CVS 3 cardio dynamics now there's something to do with cardiodynamics and then we'll also

discuss cbs4 because we're done with with the heart already so i'll be discussing the blood
vessel later on so we'll have a break first after this and then we will discuss okay the blood
vessel so before we start we can you can have um an opening prayer so you can say your own
prayer i'll give you um several seconds now for that you can start now so okay so um these
are these are the objectives now for this topic so at the end of the discussion you should be
able to define and know about the cardiac output i will also enumerate okay the determinants
of cardiac output and give the factors that will affect its determinant discuss the different
methods used to measure the cardiac output okay and discuss the indices of cardiac
contractility and then explain the frank starling's law the buddhist phenomenon the main
reads reflex and then explain the post extra systolic potentiation so those are the topics that
we're going to discuss okay this morning so i'll start with the definition of the cardiac output
okay so cardiac output cardiac output is defined as the amount of blood ejected by either the
right or the left ventricle per minute so it should be permanent because if it's per bit you call
that the stroke volume so again cardiac output is the amount of blood ejected by either the
right or the left ventricle per minute and we mentioned that the cardiac output of the right
ventricle is the same or equal to the cardiac output of the left so which means that okay if um
the right ventricle ejects five liters of blood per minute okay the right ventricle also ejects five
liters per minute okay and you know already i mentioned that already in my first lecture that
the whole cardiac output of the right ventricle will go to the pulmonary circulation and the
whole cardiac output of the left ventricle will go to the systemic circulation okay now we can
express the cardiac output using your cardiac index so what how do you how do you do that
all you have to do is get your body surface area in in square meters and after getting your
body surface area you have to multiply that with three liters so let's say for example you
determine your body surface area and you found out that that is equal to two square meters
let's say for example your computation of your body surface area is two square meters okay
now all you have to do is multiply that with three liters so it means that approximately your
cardiac output is around six liters per minute okay so that is how you express you can express
that k as your cardiac index now let us take note of the variation of your cardiac output in
different conditions what are the different conditions that can increase it or that can decrease
it or will not change your cardiac output so i have here a table okay with a different condition
or factors no so we can change that it should be different conditions or factors that will affect
your cardiac output for example you will not see um any chains with your cardiac output
when you are sleeping or if there are changes it is not clinically significant so when you are
sleeping or when there is moderate changes in your environmental temperature so these two
conditions will not markedly change your cardiac output but for the following okay let us take
note of the factors that will increase your cardiac output so one is anxiety or excitement so
you know this already because anxiety or excitement is will activate the sympathetic nervous
system so once sympathetic nervous system is activated then that will increase your cardiac
output by approximately 50 to 100 percent another one is when you are eating okay when
you are eating okay your cardiac output increases by 30 but the most important okay
increase in your cardiac output that is viscologic also because excitement and anxiety and
then eating are physiologic conditions but the most important is exercise exercise is one of
the most important physiologic conditions that markedly increase your cardiac output by
around cardiac output is 5 liters it can actually increase as high as 35 liters when you do your
exercise another physiologic factor is high environmental temperature okay pregnancy and
epinephrine so this conditions no anxiety or excitement eating exercise high environmental
temperature pregnancy and epinephrine are actually physiologic conditions that can increase
your cardiac output now what about the pathologic one okay the pathology conditions that
will also increase your cardiac output one is anemia okay that's why uh anemia is said to be
uh that's that can lead to high output failure meaning there is a failure of the okay heart okay
or there is an adequate um supply of blood to the different parts of the body okay the reason
is that the the heart is not a problem but there is only high demand no that cannot meet by
the heart that's why you call that high okay um output a failure so another one is fever no if
you have fever there is an increase in your cardiac output and of course one of the most
common conditions you have hyperthyroidism okay now let's go to the common condition
that will decrease your cardiac output okay number one physiologic condition is a change in
your position it should be from lying to standing or sitting to standing because once you stand
up from lying or sitting the blood okay by gravity will pull down to your lower extremities
therefore okay the blood that will return to the heart decreases so therefore the amount of
blood ejected also decreases so position another one is any uh problem with the heart it
could be failure but one of the most common is arrhythmia so when you say arrhythmia this is
a condition within there is a chainski in your um there is a change in the rate in rhythm either
you increase or decrease either there is a decrease or increase in your rate in rhythm okay
now as i said other heart diseases like myocardial infarction heart failure say cardiomyopathy
etc okay so these are the conditions that can change your cardiac output now another
question is that okay when the blood when the blood is ejected by either the right or the red
left ventricle okay the next question is where will it uh go no the blood and the highest
percentage is will go in what organ okay so if you will notice in this table among the organs
that will receive the highest cardiac output are the splunkenic organs when you say splunk
nick orgas that is your git including your liver okay actually that is self-explanatory because
they are one of the largest now one of the largest um organs okay in the body that is a real
the reason why it receives k the greatest cardiac they receive the greatest cardiac output no
splenic organ followed by the muscles self ex explanatory because you also have large scale
um size of your skeletal muscles followed by the kidney and then you have skin in other
organs and then of course the brain and then the heart now if you will notice in this
distribution of target output you will notice that kidneys are very small so kidneys compared
to other organs so kidneys are small and yet receiving 20 of your cardiac output and that is
the reason why if the question is who will receive the greatest cardiac output okay per gram
of tissue meaning you consider the weight okay the highest amount of cardiac output is
received by the kidney that is if you consider the weight if not then the greatest amount of
cardiac output is actually received by your splunk organs okay so we are done with the
definition we are done with different conditions and factors that will affect your cardiac
output and then the distribution of your cardiac output okay so let's go to the determinants of
your cardiac output okay so if you will notice the equation is cardiac output is equal to stroke
volume times the heart rate what does it mean if you have that kind of equation it only means
that if you increase your stroke volume you will also increase your cardiac output and if you
will increase your heart rate you will also increase your cardiac output but please take note of
the heart rate okay the heart rate there is a limitation on the average okay an increase of
heart rate okay only up to 180 bits per minute because beyond 180 you can no longer
increase your cardiac output cardiac output will decrease on the average if you increase your
heart rate beyond 180 beats per minute okay we call that the maximal heart rate for example
when you do exercise and your cardiac or your heart rate increases it's okay because that
increase in heart rate as i said will also increase your cardiac output so an increase in heart
rate will also increase your cardiac output but please take note if your heart rate is already
beyond 180 okay you have to slowly okay decrease your activity because beyond increase
your cardiac output so we call that the maximal heart rate so i told you that this one is only an
average you can compute for your own maximal heart rate okay the computation is 220
minus your age so if you are already let's for example you are okay 200 bits per minute
which means that the younger you are the higher your maximal heart rate so as long as if you
are still young your heart your maximal heart rate is higher so you can sustain a longer period
of exercise or physical activity but as you grow older you will notice that your maximal heart
rate decreases and that is the reason why many elderly individuals cannot tolerate a longer
exercise because they can easily reach their maximal heart rate unless you are an athletic
individual okay why for example let's say um manny pacquiao and i have the same age
assuming that we are both this is only an example assuming that we are both um years old
rate is 180 okay but i am not an athletic individual so my my resting heart rate is okay for
example my resting heart rate is let's say 70. okay so my resting heart rate is 17. but manny
pacquiao is an athletic individual one beneficial effect of okay training is that it lowers the
resting heart rate so probably if i have a resting heart rate of around so we have the same
maximal heart rate of 180 so which okay between us will reach easily 180. i can easily reach
that because i started at 17 but manipuls started at 50. that is one of the most important
beneficial effect okay of your training or exercise now please take note of this class okay i i
already asked this i already asked um dr pined about i dr de guzman about this i know i read
that the lower your resting heart rate the longer your life okay so the lower your resting heart
rate the longer your life now if you're going to ask me doctora what will decrease my resting
heart rate very easy all you have to do is do physical activity exercise can lower your resting
heart rate okay so starting now you have to have a enough physical activity so that your
resting heart rate will be lower than the than the rest of the individuals so that you will have a
longer life okay so as i said the lower the resting heart rate the longer your life okay of course
without considering any factors now what will affect your stroke volume so we okay this is
defined as cardiac output is equal to stroke volume times the heart rate as i said if you
increase the stroke volume you'll increase your cardiac output and what is stroke volume we
mentioned that stroke volume is the amount of blood ejected by its ventricle per bit now
since this one is per bit this one is per minute then you have to multiply this with the number
of times the heart contracts and that is your heart rate because this one is per minute okay
so that is that is the reason why stroke volume times the heart rate is equal to your cardiac
output now as i said your stroke volume is the amount of blood ejected per bit now this is
actually determined by what it is determined by the amount of blood present in the ventricle
at the end of the astole so meaning after diastole the amount of blood present in the ventricle
is known as your edb remember the end of the asteroid is the beginning of your isovolumetric
contraction phase am i right so after n days after the after the end of diastole the av valve will
close and eventually you will have iso volumetric contraction phase now during isovolumetric
contraction phase the ventricle contains the edb because ebb is the amount of blood present
in the ventricle at the end of diastole which means that at the end of ventricular filling so
normally edb is okay approximately around 120 ml per minute so this is around 120 ml per
minute now this is at the end of the now after ejection you eject already the blood remember
that you do not eject all that 120 will not be ejected all a you will only eject around 70 okay
on the average so 70. so what about the remaining 50 then you call that the esb and systolic
volume so if this one is 120 and okay 50 ml is remaining so we call that end systolic volume
then the amount of blood ejected is approximately around 70 and that is equal to your stroke
volume so therefore stroke volume is equal to end diastolic volume minus and systolic volume
now let us take note now of the changes in your cardiac output once you change all these k
parameters so once i increase the edb i will also increase the stroke volume then i will also
increase your cardiac output but if you increase the esb this follow this is preceded by a
negative sign then you decrease your stroke volume then you also decrease your cardiac
output and i already mentioned no if you increase the heart rate as long as it is not beyond
180 on the average okay you will still increase your cardiac output okay so therefore let us
again define stroke volume as i said approximately 70 ml that is the amount of blood ejected
by its ventricle per bit and diastolic volume or edb that's approximately 120 ml that is the
amount of blood present in the ventricle okay before systole before ventricular systole is the
end of the astole also okay so the end of diastole now your end systolic volume is
approximately 50 and that is the amount of blood remaining in the ventricle okay after
ventricular systole or after ejection so if you're going now by the way the heart rate is equal to
60 to 100 bits per minute so uh there is there is a range of 60 to 100 actually the average
heart rate is around 72 bits per minute so that is the frequency of cardiac contraction by the
way class since i told you that the lower the resting heart rate the longer your life how low
should be okay your your your heart rate should not always be beyond 80. it's better that
your heart rate is between 60 to 80. okay now let us take note of the cardiac output as i said
so cardiac output is the amount of blood ejected by its ventricle per minute so approximately
is around five to six liters per minute higher in males now as i said you can approximate your
cardiac output using your cardiac index all you have to do is get your k body surface area and
multiply it with 3 liters per square meter so what are now the examples so what are what are
now the determinants of your cardiac output so the major determinants of your cardiac
output are your heart rate and diastolic volume systolic volume that is actually those are the
determinants of your stroke volume okay so from our computation edb is around 120 ml esb
is around 50 ml you multiply this with an average heart rate of 72 so that is approximately
approximately five to six liters because it is higher in males okay so those are the the different
determinants k of your cardiac output now let us take note of this okay the question is what
are the factors that will affect your what are the factors that will affect edb therefore
affecting stroke volume therefore affecting cardiac output we will also discuss what are the
factors that will primarily change the esb so that that will also change your stroke volume and
cardiac output in what are the factors that will affect your heart rate therefore affecting also
your cardiac output so i will start with what are the factors that will affect the heart rate what
will increase it and what will decrease it okay so these are the factors that will affect your
cardiac output so i told you that on the average okay it is around 72 bits per minute so let us
round it off to 70 bits per minute now the major factor that will affect your heart rate is the
neural factor nervous factor the neural factor in the major determinant is autonomic nervous
system so which means sympathetic in para sympathetic that is the major determinant but
there are also higher centers that can affect your heart rate it can be affected by your cerebral
cortex but this one is voluntary this one is uh this is something to do with the voluntary
activity that also increase your heart rate that can also be affected by k activation of your
thalamus about primarily hypothalamus because hypothalamus is the head ganglion of your
autonomics that is the center for autonomic function and of course the medulla oblongata
because this is where you have the different cardiac centers located now that cardiac centers
will be discussed in cbs6 now please take note that i told you the pacemaker of the heart is
the sa node that is a pacemaker of the heart and that dictates our heart rate so which means
that if the sa node fires 100 impulses per minute then our heart rate should also be 100. if it
discharges 60 impulses per minute our heart rate is also 60 okay but class please take note of
this in humans normally in humans normally as a node fires 100 bits per minute a normal
firing of your sa node in humans so therefore supposed to be our heart rate should be 100 bits
per minute our heart rate should be 100 bits per minute why because sa node in humans
discharges but if you're going to ask me doctor if sa node normally fires 100 impulses per
minute how come our average heart rate is around 70 okay or 72 why is it lower than 100 by
the way class that is the heart rate if there is no autonomic innervation if there is no
autonomic innervation our heart rate is 100 bits per minute but since there is an activity of
parasympathetic in simpa do you know that glass even at resting state there is tonic
discharges from sympathetic and parasympathetic simultaneously to the heart at resting state
and please take note parasympathetic predominates sympathetic at resting state which
means that effect a parasympathetic to the heart is stronger than sympathetic at resting
state it does not only mean class that only simple sympathetic will act only during excitement
or emergency situation it doesn't necessarily mean that parasympathetic only have effect
okay if you are resting no even the heart is resting there is an activity of simba in para only
that para predominates but during excitement simpa will predominate with para did you
understand class clear clear so that when i say node fires 100k impulses per minute since there
is an action of simpa and aksana para and para is stronger then there is a tendency of the
heart rate rate to become lower okay now class if you danger wait the heart if you remove
simple in para your heart rate is 100 so if you remove para in simple to the heart heart will
not stop because there is a pacemaker in the heart take note of that remember i i told you
there are two innervation of the heart intrinsic and extrinsic and intrinsic is more important
than intrinsic because extrinsic is your autonomy it's just for regulation either you increase it
or you decrease it so if you will remove simpan para the activity of the heart will even
increase take note of that if you remove simply impart activity of the heart will even increase
because at resting state para predominates clearion class clear clear okay so that is a uh
impara so this is actually your zinpa you will notice that simpa okay innervates both the the
atria and in the ventricle so on the other side you also have that in the atria and the ventricle
but for the right side it probably will primarily it is primarily distributed in the sa node in on
the left side more on the av node now if you look look at the para that these are vagus nerves
okay young vega nerve mo you will notice that right also is mainly distributed in the sa node
is le and left is mainly distributed in the av node you will notice that there is very small
amount of innervation in the ventricle and that is the reason why parasympathetic activation
will least likely affect your ventricular activity because there is a very small amount no or
even not affect the activity of the ventricles so that is neural so plus look at this huh heart rate
the first factor is neural sympathetic increases the heart rate therefore increases the cardiac
output parasympathetic decreases the heart rate therefore decreases the cardiac output okay
so that is neural let's go to the hormonal okay or we call this humoral factors so casein
dilemma hormone so let us change this to humoral factory because that also include hormone
that can also include neurotransmitter in other substances no humoral let us take note of this
acetylcholine okay which is also para so acetylcholine decreases your heart rate therefore
decreasing your cardiac output while epinephrine in norepinephrine increases your heart rate
therefore increases your cardiac output thyroid hormone increases also your okay also your
your heart rate by the weight class there are several substances but i will mention only the
most common because as you as you go to the endocrine lecture because the the later part of
second semester is all about endocrine and let's say you also will discuss renal you will also
discuss git there are some substances that can also affect your heart rate never mind not i will
only mention the more common so these are the more common let us see on how the
sympathetic and epinephrine in norepinephrine increases the heart rate so we discussed this
already okay so uh where is my slide oh my god where is it okay wait long huh hannah i will i
will look for um a slide no okay it done okay let us take note first of this okay in my cvs one
lecture i mentioned that sympathetic specifically due to the secretion of catecholamines
increases the heart rate how binds with beta 1 receptor which is linked to a g protein and
then since it is linked to alpha s it activates a dna cyclase converting atp into cyclic amp you
know the cyclic amp will actually phosphorylate your protein kinase so your protein kinase
will phosphorylate your phospholipid take note of this when phospholipid is phosphorylated
classical say when phospholymbone is not phosphorylated it inhibits the activity of circa but if
it is phosphorylated phospholamban increases or activates the activity of circa so once circa is
activated you can easily sequester your calcium into your sarcoplasmic reticulum so therefore
if you if you sequester calcium easily into your sarcoplasmic reticulum then your relaxation
period is shortened so if you shorten your relaxation period then your heart rate is increased
and that is the reason why catecholamine increases your heart rate now let us take note of
the effect of acetylcholine so this is your this is your catecholamine right so epinephrine in
norepinephrine which is also sympathetic activates your beta one okay a g protein since it
activates the gs look at this one the tester gs then you you you convert 80 pintocyclic amp
and cyclic amp will activate your proteinase a phosphorylating your circa so if you postpone
electric circuit you can easily sequester the calcium that increases your heart rate now what
about acetylcholine look at this one acetylcholine when okay when acetylcholine binds with
m2 receptor it is k a coupled with a g protein but the alpha is gi so you know once it is gi not
gs it inhibits adenylate cyclase so once it inhibits adenylate cyclase then you will not form
cyclic amp so therefore you will not activate protein kinase a if you cannot activate the protein
kinase a then the phospholon bond will not be phosphorylated so therefore the activity of
circa decreases so you which which means that this decreases the uptake of calcium so if
decrease if you decrease the uptake of calcium then therefore you will also okay prolong the
relaxation period so if you prolong the relaxation period then you decrease the heart rate
class clear back clear clear hello hello clear boy did you understand now what about thyroid
hormones actually plus the effect of thyroid hormones is almost the same as that of the effect
of catecholamines because thyroid hormones is synergistic to your catecholamine so same you
will affect the gs therefore you increase the cyclic amp so that is humoral so it means that
okay um going back again to this so we are done with neural we are done with humeral
epinephrine norepinephrine thyroid hormones increases the heart rate therefore increases
also your cardiac output okay while acetylcholine decreases your heart rate therefore
decreases also your cardiac output so we're done with neural we're done with humoral and
then we also have k the effect of respiration and by the way look at this class like this
applying your applying your um knowledge about okay sympathetic or the autonomic nervous
system question column what is atrophine are you familiar with i only choose two most
common substance what is atrophine familiar familiar you know what is atrophine a class
you're done with your autonomics okay so according to geneva okay um atrophine is an anti-
muscarinic drug so if it's an anti-muscarinic drug it blocks the effect of parasympathetic
correct so it is classified as parasympatholytic drug so since atropine is a parasympatholytic
drug it blocks the effect of para then you will expect that once you block the para then the
heart rate increases so look at this one the heart rate increases okay now what about forming
a pharmacist it's a beta blocker so if it's a better blocker it blocks the activity of okay beta then
therefore it is a sympathetic blocker so we call that okay we call that sympatholytic drug so if
it blocks the effect of simpa it will decrease the heart rate so that will the heart rate decreases
so this is your your um effect now look at this this is the effect of blocking the para and this is
the effect of blocking the simpa so only the effect is opposite if you block simpa you decrease
the heart rate if you block power you increase the heart rate what did you notice the change
in the effect of parasympathetic drug is greater than this one look at the chains here you only
change the heart rate by around from 60 to 50. so you only change by 10. now what about
the the the atropine that is from 65 that increases to around 115 bits per minute it only
means that the effect of para really is greater than simpa okay so really uh sympathy
dominates in the heart okay now the next one the next factor that will affect the heart rate
are the physical factors okay now what is the most important physical factor that will affect
your heart rate the body temperature please take note that when the body temperature
increases your heart rate also increases so here so we are done with neural eumoral and
physical so in physical you have your body temperature the greater the temperature the
greater the heart rate the greater your cardiac output the lesser the temperature the lesser
the heart rate the lesser your cardiac output that is for physical factors another one another
factor is the effect of respiration so can i escape respiration i will discuss this in detail later on
okay in the next slide so i will i will start first with physical factor body temperature you know
already the effect another one is electrolyte concentration so please take note of this you
know problem because i cannot write so if i can only write so i can explain that okay um
clearly so let us take note of this you know your potassium right potassium is okay highly
concentrated inside the cell but if potassium concentration outside the cell is increased no
that is increased like in hyperkalemia what could be the effect what is the effect if you
increase your potassium level so please imagine this no comparison a homework drawing
[Music] can anybody uh do you know how to can i draw here pretty bad with my white board
singing so people in the think language whiteboard let us see complimenting whiteboard okay
oh what will happen if i will sing magaling whiteboard okay start a new white board let's say
imagine that there is a cell somehow okay you sell more more potassium inside and less
potassium outside but there is hyperkalemia so if there is hyperkalemia then there would be
less potassium efflux no magnesium potassium reflux because the potassium outside is high
so therefore if the potassium cannot leak now from inside to outside then the membrane
becomes less negative okay that will become less negative so you can depolarize the cell so
that's correct you can depolarize the cell because there is decreased potassium efflux but the
problem is this you can you can depolarize the cell but the problem is your repolarization you
cannot easily repolarize the cell so if you cannot easily repolarize the cell then the then the
then the cell will be arrested at refractory period and that is the reason why that decreases
the heart rate so high potassium concentration decreases the heart rate okay so it can even
cause cardiac arrest if it's too high in hyperkalemia did you understand do you understand
okay now what about if there is hypokalemia the same you also decrease the heart rate but
the mechanism is different in hyperkalemia you arrest the cell or the cardiac muscle cell at the
refractory period because you cannot easily repolarize because the potassium cannot easily
come out of the cell because the potassium outside is high but if the potassium is low it is
very low outside the cell then there would be more potassium efflux than what will happen
with the cell rmp it becomes more negative you hyper polarize the cell so if the cell is hyper
polarized you cannot easily excite that then the effect is the same in fact mark if it is markedly
decreased that can also cause cardiac arrest no so they both decrease your okay heart rate
the two reasons in hypokalemia you hyperpolarize okay the cell in in hyperkalemia you arrest
the cell at refractory period so that is electrolyte another one is calcium or you know that
already know the pacemaker the sa and av node there is a pacemaker potential due to
leakage of calcium if calcium is decreased then the pacemaker potential okay a magnitude is
also decreased so you can eat you cannot easily produce an action potential so that decreases
the heart rate not only the heart rate even the force of contraction but in in hypercalcemia
you increase the heart rate okay in in fact even the force of contraction but the problem is
that okay it can cause tetanic contraction of the heart okay now what about sodium okay if
sodium is decreased then you cannot also depolarize the other fibers in the cell so that will
also decrease the heart rate compared to hyper okay hyper natural so those are the effect of
electrolytes now the next one is exercise so you know this already exercise and emotion so
exercise and emotion class both of them can cause activation of sympathetic so therefore that
will also increase the heart rate okay now let's go to the effect of respiration respiration has
an effect on okay the heart rate okay the effect is it depends on the phase of respiration so
you know class that during inspiration heart rate increases and during expiration heart rate
decreases okay so this effect is explained by being bridge reflex so bin breed's reflex okay
states that if you increase the atrial volume you will also increase the heart rate so that that is
vein braids explains the direct relationship of atrial volume with the heart rate which means
that the greater the atrial volume the faster the heart rate the lesser the atrial volume the
slower the heart rate now why during inspiration please take note that during inspiration you
expand the chest wall during inspiration you expand the chest wall according to boyle's law if
you increase the volume of a container pressure decreases and that pressure is known as
intra thoracic pressure so during inspiration since the chest wall expands intrathoracic
pressure decreases okay so if intrathoracic pressure decreases remember intrathoracic
pressure is in the chest area if the pressure in the chest in in that area that is actually the
pressure in the pleural cavity so if the pressure there is low then the blood can easily flow into
the chest therefore it can easily go back to the heart so that when the intrathoracic pressure
decreases there are more about a blood that will return to the right atrium okay not only the
right atrium but also the right the left atrium then we call that if it is permanent then we call
that the venus return so that will increase the venous return okay to the heart so once you
increase the venous return meaning more blood enters the right and the left atria and you
increase the atrial volume so in this case you increase the atrial volume now in the atria there
are atrial stretch receptor in fact in the atria especially in the right you have the sa node so if
you if you increase the volume there and you stretch the the atria then you activate the s a
node you activate the stretch receptor then that causes the increase in heart rate so the
greater the greater the atrial volume caused by inspiration the greater the heart rate then
let's go okay to the effect of expiration this is opposite during expiration you deflate you
deflate the chest wall so if you did deflate the chest wall volume decreases so therefore
intrathoracic pressure increases so if the pressure in the chest area is high then you cannot
easily move the blood into the chest area okay so therefore you cannot easily move the blood
back to your right and left atrium so the venous pressure decreases so if the venus the venous
return decreases then the atrial volume is not increased so it is low so if the atrial volume
decreases then you cannot stretch the atrial stretch receptors and then the sa node then that
will cause the decrease in heart rate so that that is the main bridge reflex so again i'll repeat
that explains the direct relationship of atrial volume and then the heart rate and the atrial
volume is primarily affected by the phases of your respiration or class we are done with the
factors that will affect the heart rate any question did you understand did you understand
useful yes okay now we are done with this now we are done with the factors that will affect
this one then the next one is what are the factors that will affect edb and esb so that it will
affect the stroke volume therefore affecting your cardiac output i'll start with edb okay the
amount of blood that will go okay to the ventricle by the way class with la mona okay i will
discuss first before i go to the end diastolic volume i will discuss the principle about the
preload and afterload i already mentioned the afterload in the cvs one remembered after
load of the left and after load of the right so what is preload actually as that and one student
answer doctor preload is the load before and after load is the load after okay is either a force
force pressure or volume mistake note it is either a volume a force or a pressure that
stretches the myocardium before it contracts so that is the the volume or the force or the
pressure that will stretch the myocardium before it contracts and what will stretch what will
stretch the ventricle before it contracts the amount of blood present there right the amount
whatever the amount of blood present in the ventricle before it contracts that is the amount
or the volume that will stretch the myocardium and that will also exert a force right and by
exerting a force and then a pressure that will also increase the tension there we call that
diastolic tension am i right we call that the preload and what is that amount of blood present
in the ventricle that will stretch the myocardium that is your edb so edb or the preload is
actually equal to your edb so the best index of preload is edb now what about after load after
load is a pressure or a resistance it is either a pressure or resistance against which the ventricle
okay ejects the blood or it is the resistance or the pressure encountered by the ventricle in
ejecting the blood for example the right ventricle ejects the blood towards the pulmonary
circulation and that will actually encounter the pressure known as the pulmonary pressure so
if the pulmonary pressure is high then the ventricle can have will will have difficulty in ejecting
the blood because that is a resistance to which the blood is ejected for the for the systemic
circulation okay that is equal to your aortic pressure so whatever the pressure in the aorta
that is the pressure or resistance encountered by the ventricle in ejecting the blood and we
call that the after load okay so therefore the best index the best index of afterload is either the
pulmonary or the aortic pressure while the best index of preload is edb edb another one
another one that i want to mention is this edb is not equal to venus return because edb or the
preload is the amount of blood present in the ventricle before ejection well the venous return
is the amount of blood that will return to the right and left atria edb is in the ventricle this
one is the one that go back that goes back to the atria and that is per minute am i right and
that is permanent that's your venus door no i will ask you a question no if if the if the venus
return is the amount of blood that goes back to the heart or the atria per minute then this is
exactly equal the amount is exactly equal to what in normal condition the amount of blood
that will return to the atria per minute is exactly equal to the amount of blood that is ejected
by the ventricle so the amount of venous return is exactly equal to your cardiac output in
normal condition do you do are you aware of this whatever is ejected that is also the amount
that will return to the heart whatever the amount that will turn to that that is also the
amount that will be ejected so that is exactly equal in amount huh to your cardiac output
okay so we're done with that so clearly let's go to the end diastolic volume so i told you since
end diastolic volume is the volume of blood that will stretch the myocardium before it
contracts so therefore that is equal to your preload that determines okay the the length or
the muscle fiber length so determined by the muscle fiber length before contraction and what
are the factors that will influence the venus return therefore influencing also the edb so what
are the factors that will increase the edb okay so number one factor is ah can you can you in
your notes all you have to do is put a right two columns on the first column put there the
factors that will increase or the one that is directly proportional and put the factors that are
inversely proportional okay to the edb which means that if increase will also increase your
edb so let us take note so you have to group them together now the first one is ventricular
filling time ventricular filling time is the time it takes for the ventricle to be filled up with blood
if the ventricular feeling time is longer then you can allow more blood to return to the heart
therefore edb increases so that is directly proportional so ventricular filling time is directly
proportional to the edb because the longer the time it takes for the ventricle to be filled up
with blood and more blood okay we'll go to the ventricle but please take note that ventricular
feeling time is determined by the heart rate the faster the heart rate you have the shorter
the ventricular feeling time and in remember i told you class that diastole is longer than
systole correct correct class diastole is longer than sistole when the heart rate increases okay
the diastole uh duration is sacrificed so you shorten the diastole so if you shorten the diastole
you shorten the ventricular feeling time so heart rate should be put on the indirect relation
and that is the reason why i told you the faster the heart rate the greater the cardiac output
but if it is beyond 180 class ventricular filling time will markedly decrease and then it will
affect the edb and that is the reason why cardiac output decreases if the heart rate goes
beyond clear puyon clear clear class okay now the next one is this effective feeling pressure
if the pressure you use to fill the ventricle is high then okay edb is also increased so the
greater the effective feeling pressure the greater okay the edb so you put that in the one with
direct relationship but efp or effective feeling time is equal to central venous pressure which
means that the greater the central venous pressure the greater the effective feeling pressure
so you can also put the central venous pressure on the dia the one with direct relationship
nobody's central venous pressure the central venous pressure is the pressure in the atria so
which means that the the greater the pressure in the atria the more you push the blood into
the ventricle like in the case of atrial systole now the stronger the atrial systole the more you
the more you push the blood into the ventricle but it is inversely proportional to the
intrathoracic pressure which i mentioned a while ago the greater the intrathoracic pressure
the lesser the effective feeling pressure okay because the blood cannot easily go to the heart
you know so this is what put this okay in the column with indirect relationship same with the
heart rate another one is ventricular compliance that is sensibility okay so the greater the
ventricular compliance the greater the volume of blood that can be contained in the ventricle
then the greater the the greater the edb so that is also direct relationship so what are these
other factors so other factors are the following but remember if you increase the venous
return you will also pro okay you will definitely increase your preload also so look at this one
the muscle pump the muscle pump the thoracic pump the abdominal pump there's
something to do with muscles please take note when the muscle contracts in the lower
extremities you squeeze the blood back to the heart against gravity right so that increases
also your edb when the when the muscle in the thoracic cavity contract that is your thoracic
pump intraplure intrathoracic pressure also decrease so they also increase your edb when
abdominal when abdominal muscles contract you increase the intra-abdominal pressure then
you push the blood back to your heart so all this pump can increase your edb so muscle pump
abdominal pump and then the thoracic pump now i already mentioned the atrial systole so
once you have a stronger atrial systole the greater the edb so they're all directly proportional
another thing the blood volume of course the greater the circulating blood volume the greater
the amount of blood that will go back to the heart and that will that will also increase the edb
huh now what about the venus stone when you say venus stone it means that it favors more a
vasoconstriction okay v no constriction so when the veins contract then the amount that the
blood will go back to the heart so the venous stone is also directly proportional by the way
class you know that the counterpart of venus of being a stone that is inversely proportional
capacitance is inversely proportional same with pericardial pressure remember the
pericardium i told you it is non-distensible so that if it's high the heart cannot sustain you just
compress the chamber so therefore edb decreases so most of the factors are directly
proportional except the heart rate except the venous capacitance except the intrathoracic
pressure and then the pericardial pressure okay now this one is sympathetic you know that
sympathetic increases that will also cause venous constriction so that will also increase your
that will also increase your k uh adb but i also read that the greater the sympathetic discharge
the more compliant the heart so therefore the greater also your edb clear nepal it's really
hard to know to discuss no online because we really don't know if you are listening and we
really don't know if you really understand so your reaction is very important to us so once we
ask did you did you understand either you can unmute and say yes doctor and then mute
again or thumbs up a thumbs up [Music] no apparently i'm gonna go white board no bug
zoom you don't problem about z min i cannot i cannot explain it better because i cannot write
in a white board no punk zoom you can write in a white board now so siguro because i saw
you in the screen not all of you okay so all you have to do is just a sign okay so did you
understand all the factors that will affect adb okay now let's go to the factors that will affect e
s b or the end systolic volume okay now the end systolic volume is primarily affected by these
two important factors okay and what are the factors that will affect your esb number one is
the force of myocardial k contraction just imagine this if the ventricle contracts stay if the if
the force of contraction of the ventricle is very strong you almost squeeze all the amount of
blood am i right but you cannot eject all so what happens with esb if you have a greater force
of contraction less would be remaining please take note of that right so if if the force of
contraction is high or increase then you squeeze almost all the amount of blood then the esb
decreases so that is inversely proportional the greater the force of contraction the lesser the
esb then the greater the stroke volume than the greater your cardiac output this one if the
force of contraction is k increase esb is increased less would be remaining stroke volume is
increased then cardiac output will also increase okay now the other one is okay the other one
is the afterload for the left ventricle that is your aortic pressure load for the right ventricle
that is your pulmonary pressure load the greater the pressure in the aorta and then the
greater the pressure in the pulmonary artery then okay what happens there would be
difficulty in ejecting the blood because the pressure to in the area to which you eject the
blood is high okay but you know class will it de will it change the esb initially no if the after
load is high initially it will not affect the asb because the heart will hypertrophied the heart
will compensate by pay by increasing the muscle mass and we call that hypertrophy but if it is
persistently increased and then the heart can no longer compensate then that is the time the
esb will decrease and that will decrease also your a stroke volume and decreasing your
cardiac output let us take note of this young manga let's say you are hypertensive let's say
your blood pressure is persistently blood pressure mo is 160 over 100 but you do not feel
anything and the doctor said you are hypertensive then you have to take medication okay
what is the usual response an unusual response no it's okay i did not feel anything that's my
normal bp you are already hypertensive you have to take a maintenance drug doctor that's
my normal no i didn't feel anything so let us see what will happen if the pressure in the
systemic circulation is high then the pressure in the aorta is also high then the left ventricle
will have a greater afterload so in order to eject enough amount of blood because you have
to encounter a higher pressure then this area will hypertrophy and that is the reason why if
your blood pressure is persistently high you will have cardiac enlargement you will have left
ventricular hypertrophy okay now if the blood pressure is persistently high this will
hypertrophy take note there is a limitation for hypertrophy eventually your heart will dilate it
will be stretched because less amount will be okay more amount will be remaining that is the
time your esp will increase am i right so if more esv is remaining you put another amount of
blood then you stretch the myocardium then if you over stretch it your heart will be dilated
and that is the reason why you have two important changes in your heart if you expose it to a
high pressure or after load initially it will hypertrophy eventually it will dilate once it will
dilate it is irreversible so that is the reason why if you have a higher okay arterial blood
pressure you have to lower it okay to a normal level even if you are not feeling anything
because that will affect your heart eventually if you will not do anything about that your heart
will fail and that will cause the heart failure and that is the reason why hypertensive
individuals whose blood pressures are not controlled they're usually prone to heart failure oy
class i have so many uh i know um students medical students few many at the age of i think
25 plus they're already hypertensive will you check your blood pressure huh please check
your blood pressure there are so many medical students now who are at the ages 25 to 30
who are already hypertensive but not feeling anything so at your age you have to regularly
check your cholesterol and triglyceride and you have to check regularly your blood pressure
otherwise you will not be feeling anything but you already have problems in your heart and
also problems in your kidney medical students um okay uh i know we will ask them to have
regular exercise and diet tapos yes dog not only for the grain that's for you huh have
regular exercise okay eat balanced diet no healthy diet she will not be sleepy during the
lecture no i tried that when i was a medical student no especially when you when you know
when you study for major exams major exam is young you're always sleepy now during major
exam when you when you study you feel sleepy so oh you know avoid milk tea i mean avoid
milky is good for the heart but my limitation too much coffee is also bad for the heart huh
you know you're going to ask me dog why coffee is good to the heart caffeine increases the
activity of rayalodin so that increases the release of calcium therefore increases the
performance of the heart but too much coffee inhibits the release of calcium so that will also
okay that it is also dangerous to the heart who will who will join with advocacy of dr gomez
regular exercise healthy diet you ask dr gomez dr gomez because in our house we regularly
have exercise or physical activity we also watch our diet so most of the people during
pandemic gain okay weight but we lose weight now so so at least i know physical activity no
physical activity and diet of course next so we have two important factors that will affect the
esb so we have the force of myocardial contraction which is inversely proportional to esb and
then the after load which are your aortic and pulmonary pressure that is actually directly
related to your esb the greater the after load the greater the amount remaining okay without
the compensation okay in the heart so we are done with the different factors that will affect
the determinants of your cardiac output now based from this wait this one you will notice
that edb is 120 but only 70 is ejected okay so which means that the percentage of the edb
ejected is equal to your ejection fraction so ejection fraction is actually okay the percentage or
the amount okay a blood ejected in relation to your edb so that is the portion of the blood or
the portion of your edb ejected okay during systole so therefore ejection fraction is the ratio
of stroke volume to edb so how do you compute for this ejection fraction is a stroke volume
divided by edb since this is expressed as a percentage you have to multiply by so 70 divided
by around so ejection fraction in facial is normally 60k 60 to 65 percent under resting
condition so how do you determine your ejection fraction not through ecg you can determine
the ejection fraction by k by asking for to the echo two dimensional electrocardiogram okay
so you can determine the ejection fraction so which means that the higher the ejection
fraction meaning let's say for example out of 120 you ejected 100 the higher the ejection
fraction the better or the stronger the contraction that is the reason why ejection fraction is
used to measure the contractility of the heart which means that the greater the ejection
fraction the stronger the contractility of the heart the lesser the ejection fraction the lesser
the force of contraction of the heart so you can see a hyperdynamic heart a hyperdynamic
heart should have a higher ejection fraction a hypodynamic heart should have a lesser
ejection fraction or there are two things on how to determine already we mentioned two
things on how to determine a hyperdynamic or hypodynamic heart one i mentioned just a
while ago that's your ejection fraction and the other one is when the ventricular pressure
volume curve moves to the right and moves to the left still remember that still remember that
when the curve moves to the right or moves the left anyway i will mention that later on i think
okay okay so we are done with the different factors that will affect your that will affect the
different determinants of your cardiac output so you will know more or less or you should
know already what will cause an increase and decrease of your cardiac output so before we
okay before we go to the venus return are there any questions so my questions puba paybaco
sabino's return okay so we'll proceed now with the venus return so we said that venus return
is the quantity of blood flowing from the veins into the right atrium per minute or flowing
from the pulmonary veins going to the left atrium per minute okay now what are the factors
that will affect being returned now the amount of this is almost equal to your cardiac output in
normal condition so siguro class we will just only concentrate on the factors that will affect
the venus return so what are the factors that will affect being acetone just take note of this
equation there will be no computation so don't worry there will be no computation we'll only
we should only concentrate on what is the effect of increasing the the other factor with your
venous return so let us see the equation is venus return is equal to mcsfp mcsfp is equal it's
actually your mean circulating static feeling pressure mean circulating static feeling pressure
minor central venous pressure divided by venus resistance so it means that venus return
increases if you increase mcsfp or mean circulating static feeling pressure so if you increase
this one you will also increase your venous return now what will affect the mean circulating
static feeling pressure this is something to do with the total blood volume the greater the
total blood volume the greater the mcsfp the greater the penis return but the greater the
venus capacitance the lesser the mean circulating static feeling pressure and the lesser the
venus return okay so in this case mcsfp in total blood volume are directly proportional to your
venous return now while venus capacitance is inversely proportional because that decreases
your mcsfp now another two important factors that are inversely proportional are your
central venous pressure the central venous pressure is inversely proportional to the venous
return same with the venous k resistance so what are the factors that are directly
proportional to the venus return mcsfp in total blood volume what are the factors that will
affect okay or that are inversely proportional with the venous return the venous resistance
the central venous pressure in the venous capacitance now please take note of the central
venous pressure central venous pressure increases edb central venous pressure increases edv
but decreases venus return is that right i told you that once venus return is increased you also
increase the edb how come that the central venous pressure increases edb but decreases
venus return imagine this class imagine this where is the heart okay imagine this central venus
pressure is the pressure in the atria if the pressure in the atria increases edb increases but if
the pressure in the atria increases then the the blood cannot easily go to the atria and that is
the reason why venus return decreases clear clear po clear okay now we are done with the
venus return okay let's go to the last part a of our lecture so we're done with venus return
now let's go to the factors that will increase or decrease your stroke volume therefore
increase okay or decrease your cardiac output there are two regulatory mechanisms the
heterometric and then the homometric please take note heterometric okay is exclusively
dependent on the muscle fiber length so if you are asked about heterometric that is definitely
equal to your frank sterling's principle what about homeometric any factor that is not
dependent on the fiber muscle length is under homeometric and what is this i told you neural
humoral physical or under homeometric okay the one under with your home okay
heterometric is your front starlings law now frank sterling's law is equivalent to your muscle
tension or muscle length tension relationship so under heterometric that's your frank
starling's law this is the ability of the heart to control the strength okay of contraction because
of the changes in your fiber length so please take note of this let's say this is your ventricle
this is your fiber length and this is the tension now if you add volume if you add blood into the
ventricle which will eventually become your end diastolic volume what will happen is that if
you add volume in the heart then therefore you stretch okay the myocardium so you stretch
the cardiac muscle cells so if you stress the macarthur muscle cell without contraction that is
passive tension and that passive tension is equal to diastolic tension in the heart so when you
say diastolic tension that happens during diastole when the blood moves into the ventricle
okay that is equivalent to your passive tension in the skeletal so passive tension in the skeletal
is equal to diastolic tension in the heart now this is k because of adding volume to the heart
and one should add volume to the heart you stretch the the muscle fiber and then you
increase the muscle length so we call that a diastolic tension equal to passive tension and that
is also this image that in the skeletal that that is directly proportional to the length the more
you stretch it the more or the greater the passive tension that is directly proportional and
different slants language skeletal is that if you still remember say skeletal no chains muna but
before it reaches the resting length that is the time you increase the passive tension dito from
almost start palang my increase and i told you the reason why because there are more
connective tissue okay in the heart than in the skeletal primarily that will uh that will because
this is your fasting collagen tightening these are the the structures primarily okay that
contributes to the passive tension now if you start the muscle to contract you produce active
tension and we call that systolic tension that is your systolic tension now same with same
with your with your skeletal the greater the muscle length the greater the active tension you
produce or the greater the systolic tension and the highest systolic tension is at the resting
length or the optimal length but if you over stretch the myocardium and that happens during
heart failure we're in there are more blood in the heart there are more blood in the heart that
cannot easily be ejected you stretch it then the force of contraction increases but if you over
stretch it then the heart becomes weaker and we call that okay a heart failure so that is your
frank starling's law that is under underheterometric but how about under homeometrics so
we already mentioned this a while ago the nervous the nervous at your autonomic nervous
system so sympathetic increase the heart rate increase the force of contraction and i
mentioned that can also increase the distance ability or the compliance so that is the effect of
sympathetic will your para that decreases the heart rate that decreases the force of
contraction but only the atria because there is almost no innervation in the ventricle okay so
that is the effect okay of your nervous we also mentioned about the humeral so i will just
change this into humoral not only hormonal because hormone is also under your humoral
pain control so these are the substances we already mentioned the catecholamines that
increases the distensibility the force the heart rate through your increasing your cyclic amp
acting on beta adrenergic which also the opposite of acetylcholine because that decreases the
cyclic amp through your muscarinic two receptors but decreases only the atrial force
subcontraction i already mentioned the thyroid hormone thyroxine not only thyroxine but
also that's only four so t3 and t4 glucagon also increases cyclic am b so substances that
increase the cyclic amp can also increase the activity of the heart now i already mentioned the
effect of raspberries on the effect of agents i already mentioned the caffeine remember it
increases the release of calcium from ryanodine therefore that increases also the the the the
force of contraction theophylline just like your glucagon can also increase cyclic amp by the
way digitalis i will mention digitalis later on so temperature temperature can also increase the
force of contraction by the way class i forgot to mention doctor how the temperature
increases the heart rate in the force of contraction plus time high temperature increases the
permeability of ions ions so that increase the permeability of calcium that increase the
permeability of sodium so you can easily depolarize you can easily increase the force of
contraction okay now i forgot to mention about digitalis are you familiar with digitalis are you
familiar with digoxin familiar digoxin this is a drug given to a patient with heart failure
especially if the problem is systolic meaning weakening non-contraction so they give the
digitalis like lanoxin or digoxin in order to increase the force of contraction you know the
mechanism of digoxin digoxin is actually an inhibitor of sodium potassium pump okay why
do you increase the force of contraction if you inhibit the sodium potassium pump look at this
digitalis is an inhibitor of sodium potassium pump so if you inhibit the sodium potassium
pump you can you cannot pump out sodium and pump in potassium so what happens here is
that since you cannot pump out three sodium sodium here accumulates so there is
accumulation of sodium here because you block this one so you cannot easily pump out
sodium so sodium here increases now during contraction you release calcium during
relaxation you sequester calcium here or you extrude calcium through your calcium sodium
exchanger so you can pump out calcium out one calcium in exchange with three sodium but
the problem is since you block this and you cannot extrude the three sodium sodium
concentration increases so sodium outside cannot easily get into the cell so if it cannot easily
get into the cell then you cannot easily pump calcium out of the cell so calcium here
accumulates and that calcium increases the force of contraction clear clear po 19 okay so we
are done with that so digitally so we're done with the homeometry okay now let's go to this
one the bodace phenomenon i already mentioned being braids if you still remember i
mentioned vein braids bain bridge is actually the it is actually the one that states the direct
relationship of atrial volume and heart rate okay what is bone it's bodace is equivalent to trap
or staircase phenomenon in skeletal muscle you increase the frequency of stimulation below
the tetanizing point in that increases the force of contraction same class bodhis phenomenon
states the direct relationship of increasing the heart rate therefore increasing the force of
contraction okay so buddhist phenomenon states that increasing the heart rate into
tachycardia rains results in a greater force of contraction so the greater the heart rate the
greater the force of contraction so this has a positive inotropic effect young bainbridge class
has positive chronotropic effect casino increased donor heart rate if you increase the atrial
volume you increase the heart rate so that is a positive chronotropic effect now autonomous
that leads to a positive inotropic effect if you increase the heart rate bain bridge is the
relationship of atrial volume in the heart rate this one is the relationship of heart rate and the
force of contraction now the same mechanism in the skeletal that as you increase the
stimulation of your heart as you increase the frequency of stimulation to the heart the more
calcium you release it is easier for you to release calcium then the calcium in the intracellular
area increases and that increases the force of contraction another one is the buddhists the
another one is the is the post extra systolic potentiation because i'm imposed extra sicily
which means that there is exorcist premature beat that post extra okay that does that extra
systole or the premature beat or x-ray systole is weak in fact glass is an individual if you have
premature beat that is described as escape pits the ma the heart contracts but you cannot
you cannot feel that because it is very weak but that that premature beat should is followed
by a stronger one yeah i mean the individuals are what you individual because you can really
feel that now but you feel that your heart stops for a while but eventually followed by a
stronger one so which means that premature bit causes a stronger contraction of the of the
succeeding contraction so why because in the post exodus solid potentiation the premature
bit or excess systole is followed by a stronger beat and that premature bit or extra sicily is
perceived by a person as a skip beat why do you increase the contraction of the of the the
following one it's because during premature bit you'll read the release calcium then you have
another bit the calcium is still in your cytoplasm and that will cause the stronger contraction of
the following following a premature bit so this is attributed to an increase the availability of
calcium following the extra systole so this will also lead to a positive inotropic effect so we
are done with bodies and post extra systolic potentiation now how do you determine if the
contraction of the heart is strong or not how will you determine if there is hyperdynamic or
hypodynamic heart i already mentioned ejection fraction right so these are indices these are
indices of cardiac contractility okay now aside from ejection production we also have the so-
called peak dp dt or maximum or peak change in pressure per unit chains in time maximum k
or the peak dp dt is the tangent of upstroke a ventricular pressure pulse and up stroke down
stroke stroke that is the tangent of the upstroke at the ventricular pressure pulse which
represents the maximum okay rate appreciate pressure change if you class your maximum
rate of pressure change there's a okay an increasing pressure so there's a change in pressure
and that is increasing and this is the ability of the ventricle to generate a pressure in that
happens during iso volumetric contraction phase and this occurs just before the opening of
your semilunar valve so which means that the higher this one the better okay the buildup of
pressure which means that the greater the force of contraction so if you increase the pressure
change per unit time then the greater the peak dp dt for example divided inion class so
during isovolatic contraction you increase the pressure this is the normal so you increase the
pressure during isovolumetric contraction meaning the ventricular pressure before it contracts
now if the pressure increase is lesser if the letter c increase it means that you have a
hypodynamic heart for higher unpressured chains it means that you have a hyperdynamic
heart so the greater the peak dpdt the greater the force subcontraction of the heart then the
the more we we call that hyper dynamic heart okay now that is one that is repeat dpdt or
another one i already mentioned index of cardiac conductivity the ejection by the way class i
forgot to mention papala aside from peak dp dt this one i already mentioned this inca in
cardiac cycle if this curve moves to the right i told you if this k curve moves to the right it
means hypodynamic heart because you increase the esb if it moves to the left it means that
your heart is hyper dynamic i already mentioned that in my lecture okay a cardiac cycle so
next another one is ejection fraction so i told you that is the ratio of stroke volume to the end
diastolic volume that is the percentage of end diastolic volume ejected so that is equal to the
ratio of stroke volume over edb times 100 so the greater the ejection fraction the greater the
contractility of the heart the lesser the ejection fraction the lesser the conductivity of the
heart so normally this around 60 to 65 percent okay so young last part not then before we
have a break is how do you measure cardiac output i already mentioned the first one how do
you measure cardiac output you can use cardiac index so all you have to do is determine your
body surface area and then you have to multiply it with three liters so approximately measure
or approximately get your cardiac output another one is the fixed principle not fixed law see
you'll fix los angeles diffusion now the fixed principle okay the computation is all you have to
do is get the oxygen consumption of an individual and then you have to divide it with a
difference of arterial and venous oxygen k concentration so arterial venous oxygen difference
okay which means that the greater the oxygen consumption the greater the cardiac output the
greater the atrial venous oxygen difference the lesser your cardiac output so i have here an
example at resting state oxygen consumption is around 250 ml per minute so that is at resting
state okay so a weight loss weight loss okay so i have here a given oxygen consumption
actually class this is the oxygen consumption at rest so you're resting you're consuming 250 ml
per minute now so 250 ml per minute and in the arterial side the arterial side we have 20 ml
per 100 ml of blood we have 20 ml of oxygen per 100 ml of blood so compare 100 ml [Music]
per a ml 15 m l of oxygen per 100 ml so that is point 15 so is substitute nothing 250 ml per
minute my divided by so 250 divided by 0.05 that is approximately 5 000 ml or 5 000 liters
okay that is how you compute using your fixed method that is coming from the principle okay
whatever is delivered to the tissue that is also the amount that is actually uptaken by okay any
organ okay so the amount of taken then you add the amount that is not okay uh extracted by
the tissue so that's why you have to take oxygen consumption and the difference between
arterial and then the venus okay so we call that i i interpolate electron blood so that is the the
difference between your arterial and in the venus okay now by the way if the if the sample is
coming from the pulmonary area now from the pulmonary area ano casio and venus minus
arterial only if the sample is coming from pulmonary area casing antioxidant artery and
oxygenated eye pulmonary vein so that is one way of getting or measuring your cardiac
output so another one is cardiac index and you can also use the indicator dilution method so i
class etho i will not give this in the exam because it is too complicated but at least you know
that there is an indicator dilution method wherein cardiac output is measured by injecting a
dye tumor injecti let it circulate in your blood so all you have to do is get the amount of dye
injected and you have to subtract it with the mean concentration of the dye in the circulation
and you multiply it with a duration of the first circulation so too complicated though so at
least you know how it is computed using your indicator dilution method or you can use this
you can use doppler echocardiography parashant ultrasonography no that measures the
blood flow in a certain area of the body okay so we have around four ways so fixed principle
indicator revolution method doppler electrocard okay doppler um echocardiography and then
using your cardiac index so we are done with cardio graduated purpose

CVS 4
we will now start with a blood vessel my questions for class this topic is very long with regards
to cardio so bro very long young topic non cardio uh i'm glad that ecg is i know cinema ecg
because if you're going to discuss ecg much longer pasha so if there are if there are as much
as i want to discuss everything in cardo but we only have a uh shorter time so i cannot discuss
all about cardio if there are some topics that i do not discuss just read it and if you cannot if
you cannot understand it then you can ask me okay but if again include cupaditos i can tell
you that uh young electrical is already papano detailed i combined the three books and then
burned in levy and i think i read also some portions in the boron book so combination uh did
you understand mangaka back at 10 come back at 10 12. okay so we'll now start with the
vascular system so this is cvs4 so we will be discussing here okay the different types of blood
vessels so these are the objectives so i will enumerate the different types of blood vessels and
describe its type then differentiate arterial and vein distensibility in systemic and pulmonary
regulation discuss we will concentrate on the structural and functional differences among the
different types of blood vessels describe the micro circulation enumerate the starlings forces
that govern fluid exchange and describe age forces and give the factors that will affect the
different forces also and they discuss the formation of edema and give the factors that lead to
the formation of edema so ito if in case that we still have time then we can now discuss the
arterial blood pressure in the determinants of arterial blood pressure and then the methods
of determining blood pressure so depending on if we still have time then we can have
advanced lecture for for this okay now uh i'll start with the different blood vessels so in the
pulmonary and circulate systemic circulation we have three different types of blood vessels so
we have the veins we have the arteries and we have the capillaries okay so if you will notice
okay young arteries will bifurcate into a smaller a structure and eventually become a smaller
one so we call that the capillaries while your veins will unite and unite and that will become a
bigger veins okay but before that let us take note of hey the the factors that will affect the
blood vessels okay now your blood vessels not in class are okay very sensitive to what so your
blood the inner part of it with okay now let us take note first of the different okay um
structures you know in your blood vessels so uh we cannot compare the capillaries because
capillaries are really different from the arteries and in the veins so young arteries and veins
have similarities no have similarities so one similarity of your artery and then the vein is that
they have the same layers now they have the same layer so the innermost k layer is known as
the tunica intima tuna intima is primarily primarily made up of your weight loss so your your
tunica intima is primarily made up of this single layer of cells so we call that the endothelial
cell so both of them have tunica intima now please take note that your endothelial cells now
are okay are considered one major organelle now i think by now that endothelial cells class
that in endothelial cells are sensitive to what so the endothelial cells lining your tunica intima
are very sensitive to changes in flow rate if the flow of blood is fast or slow now these
endothelial cells are sensitive to that so flow rate another one is that this endothelial cell is
also sensitive to stretch so if you have stretching of your of your blood vessel another one is
that it is also sensitive to the inflammatory mediators okay that are present present in the
blood or the substances in the blood so if endothelial cells are actually activated by changes in
flow rate stress okay and then mediators in the blood okay endothelial cells when activated
of that will cause the release of substances so usually and the realistic substances endothelial
cells are i are vaso substances for example your endothelial cell can release nitric oxide so we
know that nitric oxide is a potent vasodilator and the effect is in the smooth muscle another
one that is being released is the product of [ __ ] so you you discuss that in cell signaling the
product of [ __ ] so you either have prostacyclin or prostaglandin now the process cycling is a
potent vasodilator also but prostaglandin is a potent vasoconstrictor but they also act on the
blood and prostate cycling is an anti-platelet aggregator while your prostaglandin is a platelet
aggregator now this substances will affect the smooth muscle so they're present in the tunica
intima okay another one is okay the tunica media by the way uh in between your tunica
media and tunica intima you have a connective tissue then they're usually elastin and then
collagen now the tunica media are the muscular portion so they are made up of smooth
muscles okay they are made up of smooth muscles okay and this is the one that responds to
the release of your endothelial cells so because endothelials as i mentioned that they release
usually vasoactive substances so the smooth muscles belong to if i still remember i
mentioned that in mass elector the blood vessel smooth muscle belong to the multi-unit type
not the unitary type they belong to the multi-unit type so they do not usually have gap
junctions and they do not usually have pacemaker cells now okay after that the outermost
portion of is a tunica externa that is also made up of loose fibrous connective tissue but it is
also made up of your elastin and collagen and lastly the epithelial cell okay that will comprise
sorcerosa so siguro a major difference in the lung between the artery and the brain and this
one is thicker than the vein and the veins have bulbs but the arteries do not have bulbs okay
so if you look at the okay the smooth muscle okay though i i mentioned some of this during
my lecture but i already told you that the smooth muscle the sources of calcium that will
cause the contraction are the ecf and then the sarcoplasmic reticulum but mainly the ecf so i
told you that the membrane of your smooth muscle sometimes early ketocalchum or they are
made up of voltage-gated calcium channels or they are made up of voltage-gated calcium
channels and i told you these are usually affected by substances substances um wedding
neurotransmitter pudding hormones spreading paracrine substances and that will open the
voltage-gated calcium channel so that will mechanically open your voltage-gated calcium
channel and that that is the one i mentioned no that this is usually uh the excitation
contraction coupling is pharmaco mechanical because the opening is not usually due to action
potential the opening is due to the presence of agents okay putting drug wedding hormones
burning neurotransmitters so once the calcium gets in i told you that that calcium can be a
trigger calcium so it could be a trigger calcium that will trigger the release of calcium from the
sarcoplasmic reticulum or it could bind already with galmodulin or sometimes can depolarize
the cell so once it binds with calmodulin i told you that this will activate the enzyme mlck
because if mlck is activated that will activate the inactive myosin to activation by
phosphorylating it so once phosphorylated your myosin light your your am i using then that
can interact now with actin and then you will have your contraction so how the smooth
muscle relax okay you have to release the calcium from your troponin from your calmodulins
sorry calcium from calmodulin so that your mlck will not be activated so that um the the
myosin will also be phosphorylated actually and the phosphorylation and myosin is because of
myosin phosphatases okay so once it is the phosphorylated then actin will cannot bind with
myosin because myosin is deactivated so that is the reason why this one is thick filament
regulated because you change the myosin so what happens with the calcium so there are two
ways so calcium can be pumped back to your sarcoplasmic reticulum through your circa or it
can be extruded out of the cell via your sodium calcium exchanger or via your calcium atpase
so that is how the smooth muscle they relax so as i said i told you that okay the artery can
bifurcate so the artery will bifurcate into smaller shorter but numerous okay blood vessel and
this will eventually give rise to your capillary and then from capillary it will unite to become
longer and larger and then become the largest gay vein that's your vina haba until it goes back
again to the heart so your cardiovascular system is a closed system so it's a closed system so
let us characterize its type of your blood vessel so i'll start with the arteries so why the
arteries are thick wool okay the arteries are thick wall because this transport blood under high
pressure casey young blood pressures artery is high so since the pressure is high the tendency
of your okay smooth muscles is to hypertrophied so that is the reason why since it transport
blood under high pressure they have thicker walls okay another characteristic of arteries that
they have high velocity flow if you will compare the blood flow velocity in other types of your
blood vessel it is actually faster in your arteries so they have high velocity flow another one
okay it is eight times less distensible than the veins because veins are more distensible okay
than your capillary so less okay eight times less dispensable than your veins and this one
transport blood okay away from the heart so this transport blood away from the heart and
the scary oxygenated blood except the pulmonary artery in the umbilical artery because they
carry the oxygenated blood now another thing the arteries have a fluctuating pressure it goes
up it goes down that is the reason why if you determine the blood pressure in the arteries we
call it arterial blood pressure it is usually written as systolic over diastolic because there are
fluctuations due to the pumping action of the heart it increases during systole but decreases
during diastole so these are the characteristic of your arteries there are three types of your
arteries so we have the large size the large size are the elastic arteries we have the medium
size are the muscular arteries and in the small size are the resistance arteries so but by the
way uh these three types of arteries have the same characteristics so you have fluctuations of
blood pressure they carry blood away from the heart they carry the oxygenated blood i i give
the exception that's your pulmonary artery umbilical artery less distensible high velocity blood
flow but okay let us take note of the specific characteristics so i'll start with the large size
okay the large size examples of your large size okay is your aorta and it's major branches
meaningful major branches and then your uh your pulmonary artery okay so example large
size so large size are known as elastic arteries why because these blood vessels are mainly
made up of elastic tissues that's why they're also known as elastic arteries and they are the
one that conducts the blood into the different parts of the body okay that's why they're also
known as conducting arteries now the major the major component are your elastic tissue and
smooth muscle but there are more elastic tissue now what's the purpose now why god okay
put more elastic tissue in your aorta in pulmonary artery in its major branches it's because the
characteristic of elastic elastic tissue is that they can be stretched they can easily be stretched
but they can recoil remember class that that your aorta receives the whole cardiac output of
the left ventricle and then your pulmonary artery receives the whole cardiac output of your
right ventricle that is a large amount of blood so but it can be accommodated by your by your
um aorta and pulmonary artery because they can easily distend because they are primarily
made up of elastic tissue now the question is will the blood stay in the aorta and the
pulmonary no because they can recoil so once they can recoil they can push the blood into the
different parts of the body and that is the reason why they are made up of elastic tissue
because if elastic tissue is decreased in that area in that is rigid then you will have a very high
pressure during the during systole but they have fluctuations and pressure of course and the
velocity of pressure below the blood flow here is very high now let's go to the muscular artery
also known as the medium size the medium size also known as muscular why it is known as
muscular it is made up of elastic tissue but it is primarily made up of smooth muscle that's
why you call that a muscular arteries now it is also known as distributing arteries because they
are the one responsible for blood distribution into the different parts of the body now the
pressure also here is fluctuating it goes up it goes down depending on the phase of cardiac
cycle and okay of course these are okay exemplified by your manga brachial artery radial
artery ulnar artery popliteal femoral etc okay now another one is the smallest one the small
size arteries are known as resistance arteries they are exemplified by your arterioles so they
are your arterioles they are also made up of elastic tissue and smooth muscle but there are
smooth muscle just like your muscular but difference is that since they have very narrow
lumen so once the smooth muscle contracts it can almost close the lumen so once it almost
close the lumen that can increase definitely your resistance that's why it is where the area
where you have the highest resistance to blood flow that's why you call that the resistance
arteries consofoset sagripo para young grip once the once the tissue needs the the blood
then it opens then once the tissue is inactive it almost closes no so then stop [ __ ] no or
control can do it of your okay vascular system but still the blood flow is fluctuating so it goes
up it goes down now let's go to the capillaries the capillaries are these minotaur blood vessels
you know plus capillaries are only made up of endothelial cells in basement membranes so
they are only made up of endothelial cells in basement membrane which means by which
means that there is no elastic tissue and there is no smooth muscle kayak there is no such
thing as capillary constriction no because they are not made up of smooth muscle they are
not affected by vasoactive substances when they say vaso active substances vasoconstrictor
and vasodilator no elastic tissue no smooth muscle but the it depends on where the capillary
is located some contains type junctions so if they have tight junction they're less permeable
some have fenestrations or pores so pugmy fenestration or pores they are more permeable
than the one than with diet junction but the most permeable are the one with intercellular
cleft okay and they're also made up of parasites but please take note since this one is
permeable this is the area it is the blood vessels that is more permeable than the rest this
where you have the exchange of gases nutrients and other substances and that is the reason
why capillaries are known as exchange vessels so they are known as exchange vessel now it
has the largest total cross-sectional area why they are very small but you have millions of
capillaries if you get the total cross-sectional area they are the largest so they exit 6 the it is
very thin so it is only around one micrometer thick now because of the presence of tight
junctions penetrations and enter circular cleft so we divided the capillary into three so we
have okay so we have um uh the continuous type sonoma pontine was type of capillary so
ima continuous type of capillary are the capillaries that have tight junction in between their
endothelial cells so if they have tight junction in between their endothelial cells then this is
the least permeable and these are the capillaries present in the brain in fact the thai test is in
the brain that is the least permanent vocabulary but cerebral capillaries um brain we have
that also in the muscles so that includes already the heart you know the heart then the
skeletal muscles that is also present in the lungs okay your pulmonary capillaries and then the
muscular capillaries in the skin so you have cutaneous capillaries so we have they have
continuous time now other areas have fenestrated type you will see the fenestration here you
have pores that's why this one is more permeable than this one so we have we call that
fenestrated capillaries and these are usually the one um present in the kidney so we have
renal capillaries they're fenestrated another one in the git so we have intestinal capillaries so
basamagasa git they have penetrated diet now the sinusoidal type are the one with
intercellular glare so aside from bigger pores or fenestra in between the endothelial system a
gap so we call that intercellular cleft and this is the most permeable capillary bed actually is in
the liver so liver has the most permeable um capillary bed but this can also be observed in the
spleen this can also be observed in the bone marrow and some uh in the lymphoid tissue and
some endocrine glands or some endocrine glands so in fact if the young conductivity [Music]
and then this one okay so these are the hydraulic conductivity of capillaries in the various
parts of the body you will know this class that the least permeable or the one with the least
conductivity okay is your brain actually class the type junction present in the in between
endothelial cells will form the blood-brain barrier so this this constitute the blood-brain
barrier in the in the brain so that substances cannot easily pass through okay the capillaries
except the cbo because it is the only area in the brain without the blood-brain barrier cbo is
circumvallate organs and i think we have four i i know that this will be mentioned in cns what
is that for posterior pituitary does not have blood brain barrier so posterior pituitary area
posterema in the in the middle oblongata another one is subfornical organ okay subfornical
organ and then the other one is the the ovlt organum vasculosum ablamina terminalis so that
those are the four areas in the brain without the blood brain barrier which which means that
this is the least from your capillary bed except those four no because they do not have blood-
brain barrier so the least permeable is the brain followed by the skin followed by the skeletal
followed by the lungs then you have your heart for the fenestrated type we have the git and
you have the kidney and then for the sinusoidal type you have the liver you have the bone
marrow the lymphoid tissue and some endocrine organs okay so those are the different types
of your blood vessels or i mean capillaries or the capillary is also classified into two this one
this one the major connection between the artery and then the vein that's your arteriole and
then the venule this portion of your capillary is known as the main keto fair so we call it the
mean thoroughfare now this k area are the true capillaries okay what is the importance of this
for example the the the tissue is inactive let's say for example the muscle is in relaxed state
so they the muscle does not need a a greater amount of blood flow you know class this one is
okay this area is the one that is open so there is continuous flow because a main thoroughfare
if the organ is or the tissue is inactive so you only have the opening of the main thoroughfare
now the the true capillaries are close because remember there is no smooth muscle in the
capillary not the capillary but this one so we call that the pre capillary sphincter or known as
the meta arterioles no meta arterioles they can contract they can close or the pre-capillary
sprinkler not the capillary itself but if the organ becomes active or the tissue becomes active
all are open so they they have blood flow in the menthol affair and in even the true capillaries
okay now let us take note now of the veins okay so young veins in contrast with the arteries
they have thinner walls so that their wall is thinner than your artery why because this
transport blood and i i forgot to mention glass the capillary in the capillary there is no
fluctuation of pressure because the blood flow no longer pulsating artery pulsatile and blood
flow my fluctuation of pressure but in the capillary it is already continuous there is no
fluctuation of pressure already okay so that is the reason why if you get the pressure okay in
the capillary you just you just say 25 millimeter mercury a 35 millimeter mercury in the artery
that is equal to in the capillary you only have one pressure okay same with the veins okay so
veins are thinner because this transport blood under low pressure in fat class the blood
pressure is lowest in the vein it is lowest in the vein and this one is more distensible than your
arteries sabinatin eight times more distensible than your the arteries venus pressure is 10
millimeter mercury and the blood flow is also continuous it is not volatile but one unique
characteristic of your vein is they have bulbs and these bulbs are highly concentrated in the
lower extremities but there are veins that have no bulbs in what are these veins these are the
largest and the smallest veins the largest are the vena cava okay and then the smallest are the
venules okay so no bulbs but the walls they are slightly thicker than your capillary okay so if
you look at the differences by the weight glass this is the one with the largest lumen this is the
one that is easily distensible so they can contain large amount of blood in fat class this is the
reservoir of blood in our body if you do not need the blood they are stored in the veins more
than 50 percent of the the blood is present in the veins that's why veins are known as [Music]
[Music] so uh if if artery they have elastic they have elastic or conducting muscular or
distributing they have resistance vessel in capillary they have exchange vessel veins are omg
[Music] capacitance vessels because they have a greatest capacity to contain large amount of
blood [Music] compliance okay so it looks like this you see the major differences so they have
narrow lumen but thicker okay small less thinner then they become larger again than thin so
important by the way i will discuss this in cvs6 now now let us take note of the structural and
functional differences of the various blood vessels actually class this is one of the favorite
questions in board reviewers so some of the board exam favorite questions usually my
question is in the vascular system which has the largest lumen which is the thickest wall which
has the greatest amount of blood which is the highest blood flow velocity so let us take note
of the differences uh for example considering the lumen diameter okay so paganito structural
and functional differences of various blood vessels but lumen diameter definitely it is largest
in the vein followed by artery smallest in the capillary please take note of blood largest in the
vein followed by artery smallest in the capillary look at the vein you know vein simply you
have to compare naman vina cabba with aorta so they thought trees and teammate 30 to 2.5
if you will compare the medium size you have to compare it also with the medium-sized vein
must greater talagang loom in diameter if you will compare an arteriole compare it with the
venul but look but generally the veins have largest lumen than the artery but pinocchio is a
capillary because micrometer micrometer it took us a centimeter okay so vein greater than
artery greater than capillary but gloom in diameter pagul thickness you will notice wall
thickness very obvious that the thickness is greater in the arteries greater than vein and vein
greater than capillary so if you will compare the aorta because they are only made up of a
single layer of endothelial cells and basement membranes so no smooth no no smooth and
then no elastic artery oh yeah glumen diameter in wall thickness but what about blood
distribution weather systemic yawn and by the way there are more blood in the systemic than
in the pulmonary overall they have the same i said overall blood flow that is the blood flow
that is circulating that does not include a static one but you include a static one much greater
talaga and blood volumes are systemic than the pulmonary but if you will compare okay uh
the the amount of blood it is really greatest in the vein that's why you call that capacitance
vessel more than 50 i got this from other books some books said it's 64 the other one 54 but
anyway greater in the vein followed by arteries including the arteriole in the least is in the
capillary but please take note that 5 in the capillary is the most important blood why this one
is the most important blood because that is the one involved in the exchange of gases and
new trends okay now but class happen in specified language specify let's say not not you do
not compare the artery the vein and the capillary but i said ayurta benacaba arteriole capillary
the list is in the artery you can see only one to two percent is in the artery but it is included in
the arteries so that is your blood distribution so we're done with that if you look at this pie
graph you will see that more than 50 percent of the blood is present in the vein then followed
by arteries and then followed by the smallness is in the capillary okay so we're done with
lumen diameter wall thickness blood distribution let's go to the total cross-sectional area so i
told you already if you are considering the total cross-sectional area definitely capillaries can
have the largest because you have millions of capillaries so largest capillary followed by veins
followed by veins in facts among the veins largest telogen venules the the smaller the the
smaller cassette the the the smaller the the more numerous and then the greatest the total
crescessional area so if you will compare uh total cross-sectional area is largest in the capillary
followed by the veins and among the veins venules have the largest followed by the medium
size and then the great veins the vena cava have the smallest now the smallest total cross-
sectional area is actually your arteries in fact the smallest is in the aorta okay now annoying
that is a total cross-sectional area what about if we will consider the blood flow velocity
blood flow velocity which has the fastest blood flow velocity the clue is a blood flow velocity is
inversely proportional to your total cross-sectional area the larger the total cross-sectional
area that's river the flow of water is slower but the narrow area in the river then the velocity
is faster so in this case your blood flow velocity is the mirror image of your total cross-
sectional area so that since capillary has the largest total cross-sectional area it has the least
flow velocity another one is the aorta has the smallest total cross-sectional area therefore it
has the fastest blood flow velocity okay so blood flow velocity greatest in artery followed by
vein followed by capillaries um slowest a capillary next okay um variable that we have to
consider or parameter aside from wall thickness lumen diameter blood distribution uh total
cross sectional area blood flow velocity the pressure so the blood pressure remember that the
blood pressure is actually exerted by the pumping action of the heart okay the more it is
nearer to the heart then the higher the pressure so considering this now considering this look
at this one ampina can you rest is actually your aorta so aorta has the highest blood pressure
followed by the medium size and followed by the smallest size you will notice that the
pressure here is fluctuating you have volatile pressure that's why you have systolic over
diastolic but the thing is a capillary it is already continuous actually started with the arteriole
the the the the distal portion of your arteriole then that becomes already continuous so there
will be no fluctuation of blood pressure here so highest blood pressure is in the artery
especially your aorta followed by capillary then followed by the veins lowest pressure and
then davina has thus paid the lowest pressure actually it started with a pumping action of the
heart so usually 120 millimeter mercury so usually i mean arterial blood pressure and
manganese and 95 millimeter mercury when it go once it goes back again to the heart by your
vena cava the pressure is almost zero but as i told you already that in the in the pulmonary
circulation okay you look at the the pressure in the systemic circulation it is really higher than
your pulmonary that's why i said pulmonary is a low pressure area while systemic is a high
pressure by the way glass i mean that the more the the more proximal it is okay to the heart
the higher the pressure okay like for example is the ascending followed by arch and followed
by ending now please take note of this that is if we do not consider gravity so if you do not
consider gravity this one is true if we will consider gravity class if we will consider gravity it is
already different like for example sabiko without gravity ascending is the highest pressure
because it is the one more proximal to the heart followed by arcs followed by descending by
the way class if you consider the gravity the highest is in the descending why because okay the
the more if the blood vessel is above the heart pressure is decreasing if the pressure is below
the heart pressure is increasing actually class you can compute for this for example if you
have if you have a paul actually class you can con compute let's say class will get not the not
the arterial blood pressure the mean average na so average systolic diastolic i will i will i will
uh teach on how to compute for the mean arterial blood pressure halimbawa class kalimbawa
the mean the mean uh arterial blood pressure is 100 millimeter mercury at the level of the
heart so you mean arterial at pressure is 100 millimeter mercury that is the average pressure
in all the segments of arterial tree so the average pressure is 100 millimeter mercury converter
that is the average my question is what is the arterial blood pressure of a vessel and 20
centimeter below the heart what could be the mean arterial blood pressure above vessel
centimeter below the heart if the mean arterial blood pressure is one hundred so on
gangovenulum class is this for every one centimeter distance from the heart okay that is
equivalent to 0.77 millimeter mercury value so 0.77 for every centimeter now since i
mentioned 20 centimeters so what will you do you multiply so for every one centimeter 0.77
since i mentioned 20 centimeter above and below so more or less 14. i'm about 15.4 let's go
15.4 what will you do so you computed 20 centimeter away from the heart whether above or
below you you have a value of 15.4 so what will you do okay you're going to subtract that
15.4 to 100 so but above the heart all you have to do is okay subtract that 15.4 to 100 so 100
minus 15.4 so that is equal to uh 84.6 yes okay so the heart so meaning that the the blood
vessel heart will have amine arterial blood pressure of 84.16 with the blood vessel 20
centimeter below you have to add young below the heart magic is 114.6 i 115.6 so much
higher and pressure back below the heart because you have a greater effect of gravity but
when i asked that question in the exam if i did not mention about gravity then i mean i mean
that the highest pressure is in the aorta okay because if i will ask you about the gravity i will
mention that in the exam if it is not mentioned meaning i will not consider the gravity now
the last one that you have to consider is the resistance to blood flow resistance to blood flow
so we're done with blood distribution lumen diameter thickness blood flow velocity total
cross-sectional area blood pressure no what about the resistance to blood flow ganito pujan
class you will notice class that when the blood flows from the aorta what did you notice when
the blood flows from the aorta blood pressure goes down it decreases so that the pressure in
the arch is different from the pressure in the ascending is different from the arch it's different
from descent being different from break it goes down it slowly goes down in fact glass in the
vein it is the lowest because the pressure drops the reason is that the pressure decreases as
the blood moves to the periphery because the blood meets resistance so which means that
the greater the fall in blood pressure it only means that the greater the resistance so let us
take note of this adito class aorta less unfollow pressure almost flat tian so lesser and
resistance but in the medium size measure greater neon fall so much greater than resistance
if you look at the arteriole this is thus it has the steepest fall you know my pinnacle rapid fall
and that is the reason why uh arterioles are the resistance vessel sorry the highest resistance
is actually present in the arteriole followed by your capillary followed by your venule then you
have the medium size and then you have the vein so if you look at here the fall in your blood
if you specifically mention the artery highest is in the arteriole okay followed by capillary
followed by benjal but if you will compare in general artery capillary and vein shampoo my
pinnacle highest resistance is in the artery specifically your arterioles followed by capillary
with the highest resistance followed by the vein but in the vein the highest fall is in your
venule so those are the different k [Music] so you know the reason why i look at the camera
you are really listening and you are taking down notes no so good signions always even if we
are online we have online lecture okay because you're already medical student no please
listen please take down notes no if you are confused you can ask the lecturer for clarification
please do that you know if during my evaluation you know young evaluation because among
students i'm glad no i'm very happy that i get good evaluation from the students evaluation
give difficult exam now somebody had give difficult exams so one time face to face i told the
students i think it about last year or young previous but fabico you know i got my evaluation
and there are two important comments for me so i asked the student is it right is it really true
that i give difficult questions [Music] it's not my trip no no i will give difficult questions now
the reason why i give that questions because i really want to evaluate if you really understand
my lecture or not now the reason i did not change that despite my my evaluation young
previous graduates once they once they i know once they approach me no but we see each
other in the hospital after the board exam you know islam and commentary you know doctor
when i was a medical student when i was first year medical student i really don't like her
questions no you know i really cried you know i read a lot but sometimes i failed i really hate
that but when i took the board exam and during my clerkships i've been assaulting that is the
time i really appreciate your questions have been please doctor don't change that please
don't change that because we are forced to study because of that so sorry i will not change
that [Music] i will not change that another thing another comment dr gomez gave a very long
lectures having a give a very long lecture then i said you are a medical student this is medicine
medicine have long lectures because we really want to understand the principle sabiko and
that is the reason why i asked you class i asked your class please have that very long patience
no dappatmeronkang patience in in in listening to a very long lecture because a bug shorter
lecture that is not medicine agree agree clear okay say actually class i received i received just
i think a week ago i received a message from a student we are not close uh and at that time
not online you know class and message yeah overwhelming then sabine hi dr i just want to
say thank you so much for all the learnings that you gave us during first year in physiology
because it makes pharmacology easier for me on the bus you know when i lecture so always
take note of that this in preparation for your pharmacology medicine and pathology okay so
okay let's move to the next one the vascular distance ability actually class distance ability is
very different from compliance now okay because the sensibility is just stretchability but
when you say compliance it is stretchability plus the recoil recoil so that is the reason why
vascular distensibility is defined as a change in volume per unit change in pressure but you
have to consider the original volume for example my vessel is okay my vessel has 10 ml
volume a 10 million volume when applying one millimeter pressure when i apply one
millimeter pressure okay it increases to 11. so what is the change in volume the change in
volume is from 10 to 11 so i have one ml chains divided by the pressure that i apply one
millimeter but since i consider the original volume i have to multiply this with the original
volume so what happens that that is one ml k divided by is 0.1 per millimeter mercury okay
an answer nothing or 10 millimeter mercury now let us compare now the distance ability of
the veins and then the artery so i mentioned that veins are eight times more distensible than
your arteries so i mentioned that veins are more distensible than arteries so that is true veins
are more distensible than arteries is it in the systemic and in the pulmonary circulation both
which means that both in the systemic and pulmonary circulation really veins are more
distensible than arteries but let us take note individually like vein distensibility which is more
distensible the veins in the systemic or the veins in the pulmonary plus they have just they
have the same distance ability the systemic veins have equal ability with the pulmonary veins
but with arterial distensibility pulmonary arteries are more distensible than systemic arteries
that is the reason why i told you that in the pulmonary area since arteries are more
distensible than the systemic they have lesser resistance therefore they have lesser pressure
than your systemic clear puyonha when i mentioned about uh resistance in the systemic and
in the pulmonary artery i mentioned that arterial vessels are more distensible i did not see all
vessels i specifically mentioned arterial i didn't mention about vein because the distensibility
of the pain is the same in the systemic and pulmonary now let's take note of the compliance
compliance is also changed in volume per unit change in pressure but i did not consider the
original volume you just remove the original volume just consider the change in volume per
unit change in pressure that is compliance okay so compliance therefore is distensibility times
the volume okay because you do not consider the original volume in your okay in your
compliance so if you will now consider the compliance you will notice that compliance sub
systemic vape is 24 times greater back it 24 times not eight times because eight times is only
the distance ability so since it is distancibility times the volume and then the volume of your
vein is three times greater than that of your artery and that makes it 24. so the compliance of
systemic vein is 24 times than that of corresponding artery because it is eight times more
distanceable in a there's a volume of three times as great as your artery upon compliance
times now the question is this what will affect extensibility in the compliance it depends on
the substances that either dilate it or constrict it and the most important thing is the
autonomics because sympathetic stimulation okay generally cause vasoconstriction but not all
vessels so generally it will cause vasoconstriction so vasoconstrict invested and volume
decreases so look at the volume it's low but the pressure is high because once you decrease
the volume you decrease the radius the resistance is high then the pressure is high compared
to your parasympathetic parasympathetic causes um vasodilation so therefore volume
increases with lesser increase in pressure pero class dito i got this from ganong i got i think i
got this from ghana or gaiton you will not see here any parasympathetic you will see here
sympathetic stimulation and sympathetic inhibition you do not see in the blood vessel
parasympathetic why because there are some books that claim that blood vessel is exclusively
innervated by sympathetic and i think one that claims that is gaiton no that claims that it is
exclusively innervated by sympathetic domicolinergic portion so my cholinergic portion okay
my questions for my question spots of indistensibility and then compliance before we go to
the micro circulation any question my questions okay if if none let us proceed with micro
circulation so i know have a deep breath okay and then relax before we will proceed with
micro circulation now it depends if i can finish the micro circulation at 11 40 plus then we'll
stop with micro circulation so if i will finish that at pressure because he's short short lung and
arterial blood pressure now so definitely we will end before 12 we will end before 12. lecturer
class if i am the lecturer don't don't count my slides always expect that we will end before uh
okay so let us start with microsoft microcirculation microcirculation is actually the the
circulation in the capillaries where you have exchange of nutrient in gases so we will be
considering here the capillaries so you have your continuous we have your fenestrated and
you have your sinusoidal type this is your main thoroughfare and these are your true
capillaries now what is the characteristic of your capillary you have actually class 7 book
millions of capillaries but i think i got this from ganon and gangnong said you have 10 billion
capillaries you know sometimes i also asked how did they count the number of capillaries no
parang did you really believe that there are 10 billions billions count numbers now let us just
believe no means so anyways you have billions of capillaries and the that is the reason why
the total cross-sectional area okay is the greatest no dito and total cross-sectional area is it
exists i've been at 6 300 but anyway don't worry i do not usually give values in my exam you
will notice that my exam does not usually contain values unless that value is very important
now so you know why i did not usually give values in my exam when i was a medical student i
hate memorizing value so what i hate during when i was a medical student i do not usually uh
do that now okay so 10 billion capillaries total cross-section total thickness is 0.5 micrometer
total cross sectional area is 500 to 700 micrometer internal diameter is 4 to 9 micrometer you
know plus the internal diameter is almost the size of the red blood cell and that is the reason
why the red blood cell do not red blood cells do not pass the capillary in groups they pass the
capillary in single file and they should be deformed so that they can pass that is the reason
why um our pieces are very flexible okay so blood flow is non-volatile so there is intermittent
vaso motion in the wind it depends not the width of the intercellular cleft depends on the
area where it is present no so why this in the liver so that's your capillary see the fenestration
here okay now the circulation in that area in your capillary is known as the microcirculation
and i told you this is the most important circulation it is a purposeful okay it has a purposeful
function and the function is to transport nutrients in oxygen to the tissues and remove the
waste products and carbon dioxide from the tissues now the question is this how is this
accomplished how the transport of nutrients in oxygen is going to the tissue and how the
transport of waste product is from the tissue going to the blood now this is due to what uh
what transport mechanism mango immune slide go you should know that what transport
mechanism is utilized by substances inside the blood vessels diffusion simple facilitated
osmosis filtration primary active secondary active co-transport counter transport vesicular
endocytosis exocytosis paracellular trans cellular so here since this is driven by hydrostatic
pressure it is filtration but you are right because filtration is also diffusion so only that this is
driven by hydrostatic pressure so the same parent that the that the diffusion rate or the
filtration rate is equal to negative negative means that the movement is from higher to lower
okay directly proportional to diffusion coefficient just change the diffusion coefficient to
filtration coefficient so just change this to filtration coefficient and then the area so which
means that if you increase the filtration coefficient in the area you also increase the filtration
now instead of concentration gradient put here pressure gradient now pressure gradient and
of course inversely proportional to the thickness okay so that if i'm going to ask you which
substance can easily pass the capillary what substance by filtration the lipid soluble because
they are permeable so the lipid-soluble substances can easily directly through the capillary
membrane examples are your oxygen in carbon dioxide so very same polynomial okay lipid
soluble now the next one is followed by the non-lipid soluble or the water soluble substances
that can easily diffuse like water like electrolyte like glucose okay and lastly the one that
cannot pass the pores the larger water soluble in charge substances like proteins and
polypeptides this is the only substance that will that undergo filtration or diffusion they
undergo vesicular transport so they undergo endocytosis or exocytosis because they cannot
pass the pores okay so in this case it is inversely proportional to the molecular weight or the
ratios so which means that the greater the molecular weight or the radius the lesser the
permeability okay so the lesser the permeability that this is the reason why and pinnacle
permeable early soluble substances peripheral things are water soluble substances water and
pineapple permeable because this one is small and uncharged small enough charge followed
by the sodium chloride though this one is small but charged cyber casing booklets must
permeable and glucose aca glucose needs a carrier they need a carrier and that is the reason
why they become less permeable without the carrier glucose can easily diffuse than
electrodes because they are uncharged but let us follow this because we will consider the type
of transport mechanism okay now how it is accomplished that microcirculation that exchange
of gases and nutrients is accomplished by the presence of starlings forces so we call that
capillary fluid shift okay so the shifting of fluid okay across your capillary so capillary fluid shift
the rate of filtration at any point okay along the capillary depends upon the balance of forces
called the starlings forces across the capillary k wall these starlings forces are made up of two
hydrostatic pressures and two osmotic pressures what are this k uh hydrostatic pressure so if
the movement of fluid is out of the vessel so if the movement of fluid and substances is out of
the vessel we call that filtration now the pressure that favors the movement of fluid out is
known as total filtration pressure so again it is known as total filtration pressure these are the
pressures that move the fluid and substances out of the vessel there are two forces here the
first one is the capillary hydrostatic pressure meaning the pressure in the capillary area this
capillary hydrostatic assay class pushing an effect but osmotic pressure pulling an effect so
hydrostatic pressure capillary hydrostatic pressure push the fluid out of the vessel so we call
that capillary hydrostatic pressure now the tissue colloid osmotic pressure attracts the fluid
out so it open capillary hydrostatic pressure pushes the fluid out okay tissue osmotic pressure
attracts the fluid out so both of them are known as total filtration pressure now what about
the total absorption pressure these are the pressures that moves the fluid into the vessel
there are two the plasma colloid osmotic pressure attracts the fluid into the vessel and then
the tissue hydrostatic pressure pushes the fluid into the vessel so you have these two types of
pressure now let us characterize its pressures i'll start with um in the wedding mcplay okay
sabine filtration okay filtration pressure filtration pressure filtration is equal to kf which
means that the greater the kf the greater the filtration then plus i times the the the difference
between the capillary hydrostatic pressure in the tissue colloidal but anyway what we
subtract is this one a capillary pressure subtract it with the plasma colloid osmotic pressure
then minus these two pressures in then the effect is if you uh if you get the difference you call
that the net filtration pressure so what is kf kf is directly proportional to filtration kf is
determined by your or filtration coefficient i change this to filtration coefficient okay so what
is kf what is filtration coefficient that is primarily affected by capillary permeability and total
cross-sectional area which means that the greater the total cross-sectional area the greater
the kf the greater the filtration the greater the capillary permeability the greater the kf or
filtration coefficient the greater the filtration please take note if you're asked what what are
the major determinants or factors that will affect kf permeability in surface area so once they
are both increased you both increase the kf you both you increase filtration once decrease
decrease kf decrease filtration so we are done with that let's go to capillary hydrostatic
pressure capillary hydrostatic pressure is the pressure of the blood that push the fluid out of
the vessel what are the factors that will affect capillary hydrostatic pressure remember that
pressure is coming from arterial blood pressure pagnasa artery arterial blood pressure once
once it goes to the capillary that becomes capillary hydrostatic pressure so if if the arterial
blood pressure is high therefore the capillary hydrostatic pressure is high so one determinant
of capillary hydrostatic pressure is arterial blood pressure another thing it depends on
arteriolar resistance so before it becomes a capillary you have an arteriole here how do you
increase arteriolar resistance constrict it once you constrict the arterioles by the weight class
in the blood vessel once you have constriction before the constriction yin young higher
pressure after the constriction lesser and pressure so that is the reason why if there is
increase in arteriolar resistance by vasoconstriction what happens with the capillary
hydrostatic pressure it decreases so because it is okay after the constriction so arteriolar
resistance by vasoconstriction decreases capillary hydrostatic pressure once it dilates it
increases capillary hydrostatic pressure okay vice versa now what about venular resistance
what happens if you have venular constriction before so what happens with the capillary
hydrostatic pressure it increases so opposition arteriolar constriction decrease and capillary
hydrostatic pressure perpendicular constriction increase in capillary hydrostatic pressure
another one is the venous pressure pugmatas and venus pressure increase the lung venular
increase the non-capillary hydrostatic pressure so we are done with the factors that will affect
the capillary hydrostatic pressure arterial blood pressure arteriolar resistance venular
resistance and venous pressure now please take note of this since this is your capillary you
have the capillary hydrostatic pressure so this is your this is your capillary i this is your
capillary okay so you have here the pressure sabina and pressures are capillary once it goes to
the vein pressure drops so that the pressure in your okay arteriolar end of your capillary is 35
it decreases to 25 it decreases to 13. so therefore class this is the only pressure that varies
along the capillary so it decreases from the arteriolar side to ventilator side this is the only
pressure that k changes okay that is your capillary hydrostatic pressure now let's go to let us
go to your okay um hydrostatic pressure capillary hydrostatic pressure minus okay because
they are they are opposing pressure okay this hydrostatic pressure now what will affect the
tissue hydrostatic pressure tissue hydrostatic pressure is primarily affected by solutes in the
interstitium because the solutes in the interstitium can push the fluid into the vessel so
usually glass and tissue hydrostatic pressure is sub-atmospheric or negative it is sub
atmospheric meaning lesser than your atmospheric pressure or negative okay like in the
subcutaneous tissue except positive telegrams are kidneys and liver in the brain the rest
meaning lesser either zero or lesser okay so except in the kidney in the liver in the brain so
we know already what is kf we know already this one we know already this one so they are
opposing so you have to subtract this now what about the plasma colloid osmotic pressure so
what about the plasma colloid plasma collet osmotic pressure are exerted by proteins in the
blood not only proteins but solutes in the blood but greater casital effect on protein so what
are these proteins in the blood so we have albumin we have globulin and other proteins but
the most important protein that exerts your osmotic pressure and that becomes your oncotic
pressure an osmotic pressure exerted by large molecule like proteins we call that oncotic
pressure is the albumin no albumin by the way class tissue hydrostatic pressure does not vary
so it does not decreases that it does not increase so same thing along the capillary same with
pro same with plasma colloid osmotic pressure the same denial because you have the same
con k what the same protein content okay and lastly the tissue colloid osmotic pressure so
what is this of color okay what is tissue colloid osmotic pressure sorry plasma colloid osmotic
pressure so a plasma quality pressure are the proteins and solutes so proteins exert out of 28
nine millimeter mercury and that is also the one that uh that um explains the donor effect in
your cell lecture and the most important k protein is albumin now what about the tissue
colloid osmotic pressure that is the one that will attract the fluid out that is also due to
proteins and solutes in the interstitial they can also attract substances but bucket eight lung
eight millimeter mercury a casino proteins cannot easily move out of the vessel hindi matala
usually move out of the vessel so proteins in this area are very small in amount that's why they
can only offer 18 million eight millimeter mercury so we are done with this forces now forces
so let us stay considered now of okay this one so etobo upon your own i cannot in the
occupating mug drawing or any way or imagination only imagination so assuming that there is
a capillary here so capillary here capillary and assuming that this area is your capillary this is
on the arteriolar end and this one is on the venular end so let us consider the forces so
arteriolar end glass and total filtration pressures arteriolar end is 43 bucket 43 casing capillary
hydrostatic pressure 35 and t so call it osmotic pressure eight so total filtration pressure that
moves the fluid out so total 43 let us take the opposing force the total reabsorption pressure
tissue hydrostatic pressure only one in some areas of atmospheric or negative plasma colloid
osmotic pressure 25 so i'm totally 26 so therefore class in the arteriolar end in the arteriolar
end in this area filtration is greater than absorption because total filtration is greater than
total reabsorption so 43 versus 26 so what happens if the blood is flowing in the arterial side
it is either coming from the the lungs the aorta or it is coming from the git so loaded ion class
non-nutrient in oxygen so it is really correct that filtration should be greater so that you can
you can push the fluid out because it contains a lot of oxygen and nutrient okay so more on
filtration in fact the net is 43 minus 26 most of the fluid are being filtered because filtration is
greater than the absorption okay let's go to the venular end so if the if the net here is
filtration what about the venular end look at the venular end the total reabsorption pressure
is the same 26 because the same tissue hydrostatic pressure the same and plasma colloid
osmotic pressure why is it that from 43 it becomes 23 it is because this one is still the same
this one varies still remember that once the fluid this one once the fluid moves along the
capillary the pressure decreases so instead of 35 it is already 15 so you add 28 then the
filtration is only 23. so what happens here is that you filter the fluid in this area you reabsorb
the fluid in this area because much higher telaga and reabsorptions of vanilla end the net is
only around three three so internet so bbc being glass of angular and total reabsorption is
greater than total filtration okay that is the reason why arteriolar your filter cell venular you
reabsorb now okay now is it really correct that you have to re-absorb fluid here yes you have
because you have to move back the carbon dioxide to the blood so that it will go to the lungs
and you have to get the waste product to move it into the kidney so you filter here you
reabsorb here okay filtration 17 17 so very high young pressure difference young reabsorption
doctor is only three that is 17 filtration only three in angry absorption so it means that more
fluid will be retained in this area because the net effect of reabsorption is only three
millimeter mercury so much greater and fluid energy filter plus there is no problem so
pressure or nothing there is no problem if there are more fluid filtered but less or reabsorbed
because the net uh pressure is only three that excess fluid that is being um filtered is
reabsorbed by lymphatic so that is drained by the lymphatic and lymphatic move it again to
the veins so wala talagang na na accumulate the fluid because you excess fluid that is being
filtered not reabsorbed is drained by the lymphatic clear po clear clear okay so siguro that
opposite we will just finish this micro circulation the rest will be discussed and next meeting
no new arterial blood pressure because your arterial blood pressure is very important casione
that is very important you are already tired that you cannot absorb the factors that will affect
arterial blood pressure so mass maganda fresh no so now this one the filtration the filtration
in that area or the diffusion in that area could be flow limited or diffusion limited what is flow
limited what why do you call that flow limited now if the diffusion is determined by flow like
for example i'll give an example i for example carbon dioxide it's a carbon dioxide glass is a
carbon dioxide lung lung pressure is 46 in the tissue then 45 so you only have one difference
one pressure difference so that when the blood moves you can easily equilibrate the pressure
so once they both become 46 there will be no diffusion so that what is important now in this
element equilibrate is this the flow should be faster so that once they equilibrate they will be
pushed by the blood then you have another 45 once it becomes 46 they will be pushed again
then for you you give again another 45 then push again once it becomes 46 so what is
important there is the diffusion is actually determined by the blood flow that's why you call
that flow limited so when you say flow limited if the total diffusion is increased by increasing
the blood flow what about diffusion limited when you say diffusion limited the transfer of
substances that do not reach the equilibrium with a t-shirt during the passage for example
you know cluster oxygen there is no need that the blood flow is faster because in the tissue
you have around 45 in the blood you have around 95 so even if the blood flow is slower you
cannot easily equilibrate with the blood because the pressure difference is very high that's
why we call that diffusion limited so the transfer of substances do not reach equilibrium easily
with the tissues during the passage of your capillary so those are the best examples of flow
limited and diffusion limited okay how can you develop edema what is edema the last slide
what is edema edema is when the fluid accumulates in the interstitium for example more fluid
is being filtered but less is absorbed then the fluid accumulates in this area then we call that
edema so we call that edema or in in layman's term manas so what are the cause what are the
causes of edema i'll start with this because this one is easily we can easily explain this one
inadequate limb flow so what happens remember excess fluid that is being filtered is drained
by lymphatics what happens if you have inadequate lymph flow for example there is
obstruction so if there is obstruction in this area you cannot drain the excess fluid in this area
so you will develop edema so one best example we call that lymphatic obstruction or
inadequate limb flow the best example is have you heard of elephantiasis or filariasis
elephantiasis or filariasis is caused by bacteria that is actually transmitted by mosquito
especially mosquito that resides in abaca plantation that's why it is very common in albay
where you have abaca plantation now that bacteria once you in you are beaten by mosquito
with that bacteria that bacteria will cause edema or that will cause lymph adenitis so there is
inflammation of the lymphatic tissue so if it is not resolved let's say for example it is not
resolved the the the the inflammation is not resolved that is converted to fibrosis so once it
becomes fibrotic it will obstruct lymphatic flow and that is the reason why if the if the
affected area is your lower extremities you cannot drain the fluid in that lower extremities so
that the lower extremity enlarges because in there is enlargement of your lower extremities
because of k because of edema and it resembles the the the feet of elephant so you call that
elephantiasis or filariasis so agrippocalyon a lymphatic blood flow agree agrippo okay now
the next one the next cause is this the effect on kf remember the kf the kf is affected by
permeability in surface area if the kf is high filtration is high if filtration is high not
compensated with absorption in lymphatic drainage edema will happen so how do you
increase the kf by increasing the capillary permeability and how do you increase the capillary
permeability by releasing vasodilators the capillary becomes very permeable okay and what
are these inflammatory mediators so these are the examples once you release substance p
histamine radicane in other related substances or kindness they they cause vasodilatation
then they cause increased permeability so you increase the kf now another one if you
decrease the osmotic pressure like the plasma colloid osmotic pressure that is very common
that is the pressure that moves the fluid into the vessel because of proteins the proteins like
albumin attracts the fluid into the vessel so what happens what will cause the edema if you
have hypoproteinemia or decrease plasma protein level in protein in the blood is decreased
like you have hypoalbuminemia another example now hypoalbuminemia let's say class you are
excreting protein in the kidney because you do not usually excrete protein in the kidney you
keep on excreting fluid in the kidney you call that proteinuria and that is the reason why your
protein in the blood decreases another one is malnutrition okay what happens if the protein
in the blood decreases plasma colloid osmotic pressure decreases so you cannot attract the
fluid into the vessel then you will have edema and that is the reason why bhagavad-gita you
know here in the philippines elderly elderly individual will eventually die because there is
edema without knowing the elderly individual they do not usually eat meat they do not
usually eat proteins what they eat are what carbohydrates fruits now see most modeling right
it's easy to what it's easy to uh mechanically digest so once they do not eat proteins they
develop hypoalbuminemia i ask why because once you eat egg white albumin uh level
increases then you increase the plasma collide osmotic pressure then that will attract fluid into
the vessel so that is one a that is another one reason so decrease plasma protein level or
accumulation of osmotically active substances in the interstitial space for example negligion
protein it's a blood vessel then the osmotically active substances proteins accumulate here
then that will attract fluid out and that happens also during vasodilation because fruit
proteins can leak out of the vessel so that's another cause now another one is this once you
have arteriolar dilatation once the arterioles are dilated so if you dilate the arterial capillary
hydrostatic pressure increases and what will cause a dilatation it could be through the release
of i know through to their list of inflammatory mediators so that will cause arteriolar
dilatation or the counterpart is venular constriction so pugna area then that will increase the
capillary hydrostatic pressure it's the capillary hydrostatic pressure that is being affected so
therefore that will cause greater filtration of fluid and that will cause also edema or increased
venous pressure so you increase the pressure in the vein i told you once you increase the
pressure in the vein you will also increase the pressure in the vanilla area that will also
increase data pressure in the capillary so recall that there is um dumbing back okay of your
pressure so that will also cause edema and that that what will increase the pressure in the
vein class heart failure so once the heart okay fails so once the heart the ventricle fails to
pump enough blood pressure here will increase pressure in the atria will increase pressure in
the pulmonary veins will increase pressure in the pulmonary capillaries will also increase but
right side that naman pressure in the right atrium will increase pressure in the capill in the
superior vena cava environment will increase and also in the vein so failure heart failure or
incompetent bulbs like for example somebody make varicose it is they already that they
already lose the complete competence of their bulbs so they cannot they cannot prevent the
backflow of blood okay going back to your lower extremities so that can be cause of
increased venous pressure and that is the reason why they also have lower uh lower extremity
edema venus obstruction one one important example of venus obstruction in pregnant
individuals of a pregnant individual enlarging uterus it will compress the inferior vena cava so
pugna compression inferior vena cava that will also increase the v that will cause venous
obstruction then that will increase venous pressure or increase ecf volume like uh ib fluid uh
the the flow is not regulated so there is massive iv administration ibf administration or intra
intravenous fluid then that will also increase the capillary hydrostatic pressure because arterial
blood pressure will increase remember capillary hydrostatic pressure is coming from arterial
blood pressure or the effect of gravity okay prolonged standing will pull the fluid down okay
that will pull the blood down and that will accumulate in the lower extremities that will
increase the venous pressure and that will increase the filtration that is that is the reason why
if you travel in a long travel a long distance okay what happens is that you will have edema in
your lower extremities all you have to do is when you reach home when you reach your house
elevate just elevate your a lower extremities now how will you prevent that sales lady the bus
sales lady prolonged standing they develop edema so all you have to do is you have to
contract the muscle intermittently contract the muscle so that you squeeze the blood up okay
to prevent edema so these are the conditions that will cause edema so we are actually done
with our lecture my questions po did you understand uh did you understand for my questions
for did you understand okay wait nala dr they will have a quiz cbs1 and cbs2 uh waiting for
the arnold park no reply yet because it based on our schedule it's already the vision for
respiratory we have is already respiratory physiology by dr but that's october 29th so the
schedule will be moved so october in two place which is the 30 item quiz [Music] uh we'll
update the on the phone uh we will update the um see kate and then we'll cascade it to the
students for through our messages so i can if there is a unit test on october 29th i cannot
finish cbs106 i will verify it with the arnold and will immediately inform the students if there
will be a quiz or there will be pure lecture coming from you can i can i ask thursday and then
the quiz of the students will only can take 40 minutes of their time it's a 30 item problem can
we start exactly we usually start part eight the the exam will be published at eight a.m and
then they will end at 8 40 plus the proctorial tradition we usually unlock a 10-minute booming
[Music] can i have the letter at eight to ten then you can you will have the exam at the end
okay i will issue again another yeah so eight to ten picture anyway i will finish at 9 30 yeah but
30 minutes break then you will have the exam at 10 o'clock is it okay yes they can be basically i
don't know uh let's go get so you can have a 30 minute review on your quiz for cbs1 agree
then it means that we can we can have the exam at 10 o'clock anyway i will stop at 9 30. okay
park i see they all agreed thank you okay so we are done we can go thank you doc arnold
thank you