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
what are the feedback mechanisms during the onset of exercise
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
metaboreceptor
kind of chemorecepotr in sk muscle that responds to an increase in the production of metabolic products stimulates increase in BF to area
27
haemodynamics are due to
LOCAL not central (neural) mechanisms
28
haemodynamics are
distribution of blood flow
29
By which 3 mechanisms does venous return increase during exercise
1. Symp venoconstriction 2. skeletal muscle pump 3. respiratory muscle pump
30
symp venoconstriction affecting venous return
* 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
skeletal muscle pump and venous return
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
respiratpry muscle pump and venous return
* **_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
pulmnonary circulation overview
* 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
how does alveolar interdependance at different lung volumes affect BF
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
perfusion differnces in the lung
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
how many zones of the lung are there in tems of blood flow
3
37
zone 1 of the lung
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
zone 2 of lung perfusion
alveolar pressure 0 is greater than Pv (pulmonary venous) and less than Pa therefore there is SOME blood flow
39
zone 3/4
Pa and Pv is greater than Pa so full flow through capillaries
40
functional (metabolic) hyperaemia
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
metabolic mechanism
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
metabolic hyperaemia can be split into 2 divisions
active and reactive
43
active hyperaemia
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
reactive hyperaemia
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
coronary circulation
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
special problems with coronary circulation
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
inactive vasoconstriction
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
cutaneous circulation; thermoregulation vs ABP
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
how does flow change in pulmonary system
recruitment- opening of vessels distension-