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281 Cards in this Set

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when dealing with an occulusion, what is happening with resistance and flow proximal to the occulsion?
increase resistance, decrease flow. as flow decreases, amt of interstitial CO2 increases acting as a vasodilator, therefore arteriole always in dilated state.
what is the "cardiac steal"?
when you have an occluded vessel and give a vasodilator (adenosine), the branching vessels will dilate more than the occuluded arteriole b/c blood takes the path of least resistance. R will decrease in the branching vssls. P will then drop in the occluded vssl, dropping the Q even more
effect of vasodilator on TPR and afterload?
vasodilator like Nitro, will decrease the R and decrease the afterload which decrases the work the heart has to do, which decreases O2 consumption
effect of vasodilator on venous circulation?
vasodilates venous which decreases the preload which decreases O2 consumption
*purpose generally of Nitro is to decrease O2 consumption
what is the effct on MAP when Qh > Qr?
increase BP
what is the effect of Qh < Qr?
decreas BP
what happends to TPR, Q and P when you decrease cross sectional area of arteriole system?
increase TPR, decrease Q, pressure increase
a pt. has normal BP, normal fluid vol, and given a liter of fluid, what happens to MSFP, VR, CO, P?
increase MSFP
increase VR
increase CO
increase P
how will local metabolic factors try to control blood flow themselves?
increase TPR by increasing flow to area to wash out metabolic byproducts
what is CVP equivalent to?
what system is for acute control of MAP? chronic?
acute: aortic baroRs (w/n seconds)
chronic: kidneys (w/n hours to days)
what is the capillary fluid shift?
such as in hemorrhage: want to decrease TPR to decrease filtration and increase reabsorption
what are the low pressure vascular sensors?
cardiac atria
pulmonary vasculature
what are the high pressure vascular sensors?
carotid sinus and aortic arch (arterial baroR's)
JG apparatus in afferent arteriole
what do the hepatic and CNS volume sensores respond to?
to the amt of Na in plasma, osmoreceptors; affect hormone secretion
what controls total body fluid level?
kidneys b/c how much vol you have in body determines BP
what is the result of taking in fluids?
increase MSFP, i CO, i VR, i MAP,- renin, i CHP, i filtration, i urinary output
*takes 1 hr to happen
what does the renal fxn curve tell us?
x axis: arterial P
y axis: urinary output
as you increase arterial P, you incresae urinary output to try to decrease MAP
what is prssure diuresis?
loss of water to try to bring MAP back to normal
what is naturesis?
loss of Na and water
in kidneys, why do local factors predom over baroR's?
b/c baroRs are acute control
they will adjust to new pressure after 24-72 hrs
what does the macula densa respond to?
Na ions: if high Na detectd, inhibit renin secretion
*increase flow, deliver more Na
what are the 2 mechanisms that control long term chronic BP?
renal fxn: changing BP by increasing output
water and salt intake: intake must equal output
what happens to the renal fxn curve in a hypertensive patient?
the renal cuve shifts right, need higher p to maintain intake/output at normal levels
if you cut the vagus nerve and eliminate right atria input to the medulla what will happen?
decrese secretion of ANP, get a total increase in total body fluid volume. secretion of ANP will effect how much fluid the kidneys retain or secrete.
what would happen to BP if the renin AA sysem wasn't working and you increased intake of Na?
increase BP to increase filtration and excretion. need a higher BP b/c intake of Na higher *doesn't happen normally b/c RAA system prevents the increase in BP when increase salt and water intake
what happens to GFR during exercise?
blood flow decreases b/c divert from kidney,
decrease inflow, GFR decreases only slightly b/c constrict efferent artery decreasing outflow: a decrease in inflow and decrease in outflow will keep GFR normal
how do you keep GFR normal when flow is low?
decrease outflow by constricting efferent artery. the decrease in inflow and decrease in outflow will restore GFR
what 3 factors regulate renin secretion?
renal nn that innervate JG
stretch of renal afferent artery
macula densa
what is the effect of renal nn when BP is low?
increase sympathetics
increase renal nn activity on JG cells in afferent arteriole
stimulates renin secretion
renin causes retention of fluids and BP will increase
effect of increased afferent arteriole pressure?
stretch decreases sym activity
inhibit renin secretion
what happens to renin secretion when a pt has a heart attack?
BP drops, renal afferent artery P drops, increase renin secretion to retain fluids
why do you want to retain fluids after heart attack?
retain fluids to increase TPR to increse EDV
a decrease in Na to the macula densa means what?
that there is a decrease in Q, so it stimulates renin secretion to increase the amt of volume
what affect does renin have on TPR?
increase renin, retain more fluids, increase TPR
*muscle tone increase: constrict afferent arteriole
effect of diuretic on TPR?
relaxas TPR by i secretion (NaCl excretion) and inhibiting renin secretion
*muscle tone decrease: dilate afferent arteriole
affect of diuretic on afferent arteriole resistance?
decrease resistance, increase secretion by - renin
ADH secreted from where? controlled by?
from pos pituitary
controlled by hypothalamus
ADH responds to?
osmotic pressures
if hypothalamic osmoR's sense hypertonic plasma, what happens to ADH secretion?
if hypertonic plasma, cells will shrink and ADH stimulated (antidiuretic)
if hypotonic plasma, what happens to ADH?
cells swell
ADH inhibited, want to get rid of fluids
what is the RAA pathway?
angiotensinogen from liver is cleaved by RENIN(from kidneys) leaving Angio I. Angio I is then cleaved by ACE(from lungs) to become Angio II. Angio II leads to aldosterone production (from adrenal gland)
why does ACE conversion occur in lungs?
b/c amt surface area available
angiotensin II is potent? action?
vasoconstrictor that stimulates the adrenal gland to secrete aldosterone, causes retention of fluids, increases TPR which increases MAP
affect of angio II on TPR?
vasoconstrictor that incresaes TPR
why does aldosterone need ADH?
aldosterone increases Na reabosorption and needs ADH secretion for aquaporin channels to move H2O to restore BP to normal
main action of aldosterone?
increases uptake of Na dragging water with it due to insertion of aquaporins by ADH
affect of ADH (vasopressin) on Na concentration?
no effect
ADH causes migration of protein channels, provides channel for H2O to come across
a Na depletion will cause what?
sensed by macula densa
increase renin secretion
what happens to renin secretion when standing up?
increase renin secretion b/c lower MAP which means lower renal afferent arteriole P
what happens to renin in cardiac failure?
decrease CO, decrease Map increase renin secretion
to get rid of the excess fluid that shifted renal fxn curve to right, what do you do?
do not have to change renal afferent artery P, only have to get rid of hormones that are affecting tubule: decrease the amt of angiotensin in blood
what happens in renal artery stenosis?
renal fxn curve same shape but shifted to the right;kidney is fine;problem is getting blood to kidney
Proximal to occulsion: P is initially low
distal to occulusion: P high
R is high and flow is low
JG sense low P and secrete renin to incrse P proximal to overcome R and return Q to normal
result: hypertension
what happens when you reduce kidney mass?
blood pressure increases very slightly as long as pt on low Na diet. If increase Na diet you exceed capabilities of kidney increasing BP: become more hypertensive
*can live w/ reduced kidney mass on normal salt diet
effect of ANP on renal arterioles?
dilates afferent
constricts efferent to get rid of fluids
what do you give pts w/ hypertension due to too much angio II?
give ACE - reducing angio II in body
explain one-kidney goldblatt.
clamp on kidney afferent causing a decrease in p distal sensed by JG to secrete renin. in good kidney, pressure will be high so renin will be inhibited. but aldosterone is being stimulated by elevated renin secretion and will affect both kidneys
explain bp in person w/ aortic coarctation?
upper extremities: high P to overcome R from coarctation stimulated by renin secretin to retain fluids *cause hypertension
lower extremintes: low/normal P
how can oral contraceptives cause hypertension?
lead to incrase angiotensinogen leading to incresae angi II- retain too much fluids
what is happening in vol loaded hypertension?
incrase fluids and Na intake, kidneys cannot control total amt fluid in body
initially thre is an incresae in Co, which incrases BP stim baroRs to decrease TPR. BaroR's reset to higher MAP. Autoreg then almost returns CO to normal while cauing increase in TPR.
incrase in MAP in vol loaded hypertension is caused primarily by wht?
incrase TPR by autoregulation (maintin Q by changig P)
what hormonal problems are associated w/ hypertension?
too much aldosterone due to adrenal tumor
too much angio II
what happens to cerebral blood flow in pts with chronic hypertension?
blood flow decreases at a higher MAP due to alterations in autoregu
what are the 2 cardiac factors that determine CO?
myocardial contractility
waht are the 2 coupling factors taht determine CO?
how will change in venous capacitance affect preload?
decrease unstressed volumes you increase preload
if you increase venous capacitance,dilate, decrease VR, you wil decrease preload
affect of afterload on CO?
increase afterload, CO decreases
what is the primary factor of physiological HR?
filling time, time for diastole
decrease filling time = decrase SV
when HR is 50-100, what happens to CO and SV?
CO increases b/c increase in HR > decrease in SV so HR overrides affect on CO b/n 50-100 b/min
when HR is b/n 120-180 what is the affect on CO?
CO is the same b/c increase in HR = decresae in SV so no change in CO
*impt during exercies
when HR greater than 180, what is the affect on CO?
CO decreases b/n amt SV decreased outweighes the high HR and now you don't have enough time to fill so your CO goes down
what does cardia fxn curve tell us in terms of preload?
increase preload will increase CO
normally do we need nervous system to change SV and CO?
NO! changes in HR will change SV and CO automaticaly
effect on cariac fxn curve w/ hypereffective heart?:
hypereffective heart is associated w/ stimulation of SNS (due to increase intrapleural p): will be elevated and shifted R
effect on cardia fxn curve w/ hypo effective heart?
hypoeffective heart is associated with cardiac disease, ischemia or loss of fxnl tissue (due to reduced intraplueral pressure). curve will be depressed
VR equn?

incrase RAP, decrease VR
affect of venous pressures in cardiac failure?
decrease CO and increase venous pressures b/c no blood pumped from heart
affect on vascular fxn curve when transfusing pt?
shift vascular fxn curve up
keep vol in aa the same, but at a higher CVP now b/n more blood in circulatino
affect on vascular fxn curve during hemmorhage?
more blood in aa, less in vv therefore decrease CVP
curve shifts down
how can you change MSFP?
changing vol or tone (compliance) of ENTIRE circulation, not jsut arterioles
affect on vascular fxn curve w/n increased tone? decreased tone?
changing arteriole tone does not change MSFP must change entire tone of ciruclation
if you give vasodilator, what happens to venous circulation?
vasodilator will increase flow in arterioles decreasing arteriole pressure, increasing venous pressures
Qh < Qr = decrease MAP
if you give vasoconstrictor, what happens to venous circulation?
Qh > Qr = MAP increases
what happens when you superimpose cardiac fxn curve and vasclar? axis?
x axis: CVP
y axis: CO
get equilibrium pt where VR = CO
elevated CVP is indicative of what?
increases in preload
in compensated H failure, you can increase your CO back to normal but will have elevated waht?
CVP is normally (#)?
LaP is normally ?
CVP 2-3mmHg
LaP 6-7 mmHg
how do you get blood from Rv to Latrium when CVP is a lower P than LaP?
need to generate a pressure gradient diff to overcome the R this is the job of the R ventricle. when in R heart failure, you need a pressure gradient generated on entire venous circulation for flow to take place. therefore kidneys retain fluids, incresae venous circulation, i CVP, i filtration which often leads to edema
in R heart failure, how do you increase pressure gradient to move blood from r heart to left heart?
increase fluid in venous circulation
*must have elevated CVP for flow to be normal
why do you want to give a pt in cardiac failure a vasodilator?
not to dilate coronary aa: these are already dilated due to metabolic prducts
vasodilate instead the periphery to decrease TPR which reduces the afterload
change MSFP to decrease preload: decrease VR by increasing venous capacitance
affect of vasodilator on cardiac failure pt?
vasodilate periphery: decrease TPR which reduces afterload
increase venous capacitance, decreasing MSFP, to decrease preload
affect of anesthesia on combinaed curves?
anesthesia cause dilation thefore get depressed cardiac and vascular curves
this is because you are increaseing venous capacitance, decreasing MSFP, VR, and Co
why don't you want to give someone that is low in volume, anesthetics?
b/c anesethetics will cause dilation, therefore causing even more drop in CVP wich can cause compenstion mech to result in edema
CO eqn-
CO = MAP-CVP/TPR compared to
how does CO change when you give someone a transfusion?
it doesnt change! putting the same vol of blood in arterial side, excess blood will be in vv
vasodilating affects CVP how? MAP?
vasodilate arterioles will cause flow OUT to increase and MAP will drop, CVP will increase
Qh < Qr
vasoconstricting affects CVP how? MAP?
decrease flow out of arterioles so decrease flow INTO venous
MAP increases and CVP decreases
in heart failure, why do kidneys start to secrete renin?
b/c CO decreases and CVP increses
MAP is low so they want to retain fluids
what is happenening in conpensated heart failure?
CO is low, and CVP is high
kidneys secrete renin to increase MAP
EDV goes up and heart responds by increasing contractility (constant incrase in sympathtics to make more Ca available for contractility)
characteristis of heart.
BF highest to meet metabolic demand
AVO2 diff is highest
*very dependent on flow to coronaries to increase O2 delivery *90% dependent on flow
02 consumption to heart is dependent on?
increasing flow! 90% depenent on flow
what percent of all venous blood will come theough coronary sinus and empty into Ra to be circulated through lungs?
95% whle 5% dumps direclty into left ventricle through Thebesian vv (venous admixture that decreses arterial 02 content)
what are the 2 ex of venous admixtures?
5% venous blood dumping direclty into left v though thebesian vv
blood from bronchiole circulation dumps directly into pulm vv
diff b/n cardiac and skeletal cell sizes? cap density?
cardiac: smaller cells and much greater capillary density
*more cappilaries means less distance for diffusion = faster O2 delivery
affect of capillary density on diffusion?
greater cap density decreases distance for diffusion
*ex : emphysema: greater distance b/c capillaries destroyed
what is the main goal in controlling circulation through coronary system?
maintain flow!
what is the primary driving prssure for coronary blood flow?
mean aortic blood pressure: p that drives the pressure into cornoary circulation
if there is decrease in perfusion pressure how is this compensated for?
decrese perfusion pressure = decrease Tm therfore dilate by autroregulation
what is the primary mech for controlling flow into heart?
metabolic activity: increses in contractility will increase metabolic byproducts, increase CO2 causing vasodilation and relaxation of vascular resistance
what is NOT the primary mch for controlling flow to heart?
nervous control of flow: even though coronaries are inervated by the nervous system this is minor to METABOLIC control of flow
what happens when cornoary perfusion pressures are too high?
they will not vasoconstrict b/c NO production overrides autoreg thefore they dilate
where does the systolic squeeze have the most effect?
left endocardial region impairing blood flow into left coronaries
what is happening to left coronary perfusion dring isovolemic contraction and beginning of ejection phase?
right before systole, there will be a retrograde flow of blood back out of coronary circulation causing decrease in blood flow and the left endocardial region will have the highest sqeeze
effect of systolic squeeze?
the squeeze to eject blood sqeezes on cornoaries and decreases flow to them
*left endocardial region is squeezed, blood flow is diminished
when does majority of left coronary blood flow occur?
80% left coronary blood flow occurs during diastole as teh ventricles relax
why does endocardial region repolarize last?
b/c it is underpefused during systolic sqeeze unlike epicardial regions therefore it doesn't have the blood supply and nutrients to repolarize tehfore it is the most susceptible to infarction
compare epicardial vessels to endocardial vessels
epicardial: alpha 1 R's
endocardial: beta 2 R's to try to vasodilate to get as much flow as possible during diastole b/c underpefrused during systole; greater ability to have decresaed R and more flow; *more compliant
what happens in cornoary circulation when the perfusion prssures are high (in terms of blood flow velocity)?
increase amt of flow increasing shear wall stress which will stimulate NO prodcution. now you increase flow by increasing change P (flow increases while keeping Tm same) **coronaries are dependent on flow; if eliminate NO production, coronary flow will decrease by 60%
why is the heart so dependent on increasing flow to meet metabolic demand?
b/c at rest the heart already extracts 75% of O2, the most it can extract is 85% thefore must incraese flow to meet demand unlike skeletal mm which can increase O2 extraction tremendously
what 4 factors play a role in helping the heart meet its metabolic demands?
1. contractility
2. HR
3. muscle mass (increase mass, increase contractility, increase metabolic rate)
4. EDV
effect of muscle mass on metabolic demands of heart?
increase number of cells you increase metabolic demand and vice versa
why is it impt that diastolic pressure in left coronary be high?
to increase blood flow to endocardial region that was underperfused during systole due to sqeeze* if pt has low diastolic prssure it results in low perfusion during diastole to this region. this decrease in blood flow is the reason this region is the last to repolarize
pulmonary hypertension causes what?
cor pulmonali : describe a change in structure and function of the right ventricle of the heart as a result of a respiratory disorder - causes R v hypertrophy
in left sided heart failure, why do you hear wheezes basally in the lungs?
b/c higher hydrostatic pressure in apices
*pulmonary edema
what are the 4 possible syndromes of ischemic heart disease?
1. angina pectoris
2. MI
3. Chronic ischemic heart disesae
4. sudden cardiac death
MI can lead to?
v fib b/c re-entry
why would you possibly develop v fib from an MI?
increased sympathetics that increases loss of K ions, now more K in ECF, takes longer to reach threshold
what is the diff b/n hypertrophy and dilitation?
hypertrophy: in response to increased afterload, chamber size NOT increased, increase amt of mm around chamber
dilatation: increase in chamber size increasing EDV, increase tension, increase O2 consumption, increase in ventricular chamber size
what is cardiogenic shock?
CO not meeting metabolic demand of the tissues
thromboembolisms are mostly due to?
infarctions, not ischemia
compare ischemia w/ infarction.
ischemia: lack of O2 delivery
infarction: death of tissue
what is the metabolic factor in vasodilatation in ischemia?
what are the 3 major factors involved w/ development of ischemia/all increase metabolic demand?
1. platelet aggregation: due to damage to endothelial cells
2. coronary thrombosis: decrease radius increase R
3. coronary vasospasms: no thrombus
normal effect of endothelial cells on perfusion pressure?
NO and prostaglandins produced increases perfusion but if the cells are damaged, don't produce products therefore platelet aggregation and no dilation
what are the 3 forms of angina?
what is stable angina?
associated w/ tachycardia, increased HR, increased O2 demand b/c occlusion can't meet demand
*associated w/ exercise
*patient relieved w/ rest and HR comes down
which form of angina is associated with tachycardia and is relieved with rest?
stable angina
what is variant angina?
associated with coronary vasospasms
*sporatic and spontaneous
Tx: vasodilators
which form of angina is associated with coronary vasospasms?
variant angina
what is unstable angina?
the worst form
combo of vasospasms, platelet aggr, and thrombus
endothelial cells damaged-no NO production
*result in MI and SCD
what are you responding to in angina?
increased prostaglandins and K
what is the stress test? what is it for?
for angina
involves exercising on treadmill, increasing O2 demand thefore increasing CO. If person has coronary artery disease the increasd demand wont be met therfore see current of injury and angina
what is the adenosine test?
potent dilator
distal to occulusion dilated due to metabolic acivity. adenosine diverts blood flow away (coronary steal). will decrease P proximal to block
*will see current of injury b/c decreased Q to blocked pathway
when are the 2 most dangerous times for fibrillation?
first 10 min after infarction (b/c BP decreasd and perfusion very low)
3-5 hours after start getting reperfusion: superoxide and hydroxy radicals damage endothelial cells and cause platelet aggregation
what are the 4 factors that increase tendency for v fib to develop?
1. increasd K leaks out
2. increased current of injury: cells can't repolarize
3. delayed afterpotential
4. dilatation of vessl: increases distance, slows down conductance
effect of heart failure on kidneys?
decreasd CO
decreased MAP
decreased kindey perfusion
kidneys retain fluids
increase EDV
what is cardiac reserve?
ability of heart to increase CO above normal resting levels
normal reserve? athletes?
normal: 400% reserve therefore increase CO by 400%(from 5-25 L/min)
athletes: 550% b/c hypertrophy they can squeeze harder, increase CO more than normal b/c more mass therefore increased ejection fraction
describe cardiac reserve in mod. coronary disease?
decreasd cardiac reserve ~150%
only 5L-10L/min
limited O2 delivery
*heart cannot generate a rate or contractile forces of the normal heart (compensated failure)
describe severe coronary thrombosis and cardiac reserve?
blood flow BELOW normal delivery rate. can't meet metabolic demand. (decompensated)
affect of diptheria on cardiac reserve?
toxins affect cardiac mm cells, can't contract as hard
EDV and ESV in compensted heart failure pt?
both elevated
same SV
P-V loops shifted right
why do heart failure pts. need increased EDV?
to increase contractility
improve sarcomere length
increase affinity for troponin C and Ca
an increase in EDV has what effect in ischemia pt?
response to EDV is impaired, won't respond as normal heart to EDV increases. Will be acidotic causing an interferene w/ troponin and Ca thefore less contractility
the ability to increase CO and maintain it during exercise is dependent on wht?
ability to increase HR, in heart disease pt. their incrase in HR is limited
what is high output failure?
due to sepsis
LOW TPR!! b/c significanly increased CO thefore decrease TPR to keep MAP constant
*skin will be red, hot b/c vasodilated
what is low output failure?
significant decrease in CO
skin will be gray and cold
in CHF, how does redistribution of CO to gut change?
decreases, hypotension wants to decrease flow to gut to divert to brain and heart *reason pts become infected
in CHF, how does redistribution of CO to muscle change? kidney?
no change in muscle
kidney: divert flow away but they dont like being underpefused so you see a decresae in renal fxn
in CHF, redistribtuion of CO to brain changes how? skin?
brain flow decreases
skin greatly decreases: low output falure-cold clammy
In CHF, redistribtuion of CO goes up in what organ?
only heart
capillary refill is a test for what?
to check of low blood flow (such as in low output failure)
*needs to turn pink right away when released
what are some acute compensatory mechanisms for conpensated failure?
tachycardia (increased sym)
ventricular dilatation (increase preload, dec unstressed vol)
increase adrenergic activity (increase contractility; enchance Ca conduction)
what are some chronic compensatory mechanims ?
ventricular hypertrophy: tries to increase muscle mass so that it can pump a given force
salt and water retention (increase renin secretion,stimulated by dec BP in afferent artery)
increase RAA activity
increase vasopressin/ADH acitivity
what is state of contractility in decomp failure?
due to incresaed sympathetics, you increase sarcomere length to point where contractility starts to drop. develop excessive tachcardia b/c the decrease in contractility you want to increase HR
in comp failure, how do we increse contractility?
change preload by dec unstressed volumes
increase Ca release by increase sympathetics
*as you increase preload, Ca and troponin have increased affinity for each other
effect of ischemia on Ca and tropmonin?
ischemia your are acidotic, impairs the afinity of Ca and troponin decreasing CO
why would you give diuretics to decomp person?
helps reduce EDV back to normal
decrease contractility
reduces ventricular chamber size reducing amt O2 reqd
why would you give vasodilators to decomp person? when wouldnt you give ?
decresae VR, dec MSFP, dec preload in venous
in arteries: dec TPR dec afterload dec work of heart
**wouldnt give to ischemic person b/c they are already vasodilated
when would inotropes (digitalis) not work?
in ischemic pt: b/c it increases O2 consumption
how can comp failure cause DADs?
require constant incresae in symp to keep SV the same which can lead to Ca store overload leading to the development of DADs
surgical methods for decomp pt?
angioplasty: seen that drugs work better now than this
bypass surgery: grafts last 9-15 yrs but only 2 chances for open heart surgery b/c of scarring
Stent: hard straws to maintain strcture, but there is the problem of re-stenosis
if reperfusion is not established what state is your heart in?
infarction (cell death)
no current of injury
no ischemia
dead tissues do not conduct electricity
what are the fxnl implications for myocardial scar structure?
infarcted area will develop fibrous scar tissue which does have some affect on ability of heart
scar tissue develops in a way that allows normal contraction to take place: maintins mechanical contraction of ventricles
affect of ACE -?
decrease TPR (b/c no angiotensin) decrese afterload
what is happeneing with lungs in decomp failure?
can't achieve CO-CHF
heart gets bigger
lungs fill with fluids (parahilar)
*generate too much fluids b/c still can't reach CO therefore renin continually released
wht is the pre-conditioning of the heart?
repeated infarctions build up chemicals, no the heart remembers and will adjust much quicker during the next one
what happens after the heart goes into reversible injury condition?
can be reperfused
goes into stunned state in which limites O2utilization
can come back to normal
*stunned state: prtotective to avoid more cell death
compare pressure of pulmonary and systemic ciruculations?
pulmonary low pressure system compared to systemic, more compliant (less muscle) *less resistance**
values of pulm press vs systemic?
pulm: 25/10
systemiic: 120/80
why do we want pulmonary system to have low resistance?
b/c if increased resistance, it will incresae afterload in right ventricle
flow from right ventricle:
pulm artery - alveolar cap system - pulm vein- left atrium
role of nervous system in tone of pulm circulartory system?
little role
*no autoreg in lungs
*dependent on NO production for controlling tone of pulmonary arteries
what controls the tone of pulm arteries ?
NO production: as incrase CO, stimulates shear wall force which stimulates NO production and vssls relax
why are the lungs dependent on NO?
to vasodilate to decrease R to prevent increase P
what if patient is not producing NO?
exogenous NO, but if they lack receptors, can't give NO
what is hypoxic vasoconstriction?
when decreased O2 in alveoli, cause vasocontriction to maintain Q to good area by closing off hypoxic area to shunt blood to good alveoli (take path of least resistance) maintain ventilation:perfusion ratio
*normall when decrease O2 you want to vasodilate, but NOT in lungs!
decribe bronchial circulation.
for nutritional flow only
true systemic flood Q
only goes as far as terminal bronchioles
not involved with gas exchange
describe venous ad-mixture of bronchial artery.
venous blood of bronchial artery dumped straight into pulmonary vv
which is leakier, pulm capillaries for systemic?
pulm thefore more devlopment of lymphatics to remove fluid
action of thromboxanes?
byproduct of varioius types of sepsis and toxins produced through diffrent kinds of infxn
action of prostacyclins?
produced by endothelial cells
inhibits platelet aggregation
describe the rate of repurfusion in treatment of heart failure
the faster the heart can be reperfused, better chance of saving mild ischemic and non-fxnl areas
which circulation system is low resistance, high compliance?
afterload of Right ventricle is what?
pulmonary artery: 15-17mmHg
what happens to right ventricle in pulmonary hypertension?
increase pressure in pulmonary artery, increase afterload of right ventricle
what is cor pulmonali?
right ventricle hypertrophy due to pulmonary hypertension
what is happening in zone 1?
alveolar pressure exceeds cap pressure (P0 greater than Pi)

*dead space: ventilation w/o perfusion in systole or diastole
when do we see zone 1?
not normally, but if we do see it at very top of apices of lungs
*created during Valsalva maneuver
*convert zone 2 -1 during hypotension or standing up too long w/o moving arround
what is zone 2?
intermittent blood flow
Q during systole but not diastole
Pi > Po
from apices of lung down to Ra
when does flow exist in zone 2?
during systole when capillary pressure exceeds alveolar pressure
what happens to zones during hypotension?
zone 2 - 1
what happens to zones during exercise?
zone 2-3 increase cross sectional area in lungs
where is zone 3?
from Ra down
what is zone 3?
throughout entire cardiac cycle, pressure in capillary exceeds pressure in alveolus
Pi > Po
*continuous flow
what happens to zones when lying down?
more zone 3 b/c less gravity
what happens to zones in space?
no zones b/c no gravity
why do you see an increase in zone 1 in valsalva maneuver?
increase alveolar prssure thefore more zone 1
if you have problems breathing how should you sleep.?
no pillows.. lie flat to increase zone 3
when would you becom short of breath and require sleeping on pillows?
when L heart failure b/c backs up into lungs need pillows to decrease preload, sarcomere lenght
what happens to cap hydrostatic pressures as go from lung apices to base?
where will pulmonary edema develope first?
in bases, as edema progresses it will move toward apices
*this is because CHP is greater in bases-more filtration
R of lungs of neoneat?
high but decreases after birth b/c NO production
where would you find Tuberculosis bacillus?
active in apices of lungs b/c likes O2 thefore in zones 1 and 2
when would you becom short of breath and require sleeping on pillows?
when L heart failure b/c backs up into lungs need pillows to decrease preload, sarcomere lenght
what happens to cap hydrostatic pressures as go from lung apices to base?
where will pulmonary edema develope first?
in bases, as edema progresses it will move toward apices
*this is because CHP is greater in bases-more filtration
R of lungs of neoneat?
high but decreases after birth b/c NO production
where would you find Tuberculosis bacillus?
active in apices of lungs b/c likes O2 thefore in zones 1 and 2
Q through the lungs is dependent on what?
body position and gravity
why are lungs leakier than systemic?
interstial fluid colloid osmotic pressure in lungs greater than systemic
why is the negative intersitial fluid prssure in lungs lower than systemic?
b/c evaporation and more lymphatics
**filtration in pulmonary system is greater
what happens as left atrial prssure increases?
rate of developing pulm edema increases
what hormone production takes place in lungs?
conversion of angi I to ang II by ACE b/c large surface area
capillaries of lungs?
high cap density
short diffusion distance
why are lung apices poorly perfused in upright subject?
b/c pulm arterial prssure is low
what is happening in pts with severe emphysema?
destroy capillary bed decreasing total cross sectional area (increase diffusion distance)
chronic hypoxic vasoconstriction can lead to?
righ sided heart failure
why do neonates have higher TPR?
less amt capillaries in parallel. but as they develop they get more in cap. bed thefore decreasing R
placenta and flow? polmonary aa?
low R to Q in placenta
pulmonary aa: high R
90% Rv output in fetus goes where?
from pulmonary artery to the aorta through ductus arteriosus
why does only 10% of blood from Rv go to lungs in fetus?
b/c pulmonary R in fetus is high
in fetus, blood that is highest in saturation goes where?
liver, heart, and upper body/ head
waht is the max fetus O2 saturation?
80% from umbilical vein
*fetus always in hypoxic condition
in fetus, where does blood go after entering via umbilical vein?
50% to liver
50% bypasses liver to IVC via ductus venosus
what is the % saturation of blood entering Ra in fetus? why?
67% instead of 80% b/c of extraction from the liver
what happens after fetal blood enters right atrium?
crista dividens diverts blood flow
majority goes from Ra though foramen ovale into La
the rest enters Ra to Rv
blood in Ra is from (fetal)?
small stream from IVC
blood from SVC
blood from carotid sinus
satruation of blood from Rv into pulm artery in fetus?
52% saturated
*only 10% of Rv output enters lungs 90% diverted through ductus arteriosus into aorta
majority of blood going into La is coming from where?
IVC though foramen ovale
small amt from pulm vv into La
is the saturation of Rv grater than that of Lv in fetus?
Lv saturation greater in fetus
how can fetus live if blood from umbilical vv is only 80% saturated?
b/c fetal Hb has greater affinity for O2
in fetus is R v afterload greater or Lv afterload?
Rv afterload b/c lungs are high resistance in fetus (no NO production yet)
at birth what immediately happens?
increase in sympathetics
increase in reticular activating systems
after birth, cutting the umbilical cord does what?
causes ductus venosus to contrict increaisng TPR rapidly** this causes arterial blood prssure to Incrase
after birth the umbilical cord is cut increasing arterial blood prssures, that happens to pulm resistance?
increased O2 decreases pulm R due to expansion of lung tissue and the presence of O2 now the afterload of Rv decreaess.
after birth, what happens to afterloads?
Rv afterload decreases b/c pulm R decreases
Lv afterload increases b/c increased R on arteriole side
now L prssure > R prssure
after birth when L v P > Rv P what happens?
this causes foramen ovale to close when left atrial pressure exeeds Right atrial prssure (hear murmur b/c turbulence)
what happens to musculature in lungs after birth?
decreases as resistance in lungs decreases (less smooth mm mass)
what maintains an open ductus arteriosus during fetal development?
if ductus arteriosus does not close after birth, can give prostacyclin inhibitor to initiate closure
the major mechanism of body heat loss is by ?
radiation and condction 70%
what is the primary flow regulator of skin?
control body temp NOT metabolism
what controls core body temp?
hypothalamus via control of A-V anastomoses
what organ acts as a reservoir in times of hypotension during hemorrhage or cardiac failure?
skin: BP drops, symp incre, dec perfusion to skin
4 funxs of skin?
1. temp control
2. reservoir in times of hemorrhage
3. barrier
4. protection against bacteria
where do you have the highest amt of A-V anastomoses?
palmar surfaces:
palms, feet, ears, lips
purpose of A-V anastomoses?
delivers arterial blood into venous plexus
involved w/ radiating heat
contrict when core temp decreases
dilate when core temp incresae to radiate heat to environment
in the cold what do you want to do with the tone of A-V anastomoses?
increase R to dec amt of blood in venous plexus to keep core warm
type of R's in skin?
alpha 2: modified constriction
negative feedback to modulate blood flow to skin
how does the skin override hypothalamic activity?
local controls: stick one hand in cold water and get vasocontriction at the same time stick other hand in warm water and get dilation
what is the problem with compression of skin for too long?
develop bed sores: compressing skin for too long, perfusion decreases, tissue becomes necrotic (old people, diabetics and fat ppl) Diabetics have poor circulation to skin
describe rythmic flow in sk mm?
blood flow varies as contract and relax during isotonic cntrxns
Q occurs when mm relax
Q stops with mm contract
capillary density in type I mm?
high density b/c slow fibers
convert type 2b fibers to 2a when training
what primarily controls cerebral blood flow?
amt of Co2, metabolic activity of tissues
effect of sympathetics on control of cerbral flow?
very little! due primarliy by metabolic: CO2
intracranial prssure is the prssure where?
Po outside arteries: generated in the brain
*normally low, less when standing up
what happens when ICP get too high?
restrict blood flow, herniate brainstem
what happens to ICP when sneeze and cough?
instant increase ICP, get lightheaded b/c incr P affect Q
what is the treatment for increased ICP?
hyperventilate (artificially) to bring CO2 levels down in arterioles causing vasoconstriction decreasing hydrostatic prssures in cerebral cappilarires. the filtration pressure will now go down
eqn for cerebral blood flow?
cerebral blood flow = MAP-ICP
to increase cerebral blood flow, want to decrease ICP, do so by dec CO2 in arteries to vasocontrict them to dec Pc
how does viscosity of blood affect cerebral blood flow?
increase viscosity decrease flow
why can't you lie down a severe head injury pt?
want to increase venous drainage out
is the grey or white matter of the brain more INtolerant to hypoxia?
white matter more tolerant
grey matter intolerant to hypoxia
why are cerebral vssls excused from baroreflex activity?
metabolic factors override
want to always vasodilate to bring Q back
blood flow to GI is impaired when?
during exercies, hypotension, and/or hemhage
is the GI tract sympathetically controlled?
NO! controlled by pre-cap sphincters that respond to metabolic acitivities
what is the problem with GI tract?
countercurrent flow patterns: in villi have artery coming up, vein coming down and capillaries all the way through up and down. the problem is that by the time the arteriole blood gets to the tip of the villi it already has very low P02 and any drop in perfusion reduces this drop even more making tips of villi necrotic-bacterial infxn*
why do hypotensive pts get bacterial infxns?
b/c decrease P02 at tip of villi becoing necrotic
why is the liver a reservoir for blood?
b/c increased capacitancde in hepatic sinuses
receptors found in hepatic artery? sinuses?
artery: B2 R's
sinuses: alpha 1 R's thefore decreased unstressed vol from hepatic sinuses
what happens to hepatic artery and sinuses during exercies?
hepatic artery dilates and sinuses constrict