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anesth
4/21
olson
cardiac arrest

causes of cardiac arrest

recognizing it
treating it

most important thing in an animal that has 
arrested is to recognize the problem immediately. seconds are crucial. 
not noticing is BAD. you must find it immediately. 

the main thing you 
are looking for,that you will notice, is apnea. once heart stops, 
respiration stops. no functional ventilation occurs. sometimes, an animal 
lies there and does a few agonal breath type things - that isn't 
breathing, it's reflex action, don't confuse that with respiration. if 
you see that as the first peculiarity it's probably too late. you should 
have noticed this before. you see an animal that:
has no respiratory 
motion, or
is trying to breathe but can't - no air flow (heart will stop 
soon)
has no functional circulation (this isn't grossly visible)

check 
for apex beat with your hand or stethescope. many people palpate for a 
pulse - this isn't correct. heart may be beating but blood pressure may 
be so poor that there is no pulse. you don't want to do compressions if 
heart is beating. 
also you will see color change - pale, grey, ugly mms 
- later change.
loss of consciousness
dilation of pupils within 45 
seconds of cessation of heart
unresponsive pupils
cessation of 
intraoperative bleeding is a late sign. usually there is venous bleeding 
for a while after cardiac arrest, although arterial bleeding stops.


causes: there are many, they are listed in the handout. some are more 
common than others. pretty much anything can cause it. it's important to 
try to recognize what might have caused it in that particular animal. you 
want to prevent recurrence.

those who have taken CPR/ACLS classes have 
seen the AHA algorithms- generally the same as ours. 

ABCDE:

A: 
assessment, airway
B: breathing
C: compression, circulation
D: drugs, 
defibrillation
E: EKG, evaluation

main things are ABC. first establish 
airway and breathing. can't start heart without oxygen. C - cardiac 
compressions. all the rest is gravy. 

AIRWAY:
depending where you are, 
the best thing you can do is place an ET tube immediately, blow up cuff, 
isolate trachea andlungs. you can, if you do not have an ET tube, use a 
mask or use mouth to nose breathing. you can't get good mask fit to face 
in general. probably shouldn't waste time trying to ventilate by mask. 
mouth to nose would work better. the problem with mask/or mouth to nose, 
is that you haven't isolated trachea - some of the breath will go into 
the stomach, which will fill up with air, and impede ventilation of 
lungs. now it is harder to ventilate, and there could be regurgitation. 


BREATHING: it's hard to give a rate - depends on size of animal, species. 
fairly rapid is good, 100% O2 is best. you must consider O2 as a drug. 
the first drug you give for cardiac arrest is O2. often intubation and 
ventilation with 100% O2 will be enough to start the heart. also can 
ventilate with room air via ambu bag if you have to. 

CIRCULATION: two 
possibilities: external or internal cardiac compression. this is huge 
part of the process. you need to get blood moving. you want it moving 
from heart to brain. maximize your forward blood flow!
during cardiac 
arrest, heart and brain are the only things you are worrying about. 
everything else can wait 20 minutes or so, but heart and brain will die 
if you don't restore blood and oxygen immediately. so, with external 
compressions - the first description of this in people was published in 
1960, in JAMA - and was huge news. before that, they used internal 
massage. but this paper talked about 20 patients that had arrested and on 
whom they used external compressions - all 20 were resuicitated, and 14 
out of those survived with no CNS damage. this was a MAJOR thing. 70% 
survival is unheard of these days. part of the thing is, though, most of 
those patients were under anesthesia, and a lot of the arresting was due 
to a halothane overdose. this kind of arrest will have a high 
resuicitation rate b/c you can quickly get rid of the drug, patient is 
already intubated and on oxygen. there you go. so after this paper people 
went nuts and started doing lots of external cardiac compression.
then in 
1976 another paper in JAMA - cited 8 people having coronary cardiac caths 
- at high risk of v-fib - and 8 of them suffered v-fib. 3 remained 
conscious during v-fib by coughing every 1 to 3 seconds. all converted to 
sinus rhythm following electrical defibrillation and survived to be 
discharged. realize, they had defibrillators sitting right there in the 
room ready to go.
the v-fib episodes lasted only 24-45 sec.  the coughs 
produced peak aortic pressures in the range of 140 or so. in the people 
who passed out and had external cardiac compression, the peak aortic 
pressure ranged from 42 to 75. the coughing generated much higher 
pressures. this caused a bit of a stir. people discussed it and figured 
out what causes forward blood flow in a cardiac arrest situation when 
doing external cardiac compression (ECC) - at first they figured they 
were compressing heart b/w sternum and spine, smushing heart, making 
ventricles smaller physically, blood has to go forward since other valves 
are shut - and they thought blood flowed b/c you made ventricles smaller 
and blood had to go out. but, that wasn't really the case. how do you 
explain the coughing? there is no compression. why did those people 
generate pulse pressure? well, there is some argument about this. cardiac 
pump theory people think it's as already described - you make heart 
small, blood goes out, you let go, heart sucks blood in. but the thoracic 
pump theory accounts for how coughing works. this says that if you think 
of thoracic pump as right heart, pulmonary vasculature, and left heart - 
they say pressure in all those areas is the same. you only get flow with 
pressure difference. they say when you push on chest you increase 
intrathoracic pressure all over, so the arteries with rigid walls stay 
open, but the veins collapse and valves close - so you increase 
intrathoracic pressure above systemic pressure, and blood flows forward 
through arteries. you're moving all blood not just ventricular blood. 
then when you release, pressure drops, blood flows into heart. the vein 
valves are important. 
which is true? probably depends on who you are 
working for :)
you can find studies to support either one. maybe it is 
both. more important may be size of patient. it probably isn't that hard 
to squish heart of dog/cat or even person. but big dog, foal, calf, 
horse, there is no way you are physically compressing the heart. it's 
just not happening. so maybe in some patients it's cardiac pump and 
others it is thoracic - or maybe it is both. we do not know. an important 
consideration is - it might make a difference which mechanism is in force 
for how you do your CPR. if you think you are squeezing the herat, you 
want to compress right over the ventricles - as in a small cat. for 
thoracic pump, it really doesn't matter, and in fact the best place to 
compress would be at widest point of thorax to create the biggest 
pressure gradient. you might want to jump up and down over widest part of 
horse thorax, but squeeze cat ventricles.

cerebral blood flow is 
important and myocardial blood flow is important. 
so, what determines 
flow to brain? cerebral perfusion pressure is related to difference b/w 
carotid artery pressure and intracranial pressure. with a high 
intracranial pressure, flow is reduced. you want high carotid artery 
pressure and low intracranial pressure. the brain is perfused during 
systole.

myocardial blood flow - perfusion occurs during diastole. the 
determinants of flow through coronary arteries is the aortic pressure and 
aortic diastolic pressure (right atrial pressure). 

studies have been 
done, and pretty much it is accepted that -
they measured aortic 
diastolic BP in animals and animals that survived cardiac arrest always 
had higher pressures than animals that didn't survive. so it makes sense 
that aortic diastolic pressure is a determinant of your success.


prognostic factors: aortic diastolic pressure and coronary perfusion 
pressure 

how you can improve those things during external cardiac 
compression is a good thing to know. 

ECC: it's important when doing 
this that the animal be in lateral recumbency (sometimes people try 
dorsal recumbency, but that probably isn't working as well) and that you 
work with your elbows locked, and use two hands for a bigger animal, or 
maybe one for a cat. push hard! you have to push hard. you should get 
tired in a minute after doing this. if you do not you aren't pushing hard 
enough. another important thing is to say you are tired when you are 
tired, and get someone to replace you. as you tire, forward blood flow 
slows significantly. 

internal cardiac compression, ICC: peter benton 
does this on ER all the time. If you are going to try it, and you might 
in a dog or cat one day (probably not a horse or foal or heifer), you 
would make a lateral thoracotomy incision above the 4 or 5 rib space 
(behind the elbow when the leg is in the normal position). make incision 
big enough to get a hand or two in, and make it down to about the 
costochondral junction - but do not go too far down or you will cut a 
brachial artery. to do internal compression, you can't spend a lot of 
time worrying about sterility. if you do you will waste too much time. 
maybe one pass of clippers, splash with alcohol, put on gloves IF your 
hands are dirty, make one big cut through skin, one through muscle - it's 
hard to do compressions w/o rib spreaders b/c ribs will hurt your wrist. 
some people open pericardium, some don't. it takes time. some people 
think opening it helps 10% or more, some people think it wastes too much 
time. it's up to you. one or two hand technique depending on size of 
heart. compress from apex to base. blood should go in that direction, out 
the aorta. 

advantages of ICC: can directly see heart, see cardiac 
filling, if there is any myocardial activity, or can make an IC 
injection. it also allows compression of aorta - you can stick your hand 
there and squeeze the aorta and prevent blood from going to distal parts 
of the body and lets you direct blood to the head/heart. this allows 
improved cerebral and cardiac blood flow. squeezing heart directly is 
obviously going to push more blood.

indications for ICC: thoracic wall 
injury, broken ribs - can't do ECC. 
barrel chested or large breed dogs

pneumothorax, pleural effusions
cardiac tamponade
ineffective ECC - if 
you aren't getting blood flow, you have to pronounce death or open the 
chest.

adjuncts to ECC: simultaneous compression/ventilation CPR 
(SCV-CPR)
interposed abdominal compression CPR (IAC-CPR)
high impulse CPR


SCV-CPR: people who believe in thoracic pump think that increasing 
intrathoracic pressure by giving a breath will promote more blood flow. 

numbers of studies have been done and we haven't seen improved outcome 
with this. some studies suggest that this increases cerebral flow but 
decreases myocardial flow. that isn't that useful. so she's not 
recommending this technique to us - don't worry if it happens 
accidentally, but don't do it on purpose.

IAC-CPR: pretty easy. two 
people. chest compression, then abdominal compression, then chest 
compression, etc. lather rinse and repeat. why do we do this? pressing on 
the abdomen will increase the abdominal pressure, reducing flow from 
aorta into abdomen, increasing aortic diastolic pressure, which we want 
to do, rmember? also helps improve venous return, we think.
studies have 
shown increased survival rates, and increased return of spontaneous 
circulation (ROSC), and increased survival without CNS damage using this 
technique vs standard CPR. 

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ways to improve forward blood 
flow - cont.

high impulse CPR was mentioned

for people, a rate of 60 
has been suggested.this wouldn't be good for a cat. we have to adjust 
this. the rate is figured out how? well, you improve forward flow if you 
increase rate. AHA now suggests a rate of 80 bpm. think about parts of 
compression that contribute to flow.

if you do it faster, you get more 
flow
if you use more force, you get more flow - regardless of if it is 
cardiac or thoracic mechanism. you don't want to break ribs or cause lung 
contusions though. 
duration of compression - as a % of 
compression-release cycle - when you increase the rate, your amount of 
time in the compression phase of the cycle is increased. 
at a rate of 60 
bpm, your cycle is 1000 msec, and your compression takes 300 msec, so 
that's 30%. at a rate of 100 bpm, your cycle is only 600 msec long, and 
your compression is still 300 msec so it is now 50% of the cycle.


different rates have been studied - they compared 60 bpm to 120 bpm in 
dogs or pigs or something, and the higher rate had a higher survival rate 
for both defibrillation and 24 hr survival.

so for people, try to do 
about 80, for a cat, go as fast as you can. for a horse, you can't do it 
at 80/min because you are jumping up and down, using your knees or your 
butt - do it as fast as you can. 40/min?

ECC vs ICC - sure, internal is 
better at promoting flow. ECC resuicitates a lot of people to a 
vegetative state. ICC produces a higher aortic pressure at all times and 
a higher mean cardiac index - drastically higher.

ECC + Epi produced 
better pressures and cortical blood flow than without epi
ICC was way 
better than either

10 dogs got ECC for ten minutes, then half got ICC 
and half got ECC then they were defibrillated - ICC had better 
resuicitation rates. way better. all the ECC ones died. 4 out of 5 of the 
ICC ones lived.

she's showing many studies - ICC produces much much 
better chance of survival is the bottom line. 

in a human prospective 
clinical trial on witnessed cardiac arrests - 49 patients, all arrested 
with witness present - some got ECC and some got ICC - but there was no 
difference in resuicitation rate. total down time for both groups was 
18-19 minutes, downtime before CPR was about 5 min for both. if you are 
going to open the chest, therefore, you have to do it right away, or you 
lose the advantage. 

DRUGS:

epinephrine - alpha/beta mixed agonist. 
this is the main drug used. why was this drug chosen as the drug to give? 
look at the effects:
alpha: arteriolar vasoconstriction (good - sends 
blood centrally), venoconstriction
beta: increased HR, stimulation of 
myocardial contractoin, increased force, etc.

so, how much do you use? 
in people they used to use a 1 mg dose for some reason. this was 
extrapolated from studies using 1 mg epi in 20 kg dogs. so someone 
thought "that's odd" and did a dose response curve type of study. now, 
there is a lot of debate about this. 

high dose vs low dose epi: 
standard dose 5-15 ug/kg IV; high dose is about 200 ug/kg IV

minimum 
critical blood flows to keep heart and brain alive - to maintain these 
tissues there are specific amounts of flow required. they did a study in 
pigs using standard epi dose, and multiples of that dose. they also 
measured flow after drug administration. with standard dose, only the 
left ventricular epicardium got enough flow. at higher doses, the minimum 
critical flow was exceeded for all the important tissues. for the brain, 
results were similar. 

so people started thinking about using more epi. 
in JAMA 1988 a case report was published on 2 people, an old guy and a 20 
yr old girl. both arrested and came in after standard CPR and normal 
protocols. after 30 min, wasn't working,they tried high doses of epi, and 
both were resuicitated after that. the old guy died later, the girl 
survived and was kind of ok. this got people more excited. 

but, that 
was two people. in 1992, two studies were published - they found no 
difference in the ultimate survival time to discharge using either dose 
regimen.

so what do you do? some people are aggressive about using high 
epi doses. some are not. plenty of times standard doses work. blasting 
epi and then getting tachycardia and hypertension is dangerous. if after 
ten minutes you're not lucky maybe increase the dose...really it's up to 
you.

there is an algorithm in the notes for how to manage cardiac 
arrest. no matter what rhythm the animal is in - v-fib, asystole, 
whatever - you always treat with epinephrine and oxygen. give it 
often,every 3-5 minutes. it is short lived. 

EKG findings - 
v-fib: 
chaotic, disorganized, squiggle
asystole: flat line
EMD - 
electromechanical dissociation: looks normal. this is induced by 
euthanasia solution. EKG continues for minutes, looking pretty normal. 
could also look kind of abnormal or grossly abnormal. but usually starts 
out looking normal, then over time degrades into wide bizarre complexes

severe sinus bradycardia - HR of 5 - pseudo-arrest

treatments:


fibrillation can be fine or coarse. based on width of waves. fine 
fibrillation probably shows more disease, less happy heart. give epi to 
fine fib cases. defibrillate coarse fib. but - defibrillation is the 
definitive therapy for v-fib and if you do not have a defibrillator you 
are screwed. v-fib isn't that common in animals though - more common in 
people who get heart attacks. in people, the faster you defibrillate, the 
more likely you will convert them. same in animals, most likely.

the 
defibrillator has two paddles  (one of which may be round and flat). you 
have to put a lot of defibrillator gel on the paddles and you can't use 
u/s gel or ky jelly - you won't get good conduction. this gel has 
electrolytes in it.
use a lot of gel!
do not ever ever ever ever use 
alcohol on the EKG leads of an animal in cardiac arrest. there is a big 
urban legend that circulates about a little yorkie where they soaked the 
leads in alcohol and when they defibrillated the dog, it caught on fire. 
so, that could really happen. so try to avoid it by not using alcohol.


as dogs get large, you really start needing to use that big flat paddle 
that you slide under it while it is in lateral recumbency. for smaller 
animals you can use two hand held paddles but we discourage this. if you 
have the paddles, it is your job to ensure no one else is touching the 
animal. tell people to get clear, and make sure they do it.

say the 
animal refibrillates. now what? give lidocaine. it will help as far as 
making it easier to defibrillate or retaining sinus rhythm. 

lidocaine 
indications: resistance to countershock; recurrence of fibrillation

bretyllium is also used for v-fib - either in place of lidocaine, or 
after lidocaine fails to help. also, if you have no defibrillator, there 
is an outside chance that ths drug will convert it back to sinus rhythm.


asystole: treat with epinephrine. also may use atropine - if you think 
animal arrested due to vagal stimulation. atropine is anticholinergic, 
increases SA node discharge, improves AV conduction - probably won't 
hurt. 
also sometimes people say "well you may as well defibrillate" but 
if animal is truly in asystole, it probably won't help. there have been 
some reports of this working but most people believe these patients 
weren't truly in asystole. try switching leads to see if EKG is flat in 
all leads. if it is, probably defibrillating won't help, but it won't 
hurt to try - animal already dead.

EMD - sometimes esp in older 
algorithms, they talk about giving calcium. you have electricity without 
contraction - so they gave calcium. but this didn't work. there was no 
improvement in hemodynamics, and sometimes people got dangerously high 
levels of calcium. so you shouldn't just give calcium because it might 
help...it isn't helpful. there might be some indications for calcium - 
but you hav eto know why the animal arrested. if animal was hypocalcemic 
prearrest, give the calcium! if a blocked cat/goat comes in with severe 
hypokalemia, calcium can also help this animal. also use calcium if 
animal has overdosed on verapamil or other ca++ channel blocker.

acid 
base balance and bicarb during CPR: early algorithms started with giving 
bicarb first. historically people thought bicarb made sense. the heart is 
stopped, there is poor blood flow, you're hypoxic, making lactic acid, 
animal is acidotic - give bicarb. but, when this was studied with blood 
gases, they found arterial blood gas values indicating respiratory 
alkalosis - they are blowing off all the CO2 by ventilating. mixed venous 
blood gases show respiratory acidosis - high CO2 - b/c tissues are making 
CO2 but it isn't being transported out well. there isn't really a 
metabolic acidosis unless they've been arrested 15-20 min. they do not 
need bicarb early during tx. 

acidemia causes  many bad things, but so 
does bicarb. so they studied giving it vs not giving it,many times. many 
studies showed either no improvement or worse outcome if they used the 
bicarb. however, those studies werne't that great.

another study was 
done with better adherence to protocols, using normal doses of drugs, and 
they found that using bicarb there was a better outcome. 
indications for 
bicarb - hyperkalemia, blocked cats. 
permitted but not recommended - 
when prolonged arrest, after failed tx

glucose: your brain likes 
glucose. there is a lot of research about cerebral ischemia and 
glucose...

ischemia -> anaerobic metabolism-> lactic acid, increased 
w/hyperglycemia -> acidosis -> increased CNS injury. 

a study done 
retrospectively - in people - people who never recovered had high blood 
glucoses. people who woke up normal had lowest. vegetables were in the 
middle. but maybe the people who never woke up started out sicker, this 
study wasn't that well controlled as a retrospective...but we suspect 
that glucose in the body when blood flow is poor is bad for the brain. do 
not use glucose containing fluids in cardiac arrest patients. use other 
stuff. they're looking now at the use of insulin in these patients.


ETCO2 monitoring during CPR:
probably here they do this in some patients. 
maybe they should if they aren't, anyway. the last breath out of your 
lungs comes from alveoli - this is ETCO2. a function of how much CO2 is 
produced, how much is delivered to pulmonary capillaries, and how good 
alveolar ventilation is. 

they've shown that with the onset of v-fib, 
there is a drastic drop in ETCO2, since blood isn't returning from the 
tissue. when you start ECC, and measure ETCO2, the higher your ETCO2 goes 
(closer to normal) the better, we think, in that the survivors in this 
study had hgher ETCO2 than the nonsurvivors did. the rise in ETCO2 
indicates that blood is moving around and perfusing tissues. 

often the 
first indication you have that heart has started is a large and sudden 
rise in ETCO2. the heart can pump better than you can - you see a sudden 
jump in ETCO2 when blood moves better.

clinical corollaries and pitfalls 
of ETCO2 monitoring:
when people tire doing ECC, ETCO2 starts decreasing, 
b/c compression is less useful. you can monitor when to change people 
this way.
if you give bicarb, it's metabolized to CO2 - giving bicarb 
will cause a rise in ETCO2 unrelated to heart function.
epinephrine 
causes a dose related decrease in ETCO2
hypothermia causes a decreased 
ETCO2
ETCO2 under 0.5% indicates esophageal intubation. if it's over 0.5% 
you're in the trachea. 

when do you stop resuscitating?
if you 
successfully resuscitate, you have restoration of spontaneous circulation 
- an audible heartbeat, palpable pulses, stable rhythm, decent BP. then 
you get return of spontaneous ventilation - maybe right away, maybe 
later. may be delayed hours or minutes. assure the adequacy of 
ventilation before extubation! also, having pounded on the chest and 
caused pulmonary contusions, you may need to ventilate the animal even if 
it wants to breathe on its own. maybe it will need oxygen therapy.
return 
of CNS function- look for presence of pupillary response, palpebral 
reflexes. pupils will be fixed and dilated under influence of epi and 
atropine but if they stay that way after return of HR, worry. look for 
return of spontaneous ventilation and spontaneous movement. 
neuro status 
of post-resuscitation patients may range from alert and responsive to 
comatose, and is not a reliable prognostic indicator during or 
immediately following resuscitation. 

most patients with good neuro 
outcome will emerge from coma within 24 hrs - tx with mannitol, etc. 


this is very frustrated. 
resuscitation rates - 15 arrests, 1 went home. 
18 arrests, 4 went home. 
in human ICU- 294 arrests, 14% went home. 
so 
mortality is going to be high.
duration of CPR correlates to prognosis. 
over 30 minutes - near 100% mortality. 95% mortality if CPR is over 15 
min. repeat resuscitations -> poor px. 

decision to stop a resuscitation 
is based on:
duration of attempt - anything over 30 min is probably a 
waste
age and general health - old patient with multiple dz - poor px. 
puppy with ball causing respiratory obstruction -> better px
cause of 
arrest - due to multisystem failure /hemorrhage? 
owner committment/owner 
desire

most animals that arrest probably will not go home.

once animal 
arrests and you get it back, you have to keep it alive. you must know 
what caused the arrest b/c if you do not fix it it will recur. also 
maintain HR/rhythm, tissue perfusion, ventilation, O2, neuro status, 
acid/base stuff, tx organ failure. feed. bills are very high.


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