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anesth
4/28
soma

ok, we were doing henderson-hasselbach 
stuff

when we add or subtract CO2, we add or subtract bicarb and H+ in 
equal amounts. if you hold your breath, you increase CO2, equation goes 
to the right

CO2 + H2O <===> HCO3- + H+

CO2 is carried in RBCs to the 
lungs.  while in the RBC, carbonic anhydrase converts the CO2 to HCO3- 
and H+. the major reaction is in RBCs. The H+ stays in RBC, and HCO3- 
moves into extravascular tissues. the H+ is buffered by the RBC. if you 
are anemic you have reduced buffering capacity.

so, when you produce 
respiratory acidosis - pH is decreasing, but you have a slight increase 
in bicarb which confuses people who see bicarb going up and pH going down 
- this is called respiratory acidosis, not based on bicarb concentration 
but based on CO2 level, not on pH or bicarb. you could have a balanced 
resp acidosis where CO2 is over 42 but there is no acidemia. but you 
still have respiratory acidosis. how do you tell apart the change in 
bicarb - you could have dual change. think about it. suppose you have 
metabolic alkalosis or metabolic acidosis - what happens to bicarb in 
metabolic acidosis? if you are infused with a low concentration of HCl, 
what happens to base? it depletes. your major base is bicarb. so what 
next? you then add a respiratory acidosis into the system for fun. what 
happens to the bicarbonate? it rises. how do you know where the bicarb is 
coming from? 

he's showing that slide of in-vivo vs ex-vivo buffer 
curves.
if you look at this slide, one line shows the change that happens 
in-vivo, and the other one is ex-vivo/in-vitro and that one is a straight 
line. when you equilibrate the body with increasing amts of CO2 you get 
the in vivo type of curve. you produce, as you move from PCO2 of 40 to 
say 60, 80 - you see a slight rise in bicarb. with metabolic acidosis you 
move down the black line, the PCO2=40 isobar - you're not changing the 
CO2, you're adding acid or removing base. 

when you add acid, what 
happens to the base, asks elizabeth? he says you reduce the base because 
it is buffering acid. you could excrete a lot of base due to renal 
dysfunction and also produce metabolic acidosis, or you could accumulate 
a lot of lactic acid like when you exercise to fatigue, and you buffer 
that with bicarb, and that also produces metabolic acidosis with low 
bicarb. as you metabolize lactic acid, bicarb goes back up and pH comes 
back to normal. this is normal when you exercise a lot (not just walking 
up the stairs, but say running a marathon.)

ok?

ok.

ok, let's follow 
this - if you move from A to B on the respiratory and metabolic acidosis 
graph, what is the situation? you have metabolic acidosis. moving b to c 
is respiratory acidosis. a pure metabolic acidosis, going a to b - your 
bicarb is about 18, then. so you have lost some base. when you 
superimpose a respiratory problem and move to C, where PCO2 is 60, you 
move the bicarb back to about 20 - adding 2 mEq of bicarb as you move 
from PCO2 of 40 to 60. that's the amount of bicarb added to plasma in our 
equation. it moves out of RBC, into plasma, then into extravascular 
compartment to buffer pH changes. but this 2 meq stays in plasma. so the 
actual bicarb doesn't define the amount of metabolic change, b/c you have 
added a small amount.  if you then go to PCO2 of 80 you add more.

so how 
do you define that component? so you can quickly indicate that you have a 
metabolic acidosis and a degree of respiratory acidosis?  look at base 
excess (that means - if you change the PCO2 from 60 to 40, the base 
excess tells you you have a respiratory acidosis or alkalosis which 
alters the bicarb, and then you have a metabolic situation which is 
adding or subtracting to the bicarb, and i want to know the degree of 
metabolic component - so i adjust the bicarb to what it would be at PCO2 
of 40. so this means without regard to the PCO2, the BE says that the amt 
of addition or subtraction of bicarb will be based on a PCO2 of 40. this 
brings you back to point b, and now you say that your bicarb would be 18, 
because you are taking out the amount of bicarb added by the increased 
PCO2 (or you would add the amount in if you had resp alkalosis and 
decreased CO2). the common situation under anesthesia is metabolic 
acidosis due to disease, and then hypoventilation causing increased CO2 
and respiratory acidosis, and the degree of hypoventilation determines - 
the more severe it is, the higher the CO2, and the more bicarb added into 
the system relative to CO2. so if you say, you have a BE of -10, that 
means (and it isn't uncommon; in an athletic event to fatigue a BE of -20 
can occur) that irrespective of CO2, this is how much of a decrease in 
bicarb you have - or, if you have metabolic alkalosis, the increase in 
bicarb you have irrespective of CO2 level.

so BE says what the metabolic 
component is. if you get a BE you should immediately in nanoseconds KNOW 
the degree of acidosis/alkalosis on the metabolic side. 

if you are 
given a CO2 of 60 you should KNOW the degree of respiratory problems you 
have. 

then if you get the pH you should IMMEDIATELY know if you have 
acidemia or alkalemia. 

very straightforward to understand and interpret


the other thing you can use is "standard bicarbonate" - same thing. this 
is the bicarb if it were adjusted to PCO2 of 40. so if bicarb goes up as 
before to 20, standard bicarb would be 18 (I think) but BE is easier, he 
says. the range of values for carnivores is b/w -3 and +3 for acceptable 
values. for equine and bovine, anywhere from 0 to +7. so equine 
especially is shifted in opposite direction. it may be the algorithm - we 
use a human algorithm. but these are the ranges we accept. with an 
equine, a -3 would be treated. also if you see a +7 in the equine you do 
not treat it. sure, it's metabolic alkalosis, but it's within the range 
of normal for horses. well, it's at the tail end of a gaussian 
distribution, but it's still within normal range. you do not treat that 
by adding acid. you would treat an equine with -3, -4, -5 b/c they have 
metabolic acidosis that needs treatment.

chart - metabolic alkalosis and 
respiratory acidosis
this is the reverse.
moving from A to B we see how 
much bicarb is added due to metabolic alkalosis, and to C, we see how 
much bicarb is added as we move from CO2 of 40 to 80. so actual bicarb is 
about 34, but standard bicarb is about 30.(i think)

on blood gas you get 
both BE and std bicarb.
positive BE = metabolic alkalosis, excess fixed 
base
negative BE = metabolic acidosis, decrease fixed base, excess acid

at pH of 7.4 and HCO3- of 24 the BE is 0.
if your O2 sat is below 90, say 
in the 80s, this gives a clue - what is going on? a shunt. a V/Q 
abnormality. if you are giving near 100% O2 and saturation is 80, you 
have a big problem. you are expecting a saturation above 97 at least. 
should be 99.999%, really. so if it is 80 something is wrong with the 
lung, or the transport system. figure that one out at the time. but you 
should know there is a shunt, transport problem of some kind, b/w alveoli 
and pulmonary blood. this is what you use O2 sat, O2 tension for. this 
will tell you that your alveolar O2 isn't getting into blood for some 
reason. the O2 tension gives a more defined relationship. 

so when you 
look at O2 sat under anesthesia, it's going to be very high if things are 
ok. when they put a probe on the tongue, and you look at O2 sat, it 
should be high. if the perfusion is normal, that is. you may have good 
plasma saturation, of your blood, but if it isn't getting into tissues 
you may hae poor oxygenation of tissue.

so how do you use BE? to 
determine the amount of metabolic acidosis or alkalosis. then, what do 
you do? 

if PCO2 is 60 and BE is -10, you do what? increase ventilations 
for fixing CO2, and give bicarb to fix the BE. you can use bicarb to 
adjust this. how much do you give? take the BE, multiply times body wt in 
kgs (not pounds!) times 0.3 to adjust for extravascular compartment. then 
infuse that much.

10 kg dog * BE -10 * 0.3 = 10 * 10 * 0.3 and this is 
what you infuse under anesthesia. it's acute under anesthesia so you can 
correct it fairly rapidly, unlike with chronic situations in medical 
cases. this will at least temporarily fix the problem. hopefully the 
surgery will fix the underlying problem. 
bicarb is measured in mEq/L as 
is BE. when you read the label on the bicarb, it's also luckily in mEq/L. 
always read label carefully - usually 5% bicarb solution. usually infuse 
in reasonable amt of time and recheck acid/base status. usually you will 
have corrected it to some reasonable level. pH will be close to normal, 
assuming you corrected CO2, and BE will be around zero. keep CO2 b/w 40 
and50. this is how you correct this under anesthesia. 

when you 
ventilate to blow of CO2, won't that lower bicarb? sure, but it also 
changes the acidosis. 

remember - it's not going to lower the bicarb by 
very much. the primary change in this case isn't respiratory componenet- 
it's the metabolic component. 

if you want to look at what the 
contributions are in the pH change, which is strictly related to CO2, you 
look at the CO2 isobar for the Co2 you have and see what pH should be. 
for CO2 60 w/o metabolic component, pH is about 7.25; and changing the 
CO2 will get rid of that component. the metabolic component brings the pH 
down lower.

so you always want to treat both the respiratory and 
metabolic component if the animal needs treating. i mean, if BE is -3, 
you can just treat respiratory component, and that's probably ok. but if 
BE is contributing to the acidosis significantly, you will treat it. this 
case we are discussing, the pH is down to about 7.1. acidosis is more 
common than alkalosis. we rarely see metabolic alkalosis. under 
anesthesia, usually you see acidosis. 

what's a reasonable amt of time 
to give the bicarb in? depends how much you give. infuse over 15-20 
minutes maybe. for a 500 kg horse with a BE of -10 maybe this takes 
longer b/c you have to give a lot of bicarb. horse may need 3 lines going 
in - one for fluid, one for bicarb, one for pressor, b/c you can't change 
fluid balance that fast in the horse. in a cat, you can fluid overload 
really fast. in horse, you'd have to give tons of fluid to do that. it's 
not easy.

if you do not correct your ventilation problem here and you 
give bicarb do youmake it worse? you do get rid of some bicarb as CO2 so 
that could contribute some, but not that big a deal. but in this 
situation we will be ventilating and correcting the respiratory problem. 
you could hyperventilate, too, to chnage acid/base balance. you still 
have acidosis - metabolic acidosis is still there. the bicarb will tell 
you. 

you don't need BE if you are moving along the middle line with BE 
around zero, not adding or subtracting alkali, just adding or subtracting 
CO2. if only the PCO2 is changing, BE isn't changing (theoretically). 


what's the difference b/w arterial and venous blood gas? 
you want to 
know acid/base balance of an animal but can't get an arterial sample for 
some reason. what are the differences? 

CO2 content in venous sample 
cannot be interpreted. you cannot interpret the respiratory side of 
acid/base status. if you try to interpret it, you will demonstrate to dr 
soma that you do not understand. the venous sample is venous drainage 
from one body part or if mixed venous sample, tells you what CO2 is doing 
all over body - you want to know CO2 status AFTER it clears the lung 
because that tells you if lung is working. but you can use venous sample 
to get an idea of acidosis or alkalosis. it's close enough to get an idea 
of what's going on and if you need to treat acid/base disorder. but you 
can't interpret CO2 tension, bicarbonate, or oxygen tension. O2 tension 
you want to know is what it is after clearing lung -to see if lung/gas 
exchange is working!

questions?

if he gives you this:

PCO2 = 60
BE = 
-3
HCO3- = 22
O2 sat = 99
O2 tension = 450

this is pure respiratory 
acidosis. this is a dog, btw. basically this is a normal dog.

same 
animal with BE = -10; this is respiratory acidosis with metabolic 
acidosis too. 

you're interpreting this based on BE, not really on 
actual bicarb. if he didn't tell you what the BE was, and he gave you a 
high CO2 = 60, and low bicarb, and low pH, and asked you to interpret, 
what would you say? well, respiratory acidosis sounds good to me but 
bicarb is low so that can't be - we are given a bicarb of 20. so, this is 
going to have to be metabolic acidosis superimposed on respiratory 
acidosis.

remember - respiratory acidosis alone causes increased 
bicarbonate
high CO2 with low bicarb is a mixed disturbance.  


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controlled or assisted ventilation - not only an 
anesthesia thing, also use this other times.

indications:

depression of 
respiratory centers *
limitations of movement of thorax and diaphragm *

limitation of movement of lungs *
interference with neural conduction or 
neuromuscular transmission **
decrease in functional lung tissue

ineffective respiratory exchange
CPR
pulmonary edema
thoracic surgery *
* 
all these may apply during routine anesthesia.
** with NMBAs

pulmonary 
edema - fluid going from capillaries into tissue.
when you have this, 
fluid goes into small interstitial spaces and then alveoli. lymphatic 
system removes fluid but if overwhelmed, edema occurs. PPV will help 
prevent some of the fluid from going from interstitium into alveoli. 


normally under anesthesia cardiovascular failure would be a cause of 
pulmonary edema, as would hyperinfusion of fluids, with increased 
pulmonary pressure, increased central venous pressure, temporary 
pulmonary edema. correct with diuretics.

many times under anesthesia, it 
is easier to maintain a more stable level of anesthesia if you control 
ventilation - spontaneous ventilation may be inadequate, erratic, or 
inconsistent, making it difficult to deliver appropriate concentrations 
of inhaled anesthetics. 

difference b/w controlled ventilation (PPV) and 
spontaneous ventilation (SV)
a while ago, he asked us what a valsalva 
maneuver was. PPV is an intermittent valsalva maneuver. you are changing 
pressure in thoracic cavity for a brief period of time. you are putting 
positive pressure in there instead of normal negative pressure. 


[interruption - numerous equipment failures - "this stuff has been here 
as long as I have, no wonder it's falling apart" - Dr. Soma]

a quick 
sequence -  spontaneous ventilation:
at end expiration there is 0 gas 
flow, alveolar pressure = 0 = ambient outside pressure. no flow, no 
pressure gradient. pleural pressure is still negative - about -7. there 
is always neg pressure in thorax. when you inhale, you create greater neg 
pressure in thorax = -17; and alveolar pressure becomes negative relative 
to outside, = -7. air flows in. passive exhalation - pleural pressure is 
-4, alveolar pressure is positive at 4, and air flows out of the alveoli, 
out of the airways. 

with controlled ventilation, you reverse this. you 
compress the bag and put positive pressure into the alveoli, and air 
flows from anesthesia circuit into alveoli. pleural pressure gets less 
negative , becomes 0 or positive, depending on how much positive pressure 
you use. 
the only time the pressure is normal again is during passive 
exhalation - the machine/hand has moved air in, then you let go of bag or 
the bellows exhales, and lung exhales - neg pleural pressure, -4; and 
positive alveolar pressure, 4. this is when you have a normal situation, 
during passive exhalation.

slide: right atrial pressure and venous 
return

if you suddenly increase the pressure in your airways, what will 
happen to venous return? remember the thoracic vessels in there, vena 
cavae, azygous, etc. blood coming from periphery, dumping into the right 
heart via these compressible veins. you increase the pressure in the 
thorax, you will compress these vessels. so you decrease venous return. 
producing positive right atrial pressure decreases venous return - rapid 
decline with increasing pressure. this will decrease cardiac output. 
we're talking about compression of vena cavae, azygous, ventral mammary 
veins. all these are affected. 

slide: central venous and tracheal 
pressure

if you look at pressure in the carina, the carinal pressure 
generally goes from +5 to +15 => based on readings on the anesthesia 
machine. you transmit your pressure from circle system to the chest. 


look at central venous pressure - measured via long jugular catheter 
threaded in to near top of heart, in inferior vena cava, or on top of 
right atrium. anyway, pressure here goes from about 0 to +7. the little 
jiggle marks on CVP chart are the heartbeat - this pattern is also 
slightly evident on the carinal pressure graph.

slide: right ventricular 
- aortic pressure and controlled ventilation

if you are measuring BP, 
and you squeeze the rebreathing bag during diastole, and you see a 
decline in BP why is that? due to increased intrathoracic causing 
decreased venous return which causes decreased CO and decreased BP. if 
you keep squeezing the bag there is a slight rebound - why? 
not 
increased HR - often HR decreases with increased thoracic pressure.
so 
what is it? well, a reduction in BP is sensed by baroreceptors and 
signals are sent to cause sympathetic increase in peripheral venous tone, 
increasing venous return, causing slight increase in CO. this is a 
sympathetic reflex mediated by baroreceptors - happens when you sustain 
an increase in thoracic pressure.

ok, so then, you release the bag 
completely - and you return to where you started. 

if you didn't sustain 
the increase in pressure, but released the bag at the right time, you 
would return to normal. then you squeeze the bag again, decrease CO/BP 
again, then return to normal - this is the cycle you see. 

well, on this 
chart of RV - aortic pressure - we see aortic pressure, esophageal 
pressure, and RV pressure on this chart. the aortic pressure is going 
down every time the ventilator gives a breath (marked by peaks/increases 
in esophageal pressure). you could palpate this as a decrease in pulse. 
when ventilator cycles off and animal exhales, you palpate a stronger 
pulse pressure. you can also see end diastolic pressure in RV going up 
and down.

so knowing this, what conditions influence the response of the 
system to PPV? 
general anesthesia - in general, alters the baroceptor 
response, promotes vasodilation, decreases BP, decreases CO. there are 
variations among the drugs but most agents have these effects. what else 
do they do? they decrease response to sympathetic stimuli. decreases 
reflex responses to changes in CV status. so under anesthesia this 
response to PPV is more exaggerated. 
what other things influence it? 
perhaps pneumothorax, hydrothorax, any condition which decreases capacity 
of lung to expand, requiring higher pressures for ventilation. also, 
mainly, hypovolemia is what he was looking for - you can't give PPV to 
hypovolemic patient; if you must, you must also give fluids; also 
cardiovascular disease is important - if there is cardiovascular disease 
present, and you put animal under anesth and give PPV you can make things 
worse. someone suggests brain stem trauma - no, if you have that, and 
swelling of CNS, PPV usually will reduce cerebral blood flow and this is 
a good thing, in fact often may want to hyperventilate to reduce CO2 and 
reduce cerebral blood flow. the other thing he wants is *position*. go 
into radiology and you may be told "keep feet down for this view" but if 
you do that while giving PPV you can markedly decrease venous return and 
cause marked cardiovascular depression.

those are the reasons and it 
doesn't necessarily mean you can't give PPV, you just must be aware that 
things are more likely to happen and be cognizant of the situation.


notice on our graph there is a quick period as ventilator cycles on that 
for 2 or 3 beats there is an increase in aortic pressure, and if you 
measured flow you would see a slight increase. why? you are pushing and 
compressing lung tissue, moving some extra blood into left heart. but as 
breath is given, you squeeze stuff out of lung then pressure falls.


slide: PPV
aortic pressure, mean aortic pressure, pulm arterial pressure, 
mean pulm art pressure. during PPV we see rapid increase in pulmonary 
arterial pressure as blood is transferred into the pulmonary arterial 
compartment; as in aorta.

slide: spontaneous ventilation: no changes in 
aortic pressure occur with respiration. pulmonary arterial pressure drops 
as negative pressure in chest increases. mean arterial pressure (pulm) 
shows decreases with each breath.

if you have a central venous line in, 
and attach a pressure gauge, you can see the pressure going up and down 
like this. a catheter into cisterna magna to collect CSF would show the 
same thing if yuo put a manometer on there. pressure is transmitted 
throughout the system. a really deep breath with lots of negative 
pressure generated will show up there too. 

so, question:
if you start 
PPV, what will happen to CO, BP and why? well, you will have decreased CO 
and BP due to decreased venous return with increased pressure during 
inspiratory phase.
you're increasing airway pressure, decreasing venous 
return, temporarily reducing CO, so BP and CO go down. when pressure is 
released there is a surge of blood coming back (there is a simultaneous 
increase in venous pressure during the time of decreased CO due to 
sympathetic reflex), then there is increased pressure.

what about PPV 
w/o anesthesia? you'd see less of a change, but still less of a change. 
what about with spontaneous ventilation? You have negative changes on 
thoracic side; but you don't really change venous return so this isn't 
transmitted to arterial side - increases in negative pressure beyond 
normal do not really increase venous return. you might even temporarily 
collapse some small veins. 

what happens when you start PPV - why do you 
start PPV? to get rid of CO2. what do you have to increase? alveolar 
ventilation. can do this by increasing rate or volume or both. if you 
increase alveolar ventilation, what else do you do? go back to lecture 
number whatever. you also give more anesthetic agent! if you're breathing 
spontaneously and suddenly take the same flows and improve alveolar 
ventilation, you are increasing drug delivery. that is another reason for 
a slight decrease in BP. it won't necessarily happen, but that is 
somethign to consider when you turn on the ventilator. also want to know 
where are you on anesthetic curve? early on, not much difference, still 
in uptake phase; or later, in steady state/plateau phase where increased 
alveolar concentration will quickly increase arterial concentration and 
make animal deeper.

so the physical aspects are important, and the 
pharmacological ones also. increasing concentration of drug in alveoli. 
number three, don't forget, the other reason - you are putting gas under 
higher pressure, putting more agent into alveoli temporarily. 
1. 
physical aspects
2. increasing alveolar ventilation
3. high pressure 
driving more anesthetic agent into alveoli/blood
4. blowing off more CO2, 
and CO2 is sympathomimetic, so you are losing that sympathetic 
stimulation, and this also contributes to the drop in CO/BP - with 
substantial hyperventilation and CO2 falling below 40. but if you are 
floating along with CO2 of 80 or 90 and you reduce that to normal, this 
also can cause a reduction in CO b/c removing sympathetic tone. 

so when 
you turn on the ventilator, look at BP, HR, try to determine if there are 
changes occurring. next thing is figure if the changes require treatment. 
just b/c there is a change from a to b, doesn't mean b is bad. b might be 
ok for now. you have to figure it out, and figure out the reason for it. 
if you drop CO2 too far, maybe ventilate a bit less. if position is bad, 
reposition. if volume depleted, give fluids. pretty straightforward. if 
animal is bleeding, stop bleeding, give blood, plamsa, fluids, whatever. 
that's what you have to consider. you cannot go to merck manual and read 
this - you need to know it right away. you should anticipate things that 
might occur, during an anesthetic episode, so you are ready to counteract 
problems. the first time you manage a cardiac arrest you will be totally 
in disarray. when you drive home tonight think of a cardiac arrest and 
what you would do during it. these can occur in student surgery, and some 
students sit there and wait for somethign to happen. it is the 
anesthetist's job to deal with it. we got a plan in our cardiac arrest 
lecture. 
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