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Physiology Kerry > 3.3 Cardiac muscle, blood, > Flashcards

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
Q

How measure blood vol

how distribu various parts system

A

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
Q

What is the central blood volume

A

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
Q

What is the role of venous system

A

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
Q

What is the role aorta and large arteries

A

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
Q

What roles various part circulation

A

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
Q

what is the role of arterioles and change resistance control circu

A

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
Q

what law can be used here

A

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
Q

what are the blood resevoirs

A

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
Q

Effects of Anaemia

A

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
Q

Increasing Co

A

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
Q

What changes 2 3 DPG

A

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
Q

How does the body compensate for signifcate acute blood loss

A

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
Q

What are they phys principle mainaging severe anaemi - not tfused for reiligous reason

A

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
Q

How minimise o2 demand

A

Sedation minmise act

artifical vent - muscle relax

external measure body temp 36

min inotrops - main co with vol if possible

39
Q

Why do patient with blood loss look pale and feel cold

A

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
Q

Venous return
Vis a tergo
mean systemic presure

A

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
Q

factors tendency for venous return

A

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
Q

Outline guyton vascular function cardiac funciton curve hypervol and hypovolm

A

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
Q

Physiology of CPR

A

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
Q

Arterial pulse contours

Pressure time contour -
root aorta

radial artery

What causes the radial pulse

A

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
Q

How is the radial pressure curve different from aortic root for same contract

A

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
Q

How radial artery pressure contour altered old

A

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
Q

What is meant by mean systemic pressure

A

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
Q

Draw vascular fuxn curve relates VR to RAP

Where is MSP represent

superimpose cardiac fuxn - relate CO to Atrial pressure

A

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
Q

What significance - point where two curves cross

What are effect change venous tone abp and blood volume of vasc fxn curve

A

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
Q

What effects change venous tone abp and blood vol on cardiac function curve

A

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
Q

Hyperventilation chest compression

A

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

Physiology Kerry (17 decks)

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