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anesth
4/6
soma

Dr. Klein - for her section, just have to 
know what the EKG shows. Don't have to treat it or know the consequences 
of it or anything.

last time, we were discussing O2 tensions, and what 
they mean, and how you decide if your arterial O2 tension is ok based on 
your delivered concentration of O2 (gradient b/w arterial and alveolar 
concentrations - if large gradient exists, arterial O2 low compared to 
delivered concentration).

transport - why are you concerned about it? 
well, when you open the GI tract if you see a blue gut you worry about 
transport of O2. what transports oxygen? blood. be concerned about 
perfusion, and the content of Hb. 

the O2 Hb saturation curve is 
sigmoidal. plot content vs partial pressure.
at 120 mmHg partial pressure 
of oxygen, the Hb is all oxyHb, 100% saturation. this is what you usually 
have going on during anesthesia. you're carrying as much oxygen as 
possible in the blood both dissolved in plasma and as oxyHb. 

realize, 
anesthesia reduces CO, and positional changes may alter regional 
perfusion, and there may be hypovolemia prior to surgery or due to blood 
loss. this can change carrying capacity despite 100% saturation of Hb.


horses on their back for a long time with low bp may have marked 
reduction in perfusion of muscle mass, causing severe myositis. also if 
lying on their side - perfusion of distal limbs is low. not in dog. 

O2 
content of Hb vs partial pressure O2 in mmHg

the saturation of Hb is pH 
dependent. at 7.2 curve is shifted to right - requires increased partial 
pressure to saturate the Hb. at 7.6, you shift it to the left. under 
anesthesia, acidosis is more likely than alkalosis. normally, muscle is a 
bit acidotic, so this promotes dumping of O2, and the lung is more 
alkalotic so you pick up more O2. this is a good scheme. but under 
anesthesia, you tend to have an acidosis. if you are hypoventilating, you 
superimpose a respiratory acidosis on top of things, and can shift 
further to the right, requiring a higher partial pressure still.

room 
air O2 159 mmHg - humidify it - mix with alveolar air - end up at about 
100 mmHg O2

see the Oxygen Transfer graph on p 5 of handout.
if you 
start with 100 mmHg and end up with 80 mmHg in arterial blood, what does 
that mean?what about if it endsup being 50? that is not good. that means 
you have an alveolar arterial gradient. ideally, you have an arterial O2 
partial pressure of nearer 100. when there is a gradient, you don't have 
a diagnosis, but you know there is some problem causing loss of O2 in 
arterial blood. normal gradient should be about 10 mmHg (8-10). So PaO2 
on room air should be about 90.
mixed venous O2 should be about 40.

if 
you have alveolar O2 tension of 4-500 under anesthesia, and arterial O2 
tension of only 100, that's ok as far as that goes, but it indicates a 
big gradient, meaning there is a problem somewhere.
i

if an animal on rm 
air has a gradient, you can supply oxygen. 
if an animal on oxygen has a 
gradient, you have to do other things.

effects of CO2, O2, and pH on 
ventilation - fig 5 in handout
this study was done a while ago and it 
shows effects of CO2, pH, and O2 on respiration. 

we see a linear 
relationship b/w increases in CO2 and increase in RMV - with a final 
plateau at the top where RMV can't be increased any further. also there 
is a flat part at the low end before RMV starts increasing. so plainly, 
CO2 is what triggers increases in ventilation. 

dr soma suggests that 
you try hyperventilating until you pass out. 

what's the mechanism 
there? the mechanism there is hypocapnia, since CO2 controls cerebral 
blood flow (?). you don't breathe for oxygen needs, you breathe to 
eliminate CO2. if suddenly you are bacteremic, and have a fever and a 
high metabolic rate, you will increase your RR.

only when O2 tension 
drops to a certain level will that drive respiration. 

your respiratory 
centers act via the spinal cord to control abdominal and intercostal 
muscles and via phrenic nerve to control the diaphragm. 

the pain 
response will act on respiratory centers to cause hyperventilation
if you 
inhale something noxious that stimulates the upper airways, local 
reflexes stimulate respiration. 
muscle proprioceptors/movement may 
trigger respiration - probably not at work during anesthesia except 
during light planes of anesthesia.
lung and upper airway reflexes - if 
you have a lightly anesthetised animal, intubation can cause 
hyperventilation, coughing.doesn't happen in the horse- the horse is 
areflexogenic as far as upper airway reflexes go. seen more in humans, 
dogs,cats, maybe cows (bovines).

in deeper planes of anesthesia, those 
upper airway reflexes are gone.

what happens to the respiratory pathways 
during anesthesia? they are depressed. the ability of the muscles to move 
is decreased. conduction isn't depressed, unless you block it with a 
local anesthetic. 
so, if you are anesthetised, you have decreased muscle 
tone, inhibiting ability to expand the chest.

we'll also hear about 
NMBAs which block transmission from nerve ending to muscle. that is 
different. we're talking about anesthetics which do not block conduction 
but which inhibit muscle function to some degree.
first mm to go are 
abdominal and intercostal, most resistant to the effect is the diaphragm. 
so the diaphragm will still move while the intercostals may be pretty 
nonfunctional. as you get deeper and deeper, you may inhibit function of 
the diaphragm, too.

things that control ventilation (that affect 
respiratory center):
voluntary control - gone under anesthesia
sensory 
input - most of it gone under anesthesia, except some surgical stimuli

pulmonary stretch receptors- herring-brewer reflex - old reflex, as you 
expand your chest cavity, chest receptors signal your respiratory center 
to trigger an exhalation. esp in smaller animals, increases in 
ventilation are due to modulation of pulmonary receptors. but mainly 
suppressed under anesth.
arterial oxygen - doesn't trigger ventilation 
unless really unacceptably low
heat regulation/hypothalamus - animals 
that cool by panting, for animals in a hot room, body temperature rises 
may trigger hyperventilation, but this is mainly gone under anesthesia

emotional influences- gone under anesthesia
arterial carbon dioxide- this 
is the key thing left assuming you have an adequate oxygenation.
arterial 
pH -

dr soma is holding his breath.
what is the stimulus for taking in 
new breath? buildup of CO2. you have to blow it off (ha ha).

respiratory 
frequency and inhaled agents:

respiration in bpm vs mac.
generally, the 
RR goes up under anesthesia except in equines. as you increase MAC, RR 
goes up. if you control ventilation, you control RR. if you give opioids, 
this effect may be masked, but under pure inhalant anesth, RR increases. 
so, TV then decreases. alveolar ventilation decreases due to dead space. 
what happens to dead space under anesthesia? it's increased, because of 
the Y piece or a broken valve in the circle (mechanical dead space), and 
physiological dead space, and anatomic deadspace which is related to the 
diameter of the airways - airways are not fixed pipes, they have 
diameters which can constrict or dilate. the diameter of the airways 
determines anatomical deadspace. anesthetic agents except 
thiobarbiturates and morphine tend to relax the airways and dilate them. 
inhalational agents are bronchodilators.  if you are an asthmatic and you 
take a bronchodilator, an inhalational agent will do the same thing.

if 
you remember this figure 5 thing showing the effects of CO2, O2, and pH 
on respiration--- linear relationship b/w CO2 and RMV. the primary 
response to an increase in CO2 when awake is to increase TV. why? because 
your dead space is remaining the same. when you ventilate an aniaml, it 
is more efficient to increase your TV than to increase your frequency, 
b/c there may be dead space and there is no point in increasing the 
frequency with which you ventilate the dead space. makes more sense to 
ventilate the alveoli :)
if you control ventilation under anesthesia, 
animal doesn't have any say in the RR or TV.

CO2 response curve:


ventilation vs CO2 concentration (p12)

increasing concentrations of 
carbon dioxide cause increases in ventilation, as previously discussed.

administration of a narcotic or depressant in an awake animal/person 
shifts the line over to the right - you need higher concentrations of CO2 
to produce a given level of ventilation. this is a change in the 
threshold.

say a CO2 of 45 produces a certain level of ventilation.

under influence of a narcotic, you may need a CO2 of 50 to produce the 
same level of ventilation.

if you anesthetize the animal, you change the 
slope of the line, instead of shifting it to the side. now, you need 
further increases in CO2 to produce the same amount of ventilation. 
usually the curve is steep, but under anesthesia it is more gradual.

CO2 
responses under general anesthesia:

saline, 1 mac, 1.5 mac, 2.5 mac. as 
anesthesia is deepened, curve slope is reduced. at 2.5 mac, you can have 
high alveolar PCO2 and the animal is still breathing, but it's not 
getting oxygen - regardless of what the CO2 is, you won't increase 
ventilation b/c the response is suppressed. so if you reduce anesthesia 
to say 1.0 mac, animal will breathe again . 

so often, under anesthesia, 
you have suppressed ventilation. under 1

suppose you look at the animal 
and the CO2 is 100 and you can't lighten anesthesia because the abdomen 
is open. well, you should ventilate the animal. control ventilation and 
reduce CO2 to reasonable level. 

if you bring it down to 45 (and they 
make you do this in surgery), when will the animal start breathing again? 
you had an animal taking a breath at 75 - it was breathing 3 breaths per 
minute. now, you ventilated, brought CO2 down to 45. when will the animal 
breathe again? when the CO2 reaches threshold. you haven't changed the 
level of anesthesia, which is what increased the threshold in the first 
place.

what happens to O2 tension?
say it's 100. then you ventilate to 
get rid of CO2, and then it takes 5 minutes
to reach threshold for animal 
to breathe again. what happens during those 5 minutes.

---break----

so, 
why doesn't O2 tension drop (much) during those 5 minutes? because your 
alveolus is full of say 90% O2, plus some N2, CO2. but near 100% O2. 
there is venous blood (mixed venous blood) with an O2 of about 40-47%. 
the desaturated blood comes into the lung, and there is a high gradient, 
so it picks up a lot of O2. so blood leaves lung with high partial 
pressure of O2. and you're connected to a circle holding 100% O2 - so 
there is a natural gradient moving O2 into the animal - so this only 
works in the anesthetized patient on a circle system getting oxygen. if 
you disconnect the patient from the circle, all bets are off. CO2 doesn't 
move in the opposite direction, b/c there isn't a gradient and CO2 is 
more soluble in body tissues. so as long as you start with a good O2 
tension you can stop ventilation for a bit.

so, if someone 
hyperventilates you to get rid of all your nitrogen, hooks up the 
anesthesia machine, paralyzes you and leaves for ten minutes, you will be 
ok as far as oxygen tension goes. your CO2 will skyrocket and you will 
get acidotic, but your O2 tension will be ok. this is called "apneic 
oxygenation".

moving on...
effects of inhalants on CO2 - all of them 
depress the CO2 response, and the higher mac the greater effect - see 
chart for specifics. using any inhalant, tendency is toward 
hypoventilation.

capacities and lung volume- 
remember the FRC?
what 
happens to it under anesthesia and what are the implications? when you 
induce anesthesia, you use the tidal volume to flush out the nitrogen.


remember what compliance is?
the relationship b/w tidal volume and 
pressure needed to create that tidal volume. a stiff lung is 
noncompliant. it requires increased pressure to produce tidal volume. a 
less compliant lung requires a greater change in pressure to produce the 
same change in tidal volume produced normally. 

the lung compliance 
curve is sigmoidal. if you increase your lung volume as high as possible 
- maximum expansion - top of lung - it takes a lot of pressure at that 
point to produce a further increase in tidal volume

at the bottom of the 
curve, it again takes a higher pressure to produce a given tidal volume. 
in the normal area, the change is linear. 

if you exhale, to the bottom 
of your lung, breathing out everything you possibly can, some of your 
small airways will collapse. at this point, you have a reduced FRC, 
because you've collapsed tiny airways, and those airways are small. to 
reopen those airways, you need a greater than normal change in pressure 
to reexpand those airways. when you get atelectatic, livery lungs, you 
need increased pressure to reexpand them. not only are the alveoli 
collapsed,but the airways are collapsed. so when the FRC drops,w hich 
does occur under anesthesia, you get into that lower, nonlinear area of 
the curve, in which greater increases in pressure are required to produce 
the same tidal volume you had before.

under general anesthesia, animal 
is asleep, ventilation is pretty monotonous, no coughing, sneezes, yawns, 
deep breaths. there is a fixed tidal volume and fixed frequency- and a 
reduced FRC. so some alveoli aren't opening with the next breath, because 
the animal doesn't sigh or take a deep breath like it normally would. 


if you smoke, you tend to reduce FRC still more. 

Dorsal position: 


when the animal is in dorsal recumbency:

head
				abdomen
	thorax


weight of abdominal contents tends to smush in on the diaphgragm, 
compressing the lungs. the animal's lungs and heart are pushed  by the 
abdominal contents - causing a tendency for airways to collapse. in the 
horse, this effect is big - horse has a wedge shaped diaphragm, a huge GI 
tract, and when you flip him over, the diaphragm which is really curved 
gets compressed downward (dorsally). this is the main reason for the 
change (reduction) in FRC. also, congestion will produce reduction in 
FRC, pulmonary edema reduces FRC, other reasons. but this is the major 
reason. positional changes - lying on side does it too. head down is 
worse than feet down.

compression of small airways, closure of alveoli, 
and collapse == decreased FRC

where is this most likely to occur? in the 
dorsal lobes. but blood flow remains the same. so you have a ventilation 
perfusion mismatch, aka a shunt. those alveoli aren't being ventilated.


remember, the lung is like a spring. if you hold a slinky up, it spreads 
out more at the top than at the bottom, right? lung is the same way. the 
compressed parts of the lung are less compliant. in the awake patient, if 
O2 tension in part of the lung drops, mechanisms will shunt flow toward 
areas of higher ventilation.

in the anesthetised patient, the alveoli at 
the dorsal areas are collapsed, but are still perfused. the mechanism for 
shifting blood flow is eliminated during anesthesia. so a ventilation 
perfusion mismatch in the anesthetized patient will persist.

what 
happens if you clamp off the right bronchus? you have a severe 
ventilation perfusion mismatch. blood continues to flow to that lung 
without being oxygenated. but if you clamp of air and blood supply, your 
V/Q ratio is fine. you can't oxygenate as much blood in the same amount 
of time, but you do oxygenate all of it. the blood will all go to the 
other lung.

but your normal mechanism for adjusting flow to match 
ventilation is lost during anesthesia.

as soon as you stop circulation 
to the lung that isn't being ventilated, and shift flow back to other 
lung, you resolve the V/Q abnormality.

so taking animals and flipping 
them on their sides or backs tends to reduce ventilation in the dependent 
portion of lung, and you've taken away the mechanism that would normally 
adjust the blood flow to compensate for it.
so, you lose gas exchange. 
you end up with venous blood that doesn't get oxygenated - a right to 
left shunt, kind of situation. that blood will now mix into the systemic 
circulation and reduce overall oxygen tension. this is a physiological 
shunt, as opposed to an anatomical shunt. we normally have some shunting 
- about 5% of total CO, or maybe 3% of CO, that's  normal anatomical 
shunt for bronchial circulation that dumps back into the heart without 
being oxygenated - blood that feeds the bronchi. but now we've created an 
artificial shunt. if you pack off the lung to create room, you do the 
same thing, unless you have also diverted blood flow.

one reason for a 
large alveolar/arterial gradient under anesthesia is a shunt.
you might 
have an alveolar O2 tension about 500, and an arterial O2 tension of 250. 
why? shunting. in severe cases, it might even be below 100. if Dr soma 
comes up to you during surgery and asks you what the O2 tension is and it 
is 100 and you say "normal" you get killed. that's not normal. it's ok, 
but it is not normal, because you are giving 100% (close to) O2.

killing 
will be verbal, not physical :)

Illustration of lung perfusion zones: p 
18 of handout. look at it.
this is from West's ABCs of acid base balance 
or something

zone 1 (top) has reduced flow, zone 3 (bottom) has 
increased flow
blood perfusing zone 2 gets normal ventilation.
top of 
lung has good ventilation and reduced blood flow (dead space)
bottom of 
lung has reduced ventilation and increased blood flow (shunt)

so, under 
anesthesia, without changing respiration, or tidal volume, if you simply 
change the distribution of blood flow and ventilation, CO2 will rise, 
because of shunting and dead space. the poorly perfused area of lung is 
physiologic dead space. the poorly ventilated area of lung is a 
physiologic shunt.

ventilation perfusion maldistribution:
another 
schematic diatgram. lots of venous flow into bottom of lung - this is 
shunt area, hypoventilated area. most of the reason for reduced O2 
tension is shunt. increases in CO2 are partially due to dead space and 
partially due to hypoventilation

so, why does a rise in CO2 occur at 
constant TV and RR? hypovetilation and dead space.

mechanical dead 
space: mask and anesthetic equipment - Y piece, etc.
anatomical dead 
space: nasal and oral cavity, trachea and bronchi, non resp. terminal 
bronchi
physiological dead space: well ventilated, poorly perfused 
alveoli

CO2 exhalation curve:

%CO2 exhaled vs volume of exhaled gas
at 
the beginning of exhaling, you are exhaling dead space gas - stuff you 
just finished inhaling. then, after that is gone, you exhale mixed 
alveolar gas which contains increasing % of CO2 because you have gas from 
dead space mixing with gas from alveoli. finally, the last part of your 
exhalation contains the maximum amount of CO2, and this is your closest 
possible measure of alveolar gas. dead space gas didn't contain any CO2 
b/c you aren't inhaling any CO2.
normally, in a normal awake room air 
breathing patient there is a PaCO2 (arterial CO2) of about 38 or 39 mmHg. 
if you measure exhaled CO2 it might be 40, or 41. so the gradient is 3 or 
4 mmHg.
in anesthetized patient, the end tidal CO2 measure might be 40, 
42. maybe 50.
however, an arterial sample may have PaCO2 of 60. 
remember,in part of the lung there is poor perfusion, so gas isn't 
picking up any CO2, and this exhaled gas is mixing with the rest of the 
gas exhaled, so the end tidal CO2 isn't representative, due to dead space 
that occurs. 

a few calculations - see p 24 - you have to look at 
saturation to see why a shunt is not a direct relationship b/w what 
happens in arterial tension when you have x amt of oxygen and if you have 
that oxygen your tension should be halved and that's not true because 
it's based - that makes no sense!! see handout.

the important things to 
remember are what occurs when you move animal into different positions 
under anesthesia.

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