Physiology: Block 2, Heart

Front 1

What does the P wave look like and represent?

Back 1

P wave is short and deflects upwards, and represents depolarization over the atria.

Front 2

What is the general progression of the depolarizing wave in the heart?

Back 2

Starts at the SA node, then to the AV node. Progression through the AV node is very slow. Then it reaches the bundle of HIS, down the right and left bundle branches, then into the terminal portions of the purkinje fibers (to the endocardial surface of the ventricles).

Front 3

What structure(s) in the heart prevent transmission of electricity through the atria to the ventricles?

Back 3

the fibrous rings ensure that the AV node gets used.

Front 4

What does the QRS complex represent? What direction is current going?

What about the T wave?

Back 4

QRS complex is the depolarization of the ventricles going from the endocardium to the epicardium.

T-wave represents repolarization of the ventricles, which proceeds from the EPICARDIUM to the ENDOCARDIUM. The t-wave is upright due to this reverse-direction flow

Front 5

What's the PR interval? What causes it?

Back 5

Delay of flow through the AV node is seen in the PR interval.

Front 6

What does the Q wave represent?

Back 6

initial depolarization of the SEPTUM.

Front 7

What things affect the PR interval?

Back 7

changes in conduction through the AV node can be due to: autonomic tone, drugs, heart disease

Front 8

What things affect the QRS complex?

Back 8

things that affect spread of depolarization through ventricles: including HYPERKALEMIA, ischemia, sodium channel blocking drugs can all LENGTHEN the QRS duration.

Front 9

What affects the QT interval?

Back 9

K+ channel blockers or mutations in channels.

Front 10

What are the phases of a cardiac action potential?

Back 10

5 phases, 0=4.

0 = big upswing, rapid depolarization
1 = rapid repolarization (notch)
2 = plateau
3 = rapid repolarization
4= diastole, resting.

Front 11

What channels are responsible for the divisions of the cardiac action potential?

Back 11

4 = inward rectifying K+ channel (resting)

0 = Na+ channels (upswing)
1 = repolarizing notch = outward transient K+
2 = plateau = L-type Ca++
3 = rapid repolarization = delayed K+
4 = inward rectifying K+ (RMP)

Front 12

What are the effects of hyperkalemia, and where can it come from?

Back 12

systemic hyperkalemia can cause it, also local from near by ischemia.

this depolarizes cells, making the RMP more positive, causing fewer Na+ channels to be in the rested, available state, This can reduce the speed of action potential propegation or completely block it.

Front 13

What are ERP and RRP? How can chronic Na+ inactivation be detected?

Back 13

Effective refractory period and relative refractory period. ERP = can't conduct an action potential, RRP = reduced velocity.

This keeps the heart from beating too rapidly.

Stay in ERP until the end of phase 3, come out of RRP in phase 4.

Lengthened QRS duration indicates chronic Na+ inactivation

Front 14

Nervous System Innervation of the Heart: what are the effects? How are the AV/SA nodes different in structure?

Back 14

AV and SA nodes have a less-negative, more depolarized RMP due to lower K+ permeability.

Depend on Ca++ INflux through L-type Ca++ channels to initiate phase 0 upstroke. Can be antagonized by K+ outflux

Front 15

Where do the para/sympa systems innervate the heart?

Back 15

Vagus innervates only the atria and the AV/SA nodes. Sympathetic innervation happens at BOTH the ventricles and atria.

Front 16

What does the parasympathetic system do to the heart?

Back 16

the r. vagus can affect the SA node (slow pacing), the L. vagus can affect the AV node (slow conduction speed).

Works through Ach - this raises the ERP and lowers the velocity/amplitude of phase 0 by activating I K-Ach channels (allowing K+ to efflux out, antagonizing action of Ca++ influx). Note: MUSCARINIC RECEPTORS.

Front 17

What does the sympathetic system do to the heart?

Back 17

Speeds it up - using B-androgeneric receptors, norepinephrine and epinephrine from adrenals, increase the activity of L-type Ca++ channels, increasing the speed/amplitude of 0 upswing, lowering ERP.

Front 18

Automaticity - what cells have it normally, and how fast?

Back 18

SA node = 70 BPM
AV = 40-60 BPM
purkinje = 15-40 BPM

outside of SA node = latent pacemakers.

Front 19

What's the effect of lowering extracellular [K] on automaticity?

Back 19

In Purkinje:
This makes the RMP more negative (hyperpolarized), which can activate Ih channels (note that they activate when HYPERPOLARIZED), which lets lots of Na++ inside, which INCREASES automaticity.
This can lead to ECTOPIC PACING and is BAD.

No big effect on SA node, as there are few Ih channels.

Front 20

How is Ca+ released from the SR, and what does digoxin have to do with this?

Back 20

Calcium-coupled calcium release:
Ca+ influx during action potential causes more Ca+ to be released into cytosol from SR.

Ca+ concentrations depend on Na/K ATPase (K+ in, Na+ out) and the Ca++/Na exchanger (Ca++ out, Na+ in).

Digoxin blocks Na/K ATPase, so intracellular Na+ goes out, so the passive Na/Ca pump stops working (too much Na+ inside, can't pump more in), so don't pump out Ca++, more is around to go into SR, so have more to release = INCREASE CONTRACTION STRENGTH.

Front 21

What are the 3 standard bipolar leads?

Back 21

1. Right arm to Left arm
2. Right arm to left leg
3. Left arm to Left Leg.

Front 22

How does the depolarizing wave movement affect deflection of what's read by the electrodes?

What about repolarization?

Back 22

Initially: at 0
depolarizing wave moves towards + electrode, get an UPWARD deflection. Once get halfway between, continued depolarization towards + electrode causes DOWN deflection, so when you finally arrive at + electrode, you're back where you started.

Repolarizing wave moving toward + electrode causes DOWN deflection until halfway point, then causes UPwards deflection. Note that repolarization takes longer and has a rounder shape.

Front 23

Why is the human T-wave inverted?

Back 23

Has to do with repolarization going from EPIcardium to Endocardium - double negative (reapolarization moving AWAY from + lead) = upwards deflection.

Front 24

What's a segment and what's an interval?

Back 24

Interval includes the beginning of a wave + the corresponding segment (so PR interval = beginning of P wave to start of R wave, the peak).

ST interval = line between two waves, not including either.

Front 25

Go through the contraction progression of the heart and explain why each wave goes the direction it does:

Back 25

1. Wave goes from SA node through the atria, going towards + lead = upward P wave.

2. Q wave = septal depolarization after AV node. Left bundle branch gets it first, then the right, so moving AWAY from + lead, = down deflection.

3. R = Ventricle depolarization goes ENDO to EPIcardium, depolarization generally going towards + side, = UP deflection.

4. S - a few late-activating parts of ventricles generally go away from + lead = downward deflection

5. T - REpolarization going epi to endo = upward deflection.

Front 26

Axis deviation: what's up?

Back 26

Left axis deviation = potential problem with Left ventricle hypertrophy, left ANTERIOR fasicular block

Right axis deviation: potential problem with Right ventricle hypertrophy, Left POSTERIOR fasicular block, right heart strain.

Front 27

Abnormal interavals: what's the cause?

PR
QRS
QT

Back 27

PR: increased = AV block, decreased = junctional rhythm.

QRS: increased = bundle branch block, hyperkalemia, drugs

QT: decreased normally in fast heart rate, also hypERcalcemia.
increased: hypOkalemia, hypocalcemia, congenital long QT syndrome

Front 28

definition of arrhythmia:

Back 28

Arrhythmia: any disturbance in the rate, rhythm, or pattern of heart contraction.

Front 29

What things can cause arrhythmia?

Back 29

ischemia, hormones, chronic heart disease, things that mess with ion channels or nervous inputs to the heart, electrolyte/hormone imbalances.

Main two things:
Disturbances in conduction
Disturbances in automaticity

Front 30

Cellular conduction issues - what are they?

Back 30

Ischemia results in lower cellular ATP.

There are Katp (K ATP channels) which are inactivated by lots of ATP. When the cell stops making ATP, they open and K+ falls out, which raises the RMP (depolarizing adjacent cells) which inactivates more Na+ channels, which makes conduction bad.

Also, systemic hyperkalemia can have the same effect, as can too much stretch.

Front 31

Simple conduction block - what happens if it's at the bundle of HIS or in a bundle branch?

Back 31

Bundle of his block = bad, can be asystole (prevents ventricles from getting any signals, and without ectopic pacing, die).

bundle branch block = normal pacing, but decreased output because the ventricles aren't squeezing with synchronicity.

Front 32

Briefly, what's a Reentry, why is it significant, and what criteria must be met to have one?

Back 32

Re-entry is an example of ectopic pacing. believed to be the greatest cause of arrhythmias.

Happens when current meets a blocked path, then all flows down the other. Strong current can then jump back over the ischemic section from the other direction and re-enter where it came from, causing a repeating circuit.

Need 1. Parallel paths of current flow
2. Unidirectional blockage. 3. Conduction time greater than the ERP of the cells involved (as in, need SLOW conductance so the cells can recover and re-fire).

Front 33

What can reentry cause?

Back 33

can cause pre-beats (either ventricular or atrial), sustained tachycardia and non-sustained, and fibrillation.

Front 34

AV node block: what's up, and what kinds are there?

Back 34

Heart disease or increased vagal tone: remember, the vagal tone serves to activate antagonist K+ channels to repolarize, and also decreases activity of Ca++ L-type channels. This LENGTHENS the PR interval and INCREASES ERP in the node.

1st degree: increase >.23 sceonds the PR interval

2nd degree: some QRS dropout
3rd degree: No QRS following the P wave.

Front 35

Disturbances in automaticity can come from what?

Back 35

Local increased sensitivity to chatecholamines (from the sympathetic system), from systemic hyPOkalemia (make purkinje fibers fire), and from stretch.

Can come from duretic therapy for CHF (causing hyPOkalemia) or from heart attack which stops uptake of chatecolamines so they hang around longer, or increased expression of Beta1 receptors.

Front 36

What are two forms of ABNORMAL automaticity?

Back 36

EAD's and DAD's.

Early after-depolarizations: happen before end of phase 3, during repolarization. Result from depressed K conductance (from drugs like quinidine), acidosis, and people with long QT syndrome. Increased by Decreases in Heart Rate.

DAD = delayed after-depolarization = happens during stage 4 and are a depolarization that just kinda happens. caused by intracellular Ca++ overload from heart disease, digoxin/catecholamines, or by hypercalcemia. Increased by Increases in Heart Rate.

Front 37

What does a 3rd degree AV block look like on the ECG?

What do you see in a 1st degree?

Back 37

See regular P waves (SA node is working) but no linked-up QRS complexes (if they occur, they're random).

1st degree will show an increased PR interval (above .23 seconds).

Front 38

What does a PVC look like?

Back 38

premature ventricular contraction: will see super-wide QRS complex, odd magnitude, irregular T wave (inverted?), and no P-wave.

Front 39

What does Ventricular Tachy look like?

Back 39

wide, quickly appearing QRS complexes without P waves.

Front 40

What kinds of arrhythmias should be treated?

Back 40

those that might cause worse arrhythmias, those that might cause thrombi (from pooling blood), and those that decrease cardiac output.

Front 41

What ECG changes are seen after a heart attack?

Back 41

get an inverted T wave for a few months, and definitely see a permanently dropping Q-wave (goes hyperpolarized).

Front 42

What are preload and aftelroad? What are they directly related to?

Back 42

preload is the degree to which a muscle is already stretched when it begins its contraction.
Prealod is directly related to END DIASTOLIC VOLUME

afterload is the force against which the muscle contracts
Afterload is directly related to AORTIC BLOOD PRESSURE

Front 43

What's an isomeric contraction and when does it happen?

Back 43

It's when a muscle exerts a force without yet contracting. In the first part of systole, the valves are closed for a short time - the force of the muscle eventually blows them open, but for a short time, there's pressure but no shortening of muscle.

Front 44

What's stroke volume? What is it equal to?

Back 44

Stroke volume is the amount of blood pumped from each ventricle each beat.

SV = end diastolic volume - end systolic volume.

Front 45

Cardiac output?

Back 45

Cardiac output is the amount of blood expelled by each ventricle during a minute.

CO = SV * HR

Front 46

What's ejection fraction?

Back 46

Ejection fraction is the ratio of stroke volume over end diastolic volume.

EF = SV/EDV

Front 47

Cardiac work?

Stroke work? Which ventricle is higher, and by how much?

Back 47

volume * pressure

Stroke work:
stroke volume * applicable pressure (left ventricle = aortic, right ventricle = pulmonary pressure)

Left ventricular stroke work is 6x that of the right.

Front 48

What is a typical cardiac efficiency?

Back 48

5-10% - rest goes to heat.

during exercise, can go up (athletes can reach 25%

Front 49

What is cardiac index?

Back 49

cardiac output divided by body surface area.

Front 50

Ischemic cardiac cells release what that's bad to their neighbors?

Back 50

lots of Ca++ and decrease pH, also lots of K+ (due to K+ channel inhibitied by ATP levels).

Front 51

What is the effect of the para and sympathetic systems on automaticity?

Back 51

Parasympathetic system works to increase cellular permeability to K+, hyperpolarizing the cell, which DECREASES automaticity.

Sympathetic system opens Ica and Ih channels to increase permeability to Na and Ca, which depolarize the cell during diastole and increase the slope of stage 4, INCREASING automaticity.

Front 52

Compare a lazy person to an athlete in terms of cardiac output and stroke volume, assuming same body size, at rest and during exercise.

Back 52

At rest, both have same cardiac output, though the sloth will have a lower stroke volume and higher HR. The athlete's rest will have a greater stroke volume and lower HR.

When exercising, the sloth will be able to up only HR, increasing CO maybe 3x.

When exercising, the athlete can increase CO much more by increasing both SV and HR, making for 6x more CO.

Front 53

What is fick's law?

Back 53

Generally, that

PVo2 = PAo2 + consumption rate. Remember, though, that cardiac output has to be incorporated:

CO* PVo2 = CO*PAo2 + o2 consumption.

OR,

CO = o2 consumption/ [PVo2 - PAo2]

Front 54

At what time do the heart sounds happen, and what do they represent?

Back 54

S1 = happens during isovolumetric contraction, and includes the sound of the mitral/tricuspid valve, oscillation of blood in the ventricle, and the sound of the ventricle contracting. Loudest

S2 = happens at isovolumetric filling. Sound of semilunar valves closing (pulmonary and aortic).

S3 = Diastole sound, usually not audible. Heard in kids and people with left ventricular failure

S4 = atrial heart sound

Front 55

What is the chronology of events in 1 cardiac cycle? there are 7.

Back 55

Atrial systole
Isovolumetric contraction
Rapid ejection
Reduced ejection
Isovolumetric relaxation
rapid filling
reduced filling

Front 56

Heart Failure: how can it be divided into subtypes, and what kinds should we remember?

Back 56

divided into systolic and diastolic dysfunction.

Systolic (left ventricular emptying):
impared contractility (MI, dilated cardiomyopathy)

increase in afterload (hypertension or aortic stenoisis)


Diastolic disfunction (impared ventricular filling):
-impared relaxation (ventricular hypertrophy, restrictive cardiomyopathy)

- impared filling (mitral stenosis, cardiac tamponade)

Front 57

What does S1 weirdness signify?

Back 57

S1 weirdness could be something to do with ventricular hypertrophy, mitral valve problems, abnormal PR interval,

Front 58

What does S2 weirdness signify?

Back 58

Note that S2 should be separated during inspiration (sound of semilunar valves closing, maybe with inhalation the PV is under higher pressure?)

weiredness includes bundle branch block, valvular stenoisis, atrial septal defects.

Front 59

Murmurs: what's up? What are the big divisions?

Back 59

involving vales, can be stenotic or regurtitation (too hard to get through or incompetent = backflow)

VSD, ASD, PDA, cotation, if bad = thrill

divided into systolic and diastolic

systolic: stenois sof aortic/pulmonary valves, regurgitation of mitral/tricuspid, VSD

diastolic: stenoisis of mitral/tricuspid, regurgitation of pulmonary/aortic.

Front 60

Describe the frank starling relationship: what happens if left ventricular output goes up? what about right ventricular output?

Back 60

All about fiber length affecting cardiac performance (as defined by cardiac output, work, stroke volume):

if left ventricular output goes up, left atrial volume/pressure goes down. this LOWERS the end-diastolic volume on the left side, meaning the left ventricle, next pump, will be less stretched and not work as well.


right ventricle: up in output causes a rise in left atria pressure/volume, raising the end diastolic volume, raising the output of the left ventricle.

Front 61

What is the treppe phenomenon (frequency induced protentiation)?

Back 61

Upping heart rate ups contractility.


raising heart rate ups intracellular Ca++, which ups contractility.

Front 62

What is the effect of raising the heart rate on contractility? what about stroke volume? what about cardiac output?

Back 62

Raising HR increases contractility (as increasing Ca++ inside the cell increases power of stroke).

Raising HR also decreases Stroke Volume, as filling is directly related to time spent in diastole...as HR goes up, time spent in diastole decreases (systole stays the same).

Because CO is related to both HR and SV, raising HR brings up CO at first...as HR keeps climbing, CO dives due to SV going down. The curve is BIMODAL.

Front 63

Where do sympathetic chatecolamines work? as in, what receptors and where are they?

Back 63

Alpha 1, Beta 1, Beta 2.

Alpha 1 is on vessels to constrict.

Beta 1 is on the heart
Beta 2 is on the lungs.

Front 64

How is blood pressure interpreted by the brain?

How does this explain why old people have high blood pressure?

Back 64

Barroreceptors in the carotid sinus and aortic arch, increasing pressure causes them to stretch, they fire.

Ascend to the Nucleus Tractus Solitarius (NTS) and causes VAGI activation to slow the heart. Also slows the sympathetic signaling.

Fall in blood pressure does the opposite.

Old people's veins aren't as elastic, don't expand as much, don't detect high blood pressure and don't shut it off.

Front 65

What's the chemoreceptor reflex?

Back 65

Work on metabolism: lots of ATP inhibits ascending fibers (and keeps sympathetics from firing), lack of ATP causes ascending fibers to fire and up the sympathetic signal.

Chemoreceptors detect rise in Co2 and also go to the NTS, cause sympathetic discharge upping heart rate and contractility. Live in CAROTID BODIES, also respond to pH, toxins.

Works on impared metabolism.

Cyanide might impare mebatolism = activate system.

Front 66

What's the bainbridge reflex?

What's the vetricular reflex?

Back 66

Bainbridge reflex: stretch atria = up heart rate, not much known about it, somehow requires vagi innervation.

Ventricular reflex: stretch ventricles = lower HR via parasympathetic tone increase.

Front 67

What are the effects of insulin and glucagon and thyroxin on the heart?

Back 67

glucagon = up cAMP and increase HR and contractility.

insulin = increase Ca++ levels and ALSO increase contractility.

Thyroxin, increases number of beta - 1 receptors.

Front 68

How does norepinephrine affect the heart biochemically? as in, how does it stimulate

Back 68

NE binds G protein (s), up cAMP, up pKA, up Ca++ channels and allow more calcium into the myocyte.

Front 69

When talking about baroreceptors, where is the most "gain?"

Back 69

between 80 and 120 - the curve here is steepest, so small changes in pressure illicit a large change in heart rate - allows for the most control.

Front 70

Blood velocity and flow: how are they different?

Back 70

Blood velocity refers to the distance covered by a single particle over a certain time.

Blood flow is the number of particles that pass per unit time.

Front 71

How is cross sectional area related to velocity and flow?

Back 71

Cross sectional area is inversely proportional to speed (lower cross section = faster speed)

The flow, however, remains unchanged- the same volume passes per unit time.

Front 72

In equation form, how are velocity (V), flow (Q) , and cross sectional area related?

Back 72

V = Q / area

or, V = Q / Pi R squared.

Front 73

Flow, Pressure, and resistance - what equation explains it?

Back 73

Flow = change in pressure / resistance.

or,

resistance = change in pressure / flow.

meaning there's an inverse relationship between flow and resistance.

Front 74

What effect does velocity have on dynamic pressure?

Back 74

P increases by the square of the velocity.

P(dyn) = [(velocity squared) (density)] / 2

Front 75

What is the trippe effect?

Back 75

Increasing heart rate causes more Ca++ to end up inside myocytes, increasing the contractility of subsequent beats.

Front 76

catecholamine receptors: where are they located, and what do they do?

Back 76

Alpha 1 - on vasculature, cause vasoCONSTRICTION

Beta 1 - Receptors on the heart, act to increase rate AND contractile force (positive ionotropic). nmenonic - 1 heart

Beta 2- on the (two) lungs: cause bronchodilation (vasodilation too?)

Beta 2

Front 77

Vasodilation via parasympathetics - what structure is/is not required on vessels?

Back 77

Parasympathetic vasodilation requires an ENDOTHELIUM lined vessel. MUSCARINIC receptors.

Front 78

What can be used to inhibit sympathetic signals? What about parasympathetic signals?

Back 78

Propranolol - first beta-1 blocker = sympathetic blocker.

Atropine = muscarinic receptor inhibitor = parasympathetic blocker.

Front 79

Baroreceptor - what kinds of signals does it cause to fire when activated?

Chemoreceptor - what kinds of signals does it cause to be fired when activated? How is it activated?

Back 79

Barroreceptor - responsive to stretch, causes VAGAL simtulation to slow the heart.

Chemoreceptors: responsive to DROPS IN METABOLISM of the carotid bodies (low 02, high Co2, up osmolarity or drop in pH) cause SYMPATHETIC stimulation.

Remember that ATP keeps afferent signaling repressed - as ATP disappears and becomes adenosine, the chemoreceptors afferents fire to the brain, causing sympathetic discharge.

Front 80

On a graph of Filling pressure vs. stroke volume, what's the normal curve like? what does adding epi/nor epi cause the curve to do?

Back 80

As filling pressure increases, stroke volume increases (preload is going up, stretching, causing harder contraction).

Epi/norepi shift the curve UP and LEFT - meaning that for any given filling pressure, the stroke volume goes up when exposed to the drugs.

Front 81

Describe the signal transduction that happens in cells as a result of catecholamine stimulation:

Back 81

G(s) -coupled protein receiver = increase in cAMP/pKA, phospho Ca++ channels and increas Ca++ intake.

Front 82

When talking about flow through a rigid tube, what factors are taken into account and how do they affect flow?

Back 82

Q = pi, delta P, r4 over 8nL


so biggest affector is RADIUS, as is a greater pressure difference.

viscosity and tube length all decrease flow.

Front 83

What about resisitance? What equations do we have?

Back 83

well, R = delta P/Q

also, R = 8nL/pi r4

So, viscosity and length all increase resistance

biggest DECREASOR of resistance is radius!

Front 84

Calculating resistance in parallel vs: series...what's up?

What's the physiological result? What kind does our body have?

Back 84

Series:

R1 + R2 + R3

Parallel:

1/R1 + 1/R2 + 1/R3...

Our body mostly has them in parallel, which keeps resistances VERY LOW.

Front 85

As vessels decrease in size, what happens to resistance?

Back 85

Resistance goes up, raised to hte 4th power.

Front 86

Laminar vs. Tubulent flow - what value tells you which you get, and what factors go into it?

Back 86

Reynold's Number:

greater than 3000 = turbulent, less than 2000 = laminar.

Diameter, density, and velocity increases cause up in # (more turbulent)

Viscosity (more viscus = syrup) makes it LESS turbulent.

Front 87

What kinds of vessels are most likely to have aneurisms? I'm thinking width, pressure, and diameter.

What artery in the body is most likely to aneurism?

Back 87

Wide, Thin, and high pressure. = Laplace Law.

The anterior cerebral artery in the circle of willis. Aorta is also common.

Front 88

What are the 3 traits of vessels that have to do with changes in pressure? What do they mean?

Back 88

Compliance: change in volume per unit change in pressure

Distensibility: qualtative measure of how much something changes upon application nof force

Elasticity: how easily a vessel goes back to its original size.

Front 89

How does compliance differ for veins and arteries? How does muscle squeezing the Vessels affect this?

Back 89

Veins are 10-20X greater in their compliance ability at low pressure, but at high pressure, they're the same.

Smooth muscle contraction results in decreased compliance (doesn't expand as much when you flex).

This increases pressure.

Front 90

How fast is blood flow through the capillaries, and why?

Back 90

Speed is very slow, because the cross sectional area of the entire capillary bed is VERY LARGE.

Front 91

As you progress from the aorta to capillaries back to the superior vena cava, how do pressure, speed, and cross sectional area change?

Back 91

Cross sectional area starts out very SMALL, gets big in the capillaries, then gets SMALL again.

Speed starts out HIGH in the aorta, slows down in the capillaries, and speeds back up again in the veins

Pressure: starts out high, gets small in the arterioles, and STAYS SMALL.

Front 92

Where is the greatest pressure drop in the system?

Back 92

at the level of ARTERIOLES.

Front 93

Veins, Capillaries, and Arteries: what percentage of the blood exists in each?

Back 93

Most of the blood is in veins (67%), 5% in capillaries, 10% in arteries.

Front 94

What changes in arteries as we age, and how does this affect sudden changes in CO? How does this affect blood pressure?

Back 94

Compliance changes. Compliance will increase the time it takes to arrive at the new blood pressure, lack of it will cause a sudden increase in pressure.

Note that compliance doesn't change the new pressure that's happening - just the time of arrival at it.

Front 95

Relaxation in vessels: what are the two main pathways?

Back 95

No endothelium:
Arachidonic acid gets converted to prostacyclin (PGl2) via COX and PGl2 synthase). This turns on cAMP and causes relaxation.

Yes endothelium:
Also, can do acetycholine mediated: causes Argenine to be turned into NO, activate cGMP and cause relaxation.

Front 96

What are the 3 ways that water can move across a capillary wall? What's the most important one?

Back 96

Diffusion, pinocytosis, and filtration.

Diffusion is 5000x greater than the other two.

Front 97

What factors affect diffusion?

Back 97

Capillary permeability, Cross sectional area and concentration gradient. All increase diffusion.

Front 98

what has higher compliance: arteries or veins? why?

Back 98

Veins: arteries have more elastic tissue and are more elastic (opposite of compliant).

This is also why veins have most of the blood - their compliance is greater and they can hold more.