3.3 Cardiac muscle, blood, Flashcards

1
Q

What is prepotential

A

Phase 4 diastolic depol occurs in PM cells -> heart - depol contin til apotent initiated - threshold reached

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2
Q

Signif prepotent in sa node cell heart

A

normal conditon not all cells have preportent -
responsible for automaticity
cells - fastest prepotent - PM heart
usually sa node -

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3
Q

Draw ap for SA node cell & super impose ventricle muscle cell

Differences

A

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

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4
Q

How are the AP periph myelinated axon & skeletal muscle - different from cardiac

A

Mian diffrence - very short duration perip 1-2 msec
muscle 5-10msec

absence platuea

absence of prepotential

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5
Q

What is the function AV ring firbous

A

Inuslation - provide speration atria from vent

structural
fibrous skeleton procides sturcutor for origng insert myocardial scell - insertion valve

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6
Q

how is it relevant to av node =

A

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

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7
Q

what is the conduction velcotiy - other parts conductuion path

A

Atrial muslce 1 msec
avnode 0.05 msec
purkinje 4 msec
ventricular 1msec

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8
Q

What is the last part of the heart depolarised - why

A

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

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9
Q

Properties of cardiac muscle

specil intrinsic property

A
Excitability - 
Automaticity
rhythmicity
conductivity
contractility
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10
Q

Define automaticty

A

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

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11
Q

Rhythymicity

A

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

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12
Q

Conductivity

A

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

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13
Q

How does AP trvvel cell to cell

A

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

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14
Q

What is exctiability

how is it measured

why is it difficult

what circustance need to be considered

A

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

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15
Q

Lusitropy

A

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

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16
Q

Dromotropy

A

speed conduction thru av node -
dig slow conduction negative droptrope
phenytoin speeds rate - positive

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17
Q

Mixed venous blood

A

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

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18
Q

How could obtain sample

A

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

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19
Q

What is the po2 cor sinus

A

Typically low - 20mmHg
high oxygen extration ration

signif - moycardial o2 consump only increase flow

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20
Q

Po2 mix venous blood

what affects

A

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

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21
Q

How determine CO - sample mix blood

A

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

22
Q

Could CO2 instead oxygen - indicator determing Co

A

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

23
Q

Comparing po2 svc ivc - which has higher po2

A

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

24
Q

Distrib blood volume

what is total blood vol

A

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

25
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%
26
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
27
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
28
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
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
How minimise o2 demand
Sedation minmise act artifical vent - muscle relax external measure body temp 36 min inotrops - main co with vol if possible
39
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
40
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
41
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
42
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
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
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