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