3.3 Cardiac muscle, blood, Flashcards
What is prepotential
Phase 4 diastolic depol occurs in PM cells -> heart - depol contin til apotent initiated - threshold reached
Signif prepotent in sa node cell heart
normal conditon not all cells have preportent -
responsible for automaticity
cells - fastest prepotent - PM heart
usually sa node -
Draw ap for SA node cell & super impose ventricle muscle cell
Differences
Page 85
0 rapid depol - rapid entry Na
Spike
Tabe comparing page 86
No platue in SA, no distinction between phase 2+3
Duration 150ms v 250
SA - slow response ap
RMP SA -60vs -80 ventricle
Depol slower in sa node
Conduction vesolocity - slow speed deol - conduction easily block
phase 4 - RMP unstable during 4 in SA- spont diastol depol
Slow SA channel can be block Verapamil
How are the AP periph myelinated axon & skeletal muscle - different from cardiac
Mian diffrence - very short duration perip 1-2 msec
muscle 5-10msec
absence platuea
absence of prepotential
What is the function AV ring firbous
Inuslation - provide speration atria from vent
structural
fibrous skeleton procides sturcutor for origng insert myocardial scell - insertion valve
how is it relevant to av node =
criticallyt imporant - conduction heart 2 reaseonn
1 only pathway - atria ventricle
Adds Delay - conduction av slow - addit delay - necc allow atrail contract finish before ventricular contract commences
two aspects related - av node- not only eletricl path - delay not provide much delay contract
specalise cell av node lower RMP - lower threhsole
slower rate ph 0 vs ventricular - very slow conduciton velocity
0.05msec
Depol ph 0 - open slow Ca channel - rather that fast Na - centrilcl & atrial
av node not conduction >230 impluses - due to refctor
what is the conduction velcotiy - other parts conductuion path
Atrial muslce 1 msec
avnode 0.05 msec
purkinje 4 msec
ventricular 1msec
What is the last part of the heart depolarised - why
Psoterbasal part LV
AP - travels
wave depol travel purkinje in IVseptum
spread left -> right
To apex and then back under endocardial surfcae - towards base heart
depol travels endocaridal to epicardial surface
wall of rv thinner - epicardial right side excited before left
Conseq last part depol - epicard surf left vent at base heart
Properties of cardiac muscle
specil intrinsic property
Excitability - Automaticity rhythmicity conductivity contractility
Define automaticty
Proerty heart - enable inititae own heart beat
some myocardial cells - sa / av node -
RMP not stable during phase 4
Resping potenti spont decrease towards therhold potential
Change proten 0 intrisnic proerty cells - not require extenral nervous chem input
external infleunce may modify rate chang
Cells fastest depol thresh set heart rate - act as pacemaker heart
normally SA node PM cells - cardiac AP inititated when firing level - threshold reach
Rhythymicity
Follow depol - membrane repol - sequence spont depol occurs again
predicatble regulartiy - gives heart regular rthythum
Ventricles normalyl have a stable RMP during phase 4 -cant act as PM - some cells have properties automat & rhythy, - not apparent - rate sa and av fast - abnormal compelte block - cells take over as ventriular PM - rate ~ 30bpm
Conductivity
Depol PM cell membrane travel cell to cell myocardial action pteotntial - propagation depol thru heart - conductivity
Some tracts cells heart - conduct ap quicker others
specialise tract cells - conducting system
Benefits cordination cotnraction
How does AP trvvel cell to cell
cardiac muscle stronglyjoined at ends - eintecalted discs
advant prevent cell pulling aprt contract
fibres in series - skeleatal muscle prpominet parllel
AP - travel cell to cell thuru low resistance pathwya along interaclated discs - here cell membrane fused gap junction
electricl signal easily cross junction
no chem transmitter
What is exctiability
how is it measured
why is it difficult
what circustance need to be considered
Ease myocardial cell responde to stimulus by depolarising
cell response smaller stimulus than another said - more excitable
Degree - assessed size minim stim necc depol cell - initiate AP
difficult measure reproducibility - depend geometric arrangement electrode cell membrane difficult constant not reliable reproduced
1 Myocardial cell during phase 4 - stim cell
resting MP - decrease to threshold potential
slow phase 0 subseq depol - index excitability
more excitable cell - larger slow higher velocity conduction
2 Following onset AP - period time cell not stimulated no matter how large stimulus - absolute refractory period 0- onset ap at threshold - midway thru repol during phase 3 - longer in atrial pacemaker
3 From ened absolute until fully repol - relative refractory period - cell stim - requires supramax stim - difficult respod measure
Response stim varies - membrane potential - time stimulus apply
closer start refractory smaller membrane potential - greater stim required initiate another
ap generated stim lower mp - slower ate rise ph 0
slower conduction velocity
excitability defined increase slow phase as slope phase 0 increase
membrane - repol during later half 3 size stim depol decrease - slope phase increase if stim
irritability
context resting myocardial during phase 4 either size stim required depol or describe ease arrhythmia induced
Lusitropy
Refers to myocardial relaxation
factor affect co -improvement realz - improv filling - increase preload
relaxation active energy consuming - active tpor ca cytop to sr
ca atpase
drugs postive lusitroph or negtaive
nitroglcy positive - improved diastolic relax account benefits in rx hfail
Dromotropy
speed conduction thru av node -
dig slow conduction negative droptrope
phenytoin speeds rate - positive
Mixed venous blood
Mix systemic venous blood drain all cap bed -
not catain blood shunted -
Present central shunt true mix blood may no be possible
pulmonary venous not comonent mix venous blood
How could obtain sample
Three maj streams - SVC, IVC, Cor sinus
po2 lowest cor sinus
Stat mix ven only obtrain Pa - no shunt - adeq mix 3 streams
adeq mixing single o2 sat thruout blood sample site
ra not adeq mix
rv maj mix chamber - not adeqate sample obtain
slow asp from PAc - best method sample
What is the po2 cor sinus
Typically low - 20mmHg
high oxygen extration ration
signif - moycardial o2 consump only increase flow
Po2 mix venous blood
what affects
typicall 40-75% sat of hb
Fick equation CO = Oxygen consump / CaO2 - Cv O2
Ca - oxygen content art blood
Cv oxygen content mix venous vood
mix ven o2 increased increase CO, incease art o2 content or decrease o2 consumption
effect change mix venou o2 content depened % sat hb in mix blood
How determine CO - sample mix blood
Using fick principle
oxygen consump - o2 uptake
art content
mix conetn
co = o2 upt / art - venous
250/200-150 = 5l min
o2 coent mix venous blood - calc from po2 and hb conc
inaccuracy introduced - assuming normalposition o2 dissoc curve
mix o2 sat - measure speac pa cath
o2 conent direct sample mix blood chem analyse
Could CO2 instead oxygen - indicator determing Co
Yes- use Co2 poss
require: -
co2 output
art co2
mix venous co2
vary signif change vent
hypernt increase
0 minimise contsant vent - difficult during sample- min control ventilation
o2 less csense change vent - most 2 carriage hb - fully sat
hypernet not alter o2 uptake or cao2 much
Comparing po2 svc ivc - which has higher po2
Po2 ivc higher so2 - 77% - ivc cinflux kidney blood low o2 extraction
change blood loss and shoch
po2 svc higer - cvf conserved renal vasocon reduced rbf
Distrib blood volume
what is total blood vol
5L
70mls / kg body weight
newborns - vary size placental transuion
positon baby relative to placenta before clamp
time interval delivery & clamping
blood vol term newborn 80-100ml kg
higher value preterm infant
adult value reach 12 months
baby held above level palcent drain blood into placenta
How measure blood vol
how distribu various parts system
Indirect - plasma vol / hct
direct radiochromium labelled red cells
plsams voul - tracer evans blue binds albumin
65% veins 13% artery 2%arterioles 5% capil 15% central blood vol
recumbent - less bood peripheral vein 55% more central blood volume 25%
What is the central blood volume
Blood heart and lungs - thorax
350 heart diastole 450 lungs
context discuion vasoactive drugs - intense symp stim - periphral vasocn 0 iv adrean tfer peripheral blood to central 0 increase size central volume
What is the role of venous system
Circ close loop return blood periph to heart
High compliance - accom lot blood if increase actuley - bbuffer adverse effect increasevol
25x complaince arterial system
veins 4x capcity artery
cmpliance 6 times artery
artery pressure rise 25mmhg accomad same bloood vol that would cause 1mmhg rise venous
ca constrict counteract adverse effect hypovol circ fxn
What is the role aorta and large arteries
Conduction - function distribution blood to circulation
auxiliary pump during diastole
body sv - delivery elastic aorta during systole
diastole potential energy stored stretched walls - concerted kinetic energy maintain blood flow
pressure drop 120-80 where ventricle 120-0
Flow ventricles intermittent flow from aorta large elastic arteries continuous - pulsatile component but still has pulsatile components
What roles various part circulation
Aorta auxil pump obtai contin pulsatile flow
muscular artery - distrbute oxygenated blood tot issue
arterioles- restiance vessel - system vascular ressistance
determine ditrsib co
capilarry
exhcange vessel -
veins
capic
return blood
heart lungs - cotrain central vol - pump and gas exchange
all togerhter closed ciruc pump oxygenator designed dsitrub & exchange
what is the role of arterioles and change resistance control circu
change restriance local control flow
Local vary resistance allows local control blood flow - match tissue requirement function - autoregulation
sum all local organ tissue flow in body co -
tissue via change art resist -control co
heart act demand pump supply required flow
general control pressure
Symp control arteriolar resistance maint art bp - stable bp required assist control tissue flow - autoreg
what law can be used here
Ohms law -
flow equal change pressure divided resistance
Q = Delta P/ R
Now if pressure relative constant - flow depend only resistance
constancy pressure venefecial tissue control local flow - tissue regulatte own ressitance
genereally unable affect systemic pressure much
if could adjust flow - affect allother organ
other adjust new pressure - adjuct local resistance - change bp - facourable level -
need altered flow one organ interefre with flow other organ
cosntant bp allows each tissue adjust flow - adjust local resitance
allows tissue indep each other control local flow - effect system mainta constant bp - nervous sys - sns
import tissue - low level neurgoenic control - flow not particularly adversely affected sympatetitc mediate casocon
tissue gain benefeit also
tissue control o cosneq autoge own supply
heart act as demand pump to delvier co
nervous sytesm maintsins constant pressure head - arterial pressure allow tissue adjust indep others
some adverse affect bascon - impratnt low level nervous otrnol and autoreg
both autoregulation sns - achieve effects change arteriolar resitance
what are the blood resevoirs
generalyl - whole veonous system
some hold signif blood - venocon increase vr increaes bv
most improtant lungs liver skin
resevor
spleen only minor blood resevor human
large veins limbs - act reservoir - important response change positive
splanchnic vcon increase effective blood vol signif
Effects of Anaemia
As hb is Major carrier for oxygen blood - anaemia decrease in oxygen content given volume blood
Three major mech tresponse maint tissue oxygen avail
Icnrease co - delivery
Increase oxy extraction - (grad increasr lower po2, increase 2 3 dpg - odc right sift
redist flow - adeq o2 deliver more crtiical
Increasing Co
Mainta deliver despite lower conent
mech 0 autoreg cuases arteriolar vdil - increase lblood flow required supply increase o2 demand
All tissue affect - vasdil all tissue - drop svr increase tendency vr
co - heart meet demand - pssible provided pump fuction main and not hypovolaemic
oxygen flux eqn
oxy delivery = CO x Hb X sat x 1.34
Presence acute anaemi - Co one four terms body increase acutely
increase CO - increased myocardial o2 consump - corpmoised if hb too - <5
Drop BP - renal retnetion Na & h20 increase blood vol
assist achive Co
kidney able tolerate decrease blood flow - allow resit
EPO increase increase pro new RCC
What changes 2 3 DPG
Red cell 2 3 dpg rise in ameia
incrase p50 hb to 30mmhg
Doesnt impair o2 uptake in lunsg - flat upper part odc - right shift improve unloading
Improve tisseu ability extract more o2 for each gram hb - some increase extraction in response to lower PO2 - even if not right shift - right shift help mintain gradient for diffusion
How does the body compensate for signifcate acute blood loss
Loss hb and decrease circ blood vol
hypovol mimit amount CO can increase
Singif acute blood loss reulst
Decrease CVP= 1 Decrease strethc low pressure baro = increase adh increase symp activity -hr vcon
2 Decrease ABP
decrease firing rate high pressure baro rec
increase sypmathetic activity - vascon aff art
increase renin jg cell - increas ang II aldo
Reflex symp stim - compensatory change limit drop in BP - help maint CO
health adult - nearly fully compensae
Redist blood kidney heart and brain improatn
Symp med remal vcon - decrease RBF & GFR
Urine flow - decrease markedly help conserve volume
increase ADH & ALdo - important renal salt and water retention
Body response max effective blood vol main co
veoncon - reseover vol
tfer ISF it IV - change balance starling
decrease urine flow
Fluid isf - main blood vol -
fall hb
oxygen content fall
vascon - decrease CO important tend maint art pressure -assist redist flow
prefernt -> myocard cerebral
metabolic autoreg organs - overrides local smypathtic mediated vasocon
If excess loss = shock decompensatory mech
logner term -plasma pretin sythn 3-4 days
epo rcc 4-8 weeks
What are they phys principle mainaging severe anaemi - not tfused for reiligous reason
Pricnple miantin o2 avail tissue - adeq norml function
repvent lactic acidos
maximise stissue o2 supply
minimise oxygen demand
CO - volume artifical
hb sat -
ensure sao2
iron tablets support marrow production
oxygen combing power hb
How minimise o2 demand
Sedation minmise act
artifical vent - muscle relax
external measure body temp 36
min inotrops - main co with vol if possible
Why do patient with blood loss look pale and feel cold
Acute sym stim - skin cascon
avute hb - pale appear
redist isf blood - drop
tufsion accel soln - csl - restore volume but drops hb
patients signif trauma - clothes removed facil manegment - heat loss
Venous return
Vis a tergo
mean systemic presure
Vis a tergo - push from behind
Pressure responsible for vr
ohms law flow equal pressure diff divdied resitance
VR = MAP -RAP/trp
Mean sytem pressure - mean pressure at quil if heart stop beating
represent measure degree filling system scirc driving force retunr blood to right side
icnrease inbcrase blood vol & venocon
Guyton curve - equals RAP @ point venous return is 0
VR = MSP-RAP / VR
MSP is about +7 - positive value - over filling
factors tendency for venous return
Muscle pump
throacic pump
intrapericardil pressure
venous tone
artrail cintrib ventric filling
posture
blood volume
factors affect VR - affect msp rap vr
neg intratho pressure decrease RAP - increase pressure grad - favour return in rap 0 thoracic pump not have affect VR veins chest collapse when pressure subatomos increase intraperidcard pressure increase RAP - restrain effect for VR
Venous tone - ceno increase return
Position - pooling blood
posutal hyptension
Outline guyton vascular function cardiac funciton curve hypervol and hypovolm
page 99
hyperbvol shift up and right - msp increase overfilling circ
cardic function not affect
net result in rap and vr - seen new euilib point
hypovol - ooppostie decrease msp rap and vr
Physiology of CPR
ABC
Clear airway adeq vent - easy intubated lungs normal
main prob resus adeq circ not contracting
mech cuase blood flow during CPR
2 theoryies
cardiac pump hypothesis
external chest compression compress heart between sternum and thoracic vertebral colum -
inc intracard pressure pressure grad flow
valves ensure unidrection
alt idea - thacic pump meach - obeser VF cv lab remain concious by repeat coughing
some co - obrain whtiout external cardiac comperssion
proposed expalnion increase ithratoacic pressure - d/t tmit heart and thoracic vessels increase pressure promote forward flow mech prevent revs3er flow - valve at thaorcic inlet equal tmision venous net pressure gradient accross circ - cause forward flow
Arterial pulse contours
Pressure time contour -
root aorta
radial artery
What causes the radial pulse
Page 101
Radial pulse - transmission pressure wave to periph
clearly disting flow blood
Pressure wave travels faster than flow blood
inded pressure wave recorded even if total disatl occulsion rad arter - no blood flow
Radial pressure wave means heart pumping - mech activity
presenve evg - presence eletrical activity
if elecrotmech dissoc pressent - ecg recorded radial pressure curve abset
How is the radial pressure curve different from aortic root for same contract
Radial curve-
delayed onset - time taken travel
distorted shape - various factors reflection resonance daping occuring arterial tre - diff speed tmsiion diff component
Radial curve
Taller - higher systolic pressure
Narrow at peak - higer velocity of higher pressure peak
does not have incisura -0 d/t damping of high pressure component
diastolic hump - reflection and resonance
Radial pressure high - mean pressure not much different than mean pressure centrally
How radial artery pressure contour altered old
change =- decrease compliance aort
decreased myocardial perfomrnaace
aortic curve-
slower upstroke - decrease contractiliy
Higher peak - lower aortic compliance
if systolic peak partic elevated - systolic htn
Lower aortic compliance - pressure wave travel faster - less distorted from contour aortic curve
change elderly different younger - diff aortica radial curve less
What is meant by mean systemic pressure
Theoretical pressure - sometimes represent force promiting VR
whole circ - halt asytole without circ reflex
equilb pressure measure is mean systemic pressure
normal est +7mmHg
Positive - degree overfilling circ system
driving force promoting VR
MSP - increased w/ increase vol, vencon
vascular fuxn curve RAP increase - VR decrease
RAP so high VR cease
RAP equal msp
Draw vascular fuxn curve relates VR to RAP
Where is MSP represent
superimpose cardiac fuxn - relate CO to Atrial pressure
page 103
`Vascular fuxn - effect increase CO - independ variable
on RAP - depend
if CO 0 RAP = MSP 7mmHg
Periph resistance not altered
Max value CO limited RAP becomes neg veins collapse
Cardiac function curve shows effect increase RAP - indep vary on CO - dep vary
hetreometic autoreg frank starlin mech
Rship mech - coupling heart and periph circ
Point 2 curve cross equil point
CO - RAP @ cvs operates
What significance - point where two curves cross
What are effect change venous tone abp and blood volume of vasc fxn curve
equil - point state cvs represented by two curve
Venocon increase MSP - moves curve up and right -
result increase vr @ given RAP
Increase blodo vol same effect
vendoiln - opposite effect
Vascon not much effect on MSP - 2% vol in arterioles
increase bp and vent after- fall VR & CO
= net result curve rotate down msp not altered
What effects change venous tone abp and blood vol on cardiac function curve
venous tone or blood volume not affect position cardiac fxn curve curve
alter positon vasculr function curve and shift position equil point
hypervol shift up equil point up and cardiac function so system working high co and hgiher RAP
Change Afterload
increase art pressure - change position both curve
cardiac function curve - different tradition frank staling curve
vent function show frank starling rship not affect change after
increase contractility - shift up and left
diagr page 104
Hyperventilation chest compression
10VC rapid succession breaths
bear hug - unconc
loss conc - crit low cbf
factor -
hypocap & valsalsva
Hypcap - dec cvf
potent linear over wide range pco2
cbf - decrease 4% per mmhg pco2
if hpyernet actuely reduce then cvf decease byy 60-lighthead not enough cause unconc
BP pressure falls phase 2 valsalva - impair vr to left heart - increase intratoacic pressure causes increased venous pressure in jugualr jug
CPP Decrease
decreaed carotid arterial pressure
incrase jug venous pressure
CBF - CPP/CVR
both affected negatively affect cbf
cbf crit reduced - unconc occurs - fall limp
hypoaxaemia not factor
recovery concious rapid
conc lost - glottis opens - expiration restores intrathoracic pressure
cbf recovers conscious return
