Control of blood flow Flashcards
Blood flow is driven by
pressure gradients (created by the pumping of the heatrt)
arterial blood pressure is kept constant moment to moment by the baroreceptor reflex
if you want to alter the blood flow to structures downstream you need to alter
upstream resistance
Darcy’s law of flow
change in BP= BF x Resistance
Therefore
BF= change in blood pressure (perfusion pressure) / R
Poisevilles law
small changes in the radius of the lumen of the blood vessels can have significant effects on the resistance of vessels
what are the 4 general blood flow control mechanisms
- local
- endothelial
- hormonal
- neural
body’s blood flow response to exercise
- 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
local mechanism for controlling blood flow
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
Endothelial mechansim for controlling BF
nitric oxide- vasodilator
prostaglandins- vasodilator
hormonal (endocrine) mechanism for BF control
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
neural (central) mechnism for controlling BF
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
Intrinsic mechanisms to control BP
“regulation of BF to an organ by factors originating from within the organ”
a) autoregulation- metabolic, myogenic, endothelial
b) paracrine
C) Endothelial
active hyperaemia
example of intrinsic metabolic control of BF
increase in organ BF is associated with increased metabolic activitity of the tissue
functional hyperaemia
example of intrinsic metabolic control of BF
due to presence of metabolites and a change in general conditions
paracrine mechnosm for BF control
example of intrinsic control of BF
vasodilator and increases myocardial contractility
endothelial secretions mechnism of controlling BF
example of intrinsic control of BF
NO- vasodilator
endothelin- vasoconstrictor
myogenic response to stretch
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
extrinsinc factors for comntrolling blood flow
“regulation of BF to an organ by factors originating from outside the organ”
A) neural
b) endocrine
neural factors for controlling BF
example of an extrinsic factor
sympathetic vasoconstrictor fibres
parasympathtic vasodilators
nociceptive C-fibres
endocrine factors for controlling BF
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
intrinsic and extrinsic factors work together to shape a
co ordinated and whole body response
with the onset of exercise the CV system has to:
increase BF to active muscles
increase BF through pulmonary circulation
increase heat loss via BF to skin
maintain ABP
central command
“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
central resetting
triggered by central command, arterial baroreflex is reset, allowing for greater hypertension during exercise
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
metaboreceptor
kind of chemorecepotr in sk muscle that responds to an increase in the production of metabolic products
stimulates increase in BF to area
haemodynamics are due to
LOCAL not central (neural) mechanisms
haemodynamics are
distribution of blood flow
By which 3 mechanisms does venous return increase during exercise
- Symp venoconstriction
- skeletal muscle pump
- respiratory muscle pump
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
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
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
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
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
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
how many zones of the lung are there in tems of blood flow
3
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
zone 2 of lung perfusion
alveolar pressure 0 is greater than Pv (pulmonary venous) and less than Pa
therefore there is SOME blood flow
zone 3/4
Pa and Pv is greater than Pa so full flow through capillaries
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
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
metabolic hyperaemia can be split into 2 divisions
active and reactive
active hyperaemia
- increase in tissue metabolism
- increase release of metabolic vasodilators into the ECF
- dilation of arterioles
- decrease resistance creates increased BF
- O2 and nutrient supply to the tissue as long as metabolism is increased
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
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
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
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
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??
how does flow change in pulmonary system
recruitment- opening of vessels
distension-
