Physiology (Cardio 1) Flashcards

1
Q

Affects of cardiovacsular issues

A

1/3 of the world is affected by hypertension

Heart failure is the leading cause of death

Corony heart disease is very common

Shows that we need to find new mechanisms for treatments

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2
Q

What does the circulatry system include

A

Blood - contains Oxygen carying vehnicles (blood cells) –> blood cells are tramted through tubes
- Tubes = create a conserved cellular envirnment
- Blod = acts as a transmission system for sonignaling between organs + carres cellular waste

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3
Q

Role of Circulation

A
  1. Provide nuterients to all the cells (each cell gets the specific nutrients it needs)
  2. Provide oxygen to cells
  3. remove wast products of cell metabolsim + put waste in a place to be disposed
  4. Maintain constancy of the internal envirnment of cells (homeostasis)
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4
Q

How do organs get provided the same nuterint supply

A

To porvide organs will all the essential nuterints the ciruclatory systen has a paraelle circuit - each of the organs receives its own blood supply where the perfusion rate is locally controlled
- Allows organs to inctease the bloood requiemnet without compromising other organs

Excpetion - lung

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5
Q

Movment of blood (overall)

A

All lood passes form the right ventricle through the pulminary circulate (oxygenated in the pulminary circut) –> goes to the left ventricle –> goes to the body

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6
Q

What does the circulatory system contain (How do you get the circulatory to do its job)

A
  1. Carrier to ship out things and take away bad things
  2. Tranportation force (pump) to trasnport things t other places in the body
    • Forece = flow –> pump to move things through the blood vessels
  3. Need a route system you can follow to transport things = have blood vessels
  4. You need to be able to control how much stuff you deliver to your end users (aka organs and cells) - chaneg where flow is needed or not needed
  5. Need some way to kow that the end users need more stuff when they need it and make chnages when they get it (need feedback)
    • Inform when something is needed by the organ –> tell brain or local system (neurons or chemical)
  6. If some of te end users need more things you need to be able to deliver this to them without cimpormising the supply of stuff to other users
    • Make sure the other organs don’t suffer
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7
Q

Solution of the circulatory system

A

A parrael circut systems carrying blood with vacular tone to vary regional flow with local and strategic snesors to know how much flow is needed and hwere it is needed and input systems to privde the good things and remove the bad things with elimination systems
- Parrellel circut = can chnage the resistnce in one of of teh ciructs and that increase in flow to that circut does not chnage the pumps force for other organs
- Can have different resistnce for each organ = each get what they need

Solution = makes sure that all of the good get delivered to the organs so they get them when they need it

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8
Q

Affect of the parrallel system

A

Allows every organ to get the same base things but can adjust teh flow to each organ
- Flow can be lower in some and higher in otehrs

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9
Q

How much of blood does each organ use

A

Brain using 14% of Cardiac Output

Kidney = gets a lot of the cardiac output

Lungs = get 100% of the cardiac output –> only serios part of the circulation - everything goes to the lungs

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10
Q

Reulst of circulatory system

A
  1. All orans revice blood with the same composition
  2. Relative flow to onw organ can be adjusted as required without neccasrily comprosing the flow of another
  3. Some organds can withsand having the flow lowered more than others as they serve blood condiiong functions well in excess of their metabolic needs
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11
Q

Changing the pump function of the heart

A

Can change the pump function of the heart to make sure the brain gets what it needs

Uses a sensor –> push on the coroted snus (contains barroreceptors - mediate distention) –> barrorepctor smeasure pulastion of the circulation + pressure (chnages in distenction) –> triggers the brain to chnage pressure –> heart pumps flow
- Vessels will constrict or not conrtict at the base of the brain (where coroted is)

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12
Q

Giraffes

A

Girafes are tall but their hearts are tall (far form their head) –> have to pump blood agaisnt gravity –> herat generates more pressure to get to brain = keep base of brain intact

***Have barrorecpetor at the base of the brain

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13
Q

Receptors for local blood flow

A
  1. When excerisze (using legs) –> skeltal muscle is working = increase demand for O2 –> creates an anerobic envirnment –> increase lactic Acid –> decrease pH –>pH is a local vasodilator
    • If need O2 = get acidic envirnment = dialted the vessels
  2. Lung - If you have a part if the ling with no O2 in aveoli –> sending blood to that area would be bad because the blood would not get oygenated –> instead the pulminary vessels constrict in areas with no O2–> only get profusion to areas with O2
    • Opposite of what happens in the leg (when acidc = constricts)
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14
Q

How can we consider the hemodynamics of circulation

A

The hemodynamics of circulation can be considered as a simple electrical circute (have a volatge that dirves current past a resister)

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15
Q

Ohms law

A

V = I * R –> Pressure = Flow X resistnce

End - dP = F * R OR R = dP/F

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16
Q

What is dP

A

dP (pressure driving systemics blood flow) = the mean artery pressure you could meaure in the promixal aorta - pressure you would measure as the veins enter the heart

Creates the tran-circulatpry pressure gradients
- mean flow = cardiac output

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17
Q

Normal cardiac output

A

Normal cardiac output is 4-6 liters/minute
- cardiac output can rise to 5X

Cardiac output scales to body size (including obesity)

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18
Q

How do arteries and vein affect the disrbution of blood _ pressure + resistnce + flow rates

A

Image - shows the distribution of different parameters in different vessles

Example - Blood volume - have little volume in the arteries ; most vilume is in the veins ; almost no blood in the capilaries
- Vein = storage (mostly in the gut/spleen = blood resivoirs)

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19
Q

Increasing volume in the veins

A

Increase volume in the veins = constrict the veins

Veins = low pressure = can put a lot of volume of blood in them
- If had same volume in arteries = then BP would get too high

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20
Q

Blood presure in ateries vs. capilaries

A

Smaller arteries = have resistnce = BP decrease and flow decreases

Capilaries = force decrease = pressure decreases
- BUT the BP does NOT go to zero becase then you have have to force to put the blood in the veins (need a pressure gradient = need driving force)
- Pressure is lowest when you get to the heart then increases again

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21
Q

Basic Principle of macro hemodynamics

A

You have a pump generating flow - cardiac output is flow

You have large artries to transports the blood to orangds (no resistnce)
- Have compliance - makes sure the pressure doesn’t drop to 0

You have smaller local artieres in the organs that get small enough to cause resistnce to flow

You have tiny capillaries and by the time blood gets there flow is no longer pulsatile and goes much slower

You regroup at the other end into large veins (have minimal resisnce) to get back to the pump

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22
Q

Scenrio where flow is 0

A

Based on P = F X R

If flow is 0 when the heart is flling then P would go to zero

BUT the BP stays 120/80 because because the large arteries stretch as the heart beats (pulse is bffered by the aorta) –> aorta expands

When there is no flpw have expansion and contactons = gives volume back = maintains pressure
- BP increases as you age becaise the aorta gets stiff
- BP is able to go higher while have refilling and no flow

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23
Q

Cardiac output equation

A

CO = Mean blood pressure/vacsular resistnce

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24
Q

What determines resistnce in small arterioles

A

restince = 8/pi X viscosity (n) X legnth (L)/radius^4

As the radius gets smaller resistnce gets higher (because diving a small number to the poweer of the fourth)
- Very sensitive especially in small vessels (radius decreased by 1/2 the resisce increase by X16)

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25
Q

Why isn’t blood pressure insanley high

A

Because you are putting 4 liters per minute of blood flow into yiou arteiers AND at some point the radits is small so you would think you would have 1000 mHg to get through the resistnce

THIS isn’t the case because you have many parallel vesslves
- Becuase all of the vessels are a paraeled branches = net is resistnce is not so high

1Rtotal = Sum of 1/Ri

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26
Q

Viscosity

A

Things in blood make it more viscous
1. Serum - more protein = more viscous = increase resistnce
- Example Fibulin or glbulin

  1. RBCs
    • Example - smoking or chronic hypoxia –> lungs don’t work for oxygen delivery = increase RBCs = increase viscosity
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27
Q

Blood flowing through teh aorta vs. smalleer vessls

A

resistnce imporsed by large arteiries (like aorta) is minimal - blood flows through these tubes with neglible loss of pressure

As artieres get smaller there is increaseing resistnce (higher receistnce when arteries are in the micron range)

Smaller vessles - resistnce is difined by restince = 8/pi X viscosity X legnth/radius^4

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28
Q

Cappilaries

A

Capilaries = where good things and bad things are exchnaged

Capilaries = a tube that is one cell thinck –> lies next to the cells that need what the capilary is carrying

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29
Q

Net Filtration rate

A

Net Filtration rate = K[(PC-Pi) - (Pic-Pii)

Pc = hydrostatic pressure in intercapicalry compartents
- Dirving pressire in the arterial side

Pi = hydrostatic pressure in intestinal compartment
- Pressure on the extrcellular side

PiC = intracapilary oncotic pressure

Pii = intestical oncotic pressures

K = constant expression of how readily fuild can move acoss capilaries

Image - cross section of capilary - shows oncotic pressure vs. hydrostatic presure

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30
Q

Pc vs Pi

A

Pc = pressure on the arterial side

Pi = pressure on the extraacellular tissue soace around teh cells

Two pressures appose each other

Pc - Pi –> driving pressure to move water and the solvents the water contains out form the capilary intertore to the fluo around the cell

31
Q

Oncotic pressure

A

Protein pressure - oppsoposes the driving pressure from Pc-Pi
- Realtes to an increaseing concentraion of proetsin that remian in teh capilary as the fluid is dirving out into the tissue space

32
Q

Albumin

A

Major protein contibuting to permability of fluids/solutes in capilaries
- Made in the liver

33
Q

Concentration of protein in tissue space

A

PiC - Pii

Rising concetarion of protein (Albumin???) in teh blood passing throuh the capialry is countered by the concetrayon (of protein???) in the tissue soace

Provides a concetration gradient to brinh fluid back into the post cailary venule

34
Q

Capilary permability at homestastos

A

At homoestais the amoint of that moves into the tissue space due to hydrostatic force is counters by protein force (osmotic force) –> tissues remian relativley dry

35
Q

What happens during heart failure

A

During heart failure the equilirbium in the capilaries falls apart
- Get water in the tisue –> water can’t get back into the capilary

Pressure in the venous side increase –> there is a stringer hydrosttic force (keeps fluid in the tissues) –> the ncotic pressure can’t compensate

36
Q

Result of heart failure

A
  1. Fluid builds up in the lungs (pulmanry edema - wet sponge lung) = hard to breath and oxygenate blood (shortness of breath)
    • Space in the aveoli sac get filled with water = oygenation is poor
  2. Interstitial Edema/Pitting edema - Fluid builds up in peripheral tissues
    • Ex. ankle and legs - gravity helps the fluid pool
    • Occurs if have issue with oncotic pressire (decrease protein = decrease vicosity = water gets trapped)
    • Can occur if have liver or renal disease –> decrease albumin = dcrease visocity = get edema
37
Q

Renal disruption

A

Renal disruption can lead to pitting edema –> get rid of too much albumin (because disrput the membrane) = pee out the protain = decrease the protein = decrease viscoity = get edema

38
Q

COVID 19

A

COVID 19 = destroys the capillary endothelium (especially in the lungs) –> get leaking vessles
- Leaking if the vessles is not because of hemodynamic pressures INSTEAD get leaks because of breakdown of membranes
- Can fix issue based on sterlings low –> lower the pressure by getting rid of fluid in pee or venodilators = removes fluid from the heart BUT won’t work here
- Heart to treat because the memebrane is permable = proteins and water can go out

results - Adult respitory Distress syndrome (aka lung white out)

39
Q

Structures of the heart

A

Shows the chambers of the heart

Pulminary valve - 3 leaflets –> when pressure drops it makes sure the blood doesn’t floow back

Right atrium - get the blood from the periphery

Tricuspid valve - Right ventricle has high pressire and pulminary artery is low pressure = blood moves from high to low

40
Q

Overall principle of blood movment in heart

A

Blood moves from high pressure to low pressure

Ex. High pressure in right atrium to low pressure in right ventricle

41
Q

How do valves work

A

Papilary muscle pulls on the valvle = keeps it closed = keeps blood form flowing back

42
Q

Basic Cardiac cycle

A
  1. Filling phase (Diastole) - ventrcile needs to fill with blood at a low pressure (doesn’t require much force)
  2. Starting of contraction - valves are still closed - muscle must stifen and contract to expel the blood
  3. Continuing contractions - valvles open and heart ejects into both lungs and arteries
  4. Heart muscle relaxes - valves remai shut - muscle needs to relax and pressure needs to fall so the ventricle can fill again
  5. Heart starts filling again
43
Q
A

Top row - big peak -> aortic valvle closes –> ventricle pressure falls to below the pressure in the atrium (blood can flow high to low)
- Left artrium and left ventrcile have a small pressure difference BUT because there is low resitnce you can have a small pressure difference and still have plenty of flow

Blue peak on top row = Pressure in the right ventrcile but the aorta is close –> when the mitral valve closes the pressure increase higher than the atrial = heart ejects = aortic valce opens and the mitral vlave closes (mitral valve closes becuase the hearts pressures higher than atrrum - once the pressure is lower thna the atrium the aorta valve will close again

44
Q
A

Green line
1. First blip is a P wave
2. Spike - ventricles are activated
3. Third blip = T wave –> hert relaxes (repolarization

Boster pumpes = the little blips in EKG

45
Q

What happens if the two chambers have the same pressure

A

If the 2 chambers have the same pressire then the atrium constricties = gives a boost pump (booster pump wull fill 15% and the rest will fill due to passive flow)

46
Q

Atrial fibulation

A

Common arthyia (chaotic herat beat)
- Often fine (vs. ventril fiberlation people die)

What happens - instead of coordiating contraction the atria is constaly quivering

A fib = big problem if have 60% of the atrium boost BUT since the boost is only 15% A-fib is survivable
- If you have heart disease (high BP + stiffer heart = can;t fil = atrium contracts more = if they have A-fib it is worse)

47
Q

Pressure volume loop in the cardiac cycle

A

Shows the pahses and teh correpsonsindg wave forms for arterial, ventricle, atrial pressures + shows the cardiac ventriculaar volume + shows the elctrical activation waveform – plots the volume in the heart chmaber (X-axis) and pressure in chabe (Y-axis)

A - mitral valve closes
A -> B ventrcile pressure rises
B –> Aortic valve opens
C –> Aortic valve closes
D -> mitral valvle opens

During filling = have stertching = volume increases but the pressure does not increase

48
Q

Distaly vs. Sistaly

A

Sustaly = Actvation
Diastly = Deactivation = low pressure = filling

49
Q

Ventrcile Cardiac Cycle

A

Viewed as a spring with time varying stiffness

Left - Slope = stiffness –> goes from bottom where it os not stiff ; top red line is the stiffest

If have more stiff = it is able to contract t generate pressure = get forve to put to arteries with enough flow to get all of the blood profused THEN will relax in diastily

50
Q

Ventrcile Cardiac Cycle (image 2)

A

Top = peak - heart is stiff even if pressire doesn;t chnage = move the activation of the muscle

Middle - peak = shows the muscle is stiff until teh aortic valve is closed

Bottom = relaxation

51
Q

Stroke volume

A

The volume that is ejected with eat heart beat

Stroke volume X number of heartbeats per minute = Cardiac output

52
Q

What affects stroke volume

A
  1. Heart contraction strength (contractility)
  2. Arterial load (resistnce) against which the heart beats
    • Dilate the arteries = decrease resisnce = increase CO
  3. How much blood volume is in th heart before it contracts
    • Heart is designed to start with more volume = ejects more colume = stroke volume increase = cardiac output increases
    • Cardiac output as a linear relationship with endiastolic volume (higher CO = Higher volume)
53
Q

Cardiac Output

A

CO = mean flow rate form the herat = heart rate X volume ejected per beat
- Volume ejected per beat = Stroke volume

54
Q

Effect of excersizing

A
  1. Decrease the amount of resistnce during excersie
  2. Increase contraction strenhth
  3. Preload is higher = incerease cardiac output
    • Preload is higher becasie body adpated to have a lowere HR = higher stroke volume
55
Q

INcreasing Cardiac output

A
  1. Increase the HR - Cardiac output can increase with a higher heart rate as long as the stroke volume dosn’t fall BUT at really fast heart rates the stroke volume does fall because the heart does not have enough time to fill between hartbeats
    • In a range from 60-100 beats per minute you can increase cradiac output with heart rate
  2. Cardiac output increases if you increase the stroke volume
    A. Heart cintraction strength - Stroke volume can increase if the instrincic contractility of the heart muscle increases(increase contractility)
    B. Arterial resistence against which the heart beats - if you lower the arterial resistrnece to amke it easier for the heart to eject (lower reistnce)
    C. How much blood volume is in the heart before it starts to contract - if you fill the heart with more blood OR f you streatch the herat muscle
56
Q

What does intrinsic contractality do?

A

Contractility = how strong is the heart when it contractions (measure of stiffness)
- Increase excersize = increase conractility + have drugs that increase contractility

At decreased contractility vs. increased
- Not chnaging the amount of volume being filled at reast but increase contractility = increase stroke volume = increase cardiac output

57
Q

Why does stretatching heart muscle increase stroke volume

A

Stretching heart muscle incerases its contraction force and strole volume - based on Frank starling Law

58
Q

Situations where higher CO is found

A
  1. Excersize
  2. Normal growth
  3. Pregnacy
  4. Lung disease (oxugen diffision is reduced_
  5. Obesity (most common)
  6. Hormonal stimulation (often hyperthyridsm)
59
Q

How does the heart muscle contract

A

Deporlarization of the muscle cell causes the Ca2+ chanels to open –> ca goes into the cell AND the SR lets Ca2+ into the cell because Ca from th eoutside binds to the Rynosin receptor –> Ca2+ binds with the tropinin complex

60
Q

How does heart muscle speed up the contrcaction

A

Ca neds to go from the outside of the cell to the Tropinin

To speed this up = have Ca2+ going from the outsisde of the cell AND have paralel local delivery so the Ca does not have to go all teh way in for each beat
- Helpful because the msucle = have a fast HR –> most Ca comes from SR

Instead - T tubule network has ca2+ = releases locally to the sacromeres
- Have rynoninde receptors = actiaved by teh Ca2+ from the outsde = ca leaves teh SR Ca binds to teh sacromere = get contraction

61
Q

Ca2+ leaving the cell

A

SERCA2a - Takes up Ca2+ back to the SR

Ca/K chanel - take Ca out if the cell and brings in Na
- Maintains the elctricochemical balance

62
Q

Actin and Myosin complex

A

Thick filaments = myosin
thin = Actin

At the ends = Have Z-disk –> have signing molecule –. force is sensed and trasnduced = corrdinates everything

Shortens when activated

63
Q

Mitocondria in Muscle contraction

A

Mitocondira = fuel

Sacromere happening all happens around mitocondria because mitocnidra has ATP

Ca2+ goes through mitocindra uniporter = tells mitocindra how much ATP is needed
- Increase Ca2+ = increase actin/myosin = increase contraction = Increase ATP needed

64
Q

Tropinin complex

A

Rope = troponin –> blocks the myosin binidng sites on actin
- Need Tropomysin to move –> Ca2+ binds to tropinin complex on tropomysin –> allows the rop to roll off
- When Ca2+ decreases = tropinin rolls back and blocks sites = stop contraction

Need the mysoin helix to go from relaxed to activate to string activated so it can bind to myosin –> get contraction

65
Q

PKA activation

A

PKA activation increases both myocyte formation and calcium transients

Isoproterenol = activates heart muscles (increases and decreases calcium)
- Top right = peak have increase in Ca2+ - goes up and down quickly (fatser when activates sympathetic nervous) ; get higher force + faster force

66
Q

Myofilament response to calcium

A
67
Q

Regulation of scraromere

A

Beta receptor aginists binds to alpha subunit of the GPCR recetor –> breaks up the heterodiner –> activates the alpha subunit = actiaves adeylate cylcalse –> uses truns ATP into cAMP –> cAMP intercats with protein kinase A -> get phospherylation

  1. Phosphoylates the Ca2+ chanel
  2. Phosphorylate Rynein
  3. Phosphorylates myPBC and titan (mcrofilaments)
  4. Phosphorylates PLB
  5. Phosphorylates Tropinin 2
68
Q

Phosphorylation of Ca2+ AND phosphorylation of reynein recpetor

A

Protein kinase A phospherylates the Ca2+ chanel = get increase of Ca2+ = get increase of Ca2+ from SR

ALSO phosphorylation of Runein receptpr = get increase in Ca2+

Ca2+ goes to troponin –> actin can bind to myson = increase contraction

69
Q

Phosphorylation of myPBC and titan

A

Phosphorylate titan - titan acts like a molecular spring = causes stiffening BUT can chnage the stiffeing by phosphorylation

Phosphorylation - makes less stiff = easier to fill

ALSO phospherylation myPBC
- myPBC iteracts with Actin = keeps pace of the scaromere shortning (acts like a break) BUT when phosphorylated = decrease the break = increase movment of the sacromere

70
Q

Phosphorylation of PLB

A

Makes it easier to bring calcium to the SR

71
Q

Phosphorylation of Tropinin 2

A

Tropinin 2 = inhibitory = reduces the response of microfilamenrs to Ca2+

When phosphorylated = Trponin 2 is less inhibitory
- Phosphorylation allows the heart to release cross birdges as Ca2+ falls

Counter balance effct

72
Q

Higher stiffness

A

Higher stiffess = pump more blood if everything else is connstant
- Contracts more = more blood out

73
Q
A