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Note: This is unedited (too tired to edit) – may post an edited version later if I get energy.

I can’t post the


Guyton-Hall figures, so I just put in ref’s for those.

• Heart as a pump - at rest only works at 1/3 of max CO


o PV loops - before
o Wigger's - before
o Frank-starling

• Red equals normal range


• Pre load - describes how long heart sarcomeres are - the more the heart fills up the more
the heart pumps out
 What comes in must come out
 Described by end diastolic volume (for this test) or right atrial pressure (main
one) or central venous pressure or sarcomere length
• Transport into tissues
o Diffusion vs bulk flow
• Getting things from vasc sys to tissues where they are needed
• Diffusion is through cell mem
• Bulk flow - goes with water between cells
diffusion
bulk flow
small
big
lipophilic
hydrophilic
uncharged
charged
fick's law
starling's eq
• Fick's : Qnet = -DB/ΔX x A x ΔC
• Starlings Law – capillary – gh fig 16-5 pg 185
 Jnet = Kf(ΔP - Δπ)
o Lymph
• Water only goes across capillary membrane (in circulatory sys)
• Net filtration pressure of 0.3mmHG outward
 Meaning fluid is building up
 Lymph flow returns to venous system
 Π forces are due to proteins
• Inside capillary is function of albumin
 Pif can be negative due to lymph pump
 5 factors to increase lymph flow
• Inc Pc -
• Dec πp
• Inc πif
• Inc capillary permability
• Lymphatic pump - pulls it out

• Hemodynamics
o Compliance - ΔV/ΔP

 Arteries - red - low compliance


 Veins - blue - more compliant
• Vasoconstriction - dec compliance - rigid
 Atherosclerosis - dec compliance
• Vasodilate - inc compliance - relax
o Ohm's - V= IR
• For blood: ΔP = Q * R
 Q = flow, R = resistance
 Q actually equals arterial conductance
• Has been a prob in past w/ cowley's Q


o Poisseuille's
• 4th power law
• Q = ΔPπr^4/8ηl
 η - viscosity
 l - length
• Thus even small constriction / dilation can have large influence on blood flow
• Anemia - dec viscosity - inc blood flow
o Autoregulation - Tissues does it itself
• Blood flow is extremely constant over a range of pressure (~60-160)

• This is referring to circulation as a whole (poisseuille's / Ohm's is for a single capillary)


• 2/3 theories to how it happens
 Blood flow is related to metabolism - linear

• Regulated by precapillary sphincter


 2 theories to what stimulus is
• O2 demand theory - if O2 dec (due to metabolism in tissue), can't generate
ATP, can't constrict
• Vasodilator feed back
• Adenosine - directly relaxes vasc smooth mm - heart
• CO2 - brain
• Lactic acid - muscle
• K+ - FOR PHYS SMALL changes - muscle
• Ek = -60 log Ki/Ko
• Normally 140/1.4
• If go to 14, it depol (if inc extracellular k+)
• Would get vasoconstriction - this is when
something is seriously wrong
• BUT for small inc in K+, through sustrate level activation
of ATPase of Na+/K+ pump and when you run Na+/K+
pump faster you get net +1 out and get hyperpolarization
o Myogenic autoreg - if you have an acute inc in BP, keeps you from blowing out eyes

• Diameter dec to prevent pressure from having negative effects on important organs
• Note
 Flow = P1-p2 (Part - Pven)
 Compliance = Pin - Pout
• EKG's
o Fast response- contractile cells – see lectura for pic
o
• Phase 0 - Na+
• 1-
• 2 - Ca+ : L-type
• 3-K-+
• RMp - mostly K+ diffusion
o Slow response - SA node, AV node

• 0 - Ca+ T-type
• 3- K+
• 4 - 3 parts
 A - slow Na+
 B - ca++ leak
 C - K+ close - MOST IMPORT
o Normal vector

o Process
• SA - AV = atrial depol
• Stalls at AV node
• Av -> purkinje -> vent = vent depol
o Normal EKG

• GH figure 11-1 pg124


• P wave - atrial depol
• PR interval - AV node
• QRS - vent depol
 Q wave - septum depol - depol quickly before ventricle depol
 R wave - ventricle depol
 S wave - upper left of heart - last to depol
• ST segment - Ca++ influx through L type ca++ channels during plateau of fast response
• T - vent repol
o Einhoven's triangle
• Measured resistance through 2 buckets of water - mapped out theoretical triagngle

 GH fig 11-6 pg127


 gh fig 12-3 p132
 Put them so they meet in middle and make vector to make hexangonal reference
system
 If you add up any 2 leads the distance btw them is going to be another lead - ie
lead II + III = aVF
 But in general -> I + III = II KNOW
• Axis of depol
 NOTE: On paper pretend you are looking at heart, so right side of paper is left
side of hear
 QRS tells which direction ventricles depolaried
• If it is positive goes towards right of graph
• If it is negative goes towards left of graph
 From 0 map to right
 Anything above -30 is left axis deviation
 Anything on right side of heart is right axis deviateion
 Determing axis of deviation (up = positive, down = negative)
• Normal : I up, aVF up
• NW axis : I down, AVF down
• Right axis: I down, aVF up
• Left axis: I up, aVF down
• AND lead 2 is negative (if it is positive you are below -30)
 Heart attack
• If ST is depressed or elevated heart is having problem repolarizing
• You can map the depression/elevation (ie leads I and III) and see
where heart attack is occurring (book calls it "current of injury")
• AV nodal block - aka Heart block
 SA node block - P wave abnormalities - rare doesn't come up
 See AV node block in PR interval (normally is 0.2ms) which effects downstream
complex
• Type I block - long PR interval - all Ps are followed by QRS
• No prob, don't do anything
• Type II block - (wenckebach)
• Wencke bach - Mobitz 1 - PR gets longer until QRS is dropped
• See YouTube "diagnosis wenckebach"
• Dropped QRS - have at least type 2 maybe type 3
• Mobitz 2 - PR stays the same, just randomly drop QRS
• Type III block
• Easiest to comprehend, hardest to recog
• Aka complete AV block
• Eventually ventricles catch on own rate
• Thus you have reg P waves and regular R waves - but have
NOTHING to do with each other
• Basically look to see if you equally spaced Rs and equally
spaced Rs if it looks really funny
• May look like you are dropping QRS's all over the
place

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