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anesth
4/14
perkowski
hypotension, CV depression

for those 
of you who were here yesterday, we were talking about recognizing 
cardiovascular depression. the pros/cons of auscultation vs doppler flow 
vs oscillometric measuring devices were discussed. 

what about direct 
measurement of arterial wave form with arterial line and transducer? 
gives continuous, accurate information if used correctly, allows you to 
visualize the wave form and allows ready access for arterial blood 
sampling. downside: it's invasive, requires skill and can be expensive 
depending on your transducer. 

point: depending on where you are looking 
at the waveform, it can change - the aorta, the femoral artery, the 
dorsal pedal artery - all are different. more distally the wave starts 
later, which makes sense, and it increases in amplitude and gets more 
narrow - for reasons of physics - if you put pulse wave through a tapered 
tube, it increases in amplitude as it goes along the tube, and also you 
get summation of the waveform - as arterial pulses move out, each time it 
reaches a branch part of it is reflected, and the reflected wave adds on 
to the original waveform, so more distally the amplitude is increased for 
this reason as well. other things - dampening, harmonics, frequencies - 
who cares, just know that it changes. normally if you look at dorsal 
pedal artery, 80% of that is reflected waveforms. if you increase 
vascular resistance, the % reflected increases, and amplitude increases 
more. so be aware that things aren't the same all the way through the 
body. it depends where you are measuring. also on the size of the 
catheter.

in horses, arterial catheters are placed often in facial 
artery. also can be on transverse facial a (branch of carotid), or in 
metatarsal. we use the head more b/c it usually is easier to reach. 

in 
cows and pigs and sheep, we often put the a line in the auricular artery 
(ear). in dogs, sometimes we do that in dachsunds which have long ears 
and short legs. 

in dogs/cats usually we use the dorsal metatarsal 
artery or sometimes a cutdown on a femoral artery. cats are hard to get a 
lines in b/c they spasm.

so you get the line in and you get lots of 
information. you can see waveform, can run it along with your EKG and see 
what is going on. now, we do not always have fancy transducers. you can 
use an extension set of tubing hooked to the catheter with a hand held 
pressure gauge thing.

all the monitors in the world aren't helpful if 
you do not know what htey mean. why is the patient hypotensive? it can't 
contract heart? it's dehydrated? it's vasodilated? you have to know. 


look at waveforms. 

normal waveform - pulse pressure is difference b/w 
diastolic and systolic pressures. pulse pressure gives info on stroke 
volume (directly related) and arterial compliance - if artery isn't 
compliant, upstroke will be sharp; if it is, there will be a slower 
upstroke. in systole, volume moves out into arterial bed, extending the 
elastic arteries, then blood moves through and arteries snap back, 
creating the dicrotic notch on the downstroke of the pressure wave. 
depending on peripheral resistance, diastolic pressure may fall off more 
betwen each pulse. mean pressure depends on CO and SVR, and is always 
closer to diastolic than systolic pressure. 

decreased CO causes 
decreased mean pressure, decreased rate of rise of pulse wave, 
prolongation of inotropic phase (from start to peak of upstroke) and 
decreased pulse pressure.

decreased SVR (vasodilation) - increased rate 
of rise due to less afterload - inotropic phase is shorter, pulse wave is 
narrowed, your dicrotic notch comes further down on pulse wave or 
disappears, and pulse pressure increases since diastolic pressure is 
lower.

normal, hypertensive patient: increased CO, increased SV, 
increased SVR - you see this when the patient is a little light, lots of 
SNS stimulation.
systolic, diastolic and mean pressure all above normal. 
upstroke is rapid, dicrotic notch occurs early in diastole.


hyperkinetic, bounding - increased CO and SV, decreased SVR
post 
vasodilator, sepsis, AV shunts
systolic pressure is increased, diastolic 
and mean pressures are decreased b/c resistance is down. pulse pressures 
are increased. the rate of rise and descent are rapid, and dicrotic notch 
is low or absent. you see this with AV shunts too - here is a slide from 
a PDA puppy where you see that after the PDA is tied off, the pulse wave 
changes drastically. this is like what you would see if a patient was 
very vasodilated and then returned to normal. 

hypokinetic, thready 
pulses - decreased CO, SV; increased SVR b/c body tries to maintain BP. 

systolic, diastolic and mean pressures lower than normal
pulse pressure 
decreased. 
upstroke slow, prolonged
dicrotic notch higher than normal or 
normal
rapid heart rate, decreased diastolic phase
seen with shock, 
myocardial depression

that's all fine but we're not going to always have 
this information. you have to palpate pulses. you need to start feeling 
the pulses in between each wave also, to see what goes on in between. 
thready pulses - small pulse pressures, peripheral constriction - if 
shocky, mean pressure also will be low - won't feel artery well between 
beats. but if you are vasoconstricted b/c a vasopressor is on board you 
will feel a hard rigid tube beneath your finger between pulses.

a 
bounding pulse probably means you are dilated or dry.

volume status:


changes in arterial pressure or wave form - what else can you look at?
if 
you have an oscillometric device giving you systolic, diastolic and mean 
pressures, look at diastolic pressures - if those are really low, say 30, 
but systolic is ok - that may mean that you have a big runoff b/w each 
beat, and your patient is vasodilated or hypovolemic. 
positional changes 
- moving patient from lateral to dorsal - if this causes pressure drop, 
animal may be dilated or dry - you've just reduced the venous return by 
pressing on vena cava. if large changes in BP occur with changes in 
position patient likely to be dilated or dry. also positive pressure 
ventilation - each time you give a breath, if a pulse wave goes away, you 
are really affective venous return with each breath - patient is dilated 
or dry.

can also look at central venous pressure CVP - cath jug vein, 
measure right atrial filling. CVP will drop with vasodilation or 
dehydration. 

also you can look at PCV/TS, urine SG, BUN.

contractility 
assessment: look at changes in waveform, pulse pressure. when 
contractility isn't so great - slow upstroke, kind of prolonged. when 
contractility improves, gets steeper, faster. 

can auscult for changes. 
use esophageal stethescope. as heart beats better or worse the sounds 
change. 

CVP can also change with changes in contractility - heart doing 
good job sucks blood from venous side to arterial side. if heart fails to 
suck as much blood out, CVP will increase.

adequate BP doesn't guarantee 
adequate tissue perfusion - animal could be severely hypovolemic and 
vasoconstriction. volume is really important (but don't overload them - 
CHF)

most common cause of hypotension in anesthesia is inadequate volume 
due to preop deficits, bleeding, or not enough fluids given to compensate 
for increased losses during sx.

fluid therapy:

IV is optimal - here, we 
always place an IV for anesthesia. you really must do this, you must have 
IV access for emergencies, at least. 
rate of administration depends on 
the case.
volume also depends on the case and the ongoing losses.

maintenance fluid rates in anesthetized patients are more than in awake.

awake: 2-4 ml/kg/hr
mild sx trauma: additional 2-4 ml/kg/hr (eg, quick 
lumpectomy)
mod sx trauma: additional 4-6 ml/kg/hr (eg, spay)
severe sx 
trauma: additional 8 ml/kg/hr (eg, intestinal anastomosis)

surgical 
maintenance fluid rates: 6-12 ml/kg/hr
in small animals, frequently we 
give 12-24 ml/kg/hr for the first hour to make up for preop losses. at 
least 10 ml/kg/hr. this is easier in small animals. large animals are 
bigger, need more fluid faster.

also - blood losses may occur. normal 
blood volumes:
dog 90 ml/kg
cat 60 ml/kg
horse 90-100 ml/kg
allowable 
blood losses - people say you can lose 15% of your blood before you hve 
to replace it, but it depends on what is going on with the patient in the 
first place.

shock rates of fluid - you dilute out the normal blood 
volume by giving one isotonic blood volume in an hour. so dog shock rate 
is 90 ml/kg/hr.

type of fluid - 0.9% NaCl, LRS, etc. very similar, minor 
differences. remember that the fluid you give isn't all going to stay in 
the vessels. some will, and some will equilibrate with extravascular 
space. so when you give crystalloids to replace blood, you must give 3 ml 
crystalloid for every ml blood you are replacing. 

colloids - hespan, 
hetastarch, dextran - larger molecules in fluids, tend to keep fluid in 
intravascular space. if you have a patient with a very low TP and you are 
trying to give a lot of volume, crystalloids will dilute out the protein 
and cause more fluid shift into extravascular space. so you would 
consider colloid administration. if you have to get volume in quickly - 
colloids can be given 1 ml per 1 ml of blood loss since it stays in 
vessels. so you use it in emergencies, and with low TP animals. 

another 
colloid you could give is plasma. this is a nice colloid but the problem 
with it is hard to get in large volumes, and it doesn't stay in the 
vessels as long as the synthetics do - but it offers a lot of valuable 
proteins for coagulation and so forth.
packed cells and whole blood are 
also options.

treatment of cardiovascular depression:
you've replaced 
your volume, your pressure still sucks. now what?
adjust the depth of 
anesthesia first. flush your circuit with O2. remember we said that the 
inhalants we use have a direct effect on arterial pressure. lightening 
the plane of anesthesia should offer some improvement in pressure. in 
small animals, it is easy to flush them out and let them wake up a bit 
and you can hold them down - but a horse you can't let it wake up at all 
because it can really hurt someone (you) or hurt itself. horses you have 
to use pressors.
also you can try changing from inhalant to injectable 
anesthesia - 
opioids are nice to the cardiovascular system, although can 
cause vagally mediated bradycardia (treatable with atropine, 
glycopyrrolate) - except demerol, morphine =- these cause histamine 
release, may worsen the pressure. esp in dogs do not give meperidine 
(demerol) IV. horses aren't as prone to this as dogs are but can get 
excited from opioids, plus require large doses and can cost a lot. but 
sometimes you can used a mixed technique in horses.
etomidate - IV 
hypnotic agent used in small animals more than horses b/c it is very 
expensive. in dogs, can use this, causes almost no change in HR or MAP. 
we'd use it more if it cost less or had fewer other effects.

ketamine - 
in general considered to be sparing of cardiovascular system but remember 
this is due to catecholamine release - causes increased HR, increased or 
same MAP. in sick cats/dogs, worry about too much ketamine unmasking 
direct negative inotropic effects. in horse, you are kind of out of 
options. colic horses often induced with ketamine. benzos like valium are 
also cardiovascular sparing so you can mix them with ketamine.

also you 
can try to lighten the animal up a bit and use an NMBA like atracurium 
(cis atracurium to prevent histamine release), vecuronium (in ICU, bypass 
patients), pancuronium (most often for eye procedures in small animals; 
is vagolytic and produces tachycardia)

also: correct electrolyte 
abnormalities
change body position (tilt head down)
treat arrhythmias



what are we doing when we put patient on pressure support? manipulating 
SNS.
a1 receptors on peripheral vessels cause arterial and venous 
constriction - more on arterial. a2 receptors cause more venous 
constriction, some arterial.
beta1 receptors on heart increase rate, 
contractility. beta2 receptors cause vasodilation and bronchodilation (?)


how we use sympathomimetic amines:

phenylephrine: alpha agonist - 
vasopressor. we use a lot of this. remember, one problem is we have 
decreased sympathetic tone and vasodilation in anesthetized patients. 
blasting with fluids and waking patient up a bit isn't always good enough 
so phenylephrine is used to support pressure. it comes in a 10 mg ampule, 
you stick it in a 250 ml fluid bag and drip it to effect. don't use as a 
bolus - could increase BP too much and decrease HR, or stop heart. "to 
effect" means that you get off the knee of the curve, get your pressure 
up into 60s/low 70s. phenylephrine causes arterioconstriction and some 
venoconstriction. be careful - if patient is dry, don't give a pressor, 
because you cut off blood flow. in general, if used judiciously, works 
really well. in horses, again, you worry about myopathy, neuropathy, 
peripheral perfusion - ensure good hydration. used in colic cases a lot.


if phenylephrine isn't working or HR is low to start with, you can use 
epinephrine to get some B1 and B2 effects with your alpha effect. epi has 
mixed a and b effects. at low doses to effect, beta effects predominate. 
when you bolus it in to tx cardiac arrest, alpha effects predominate. it 
depends on dose. anyway, this works well, esp in some septic patients. HR 
increases, systolic pressure increases

norepinephrine - not used as much 
- causes large increases in SVR. will increase BP nicely but also large 
increase in SVR and can cut off blood supply to kidneys or something. 
remember norepi has no beta2 effects and epi does.

dobutamine - 
fascinating drug. a beta1 agonist with some beta2 activity. at NBC they 
use a lot of this. 1-10 ug/kg/min. horses - if you use .5-1 ug/kg/min you 
see pulse wave change, increased contractility, increased pressure, 
increased HR, huge BP effect. often used with phenylephrine. in small 
animals, often you see HR increase but BP drops. dogs are less responsive 
to this drug. you must give about 5 ug/kg/min before you see an effect, 
and effect is frequently tachycardia. why? different sensitivity of 
canine beta2 receptors? 

isoproteronol - not used much. pure beta 
agonist with no alpha effects. "isoprokillemall" - because of beta1 
effect, you increase HR, but because of beta2 effect, you decrease SVR, 
you get a decreased BP and reflex tachycardia.

dobutamine in dogs kind 
of acts like isoproteronol.

dopamine - another interesting drug with 
different effects at different doses.
low doses - renal dose dopamine - 
dopaminergic effect of renal vasodilation and some dilation of mesenteric 
and coronary vessels. as dose increases to 3-10 ug/kg/min you start 
seeing beta effects - binds b1 and b2 receptors, causing increased HR and 
contractility. over 10 ug/kg/min you start seeing alpha effects with 
vasoconstriction. so effect is highly dose dependent. so - if animal is 
not peeing well - foal in ICU - they give a bit of dopamine to increase 
renal blood flow, that doesn't work, you give more dopamine, increase CO, 
maybe it will help. we don't use it that much, some other schools do. in 
small animals, usually we don't really need anything unless the animal is 
really sick - and dopamine's effects depend a bit on norepi release, so 
not good in sick animals.

ephedrine - has some mild direct beta effects 
but primarily acts indirectly by causing catecholamine (norepi) release 
from nerve terminal. generally give ephedrine as a bolus, takes a few 
minutes to work, you get alpha and beta effects for 5-10 min until norepi 
is taken back up. not used that much here but at NBC is used b/c you may 
anesthetize a horse and it's lying on its back and waiting for surgery 
and the surgeon isn't ready yet - what do you do? you have horse 
anesthetized, you don't have any surgical stimulation - can give some 
ephedrine to buy some time.

vasopressors:
alpha agonists:
phenyleprhine, 
epi, dopamine, norepi, methoxamine (not used, some beta effect)

inotropes: beta1 agonists: epi, dopamine, dobutamine

anticholinergics: 
atropine, glycopyrrolate (small animals better, horse - worry about 
ileus)
phosphodiesterase inhibitors - used very rarely - amrinone, etc - 
increase cAMP levels and contractility
calcium - use if animal is 
hypocalcemic, hyperkalemic, hypermagnesemic, or on aminoglycosides. be 
careful - hypercalcemia can make ischemia reperfusion injury a lot worse. 

blocked hyperkalemic cat - often tx with calcium.

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soma


congratulations. you did well on the exam. if you got under 70, you are 
failing. there will be a review session prior to the final. usually it is 
the day before. this year the exam is on thursday. regarding the essay - 
you had to say that the major difference between the drugs was the method 
of administration if you wanted to get a really good grade - that was how 
to get his attention. if you just explained how one worked, and then how 
the other one worked,that wasn't good enough b/c it didn't demonstrate 
thinking, it just demonstrated giving back the material discussed in 
class. you had to say specifically that the only difference was the 
method of drug delivery.

anyway - acid base balance is the topic for 
today. the goal is to be able to read a strip of CO2,O2, pH, bicarb, BE, 
O2sat results, and say "oh, i know what the problem is and I know what to 
do!" there are some other things to explain too, but this is the basic 
goal. look at blood gas results and come up with rational diagnosis and 
treatment plan.

henderson-hasselbach equation - pH =pK + log 
HCO3/CO2*solubility

usually pKa is 6.1 - that's pretty much a constant 
for the hydration of CO2 and ionization of H2CO3. HCO3 is actual 
bicarbonate in mEq/L

PCO2 is partial pressure of CO2 in mmH
S = 
solubility of CO2 in plasma (0.03)

changes in pH and acid base balance 
can be due to addition or subtraction of CO2. hyperventilation --> 
respiratory alkalosis ; hypoventilation --> resp acidosis.

additions of 
fixed acids or bases can also cause changes in pH and acid/base balance - 
exercise --> lactic acidosis --> metabolic acidosis
changes in pH can 
also be due to changes in both fixed or respiratory components.

pH of 
7.1 = severely acidotic, acidemia
normal = 7.35-7.42
what causes this? an 
infusion of acid could do this. retention of CO2 could do this. you don't 
know what the problem is just from the pH. could be metabolic, 
respiratory, or mixed. 
pH of 6.9 is extremely low. animal could have a 
pH this low and survive, but you have to do something.

CO2 and 
bicarbonate.
when a gas dissolves in a liquid, the concentration is 
directly proportional to its partial pressure. this represents the PaCO2

equilibration of CO2 in plasma:

CO2 + H2O <=> H2CO3 <=> HCO3 + H

PCO2 * 
S = dissolved CO2 + H2CO3
therefore

[something - he changed the slide]


pure respiratory acidosis
if you fix your bicarb - say you have bicarb of 
24, and PCO2 of about 40, what's your pH going to be? 7.4
if you deviate 
from this by adding or subtracting bicarb or CO2, you will change the pH. 
so, with the bicarb fixed, any change in pH results from changes in CO2.


changes in pH related to CO2 
if you fix the bicarbonate at 24, and add 
CO2, you develop a pure respiratory acidosis - with a PCO2 around 80, pH 
is about 7.1
if you remove CO2 with bicarbonate fixed, you get a pure 
respiratory alkalosis - with pCO2 of 20, pH is 7.7

ok, now, how about 
changing the bicarb? if you increase bicarb to 32 meq/L, you move the 
curve to the alkaline side - now, if you vary the CO2, you can have a 
mixed acid base disturbance - with the curve shifted you have metabolic 
alkalosis and either a respiratory alkalosis or acidosis - this is the 
combination of adding fixed base and moving the CO2 around. 
if you add 
acid so that bicarb is down to 16 meq/L, you have a metabolic 
acidosis,with respiratory acidosis or alkalosis.



pH - HCO3 diagram - 
see handout! the thing is split into quadrants. the big line is a pCO2 
isobar where pCO2 = 40. anything along that line has a pCO2 of 40. if you 
move to either side you create a respiratory acidosis (if you increase 
the CO2) or alkalosis (if you decrease CO2). 

if you move along one of 
the lines, you have a pure disturbance. everything in the quadrants is a 
mixed disturbance.

if dr soma put kirsten on a ventilator and maintained 
her pCO2 at 40 and then infused HCL, she'd move down the metabolic 
acidosis line.

so how do you interpret mixed disturbances? check out the 
nifty pH - HCO3 diagram with PCO2 isobars and buffer curves. woops - the 
pointer died. hmmm hmmm. Tripp is donating his umbrella to the cause. 
would this happen at cornell.
if your pCO2 is 20 mmHg, and your pH is 
about 7.48, you have a respiratory alkalosis and metabolic acidosis, even 
though the pH is near normal. this is probably some compensatory 
mechanism at work here, but you don't know which came first...underlying 
respiratory problem with compensatory acdosis or underlying metabolic 
problem and compensatory hyperventilation.

usually you do not compensate 
to as great a degree as there is on the graph, but this is just to get 
the idea.

if your pH is acid, there is an acidemia. you don't know what 
the acid base disturbance is. if you have pH 7.1 and pCO2 80, you have a 
respiratory acidosis. there may be a metabolic component though - you 
need to know what the bicarb is. unless of course you memorize the graph.


slide: graphic representation of respiratory compensation:

if you follow 
the lines, you can see how you can get a metabolic acidosis, and then 
hyperventilate to compensate that and develop a respiratory alkalosis, 
and have a normal pH of 7.4 - but there is still an acid base 
disturbance. usually it doesn't balance out exactly, you just have a less 
severe metabolic alkalosis, but it is still a mixed acid base disturbance 
where you develop a second disturbance in response to a primary 
disturbance. if you take this animal and anesthetize it, it will then end 
up with a worse problem, because it will stop hyperventilating, will 
accumulate more CO2, and will be more acidotic. if you then choose to 
hyperventilate the animal, you can correct the pH and you still have a 
metabolic acidosis with respiratory alkalosis compensation. to fix the 
acidosis, give some bicarb. again - note that from the graph alone, you 
can't tell if the primary problem is the metabolic one or the respiratory 
one. you need history to figure that out. 

this stuff is fairly 
clear...it's not difficult <-- dr soma, quote of the day

in vivo vs ex 
vivo buffer curves:

look at the normal buffer slope - when accumulating 
CO2, you are getting acidotic, and bicarb is going up. why is bicarb 
going up? also pH is going down - you are getting more acidotic. moving 
from pCO2 of about 20 to 80 you go from bicarb of about 20 to 26 and a pH 
of about 7.6 to 7.2

so, if you have high CO2 you have respiratory 
acidosis. that is the definition of respiratory acidosis. so why is 
bicarb going up? henderson hasselbach...
in vitro if you equilibrate 
blood and CO2 you get a straight line - no curve - because there is no 
buffer system. in vitro, you take CO2 and mix with H2O, you get H+ and 
HCO3+ and the H+ goes into RBCs to get buffered, and bicarb goes into 
extracellular compartment to buffer changes at the cellular level. so 
there is a small increase in bicarb b/c red cells are a major buffer for 
H+ and bicarb moves into extracellular compartment - out of blood, into 
interstitium. what happens to CO2? it moves into RBCs where it meets 
carbonic anhydrase, becomes bicarb and H+, H+ stays in RBC, bicarb moves 
out into plasma, and then into extravascular compartments. but you have a 
respiratory acidosis with a slight increase in bicarb. this confuses 
people but try to remain calm.

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