pul vessels measn that gravity causes regional differences in BF (affected by exercise and posture)

upright- flow greatest at bae of lung due to the hydrostatic pressure effect of the column of blood above it

36
Q

how many zones of the lung are there in tems of blood flow

A

3

37
Q

zone 1 of the lung

A

arterial pressure is below 0 due to the height of the lung and the hydrostatic pressure effect

pulmonary venous pressure is more negative than arterial

intraalveolar is 0 everywhere as it is in equillibrium

Palveoli is greater than Pcap so ventilated but not perfused

38
Q

zone 2 of lung perfusion

A

alveolar pressure 0 is greater than Pv (pulmonary venous) and less than Pa

therefore there is SOME blood flow

39
Q

zone 3/4

A

Pa and Pv is greater than Pa so full flow through capillaries

40
Q

functional (metabolic) hyperaemia

A

increase blood to active skeletal msucle during exercise

resultant Bf washes away metabolits at a fatser rate

works under the principal of metabolic mechanism

41
Q

metabolic mechanism

A

in certain organs, BF is regulated to match the metabolic activity of the tissue

a decrease in blood supply or an increase in demand of oxygen (e.g., in exercise) causes the tissue to release vasodilator metabolites such as:

K+ phosphate prostaglandins H+(lactic acid) CO2 and adenosine

acts locally on smooth muscle

always some metabolites present– autoregulation

42
Q

metabolic hyperaemia can be split into 2 divisions

A

active and reactive

43
Q

active hyperaemia

A
  1. increase in tissue metabolism
  2. increase release of metabolic vasodilators into the ECF
  3. dilation of arterioles
  4. decrease resistance creates increased BF
  5. O2 and nutrient supply to the tissue as long as metabolism is increased
44
Q

reactive hyperaemia

A

transient increase in organ blood flow that occurs following a brief period of ischaemia

decrease BF due to occlusion

metabolic vasodilators accumalte in ECF

dilation of arterioles but occlusion prevents BF

remove occlusion

decrease resistance increase BF

vasodilators are washed away

45
Q

coronary circulation

A

increased cardiac work due to exercise= increase oxygen demand of myocardium

change in BF mirrors cardiac metabolism

coronary perfusion is autoregulated

perfusion pressure is determined by diastolic pressure not MAP

coronary art located in the subendocardial region so flow is during diastole moving by the art-ven pressure gradient

during systole myocytes squeeze cor vessels from the outside, eventually the p outside of the vessel is greater than the coronary art. BP so vessel collapses and narrows during systole. BF to myo during dias – mechanical compression is lowest and aortic pressure is still high

46
Q

special problems with coronary circulation

A

HR increases then whole cardiac cycle shortens- diastole shortens more than systole therefore less O2 for myocardium when demands are high

Increased EDP is transmitted to coronary vessels. Therefore the pressure gradient to drive blood back through the coronary circulation will be decreased and BF to myocardium will be decreased

a decrease in arterial BP will decrease the pressure gradient forcing blood through coronary circulation

these problems are magnified by coronary artery disease due to narrowing and increased resistance

47
Q

inactive vasoconstriction

A

inactive sk msucle undergoes sympathetically mediated vasoconstriction during exercise

TPR and therefore ABP is maintained when some arterioles supplying active muscles dilate and those supplying inactive muscles constrict

due to central resetting of the baroreflex a small increase in pressure across the whole body so even these inactive muscles dont have fully comprimised BF

48
Q

cutaneous circulation; thermoregulation vs ABP

A

cutaneous symp vasoconstrictor activity kicks in to help maintain ABP, by preventing TPR from decreasingtoo much when Sk. muscle arts vasodilate.

cutaneous BF rise linearly with rising core temperature until a certain point- sacrificing thermoregulation for CV stability

this set point varies with hydration levels- cardiopulmonary barorecptors??

49
Q

how does flow change in pulmonary system

A

recruitment- opening of vessels

distension-

Unit 12 Week 1 (Sam) (6 decks)

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