Physiology: Shelf Review #3: Cardiovascular

Front 1

what's the stressed volume? unstressed?

Back 1

blood contained in the arteries is stressed.

veins have unstressed volume. note that there's a whole lot more unstressed volume in the body.

Front 2

what's the site of highest resistance in the cardiovascular system? what receptors are on arterioles?

Back 2

arterioles!

Alpha 1 andrenergic receptors are on the skin, splanchnic, and renal (think of all the ones that will VASOCONSTRICT). Also on veins.

alpha 2 receptors are on the skeletal muscle (the ones that vasodilate when under stress)

Front 3

what part of the system has the largest area?

Back 3

capillaries

Front 4

what are our equations for velocity and for blood flow? where is velocity highest and slowest? how can we calculate cardiac output from this?

Back 4

velocity = Q/A

flow over area.
So the higher the area, the slower it goes - that means that velocity is slowest through capillaries and highest through the aorta. this is good because slow facilitates exchange.

flow:
Q = delta P/R

change in pressure over resistance.

resistance = Delta P over Q

CO = [MAP - RAp] / TPR

mean arterial pressure - right atrial pressure / total peripheral resistance.

Note that flow is inversely proportional to resistance.

Front 5

what's another equation for resistance? how does changing hematocrit change resistance?

Back 5

R = 8nL/Pi R^4

so, resistance is directly proportional to length and viscosity (raising both raises resistance). So, raising hematocrit will cause more resistance, decreasing flow.

note that it's inversely proportional to the fourth power of radius - so the most dramatic effect one can have on resistance and flow is by changing radius.

Front 6

talk about resistances in parallel and what this means for the body.

what about series resistances?

Back 6

parallel resistances add reciprocally.

1/R = 1/R + 1/R + 1/R ...

because the organ systems are generally in parallel, going further from the heart lowers resistance.

series resistances are added regularly, so they're combined additive.

within a specific organ, blood is in series with the highest resistance at the level of arterioles.

Front 7

in parallel and series vessels, how are pressure and flow down the chain?

Back 7

in parallel systems, the pressure is the same in all parts. (think Parallel has equal Pressure)

in series systems, the flow is the same the whole way down the chain

Front 8

what's reynolds number and what changes it? how does hematocrit fit in?

Back 8

it's the chance blood will be NON-LAMINAR and hence more turbulent.

higher number = more turbulent.

this is predicted by having LOWER VISCOSITY and HIGHER VELOCITY.

think that thick fluid has trouble being turbulent.

so, the most turbulent fluid would be water through a constricted vessel.

SO: low hematocrit = low viscosity = higher reynolds number

Front 9

what's capicatance and what's inverse to it?

Back 9

capicatance is inverse to elasticity. the more elastic tissue something has, the harder one has to push on it to make it distend.

capicatance = Volume / Pressure.

So, the highest capacity vessels will store a lot of fluid under very low pressure (they distend readily).

Front 10

how does elasticity change with age?

Back 10

it goes UP - capacitance goes down with age. Arteries get stiffer and require higher pressure to get the same distension

Front 11

how does pressure change through the system?

Back 11

pressure is highest at the aorta and lowest at the vena cava. it drops because of increases in resistance.

So, the greatest pressure drop is along arterioles (that's where the highest resistance is)

Front 12

what's pulse pressure? how does this change with aging?

Back 12

systolic minus diastolic. it goes up with age as arteries harden. With lower capicatance, a higher pressure is generated in the aorta during systole, increasing the difference between systole and diastole.

Front 13

EKG: what's the P wave? What's the PR interval? how does normal increased heart rate affect the PR interval?

Back 13

atrial depolarization. Note that repolarization isn't seen 'cause it's buried by the QRS complex.

PR interval is the time between atrial depolariztion and the beginning of ventricular depolarization - so it must represent the time through the AV node.

Things that decrease conductance through the AV node increase the PR interval.

normal upped heart rate will decrease the PR interval (so it's not necessarily pathological).

Front 14

what's the QRS complex? What's the T wave? what's the QT segment?

Back 14

depolarization of the ventricles is the QRS complex.

T wave is repolarization of the ventricles.

The QT interval goes from the beginning of the Q wave to the END of the T wave - this represents the entire time to depolarize and repolarize the ventricle.

Front 15

what's the ST segment?

Back 15

End of the S wave to the beginning of the T wave (note that segments are times BETWEN waves, interval include two waves).

ST segment represents the entire time the ventricle is depolarized.

Front 16

4 phases of an action potential: what are they?

Back 16

0 = rapid depolarization straight up, caused by Na+ channel opening (I Na)

1 = rapid but short depolarization caused by Transient Outward K+ (I to)

2 = Plateau from L-type Ca++ (I Ca)

3 = rapid depolarization from delayed rectifying K+ (I K)

4 = steady state hyperpolarized by I K1 also called inward rectifying.

Front 17

describe the SA node with respect to its phase 4

what else is kinda like this? how are their speeds relative to each other?

Back 17

phase 4 depolarization = automaticity, so it's a pace maker.

the AV node and the purkinje fibers exhibit the same behavior and can become dominant if the SA node is suppressed.

SA > AV > Purkinje

Front 18

go through the 4 phases of the SA node:

how does the AV node work?

Back 18

Phase 0 (upstroke) caused by inward Ca++ (unlike the rest of the heart except the AV node, including the purkinje fibers, where upslope 0 is caused by inward Na++ channels)

phase 3 is the same, increased K+ outward current.

Phase 4: has slow depolarization. Due to slow Na+ conductance that increases. Called I f channel, which is activated by the depolarization of the previous beat

AV is pretty much the same - the upstroke depolarization phase 0 is caused by Ca++ conductance.

Front 19

conduction speed through the heart - what determines this and where are important intervals located?

Back 19

determined by HOW MUCH current flows in during phase 0. More current = faster conduction.

fastest in the his/purkinje system.

Slowest through the AV node, which gives the ventricles time to fill. If it goes too fast through the AV node, get decreased ventricular filling and bad CO.

Front 20

what is Chronotropic and Dromotropic effects?

Back 20

Chronotropic effects are those carried out at the SA node to change heart rate based on its firing.

Dromotropic effects are those which alter conduction through the AV node.

Front 21

describe parasympathetic effects on the SA and AV nodes:

Back 21

the AV and SA nodes and atria have a lot of parasympathetic innervation - the ventricles don't.

parasympathetics on SA node: work through MUSCARINIC receptors and DECREASE the rate of phase 4 depolarization by blocking that I f Na+ channel.

Parasympathetics on AV node: work through same receptors, but this time they stop the rate of Ca++ current during phase 0, decreasing the speed of action potentials (not of automaticity)

sympathetics work through Beta 1 receptors

Front 22

what do sympathetics do to the SA and AV nodes?

Back 22

norepinephrine acts on B1 receptors.

it increases the Na+ channel in the SA node that makes the phase 4 line steeper

it increases the Ca++ channel that makes phase 0 happen more intensely in the AV node. This should decrease the PR interval.

Front 23

what does botulin toxin do?

Back 23

blocks ACh release from post-synaptic terminals.

Front 24

what's ionotropism and what changes it?

Back 24

it's the contractilty of the heart. generally related to Ca++ concentration (higher = harder contraction). Generally reflected in the EJECTION FRACTION (SV/EDV)

positive ionotropes tend to keep Ca++ high in the cell: this can be from increased heart rate (more Ca++ enters myocardial cells causing coupled-increased release of Ca++ from the SR).

sympathetic stimulation also causes increased Ca++ influx during plateau. also increases the activity of the SR Ca++ pump, so more is sequestered and ready for release when it's needed.

digitalis is a good positive ionotrope.

parasympathics are negative ionotropes. they decrease Ca++ influx during plateau.

Front 25

what's preload and afterload, and what does this represent in the ventricles? what's frank staling?
what do ionotrops do?

Back 25

preload is the EDV, and is how much the heart fills. afterload is the pressure the heart pumps agains: so afterload on the left ventricle is aortic pressure.

afterload on the right ventricle is pulmonary pressure.

a higher EDV or preload causes a stronger contraction - so the input and output of the heart are kept constant. that's frank starling.

positive ionotropes shift the EDV to SV curve up, negative shift it down.

Front 26

starting at a full ventricle, go through the cardiac cycle:

Back 26

the ventricle gets excited and begins to contrat. pressure immediately exceeds that in the in the left atria and the mitral valve closes. begin isovolumetric contraction.

once aortic pressure is exceeded, the aortic valve is forced open and blood enters the system.

once the venricle relaxes and pressure goes below the aorta, the aortic valve closes and the ventricle begins isovlumetric relaxation.

then the mitral valve opens, and begin ventricle filling.

Front 27

what's mean systemic pressure and what changes it, and how is it graphically represented?

Back 27

on the cardiac/vascular function curve...where vascular function curve crosses the x-axis.

this is measured experimentally with a stopped heart - it's the pressure with no blood movement.

it goes to the right when blood volume is expanded or there's a decrease in compliance (blood vessels don't expandas much)

shifts left when there's a decrease in volume or compliance goes up.

Front 28

heart and vascular function curves - talk about the effects of volume expansion and loss, of ionotropes, and of arterial constriction/relaxation

Back 28

volume expansion moves the vascular function curve out while contraction moves it in.

VENOUS dilation acts like volume CONTRACTION.

arterial contraction pivots both the heart and vascular function curves down, where as arterial dilation pivots them both up

ionotropes affect only the heart curve (pivots up).

note that the heart curve never seems to shift up or down - only pivots.

BRS calls arterial constriction "total peripheral resistance)

Front 29

cardiac output, stroke volume, ejection fraction, stroke work work - what are our equations?

Back 29

stroke volume = EDV - ESV

CO = SV * HR

EJ% = SV / EDV

stroke work = SV * aortic pressure

Front 30

what increases 02 consumption in the heart?

Back 30

think about anything that makes it work harder:

increased afterload (aortic pressure)
increased contractility
increased heart rate
increased size

Front 31

we have three equations for cardiac output: what are they?

Back 31

remember that q = delta p / R

so MAP - Right Atrial Pressure / TPR = CO

also, our easy one: SV * HR

also, oxygen consumption:

CO = o2 consumption / ([02 pulm. v] - [02 pulm A])

Front 32

what's the first heart sound? second?

Back 32

the closure of the AV valves as the ventricles begin to contract, quickly overcoming the atrial pressure and slamming the AV valves shut.

the second heart sound is the closure of the semilunar valves (pulmonary and aortic). Note that this gets split on inspiration (high lung pressure causes the pulmonary to close after the aortic)

Front 33

what's the first regulator of arterial pressure? how do they work?

Back 33

barroreceptors in the carotid sinus right near the bifurcation of the carotid arteries.

decrease in pressure will cause a DECREASE in the firing rate of the barroreceptors up CN 9. The brain detects this and DECREASES parasympathetics and INCREASES sympathetics. As a result, HR goes up, SV goes up, the veins and arterioles constrict (veins increase venus return which will increase CO).

Front 34

later regulator? what does the aortic arch detect?

Back 34

aortic arch responds only to INCREASES in pressure - doesn't detect low pressure.

later regulator is the renin/angiotensin system.

Front 35

what's the cushing reaction?

Back 35

there are other chemoreceptors in the brain that detect high Co2, as in during ischemia.

when ICP goes up, vessels get forced closed and C02 goes up, which the brain detects and sends out a massive sympathetic signal to the body causing dangerous vasoconstriction and increase in heart function.

if it's caused by a stroke, this makes life worse 'cause more blood goes up to the brain.

also later causes parasympathetic response in the heart.

cushing's triad is high blood pressure, low respiration, and bradycardia. weird.

Front 36

what are chemo receptors?

Back 36

also located in the carotid bodies. They have high 02 rates of consumption - so when partial 02 pressure goes down, they pick it up fast.

Drops in 02 cause a sympathetic response, raising peripheral resistance and pressure.

Front 37

ANP? affect on renin?

Back 37

released from hyper-stretched atria.

relax blood vessels and increase Na+ and water excretion from the kidney. Stops renin secretion.

Front 38

what controls flow through the capillaries?

Back 38

arteriole constriction and the PRE CAPILLARY SPHINCTER

this should be where high pressure is detected, causing clamping down and prevention of damage.

Front 39

where can protein get in and out of capillaries?

Back 39

really only in the liver and intestine - any place where there are SINUSOIDS. everywhere else, generally only fat soluble things can get across, or small water solublet things (glucose and AA).

blood brain barrier comes from super-tight epithelial cells.

Front 40

what's our equation for describing flow of stuff across capillaries?

Back 40

starling equation (not frank-starling!)

J = Kf [ (Pc - Pi) - (Pi c - Pi i)]

so, higher capillary hydrostatic pressure and lower capillary ontotic pressure lead to higher flow out of capillary into interstitial fluid.

Front 41

The Pc value from above - what affects it?

What about Pi C? What does liver failure do to filtration?

Back 41

arterial and venous pressure. Note that VENOUS pressure increases it more, but both make it go up.

ontotic capillary pressure tries to keep filtration from happening. Increased protein concentration (as in DEHYDRATION) causes this value to go up and oppose filtration. So dehydration = less filtration.

liver failure lowers the number of proteins floating around, which decreases Pi C, which makes MORE filtration happen.

note that Pi is ONTOTIC Pressure and is exerted ONLY BY PROTEINS.

Front 42

so overall, what will INCREASE filtration?

Back 42

increases in venous/arterial pressure (up Pc)

decreases Pi C (lower plasma protein)

increase in Pi I (increased proteins in the interstitum - this comes from LYMPH FAILURE)

so when the lymph stops moving, get protein accumulation and net filtration. edema?

Front 43

what's the purpose of lymph? where does edema come from?

Back 43

fluid filtered out of the capillaries is greater than that filtered in, so it's up to lymph to clear it. also gets any proteins that happen to filter.

has one way valves so anything that enters doesn't make it back.

get edema when there's too much filtered or too little moving through lymph (blocked).

Front 44

list the conditions that cause edema:

Back 44

art dilation (weird), venous constriction heart failure, volume expansion, standing,

decreased colloid plasma pressure (Pi C) : liver failure, protein malnutrition, nephrotic syndrome (peeing out protein)

upped Kf (inflamation or burns)

Front 45

what's autoregulation and what systems show it?

Back 45

the "you stretch, i squeeze" myogenic response. seen in brain, kidney, and heart.

Front 46

what does histamine do? what about bradykinin?

Back 46

arterial dilation and VENOUS CONSTRICTION, which increases Pc and causes net increased filtration (edema, locally).

bradykinin does the same thing.

Front 47

coronary circulation - how is it controlled?

Back 47

mostly autoregulation, showing active and reactive hyperemia (higher 02 demand = vasodilation)

sympathetic-mediated dilation is a minor thing in the coronary arteries.

Front 48

what are the mediators in the heart flow?

Back 48

hypoxia and ADENOSINE.

Front 49

what about cerebral circulation control?

Back 49

local metabolites. the most important local vasodilator is C02 - when occlusion happens, lots of C02 builds up and vasodilation happens like crazy.

sympathetics are minor, like in the heart. though in the heart, local metabolites are adenosine

Front 50

what about skeletal muscles? what receptors are there?

what are local vasodilators?

Back 50

sympathetics more important here, still have local factors.

both ALPHA 1 (constriction) and BETA 2 (vasodilation).

what are muscular vasodilators?
adenosine, K+, and LACTATE.

Front 51

skin?

Back 51

lots of sympathetics. temperature. High temperature = vasodilation to get rid of heat.

Front 52

exercise vs. hemmorage - what's a big difference in body resposne?

Back 52

exercise will cause TPR to go down (due to vasoactive substances in the muscles being produced like lactate).

hemmorage will cause it to go up due to massive sympathetic outflow.

Front 53

what happens during hemmorage, specifically?

Back 53

increase in sympathetic tone (due to barroreceptors detecting low pressure and slowing their pulse firing to the brain).

increase in heart rate and contractility and TPR. Get low unstressed volume and high stressed volume.

get higher renin, ANGII, aldosterone, epi/norepi.

chemoreceptors in brain and periphery respond to Co2 and dump more sympathetic tone out.

all that extra arterial constriction favors a lower Pc, which stops filtration out of the capillaries and pulls more in (restoring volume)

Front 54

what's an equation we have for arterial pressure?

Back 54

arterial pressure = Cardiac Output * TPR

Front 55

what's a good indicator of pulse pressure? as in which cardiac value moves with pulse pressure?

Back 55

stroke volume.

Front 56

what's propalanol and what does it block?

Back 56

beta blocker, blocking beta 1 and beta 2.

it should cause decreased rate of firing and decreased contractility

Front 57

describe going from sitting to standing:

Back 57

blood pools in the legs, decreasing venous return to the heart.

this causes a decrease in cardiac output and a decrease in pressure that's picked up by the barroreceptors.

this send a signal to up sympathetics and everything begins to creep up.

Front 58

what kind of nervous receptor slows the heart down?

Back 58

muscarinic receptors for ACh coming from the parasympathetic system shut it down.

Front 59

when does the mitral valve open? as in what stage of heart movement?

Back 59

isovolumetric ventricular relaxation.

think that the valve's default position is to be opened and closes only when the ventricle ejects fluid and forces it closed.

as soon as the ventricle's stroke is finished, the mitral valve will open