3.2 Myocardium & Blood flows Flashcards
What is Myocardial oxygen comsupmption
7-9 mls/100g/min 21-27mls normal heart 300g
Major determ myocardial oxygen consumption
Other factors
Myocardial wall tensions
Contractility
HR
Basal energy metabolism (25% total consump)
Energy work performed
Energy for electrical activation
- 0.5-1%
Work is mauresured as product of pressure & volume
Oxygen cost work - depenedent on way work performed - pressure work - requires high myocar than boule work
Increase afterload causes greater increase O2 than icrease Preload
What is tension time index
Are under systolic part of LV pressure curve
Correlate well w/ oxy consump when contractility not altered
What substrates metabolised
- Heart use whatever available
- Can metabolise glucose, lactate, keto FA
Amiunt each used - related arterial concntrations of subrate
40% carbs 60% other
Uptake gluc incrase insulin
brain diff - excluse use glucose
How measure myocard o2 consump
not practical - require meausre flow - sampl cor sinus
Valsava
Close off moutj nostrils strain
increas intrathoacic pressure
Every time strain -
fly pop ears
effects on CR - tidal ventail interptad
impercetible pulse
blow mercury column to ~40mmhg hold 10 sec
Essential ft - increase intrahtoracic pressure
Changes bp valsva
1 - increased pressure - pulse steady - intraopuilm vessel - increase VR
increase sv - starling
rise bp few beats
2 Strain - bp falls - decrase Co Barrecpto - sense reflex compens symp stim - incrase HR symp stim - vasoconstric maintain bp - organ flow compromised low co
3 BP dips - after release straing
removes squeeze vessel - increase size - decrease return blood - drop co & BP
4 blood left increase normal - restore co deliver normal co - vasoconstrict bed - overshoot bp
barorecptor sense - vagal slowing hr - lower previous resting
periph relax - return normal
Valsalva ratio
Ratio between ongest RR interval phase 4 and shortest phase 2
haert response secpndary events - occur d/t cartoid barorecptor
nromally >1.5
Decrease incrasing age - less in elderly
d/t decrease baro responsivness
Main cause increase pressure
increase pulmonary bv - resoevor
significat beta block - how alter
small overshoot bp in phase 5 - absne hr response pahse 2 hr not eleavted at phase 4 so co and bp not increase rapidly
Alpha blocked
lower bp phase 2 - incrase bp overshoot phase 2
Hr increase - unoopsed beta stim abense vascons to increase bp
Clin uses valsalva
Reversion SVT
-increased vagal activity
Autonomic function testing
Aids murmurs - hocm mv prlaopse increase
CVS response to standing
Immed reponse - blood pooling lower extreme
= VR & CO decrease - BP drop
Sense carotid barorec - vasomotor & cardiac centre medulla stimulated
Sympathetic stim 1 Perip vasocon - incr svr 2 Periph venocon - inc vr 3 Incr HR 4 Incr Contract
Change - restore bp & maint CP
Hydro-static effect - decreasing CPP
D/t brain higher heart erect position 30 cm
arterial pressure brain lower aorta
MAP at brain level is less after change response
Acitivity after moving
-Moves briskly - msucle pump - prevent pooling
How is standing response different in elderly
Sympathtic response slower & less effective
Baroreceptors less responsive
Experince lighthead/faint - decr CPP
Autoreg doesnt have imeediate onset
Soldiers collapsing
Decrease CPP - Decre CO
Blood pools - exstemities decrease VR
Standing still remove muslce pump
Hot - veodilates
Cartoid sinus not as effective in venocontsiction
CVS response rapid loss 1000mls blood
Mjaor acute BLood loss
Decrease CO & Decrease ABP
Change detected
1 high pressure barorecptor in carotid sinus
2 Low pressure (Volume) in RA & great veins
Compensatory -
Minimise effective blood change Venoconstriction transfer ISF-> plasma Decrease RBF Decrease Urine volume Mobilisation resevoir restless - increase muscle pump activity
Maintian ABP
Peripheral vasocon
Tachy
Sense carotid sinus
Reflex sympathetic stim
Increase HR Contractility - vasocon & venocon
Blood lungs Liver - mobilised -
Redistr - CO
Peripheral vasocon - decrease muslce
Renal vcon
olugira - min fluid oloss
CVF
perferent maintain
craotid sinu, pressure autogerg, metabolic autoreg
Changes in starling forces accorss capil - net reabs ISF into blood -0 incrase blood vol
~~1000ml / hr - transferred
Drop BP - oliguria - retnet salt water
Increase ADH - voulme rec
Increase ang & aldo
Increase thirst
Rapid loss ~~>shock
CO insuff - meet tissue demand - neurohumora l decompensating large / rapid loss - limited capacity response
Lactic acidosis arryht hf - older depress function
Hypotensi may sevcere - decr CPP - ischameic cns response - msmyph outflow ischameia medulla - last dithc mainta CPP - adernline medulla
What are delayed repsonse to major losses
Plasma volume should return normal 12-72 hours
Increase in plasma proteins - synthesis liver
Days retun plasma proteins to onormal
Incrase RCC production
EPO increase - poiesis - retuc level peak 1- day - fully restore 4-8/5
What is a reticulocyte
Erythroycte at final stage maturation
Cells enter blood * basophlic cell debri (rna, mitochandria & oorganelle)
extruded in couple days
normally only 1%
Increase epoiesis - more reticulcytes - readily detced exam
fine retic basophil material
Increased- increase epoesis
What are the effects of transfusion 1l autologues blood into normvoemic health
Blood vol increase 20%
Circulation overfilled - mean systemic pressure increases 15mmhg
RAP increase
CO increase 10-15l min d/t preload (starling) & increased HR
SVR init normal - increase CO - increase ABP
Short lived -
Venous pooling
increase BP - sense carotid sinus - result increase inflow - sinus &
decreased outflow vasomotor - cardiac centre medulla = periph venodilation & decrease systemic pressure
Increased venous pooling decrease VR & CO - retunr bp normally
Sustain increase CO - not occur - pressure autoreg - meatolic autoreg - adjust vascular resistance - maintain cosntant blood flow
Marked in brain heart kidney
Increase capillary hdydrostati c- increase tissue fluid formation - limited d/t similar oncotic pressure
How is the extra fluid extra
Increase in BP - pressure Diuruesis & natiriresis - increase
Increase urine flow - bp elevated -
autog - various tissue mainta blood flow normal level - increase periphral vasocon - rise arterial art bp
Beneficial - promotes excretion fluid salt - renal body fluid mechanism - maintain ECF
20% increase in volume - above thresld stim low pressure / boulme receptor
ADH secretion decrease - diuresis
Osmorecpt in hypothal - not stimm plasma osmolal - not alter
Increase o2 carry capactiy - remove epo stimulus
Rapids infusion of litre 5% dextrose
Haemodynamic effect - increase blood volume
Mean systemic, rap, co bp
rapidly lost IV compartment- haemodymaic change limited speed
Inital changes - ltd speed loss occurs
Venous pooling occurs
At infuson 5% isosomolar
fluid oncotic pressure -
balannce starlings - alter lower onctoic fluid lost interstital flud
gluco taken up
net effect
distrib all fluid compration
proportion contrib total bod water
Ready mobilised fluid - ratio ICF:ECF 2:1 ECF - approximate ratio:IV 3:1 Distrib 1l 5% ICF - 660 ECF 340 - ISF 255 + IV 85
Final increase blood vol <2%
Not sufficent acti volurecports
not suffic cause hd change
plasma oncotic not altered - incrased not sufficnet adverse oefefct cell fxxn
Change ISF - no effects not suffic oedema
Osmolality decrease 287->280 2.56% osmolaity Aobve threshold hypothal osmorec - adh dcerease short half life 15mions - effect 1h excess water excreted urine
What effects rapid transfusion 1l NS into patient
Acute haemodynamic - depend magnitude actue increase iv volume
speed transufion - rate fluid lost inv volume
rapid trfsion - incrase mean systmic pressure rap co incr incr hr svr normal - increase abp
[Na} ~~ ECF
no increase ICF volume
ECF 0 fluid distributed ISF & IV - proprtion contriub ecf volume fluid distirb Intracell - nil ECf ISF 750 IV 250 explains why ~ 3l need for 1 ?less- glycocaylx
Osmolaltiy not altered - no osmrecptor stimulation
IV voume increase 5% - below 10% voulume stim - no adh change
mechanism excretion fluid
Fluid & salt - d/t 2 factors
Floumerultoublar imbal
pressure volume control mech
Increase blood vol - saliene - small drop oncotic pressure
Gloerulotubular imbal - kidney & GFR increases slightly less fluid & na reab prox tube
Increase Urine flow 0 excertion excess fluid and salt
Immed - no lag 0 urine flow increase
no sense hormone level change / adh
Pressure volume - powerful but slow - onset reflex minmise effect saline loading
Rapid infusion 5% normal ablumin
Fluid IV compartment
Similar autologus blood
Incr CO + Bp
capactiance vessel relax -venous pooling increase loss ISF - increase capilalary hysdrstatic pressure
elevated abp - pressure natriuresis diuresis p renal volume control
osmalilty ecf not changfe osmrec hyptol not stim
low pressure baro stim
adh falls - favour ecretion
o2 carry capiacty decrease - hb decrease
tissue increase floow - meet req
1 autoreg - art vadola
2 decrease vlood biscotisty
Which fluid excreted quickest
N saline - gloerulotublar mbalnce - ovvurs immed renal exretion occurs
water 5% dex & abl - decrease adh - not immed
Cerebral blood flow what is it
750mls min
50mls 100g min
15% CO
CMRO - what
typical vale
significance
Cerebral metolbic rate o2 consumption
3-3.5mls o2 100g min
50mls in total
brain weight 1.4kg - use 20% basal o2 conspump
hgih level metbolic activty - not tolerate momentray o2
Is CBF alter in exercise
No -global flow ulatered
change distrib - motor cortex increase
flow small - other receive less
Factors involve in cotnol cbf
CPP / CVR
MAP-CPP
Factors affecting CVR Metabolic autoreg pressure autoreg chemical factors nervous system
Metabolic control -
draw cbf & metolic control
autoreg - ability tissue adjust blood supply - recive flow carry fxn
local vasodil metbolite
impratnat min min reg control cbf
exampls
admin indction tho- decrease cbf - decreae cmro2 cbf decrease
fitting causes incrase work - cbf increase
supply meets demand
metbolic regulation - moment moment reg cbf
glocal may reman constant
draw curtve metabolic ontrol cbf - page 63
flow metabolism coupling
Pressure autoreg
draw effect change mean bp - cbf
rel constant cbf - despite map 50-150
page 63
Myogenic theory
Pressure arteriole increase - increase stethc vessel
vascular sm responds -> stretch contract - resting tone higher
results decrease redius - increased resistance vells - return blood flow to normal
despite continuation pressure
quickly - seconds
what circumstance autoreg pressure shift ight
Chronic htn & acute sympathetic stim
Main point - lower limit shift to right
not tolerate drop bp - without decrease cbf
Low BP not tolerated espec i fealvated ICP
Neonates - pressure reg left shift platue anrrow 30-90 slopes upward to right
lower bp - phys approp left shift
decrease upper limit neonate less toerate higher bp
Curve art PCO2 & CBF
What is the shape of the curve
from what to what
page 64
Curve almost liner 2.6-10.6
CBF linear change over pco2 wide rang
Where is the normal Pco2
Decrease CB F - sustain hypocanpoa - dimish time - bic equil across bbb
brain ISF pH - normal thus so does CBF
Effect - advance 4-hours
Sudnden return normal art pco2 - excess CBF & Rise OCp
What is factor level curve lower limit curve
Cerbal vasoldtion in response hypoxia
low flow limits amount ocygen deliver - vasodilation causes prevent further decrease cbf- with decrease art pco2
Proven in hypernaric chamaber
Sifficenmt o2 dissovled - oxygne receive adeq o2 despite low cbf - acute hypocapnic vasoconsitrciton
counter ewffect hypox vosdil remoced
further decrease cbf
Daw arterial po2 & CBF
Why is it that shape
Page 65
CBF not affected until po2 <50mmhg 6.6kpa
Shape odc for hb
po2 falls o2 content not alter much upper part
as falls <60 oxy content falls rapidly - steep odc
not much decrease o2 supply in level reach
cerbrel arterioles - vasodialte cbf incrases to maint o2 delivery
Nervous control cbf
cartoid sinus cbf
SNS - not import chang cerebral circ - change CVR
autonomic stimulation allter cvr small amount
Improtant in CBF - effects on CPP
Barorecporor monitor mean carotid arterial pressure
BP falls - neuroanl firing cartoid sinus diecrase
reflex - rapid powerful sympathet stim - hr contract
vasocn attemp maintain map
Barorectpor
Stretch receptors walls heart blood vessel
Carotid sinus aortic arch
Arterial Ra LA Pulm veins
small dilation ICA - increase rate firing distention - decrease sympathehtic increase vagal response
Carotid aortic baro - end NTS at medulla - releaseglutamte, siognal go caudal ventrolaterral medulla
Carotid sinus reflex & pressure autoreg - aim mantain constant cbf - despite change map
Carotid sinus reflex - responds rapider - improtant moment moment activ - chjange positon
pressure autoreg - minutes
Under cond extreme hypoxia - ishaemic response - chusin reflex
Max sympathetitic stim - last ditch resore CBF & o2 2supply
What is the CPP - how measure
CPP CVR
CPP - driving flow blood
perfusion organs - diff map & venous draing tissue
added consideration brain - icp
icp higher cenous pres
then map - icp
type something occurs lungs heart - starling resistor
CPP i MAP minus greatr CVP or ICP
dterm - CPP require all three measure
Pressure autoregulation - brain MAP x acis
Curve drawn map x and cbf y - reason MAP est CPP
larger than ICP & JVP
Easy measure
Meausre ICP - more incasive
Path condition ICP high - high map low
Why would we want tor reduce CBF intraop
Decrease ICP
Mimise blood loss
What is monro kellie doctine
Brain ecnlsoed righid bony skull
total volume conents fixed
attempt increase volume any conents - rapid icnrease pressure
Diagr pg 67
Presuure not rise much initally csf out ventricle into extracran SA space
vuffer exhausted - rise very abrupt
Intracrain coent normally - 85% brain 10% csf blood 5%
What are methods manipulate CBF & ICP cranitomy
Head up tilt
No obstruction drainage
avoid vdilator cerebral
Hyperventilation
Mannitol
Contolled hypotension
How head til & no ostruction alter CBF
Decrease CPP - hydrostitc effect
keep jug veinbs collapse - no congestion
Min venous bleeing
Addit - decre VR - pool blood extermity - hypotension activated carotid sinus - icrease bp
fianl efect perfusion - effectie pressure & metab autoreg
Idisag - increase risk venous air ebolism
drop cpp & cbf may not be warranted
Why is hyperventilation beneficial on ICP
Rapidly reduce art pco2
Decrease 4% every mmHg decrease art pco2 from normal
intracerbral pressure decrease - desired effect
Advant -
rapid reliable
potent
easily control
disadv
not lasting
-less 4-12h -> decrease bic brain ECF - restores ecf pH to normal & vascon - decreased
allow art pco2 rise - tend excess increase cbf
How does mannitol work reducing ICP
Hypertonic - not cross cell membrane
draws water all cells
doesnt direct affect CBF - does decrease intrcerbal
decrease volumes
- rapid
IV volume
expanded water ICF - osmotic diruesis - loss fluid & decreae IV fluid
benefical - not direct depend on diuresis
Hypertonic urea also dcrease ICP
Urea less able cross bbb
hpyeronic urea - cause cerebral dehydr - reduce icp
rapid excrete kidney
What inter jug vei n pressure in erect positon
RAP low & Vp in vein above RA falls - hdyrostic pressure effect -
pressure drops almost 0 & veins collaprse
jug vein in erect position normally collapse
Jug veins collapse in sitting neurosurge
How at risk air ebolsim
Pressure grad - favours entry air cerbral dural sinus - despire fact jug vein distended
Dural sinus not collapse rigid walls
-presure can subatmopher - air can sucked in - during caniotomy in sitting
venous air embolism - large & rapid
Coronary blood flow - what is normal
How does it relate to Cardiac cycle LV/RB
200- 250 mls/min 5% CO
Supply LV - predom diastole - subendo flow to LV cease to LV during systole (commonest site MI)
Lower pressure in RV - differences less
Draw flow curves related to cardiac cycle 69
What is CPP
Driving pressure for coronoary circulation
Aortic diastolic pressure - larger of LVEDP or RAP (cor sinus pressure)
LV diastolic pressure & rap smaller than aortic - CPP is stating aortic diastolic
Intraop - peripheral arterial disatolic pressur - index co pp
Difficult acurate diastolic pressure peripher - niv & Invasive
Why is CPP defined like this
Starling resistors
Three pressures i heart
Arterial pressure
IV pressure
Cor sinus / RAP
CPP - perfusion pressure during diastole - highest most flow - lv occurs
Exa,[;s
LVV - systole
Aort - intracetric pressure =120-120= 0
LV duastole Aorti diastolic - RAP 80-5=75
RV during systole = Aortic - intraventricular 120-25=95
RV during systole Aortic - RAp 80-5 =-5
LV larger flow - larger mass - effects improtant
Subendo vsesles - subject ffull impact iv pressure - ceases during systole maj artery epicardial surface
How does venous drain heart return circ
What percet of cor flow returns via sinus
Po2 cor sinus blod
Cor sinus drain in RA 90%
Thebesian vessels
pO2 cor sinus blood 20mmHg
- myocardium high extracion ratio 55-65%
What is the myocardial extraction ratio
What is the significance
55-65
Blood supply low relative to oxygen conumsption
myodacridum extract a lot of oxygen for unit blood flow
Signif - heart requires more oxy
cor blood flow must increase
Extraction high - no reason extraction increase
Increased myocardial consumption must be acomp by increase flow
What happens cor blood during exercise
Mechanism
Cor artery flow increases to supply oxygen to match demand
Normally high extraction increased - provide more oxygen
High extraction ratio remains high - rest exercise anaemia
Heart cant devleop oxygen debty
cor flow can increase 5 times
1250
Increase
metabolic autreg in arterioles
counteract symp med vasocon
- increase mostly during ddiastole
Hypox hypercarb increase h ion, lactate, k adenosine
What is oxygen debt
During strenous exercise - energy skeltal muscle exceed supply atp - aerobic metbolism - o2 deilvery insufficient
energy atp anaerobic metab
Lactate prod
After exercise increased - increased o2 ptake
Metabolise excsess lactate & replace atp stoore
Size o2 determ measure excess o2 consumpt end exercise until basal levels
Myocardial cannot accum o2 debt - all aerobic
Hepatic blood flow
What is blood supply to the liver
where is it derived
factors control hepatic flow
Total hepatic flow 1500mls/min 30%
Hepatic artery 300-500ml min press 90-100
Portal vein 1000-1200mls min - 10mmhg
Some autoreg in artery
portal - not autoreg
Recirpocal relationship -
increased sympathetic active - increase portal flow - decrease heptaic artery
liver reseovr - 500mls - deliver cirulation - vasocon
How much oxygen from two liver sources
40-50 hep art
50-60 portal vein
Liver - cannot supply artery supply removed
What is hepatic oxygen consumption
50mls o2 mn 20% o2 cinsumption
well maintained - increased extraction if blood supply changes
How is blood flow measured in an adult
Fick prince - ICG - co also
Dye removed circ only in liver - total excr bile
doesnt have enterohepatic circulation
level blood spect 805nm
Dye given contatst infusion - steady concnetration - rate infusion = uptake
Hep arter conc - same as peripheral artery
Hep vein - determ sample catheter
Why dont amnt oxygenation of hb interfere icg
does icg interfere pulse ox
measure 805 - isobest for hb - amount light absorb hb - not vary with oxygen
reduced o2 & oxy absorb same wwavelength
True sat not altered
Renal blood flow
What is normal RBF
How is it distributed
How is it measure
1200-1300mls - 25% CO
Majority 95% flow - cortex 5% medulla
Measured clearance PAH - para aminohippurate
low plasma conc - renal blood almost completely cleared PAH - PAH equal renal plasma flow
RBF - can be calc if HCT known
What are properties indicator measure RBF
Freely filtered at glomerulus & secreted - not reabsorbed
Indicator cleared from blood single circulation
Stable easy measure non toxic not cause alteration in flow
PAH has properties
also measure eceltromagnetic othery type flow meter
How is this related to fick princeiple
Fick principle underly principle - application law conservation matter
Uptake substance tissue - difference amount entering = flow x art conc
amount leave tissue flow x venous
rearrangement
Flow = uptake / a-v conc diff
Kidney
Renal plasma
PAH uptake / renl art pah - ren ven pah
Pah totally cleared - renoul venous pah -
arterial not required - not taken up any tissue
venous pah should be idntical
Renal PAH uptake - urinary pah times volume produced
Effective renal = urinary pah xbol urine / periph venous pah
Insepction eqn reveals - same quation clearance UV/P
Low pAH conc - not all PAH removed
Correction factor convert effective renal plasma flow into renal plsam flow
divide by 0.9
above 90% extraction PAH
Why does the euqation calculate renal palsma flow and not rbf
sing plasma conc and plasma cleared pah - follows it is plasma not blood filtered glomerulus
volume calculated is clearance volume PAH for PAH removed plasma
What is renal oxygen consumption
Significance value
18mls/o2 min
Renal blood suppl 25% co
weight 0.5 body weight
Renal o2 consumo 7% total baody consumpiton
dont correalte
kidney very meatbolic active high o2 consump compared weight
RBF higher predicted oxygen consumtion
- o2 extraction ratio low
Tissues receive flow needed to carry out function
most - oxygen metbolite maginatue flow -
excretory & homestoatic functions - determine large blood rather than oxyegen consumption
How is it autoregulated
MAP autoreg 75-105
Myogenic - glomerular arterioles
tubuloglomeural feedback - involving juxtglom app
Sitatuion
myogenic mech -intrinsic mechansim - primary control rbf
tubuloglomerular feedback - involved primary maintain constant filtration rate - effector vascon / vasodil afferent arteriole - assist maintain constancy of blood flow - indirect consqew
What is tubuloglomerular feedback
Imporatnt feedback autoreg GFR - too much fluid or electrolyte reaches early distal tubule - sensed macula densa - feedback signal vasocon - glomerual afferent arteriole decrease rbf and gfr = decreased delivery fluid * electrolytes in distal tubule
Two componenets to tubuloglomerular feedback - feeedback signal cause
vasocon / dil
details - not fully elucidated
signal sense macula desna - change na flux accross membrane
change content early distal tubular fluid
macula densa cells - compound acts signal
vasoconstrictor mechanism act efferent arteriole - vasdil afferent - renin angII not fully workled
Mech effect gfr change - few percent between map 80-160
Urine flow regulation
Pressure dependent
Mechnism
autoreg GFR not perfect
GFFR does increase little increase MAP
Small increase GFT - a/w larger increase urine flow
Estimated GFR - controlled controlle dfew percet maintain normal levels ater & solute reab / excretion
Nt apprecated how tight control GFR - minimise change water & solute excretion
Tight control GFR - water excretion vary w/ autoreg pressure rang
Outside range - extremely large incrase/ decrease urine flow occur
small perfect change is a lrage voulme change
5% increase gfr - 9L day
large volume - too much reabsorb mainta noirmal volume
Pressure diruesis - intrsice system control bp
presure volume control system
Effect change renal water na excrtetion response change art pressure
Most imporatnt mech control blood vol - vital part pressure depend urin e flow
autoreg urine flow - not consistent survival
What is typical po2 renal medulla
20 mmHg similar coronary sinus
Hormonal affects in kidney
Norad
AtII
Pg
ACh
Norad - contrict renal vessle - interlobaeral artery & aff aterioles
At II casocon - effect both aff + EFF arterioles
PG = Increase cortex flow decrease medullary flow
Ach - vasodilation
Micorcirculation
Smallest blood vessels in body
smallest arterioles metaarteroles precap sphincter cap small venules
arterioles - vascular sm major site sttem vasc resist
many tissue remain closed wiout flow
reserve capacity - open quickly local don fall po2 when addit flow reqd
Some tissue - contaains direct av connex shunt
flow under great control nervous system
now partic tfer gas
skin - heat regulation
Capilarry flow intermittent or contin
sm metart - precapp contract & relax - intermittent flow in capillary - vasomotion
local drop PO2 - impratnt factor rrelax precaiplly sphincter
intermitt cap flow - not cycliac rise bp - flucation smooth out arterioles
What is the importance of micorciulation
How do dif substance cross cap wall
System cap 5% lbood vol extreme imporatn - exchange water electolyte gas waste nutrient cap membrnn
most drug need cross reach site action
intracsular volume contaact ISF - baths all cells body
transfer substance principl fucntion microcir
Movement water accross cap membrane - 2 proccess diffusion
filtration
water molecuesl smaller size of pores in capilalry -c ross wall easily
cross gap enotheilail cell
electrole small mol - cross membrane thru pores - via intercell gaps
lipidsouilbe sub - o2 co2
cross thin wall endothial cell
protein large do not easily cross
some transfer pinocytsosis
What is the magnitude capilary fluid exhcnages
Water movement //t tow process
diffsuion
otal daily diffusion water across cap hgh 80000l day
larger total cap blood flow
co 8000l day
Diffusional movement water large both direction not result net movement across cap - no osmotic gradient
FIltration
Accross capillar also occurs - ultrafiltration plasma proteins do not cross
Imbalance hydrostitic & oncotiuc pressure - along capillary memnbrane - starlings hypotehsis
UF 20ml min - body whol
18mls reabs in capillary rest retuend as lymph 2ml min
No net movement water d/t diffsuion accross membrane net diffsuon depnd conc gradient - orinaryl no water cocn differece cap mebrane
Filtration does = net movement water d/t imbalance between force out and inward - different times tissue net move in or out
forces change in value along length capillary - typical sitaution net movement out at arterial end - net movement in at vbenous end
Diffsuion
Large volume
bidirection whole length
concntration gradtion
hydrostaic oncotic pressure - not involve
reponso net movement gas nutrients waste - move down con grat
Filtration
Ultrafiltration - protein not cross membrane
volume msaller
inward or outward at position along capillary
net movement gover starling forces
not important gas nutrient waste -
is improitant water
Starlings hypothesis fluid exchange
Fluid movement d/t filtration accross wal cpaillary depend balance hydrostraic pressure gradient & oncotic pressure grdient across capillary
Pc Pi Tc Ti
hydrstrric capilary
oncotic interstitium
Net driving pressure =
Pc-Pi - Tc - Ti
Net fluid flux - proportional to net driving pressure
Reflection coeff
filtration coeff
Capillary hydrostatic pressure falls along legnth of arterial to venous end
driving pressure - decrease become neg
Reflection coefficient
Correction factor - apply to measured oncotic pressure ghradient accross capillary wall
Small leak protein accross capillary membrane two improtant effect
Itnstertial fluid oncotic pressure higher than would be
Not all protein effective retain water effective capillary oncotic pressure lower measured oncotic presure
Both effect decrease pressure grad
Instit oncotic pressure - acount included cal grad
Used correct magnitaute of measuredgraident ake account ineffectives some of oncotic pressure grad 0-1
eg
CSF & GF - low protein - reflection coeff close 1
Prtein cross wall hepatic sinusiod - protein cocn lymph high
reflection coeff low - walls do not reflect all protein ack - formula for net driving pressure include reflection coeff
Filtration coefficient
net flud flux d/t filtration across capillary wall - proportional to net drving pressure
fitlration coefficient k is contstaing of proortioanlity in flux starling equn
net flux = K x (net driving pressure)
K x {(Pc-Pi)-d(Tc-Ti)}
k fitlration coeff d reflection coeff
filtration coeff two compnents net fluid flux depned
area capillary walls where transfer occurs
permeability capilary wall to water -
K = area x hydraulic condcutivty
leaky cpailly - high filtration coeff
glomeuralr capilary all leaky naturally
Filtration coeff - leaky capil membrane h20
reflection coeff - protein
Typical values for starlings forces
Art end Venous end
Pc 25 10
Pi -6 -6
Tc 25 25
Ti 5 5
Net driving pressure out at art end & ion venous end
Change in net driving pressure d/t decrease capillary hydrostatic pressure - asummes reflection coeff high
How are forces diff glomeurulus
sitatuion different remarkable
body whole net uf reabso 2-4l day
net excess capil gfr - 180l
Gloemrueres
Filtration coeff hih - high perm water
reflection coeff high - 1
filtrate true ultrafiltre - essent imperprotein - oncotic pressure filtrate 0
hydrostat pressure in capill high - not decerase along legnth
large loss fluid & imperm to protein - onctoic pressure in capillary icnrease along length of capillary -
Net outward filtration along whole legth capilary
hydrostatic pressure gloermural capill affect balance aff & efferetn constriction
How diff in pulm capilly
Balance twoard reabsoprtion cap hyrstic pressure lower - genreally lower pressure in PA
Cerebral
Cap membrane in cerebral Relatively impermeable to most low molecular weigh solutes present in blood as well as plasma proteins
Ions N Cl make up most solutes
solutes effective exert osmotic force acrros menbrae
Starling force cerbral cap & hyydrstat pressure and osmotic pressure d/t effective solutes
oncotic pressure small vs high osmotic pressure effectgive samll solutes
small leak solutes - reflection ceoff - plasma & other cap bed
1 milosm increase icrease osmotic gad bl and brain exert 17-20mmhg
small change tonicity marked effect on cerebral vol
Pulmonary microcirulation
What is lung main fxn
what is the role of the circulation of this fuxn
Gas exchange
Moves pulmonary blood flow close a/w alverolar gas at bl gas barrier - gas exchange facil
large amt of flow pulmonary = co
Membrane thin - Large surface area
1 Pul capil - thin wall
Alv wall - cap dense network - continous film blood - large cap surf area
pressure pulm lower - system -
pvr low - pressure sufficent perfuse apical areas - erect healthy adult
Values for starlings in pulmonary
Cap hydrostat 13 art 6 venous - vary effects gravity erect lung
instital hydrostatic pressure - vary 0 to negative value
Cap oncotic pressure 25mmh
instital oncotic 17 - est collection lung lymph
Oncotic pressure grad - interstital - oncotic pressure high - signif protein leak - albumin - normal circ - refecltion coeff low - est 0.5
Considering typical value -e st net oncotic snmall - favours reabsorption
Hydrostatic press grad
capil - intra alv vessel [ presure expose close alv pressure - actual measure - slight neg - closer holum more neg - favour flow alverolar intestium into lymphatics
Capillary hydrostatic pressure lung
Capillary hydrstatic pressure vary - effects gravity
erect lung - suspend gravitato field - pressure veseel high than apex
pressure difference - static water column
Distance 30cm 0 pressur diff 30
typical pa press 25/8
Pressure barely adeq - prefusion apex
low resistiance - half d/t capil - no muslce wall
cap hydrstoatic quicl;y affect change pap & lap without buffer
normal - smell net forward movement fluid
est = pulmonary flow rate
use 10-20mls hr
How is it useful to patient care
not uself - not possible measure value
estimate - plasma protein as index cap oncotic
and pa cather
How is excess fluid removed
Large surf area & thin walls - faciliatte filtration cap to interstitum
intertsil moves wtoward hilum along space beside vessel airway
hydrostaitc instet - more neg apporaching hilum - excess filtrate removed lymphatics
flow premoted vetilatiy cycle & 1 way valves
What are factor protect lung from Pulmonary oedma
For it to occur - excess fluid accumulate in iterstitum - then move into alvoeli
lung resistant - usually absorbed
1 increase lymph flow - increase filt increase flow
2 decrease intertstitial oncotic pressure - oncotic buffering
filtration icnrease - albmuin loss in filtrate decrease -
combined increased flow 0- washses albumin out interstitum & interstitial oncotic pressure decrease
3 High interstitial compliance
Large volume fluid - acumulate gel intestium without much pressure rise
tissue full fluid - pressure rise - alveolar flooding
bathtub effect - analogy tub take lot fill - point full suddnely overlys
safety - effective
capillary hyosratic rise x3 before flooding
surfactant also has a protective role
Autoreg
What is it
what are diffrent ways tissue blood supply autoreg
Tissue ability regulate own blod suplly - so recieved bloof flow requires for function
intrinsic & local - each tissue
eprate nervus/ humoral factors affect arterioal resistance
Heart brain kidney - low neurogenic control circ 45% co to them
Pressure autoreg
metabolic autoreg
Pressure autoreg
What is the mechanism responsible pressure
anywhere it doesnt occur?
blodo - tissue cosntant despite change system art pressure
blood flow - most tissue require dont alter w/ rise fall pressure -
tissue arteriolar resitrance change to compenase & hold flow coontsant
- effective wide range map - many tissues
cerebral blow flow for 50-150 in carotid
Myogenic mech increase pressure - increased strethc walls - vascular SM - repond contract
increased tone locally l- increase resist -drop blood flow
Uterine cirulatuion during preg
vasc bed preg utereus flully dilate - autoreg not present
uter blood flow late preg pressure depenedent - anaethit implication
decrease half normal before oxygenation affect
Hepatic portal supply venous drain bowle - not autoreg liver- heaptic art supply autoreg
Metabolic autoregulation
whats the mech responsible
Varies depending on metabolic needs of organ or tissue
active nearly all tissues all times-
vasoidlator mediator considered cause
identiy not est certrainty mos ttissue
possible
adnosie
nitric
h ion
increase demand blood 0- increased metabolic activity - local increase in mediator - causes local arteriolar vasodilation
increase blood flow
