3.2 Myocardium & Blood flows Flashcards

1
Q

What is Myocardial oxygen comsupmption

A

7-9 mls/100g/min 21-27mls normal heart 300g

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2
Q

Major determ myocardial oxygen consumption

Other factors

A

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

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3
Q

What is tension time index

A

Are under systolic part of LV pressure curve

Correlate well w/ oxy consump when contractility not altered

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4
Q

What substrates metabolised

A
  1. Heart use whatever available
  2. 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

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5
Q

How measure myocard o2 consump

A

not practical - require meausre flow - sampl cor sinus

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6
Q

Valsava

A

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

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7
Q

Changes bp valsva

A

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

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8
Q

Valsalva ratio

A

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

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9
Q

Main cause increase pressure

A

increase pulmonary bv - resoevor

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10
Q

significat beta block - how alter

A

small overshoot bp in phase 5 - absne hr response pahse 2 hr not eleavted at phase 4 so co and bp not increase rapidly

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11
Q

Alpha blocked

A

lower bp phase 2 - incrase bp overshoot phase 2

Hr increase - unoopsed beta stim abense vascons to increase bp

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12
Q

Clin uses valsalva

A

Reversion SVT
-increased vagal activity
Autonomic function testing
Aids murmurs - hocm mv prlaopse increase

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13
Q

CVS response to standing

A

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

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14
Q

How is standing response different in elderly

A

Sympathtic response slower & less effective

Baroreceptors less responsive

Experince lighthead/faint - decr CPP

Autoreg doesnt have imeediate onset

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15
Q

Soldiers collapsing

A

Decrease CPP - Decre CO

Blood pools - exstemities decrease VR

Standing still remove muslce pump

Hot - veodilates

Cartoid sinus not as effective in venocontsiction

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16
Q

CVS response rapid loss 1000mls blood

A

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

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17
Q

What are delayed repsonse to major losses

A

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

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18
Q

What is a reticulocyte

A

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

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19
Q

What are the effects of transfusion 1l autologues blood into normvoemic health

A

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

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20
Q

How is the extra fluid extra

A

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

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21
Q

Rapids infusion of litre 5% dextrose

A

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
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22
Q

What effects rapid transfusion 1l NS into patient

A

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 &amp; 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

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23
Q

Rapid infusion 5% normal ablumin

A

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

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24
Q

Which fluid excreted quickest

A

N saline - gloerulotublar mbalnce - ovvurs immed renal exretion occurs

water 5% dex & abl - decrease adh - not immed

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25
Cerebral blood flow what is it
750mls min 50mls 100g min 15% CO
26
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
27
Is CBF alter in exercise
No -global flow ulatered change distrib - motor cortex increase flow small - other receive less
28
Factors involve in cotnol cbf
CPP / CVR MAP-CPP ``` Factors affecting CVR Metabolic autoreg pressure autoreg chemical factors nervous system ```
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
Why would we want tor reduce CBF intraop
Decrease ICP | Mimise blood loss
40
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%
41
What are methods manipulate CBF & ICP cranitomy
Head up tilt No obstruction drainage avoid vdilator cerebral Hyperventilation Mannitol Contolled hypotension
42
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
43
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
44
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
45
Hypertonic urea also dcrease ICP
Urea less able cross bbb hpyeronic urea - cause cerebral dehydr - reduce icp rapid excrete kidney
46
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
47
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
48
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
49
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
50
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
51
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%
52
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
53
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
54
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
55
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
56
How much oxygen from two liver sources
40-50 hep art 50-60 portal vein Liver - cannot supply artery supply removed
57
What is hepatic oxygen consumption
50mls o2 mn 20% o2 cinsumption | well maintained - increased extraction if blood supply changes
58
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
59
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
60
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
61
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
62
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
63
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
64
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
65
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
66
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
67
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
68
What is typical po2 renal medulla
20 mmHg similar coronary sinus
69
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
70
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
71
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
72
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
73
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
74
Diffsuion
Large volume bidirection whole length concntration gradtion hydrostaic oncotic pressure - not involve reponso net movement gas nutrients waste - move down con grat
75
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
76
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
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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
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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
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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
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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
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How diff in pulm capilly
Balance twoard reabsoprtion cap hyrstic pressure lower - genreally lower pressure in PA
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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
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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
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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
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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
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How is it useful to patient care
not uself - not possible measure value estimate - plasma protein as index cap oncotic and pa cather
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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
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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
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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
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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
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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