# Antiarrhythmic confusion.........



## Sharktooth (Jul 18, 2011)

We briefly started covering ACLS in class  . I thought I had a good handle on it until after class another student posed a question to me . 

During pulseless fib/tac , if you get down the algorhythm to amiodarone  , you give both doses with no conversion.....you get to where its time to give another epi , administer and bam....you get ROSC  . My friend thinks you don't hang an amiodarone drip because they converted on epi not amiodarone? What?  Wouldnt you still hang the drip?


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## Smash (Jul 18, 2011)

They didn't convert on either.  What is their rhythm post ROSC? What is their blood pressure? How long were they in arrest?  How well are they being oxygenated and ventilated? What is their temperature? 

Why would you just automatically start an infusion of amiodarone without considering any of the above?  Amiodarone has significant side effects that you may not want to see happening in the post arrest patient.  It is something that has to be used with great care and only in the right situation. Honestly it is unusual to see VT as the post ROSC rhythm, and if it is you need to consider whether you really want to be pouring more amiodarone into that patient.


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## Sharktooth (Jul 18, 2011)

lets say the rhythm was normal sinus when pulses returned post epi and ,  defibrilation ,   and they had a decent BP , say 102/78 .


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## Smash (Jul 18, 2011)

Sharktooth said:


> lets say the rhythm was normal sinus when pulses returned post epi and ,  defibrilation ,   and they had a decent BP , say 102/78 .



Ok, that BP is not really decent in this setting.  So what do you want to achieve with this patient?  What are their problems and what are your treatment goals to fix those problems?  What does amiodarone do, and how will it address any of those problems?  

I could give you an answer, but it's better to think it through and problem solve.


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## Handsome Robb (Jul 18, 2011)

Can I play?

Amiodarone would be inappropriate in this situation. It is a class III anti-arrhythmic, it prolongs the refractory period as well as has some beta receptor and calcium channel blocking properties. Also, with a half-life of 45 days and 450 mg onboard already and their rhythm being SR post ROSC, I would not even consider an amiodarone drip.

This person's cardiac output needs to be increased and this can be achieved by an infusion of a pressor. I would be tempted to try a dopamine drip at somewhere around 5-10 mcg/kg/min. You could also go with Epi or Norepi at 0.1-0.5 mcg/kg/min.

Alright Smash, be gentle please


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## squrt29batt12 (Jul 18, 2011)

Sharktooth said:


> We briefly started covering ACLS in class  . I thought I had a good handle on it until after class another student posed a question to me .
> 
> During pulseless fib/tac , if you get down the algorhythm to amiodarone  , you give both doses with no conversion.....you get to where its time to give another epi , administer and bam....you get ROSC  . My friend thinks you don't hang an amiodarone drip because they converted on epi not amiodarone? What?  Wouldnt you still hang the drip?



epi doesn't convert the rhythm, it's an alpha1/beta1 agonist. 

yes you would hang the amio maintenance @ 1mg/min since you initially used the boluses(300mg->150mg). you wouldn't want the patient going back into what caused you to give the boluses in the first place would you? and just because it didn't convert right when you pushed the amio doesn't mean the amio wasn't what converted the rhythm.

just my two pennies lol


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## Smash (Jul 19, 2011)

*Grab a coffee, sit back and relax, this could get long-winded...*

OK, let's talk about the post arrest patient.  I'm not going to reference this at this stage as I don't really have time before night shift to go through all the papers.  I can find some later on tomorrow or the next day if people really want them (or you can find them yourselves!)

Let's assume for the purposes of this discussion that we are dealing with a primary VF/VT arrest in a patient who is otherwise young, fit and healthy with no co-morbidities.

Right, we have gone through our ACLS cook book.  Someone has done some good CPR, we have arrived and given some electricity, given some drugs, some more electricity and bingo! we have ROSC.

First of all, the patient did not "convert on" epi or amiodarone.  Epinephrine is given in cardiac arrests for it's alpha-adrenergic effects.  Back in the dim dark ages of the 60s and 70s it was discovered that in animal models (dogs), giving epi increased the pressure gradient in the aorta through vasoconstriction, presumably increasing coronary perfusion, and this then resulted in an increase in the likelihood of gaining ROSC.  Ever since then we have given it willy-nilly to all arrests we come across.  What it does not do is "start the heart" or any such nonsense.  In fact there is a reasonable body of evidence that it is associated with poor outcomes from increased myocardial dysfunction and poor cerebral blood flow.

So what about amiodarone.  As NVRob points out amiodarone is classed as a Class-III anti-arrhythmic, although it is really a class everything anti-arrhythmic.  We give it in cardiac arrest essentially to suppress the irritability of the myocardium, which in theory would make it less likely to want to go back into fibrillation.  (Does anyone see a problem here with using epi and amiodarone?  One increases irritability and the likelihood of VF, the other suppresses it, but at the same time makes the one intervention that works - defib - harder because it raises the defibrillation threshold.  Round and round we go in a rather pointless cycle)

Once again the problem is that there is not any particularly good evidence that amiodarone improves outcomes.  A small trial (the ARREST trial) looked at amiodarone versus lidocaine in cardiac arrest and found a reported 12% versus 24% improvement in survival to hospital with amiodarone.  This is of course a bull:censored::censored::censored::censored: outcome.  The only outcomes that matter are whether the patient gets out of hospital and whether they have any neuro function left, and there was no statistical difference noted in survival to discharge (neuro function I don't think was tracked)

Right, we have ROSC, we have a blood pressure of 102/78 (a MAP of 86mmHg) and the patient is reportedly in a sinus rhythm.  We will assume that the patient is comatose.
So what are our treatment priorities and why?

Lets get the basics out of the way first:  Secure the airway if this hasn't been done already.  (We won't be discussing how, lets just assume the patient is intubated)  Suction the ETT and oropharynx carefully as required.
Ventilate:  I think there is a good thread on EtCO2 running around here, but I aim for a lowish "normal" of around 30-35mmHg (this allows for a small EtCO2 - PaCO2 gradient which in the absence of ABGs is the best I can do really)  We should probably be aiming for an SpO2 of around 95% at this stage as hyperoxia probably helps kill these patient's brains.

Ok, now, circulation.  This kind of gets rolled in with D for disability as well.  This patient has a BP of 102/78mmHg.  That might be fine if they were alive and well, but it is sub-optimal in this situation.  Why is this?  Well there are a couple of reasons.
One is that is a 3 phase alteration in BP following arrest.  First of all as we get ROSC we have a surge in BP as endogenous and exogenous catecholamines go flying around the circulation (all that epi finally gets somewhere!)  We often see high or at least "normal" blood pressure in the immediate post RSOC setting.  However this rapidly falls to low levels before slowly rising again over some time (assuming the patient survives.  We need to avoid this rapid fall and slow rise as much as possible.  Why?

We can think of the post arrest state as being the same as septic shock, with some added nastiness in the brain that is essentially a re-perfusion injury.  Following successful resuscitation there is a widespread inflammatory response (SIRS) much as we see in the septic patient.  This leads to inappropriate vasodilation and constriction, third spacing of significant volumes of fluid, coagulopathy and myocardial dysfunction.  Coagulopathy and increased capillary permeability and inappropriate constriction/dilatation causes regional areas of "drop-out" of perfusion to organ beds which eventually becomes global.
The gut gets angry and lets the poo out (well the bacteria anyway as normal gut flora migrates though leaky gut) and exacerbates this inflammation.  The kidneys say "No Sir! and stop working as effectively as well as poor perfusion and renal vasoconstriction decreases GFR.  The liver also packs up, causing a build up of ammonia and adding to coagulopathy as less clotting factors are produced.  The heart gets "stunned" and cardiac output falls, although this is not permanent if the patient survives.

Now the brain:  Damage to areas of the brain releases a stew of excitatory neurotoxins like glutamate and calcium.  Swelling occurs which impairs cerebral blood flow and can increase ICP.  Ongoing hypo-perfusion exacerbates this and we start to see cells undergoing apoptosis, which of course furthers the release of excitatory transmitters.

So lets sum up - Post arrest we have an initial hyper-dynamic state, followed by crap perfusion, SIRS, lots of excitatory neurotransmitters revving the brain up and burning it up, swelling in the head and poor cerebral blood flow.  Crap, he's sick!

So what can we do about it?  First of all - perfusion.  Lets get some decent blood pressure going.  We really want to perfuse the brain as well as we can, we need to get GFR up to keep the kidneys going, if we can get the gut going maybe it will stop letting the poo out, and start providing energy for the patient again, the liver might give us some more clotting factors, and maybe we will have a chance at getting out of here in one piece.

So lets get some good blood pressure going by giving some crystalloids (and probably quite a lot of them) and starting some pressors.  I personally don't think it matters what pressor we use; there are theoretical differences, but as long as we are giving something as soon as possible I don't think the patient cares.  But we want to aim for a BP that is a lot higher than 102/78.  I aim for a bare minimum diastolic of 120mmhg, and if I can have it around 150mmhg without flogging them too much I'm happy.  We need to get good CBR and CPP going as soon as possible.  I always have some push dose pressors ready to go during the arrest so I can jump on that BP ASAP post arrest, and I get an infusion ready as soon as practical.

So what about this reperfusion injury in the brain?  Well, we essentially have too much.  Too much nastiness in the form of glutamate and calcium and so forth.  So what do we do when we have too much something?  We dilute it.  So again, lots of fluid.

But these things are excitatory - they are increasing neuronal energy demands at a time when it can't be met.  This is obviously bad.  So how do we slow things down?  We make them colder - so lets use some ice-cold crystalloids and get the patient's temperature down to about 34 degrees Celsius.  This temperature reduces metabolic demand significantly (every one degree drop in demperature reduces basal metabolic rate by about 7%), but is not pro-arrhythmic, and therapeutic hypothermia is an absolute must now as it is well established to improve functional outcomes (outcomes the patient actually cares about, like whether their brain works or not.) 

So our goals for the post arrest patient are: 
Hypothermia (Slow it down)
Hypertension (Perfuse it well)
Hemodilution (Flush it out)

So, how does amiodarone fit into this equation in post arrest patient?  Well, what would happen if we give amiodarone?  It would prolong the refractory period of the myocardial cycle.  Do we need to do this?  Will it help?  Our myocardium is already depressed and we don't have an arrhythmia to fix so I would say no.  It will also drop blood pressure.  Do we want this?  No, of course not, the thing we want is good perfusion, not crap perfusion.

What if they do develop VT again?  Well, in my admittedly limited experience, this is rather rare.  However, I would consider this patient to be unstable - they are post arrest with tenuous perfusion in a peri-arrest rhythm.  I would consider cardioversion to be the first course of action here.  If they did stay in VT, then I may consider a very cautious infusion to attempt to quieten things down, but this is going to be difficult and fraught with danger.

So, I hope this answers your question SharkTooth.


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## Smash (Jul 20, 2011)

Well, I'm pleased I wrote all that up....


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## Handsome Robb (Jul 20, 2011)

I'm still trying to process all of it.


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## Smash (Jul 20, 2011)

NVRob said:


> I'm still trying to process all of it.



 
It's ok, I'm post night shift grumpy is all!


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## MrBrown (Jul 20, 2011)

Brown thinks Smash is looking more and more like some sort of super intelligent non human robocop type cyborg ambo who has scanned every research article into his computer memory

Good post mate


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## Aprz (Jul 20, 2011)

I agree with Brown. Good post Smash. Thank you for your time.


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## fma08 (Jul 20, 2011)

Why is it every time I see GFR, I can only think of Grand Funk Railroad and not glomerular filtration rate? :wacko:


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## abckidsmom (Jul 20, 2011)

Aprz said:


> I agree with Brown. Good post Smash. Thank you for your time.



Agreed.  Thanks!


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## Smash (Jul 21, 2011)

Thank you, you are all too kind for humoring a ranting angry ambologist who doesn't deserve it!  Sorry I was just a bit tired and grumpy yesterday. I hope I haven't scared sharktooth off!


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## Melbourne MICA (Jul 31, 2011)

*I'm not dead  -I'm getting better*

Whats amazing about all this is:

a) I think that's the longest and most explicit speil you've ever regurgitated Smash - well done

b) so much effort, time and money as well as brain cells is put into procedures for a cohort of patients, the vast majority of whom are having end of life events

c) it is trully amazing that despite our best efforts to kill patients with untested/un-proven procedures or best guess approaches a sizeable proportion (especially here in sunny Melbourne ) decide to kick on for a bit longer, survive us and the ED's annoying interventions and go home for a coldie and a nice feed.

That's the real miracle in all this. The human body (and human spirit?) never ceases to amaze.

MM


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## Trevor (Aug 3, 2011)

hmmmm.... I like the idea about push dose pressors... I've heard a little about push dose pressors on EMRAP, however didnt know anyone pre-hospitally was/can do this. Do you have protocols for this? Or is it more of a "lets do the right thing for the patient" type of thing? My system is pretty progressive, and i can do a lot if its medically the right thing, BUT i think i would have a hard time doing that...

Awesome post btw!


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## Smash (Aug 3, 2011)

Trevor said:


> hmmmm.... I like the idea about push dose pressors... I've heard a little about push dose pressors on EMRAP, however didnt know anyone pre-hospitally was/can do this. Do you have protocols for this? Or is it more of a "lets do the right thing for the patient" type of thing? My system is pretty progressive, and i can do a lot if its medically the right thing, BUT i think i would have a hard time doing that...
> 
> Awesome post btw!



Thanks.

I try not to let protocols get in the way of good patient care, whilst at the same time keeping the QA/QI monkeys off my back.  It's a fine line to walk some days!

I don't have anything nice like phenylephrine which is what I think Scott talks about as push-dose pressors, although I think that was in a different patient context anyway.

The way I see it is if I can run an infusion of whatever, then push dose is the same thing, just spread out a bit.  I do make an effort to get an infusion running a soon as possible, so push doses are just a temporising measure for me to keep that BP around 120-150 systolic until then.

I typically just draw up some extra epi, although 1:10000 rather than the 1:1000 I use during the arrest.  Then if the BP dips I'll give 10 - 100mcgs or so depending on the patient/situation.  Sometimes more, sometimes less, depending on how many rounds of epi they had during the arrest.  If they have already had a bucket load I'll just go straight to 50 or 100mcg boluses as 10 won't even touch the sides as it goes by.

The peaks and troughs associated with this probably aren't ideal, but having a BP fluctuate between 120-170mmHg or whatever has to be better than ambling along with a BP of 70/30 for the next ten minutes.


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## ah2388 (Aug 4, 2011)

Dr. Weingart talks a lot about push dose pressors in the intubated pt when related to sedation..applies to the hypotensive trauma pt also

regards to the last part, it is sort of his solution to the cant give analgesia/sedation because the pt is hypotensive argument


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## Trevor (Aug 4, 2011)

Ya, i know he wasnt talking about a post arrest patient. I just havent heard many other lectures about this particular topic... 

Smash- I know what ya mean about trying to keep the QA guys at bay... By the way, why do you choose to use 1:1000 during arrests?


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## Smash (Aug 4, 2011)

Trevor said:


> Ya, i know he wasnt talking about a post arrest patient. I just havent heard many other lectures about this particular topic...
> 
> Smash- I know what ya mean about trying to keep the QA guys at bay... By the way, why do you choose to use 1:1000 during arrests?



Ease of use. I draw up four or five ampules (4 or 5mg and mls) and just give 1mg (1ml) at a time during the arrest.   We don't carry any prefilled syringes of anything except naloxone, and this is the way it has been done since Moses was a choirboy.


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## Melclin (Aug 4, 2011)

Scott Weingart's pod-casts make me moist.

Honest to god, I've listened to most of the 50 or so podcasts 2-3 times.


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## Trevor (Aug 4, 2011)

ya he seems to know what hes talking about...


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## hyperlyeman1 (Aug 18, 2011)

Sorry to bring this one up smash...
But what about a lido drip instead? Same principle, because it is trying to accomplish the same goal? or different outcome because of a different MOA? We don't carry amiodarone.


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## Smash (Aug 18, 2011)

hyperlyeman1 said:


> Sorry to bring this one up smash...
> But what about a lido drip instead? Same principle, because it is trying to accomplish the same goal? or different outcome because of a different MOA? We don't carry amiodarone.



No need to apologize. I would consider this the same principle/problem as amiodarone.  We are aiming for the same thing with both, and although the Na channel blocking with amiodarone is augmented by a bit of everything blocking, you will still see the same problems of hypotension and myocardial depression with lidocaine. 

The actual evidence for any difference in meaningful outcomes between the two is essentially negligible, and for that matter between either and nothing.


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## hyperlyeman1 (Aug 18, 2011)

Now what about lido/amiodarone in conjunction with a vasopressor? Would you consider that to be counter-intuitive?


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## usafmedic45 (Aug 18, 2011)

How about calling organ procurement and letting them know you have a new case for them?


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## Smash (Aug 19, 2011)

hyperlyeman1 said:


> Now what about lido/amiodarone in conjunction with a vasopressor? Would you consider that to be counter-intuitive?



In a word: yes.

It's kind of like the seesaw that some people like to get on with giving fluid to a right ventricular infarction and then giving nitrates: increasing preload to allow you to decrease preload is strange and frightening to me.  This is the same sort of thing.


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## usalsfyre (Aug 19, 2011)

Smash said:


> It's kind of like the seesaw that some people like to get on with giving fluid to a right ventricular infarction and then giving nitrates: increasing preload to allow you to decrease preload is strange and frightening to me.  This is the same sort of thing.



I'm glad I and the American College of Cardiology aren't the only ones.


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## Hunter (Aug 19, 2011)

Smash said:


> It's kind of like the seesaw that some people like to get on with giving fluid to a right ventricular infarction and then giving nitrates: increasing preload to allow you to decrease preload is strange and frightening to me. This is the same sort of thing.


 

I think moe acurate description would be; increasing preload, to decress preload and cardiac oxygen demand.

do one positive thing, so that you can do 1 negative and 1 positive?


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## usalsfyre (Aug 19, 2011)

Hunter said:


> I think moe acurate description would be; increasing preload, to decress preload and cardiac oxygen demand.
> 
> do one positive thing, so that you can do 1 negative and 1 positive?



Except the way NTG reduces MvO2 is by reducing preload.

So why increase it to decrease it :wacko:?


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## Hunter (Aug 19, 2011)

usalsfyre said:


> Except the way NTG reduces MvO2 is by reducing preload.
> 
> So why increase it to decrease it :wacko:?


 
I'm not a 100% on this but here goes

You increase preload by increasing blood volume, and then decrease it by vasodialation, the vasodialation delivers more Oxygen to the mycardium...

So I think the result is just a bigger container with out having the patients BP drop way too low?


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## usalsfyre (Aug 20, 2011)

Hunter said:


> You increase preload by increasing blood volume, and then decrease it by vasodialation, the vasodialation delivers more Oxygen to the mycardium...
> 
> So I think the result is just a bigger container with out having the patients BP drop way too low?



Problem with this theory? NTG has very little effect on the coronary arteries, EMT and paramedic books aside. NTG has a much more pronounced effect on the venous side of the vascular system (hence the preload reduction). To vasodilate the arterial side of the system your looking at something like Cardene or nitroprusside, which besides making me shuddder at the thought of some of my coworkers playing with is actually somewhat counterproductive in the setting of MI as it may reduce coronary perfusion pressure. Decreasing preload reduces left ventricular wall tension(the main determinant of coronary perfusion, lower tension=better perfusion) however in the setting of right sided MI left sided preload is going to be crappy anyway. Meaning you won't have enough preload to generate a decent stroke volume.

The American College of Cardiology states NTG is a Class III intervetion (not helpful and may be harmful) in the setting of right sided MI. Any paramedic who thinks "balancing" fluid and NTG in this case is a good idea is going against the reccomendation of the largest body of cardiologist in the country.


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## Hunter (Aug 20, 2011)

usalsfyre said:


> Problem with this theory? NTG has very little effect on the coronary arteries, EMT and paramedic books aside. NTG has a much more pronounced effect on the venous side of the vascular system (hence the preload reduction). To vasodilate the arterial side of the system your looking at something like Cardene or nitroprusside, which besides making me shuddder at the thought of some of my coworkers playing with is actually somewhat counterproductive in the setting of MI as it may reduce coronary perfusion pressure. Decreasing preload reduces left ventricular wall tension(the main determinant of coronary perfusion, lower tension=better perfusion) however in the setting of right sided MI left sided preload is going to be crappy anyway. Meaning you won't have enough preload to generate a decent stroke volume.
> 
> The American College of Cardiology states NTG is a Class III intervetion (not helpful and may be harmful) in the setting of right sided MI. Any paramedic who thinks "balancing" fluid and NTG in this case is a good idea is going against the reccomendation of the largest body of cardiologist in the country.


 
Unfortunatly what was taught to me was that a, + V4R means you check the BP(Which you would anyways for NTG)  if it's less than 100 you increase preload so that when you administer NTG it doesn't drop the BP way too low... it seems that any medics I've spoken to in ride alongs agree with this...


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## MrBrown (Aug 20, 2011)

GTN is used in the setting of cardiac ischaemia to reduce preload and increase cardiac perfusion.  Preload is reduced by dilatation of the large veins resulting in venous pooling and reduced venous return to the heart.  By reducing preload there is a negative domotropic effect on the heart muscle and possibly some dilatory effect on cardiac vessels.  These effects reduce workload of the heart and increase oxygen delivery to the myocardium.  

GTN > (mitochondrial aldehyde hydrogenase) > NO2 > cGMP > decrease Ca++ > venous smooth muscle relaxation

There is little role for GTN in STEMI and almost certainly no role in right ventricular infarct.


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## Melclin (Aug 20, 2011)

Hunter said:


> Unfortunatly what was taught to me was that a, + V4R means you check the BP(Which you would anyways for NTG)  if it's less than 100 you increase preload so that when you administer NTG it doesn't drop the BP way too low... it seems that any medics I've spoken to in ride alongs agree with this...



"9/10 American paramedics agree" is pretty much at the bottom of my hierarchy of evidence, just bellow "I once heard Alice Cooper say it" and only slightly above "the people write sexual advice on the toilet doors in pubs".  (Mods relax, I'm just taking the piss).

Anyway, the above sounds like a pretty good recipe for iatrogenic cardiogenic shock. You don't seem adverse to learning so I'd recommend reading a detailed script on Nitro pharmacology, like that from Goodmans and Gilmans. I'll send you an excerpt if you're interested and wanna PM me.


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## Melclin (Aug 20, 2011)

Hunter said:


> You increase preload by increasing blood volume, and then decrease it by vasodialation, the vasodialation delivers more Oxygen to the mycardium...



Oh and I was ganna address this. 



> When nitroglycerin is injected or infused directly into the coronary circulation of patients with coronary artery disease, anginal attacks (induced by electrical pacing) are not aborted even when coronary blood flow is increased. However, sublingual administration of nitroglycerin does relieve anginal pain in the same patients. Furthermore, venous phlebotomy that is sufficient to reduce left ventricular end-diastolic pressure can mimic the beneficial effect of nitroglycerin.



From G&Gs. 

Basically this is part of a paragraph that I think can be summarised by saying this: While nitro does cause a degree of coronary artery dilatation, it doesn't ultimately have any clinical affect on ischaemia and injury. Ischaemia is all about a supply/demand deficit. Too much demand, not enough supply. Instead of increasing supply like it was once thought to, nitro probably causes its affects my reducing demand. It does this through preload reduction. Essentially the less it has to pump, the less it has to work.

So you can see then, if you take the coronary artery dilatation out of the equation, the preload increase with fluid only to reduce it with nitrates is a bit pointless.


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## usalsfyre (Aug 20, 2011)

Hunter said:


> Unfortunatly what was taught to me was that a, + V4R means you check the BP(Which you would anyways for NTG)  if it's less than 100 you increase preload so that when you administer NTG it doesn't drop the BP way too low... it seems that any medics I've spoken to in ride alongs agree with this...



The medics your speaking with are, quite simply, wrong. This is what's been taught for years (heck, may still be taught in places) but it's not current science. For recommendations I give you, on page e35 of the _ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction_


> Class III
> 1. *Nitrates should not be administered to patients *with
> systolic blood pressure less than 90 mm Hg or greater
> than or equal to 30 mm Hg below baseline, severe
> ...



The document is available here. (you may have to register to view it). 

Choose the medics you learn from carefully. There's a ton of bad info out there.


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## silver (Aug 20, 2011)

Melclin said:


> Basically this is part of a paragraph that I think can be summarised by saying this: While nitro does cause a degree of coronary artery dilatation, it doesn't ultimately have any clinical affect on ischaemia and injury. Ischaemia is all about a supply/demand deficit. Too much demand, not enough supply. Instead of increasing supply like it was once thought to, nitro probably causes its affects my reducing demand. It does this through preload reduction. Essentially the less it has to pump, the less it has to work.



The coronary dilation does have some clinical effect, though at those dosages (like a SL tab) it will only have a very very mild systemic one. The reduction in diastolic ventricular free wall stress caused by the venous dilation is the significant one. In the cath lab we give nitro directly into the coronaries (as well as nitroprusside), but its mostly for diagnostics or what they call no reflow phenomena.


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## ekgpress (Aug 31, 2011)

To get back to Sharktooth's original question - whether or not to hang the IV Amio drip after ROSC - I think it gets down to one's understanding of the arrest - What caused it? (if a cause can be determined ... ) - Have you "fixed" whatever predisposed to the arrest, or is it likely to recur? - and What was it that resulted in ROSC? (was it the Epi? - doing good CPR? - correcting some underlying disorder(s)? - enhanced oxygenation? - or was it antiarrhythmic effect that corrected an arrhythmic electrical disturbance with the IV Amio doses that were given?). Whether or not I would consider use of IV Amiodarone infusion in the situation posed by Sharktooth should depend on the "Gestalt" of the above by the on-the-scene provider - with there being no "right-or-wrong" answer.  That said - morbidity from cautious institution of IV infusion of Amio in the setting described should be minimal, with ability to immediately stop the drip should adverse effect occur.  The IV boluses that have already beengiven will in any case remain on board for a few hours - so there WILL be "amio effect" for a while regardless of whether an IV infusion is started. My Gestalt from what I glean in this particular case however is similar to what I think Smash is saying - namely, that it seems less likely that the reason for ROSC in this case was antiarrhythmic effect - therefore I probably would NOT start an IV Amio infusion in this case with what I know.  That said - it is the capable provider "on-the-scene" who has the BEST insight as to likely cause and effect for any given code case - Ken Grauer, MD


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## usafmedic45 (Aug 31, 2011)

> The medics your speaking with are, quite simply, wrong



No, wrong is too much of an understatement.  They are dangerously :censored::censored::censored::censored:ing stupid.


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## epipusher (Aug 31, 2011)

other than an allergy or a bp less than 90, our medical directors repeatedly stress to never withhold ntg. this is brought up time and time again at our audit and review sessions.


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## usalsfyre (Aug 31, 2011)

epipusher said:


> other than an allergy or a bp less than 90, our medical directors repeatedly stress to never withhold ntg. this is brought up time and time again at our audit and review sessions.



Ummm, yeah....no.....

See previous discussion for why.


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## epipusher (Aug 31, 2011)

so our team of medical directors with local cardiologist and heart hospitals/centers approval, must all be wrong?


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## usalsfyre (Aug 31, 2011)

epipusher said:


> so our team of medical directors with local cardiologist and heart hospitals/centers approval, must all be wrong?



According to the ACC....yes. Or more likely, they're considering paramedics too uneductaed to make a nuanced decision about NTG.


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## epipusher (Aug 31, 2011)

usalsfyre said:


> According to the ACC....yes. Or more likely, they're considering paramedics too uneductaed to make a nuanced decision about NTG.



i love it when folks such as yourself have these type of discussions with our area medical directors. always entertaining.


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## usalsfyre (Aug 31, 2011)

epipusher said:


> i love it when folks such as yourself have these type of discussions with our area medical directors. always entertaining.



Ahh yes, because I'm a jack@ss who thinks he's smarter than the physician

I've had these discussions with my medical directors before. I've never once gotten "because my mad physician skills are better than the large body's reccomendations". I've usually gotten one of two answers. 1). The consensus standard hasn't been updated recently and there's newer science out there, or 2). I don't trust the lower-teir providers in our service's judgement. 

How about since you now know what your service is doing with regards to NTG runs contrary to what the ACC's consensus standard is *YOU* ask him why your doing it that. You might be supprised and disapointed by the answer.


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## the_negro_puppy (Sep 1, 2011)

If NTG/GTN has little effect on myocardial ischaemia why risk giving it to possibly pre-load dependent patients? This is where clinical judgement comes into play. It's a shame that some services have hard and fast protocols with know room for judgement.


For us, GTN is contraindicated by a systolic BP < 100 mmhg and a heart rate below 50 and above 150. An inferior M.I is a precaution due to possibility of RVI. I personally would not give GTN to a pt with  S-T elevation in V4R and would be very wary giving it to any infarcting patient with a BP close to 100mmhg. If i withheld GTN from an infarcting pt with a systolic bp of 105 I would not get audited or 'in trouble'. Our service allows room for clinical judgement and evidence based medicine.

As other have said, there's not much point giving GTN then pushing fluids to try and save your patient's preload. Withold the GTN, make sure they have had their aspirin, O2 and morphine and spend the time packaging them and tx to definitive care.


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## MrBrown (Sep 1, 2011)

Our position has recently (2009) changed: GTN has little role in STEMI however most clinical people will have given some GTN before acquiring a 12 lead ECG (Paramedic or Intensive Care).  Technicians (volunteers) do not have 12 lead ECG.  GTN has no role in repeat doses unless clearly associated with improvement.


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## Smash (Sep 1, 2011)

epipusher said:


> i love it when folks such as yourself have these type of discussions with our area medical directors. always entertaining.



I love it when people use capital letters. Capitals are important. They are the difference between helping your Uncle Jack off a horse, or helping your uncle jack off a horse...

Regardless of that, if you disagree with the ACC, or you disagree with the rationale some of us have given for withholding nitrates in RVI, can you share your reasoning with us?  I don't mean by saying "my medical director told me so" but by actually providing some evidence or some physiological rationale why nitrates are appropriate in the given circumstance. 

Maybe we can learn something, which is, after all, the reason we post here.


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## epipusher (Sep 1, 2011)

I worked for a previous service where we never gave NTG for RVI. Then I moved and started working for my current service, of which I consider a progressive service, and my partners would look at me funny when I stated I was going to withhold NTG with this particular finding. This would be followed by looks of confusion, followed by them wishing me luck when I explained to the er docs why I withheld nitrates. Keep in mind that when we have cardiac patients, we go above and beyond the usual standard of 3 sprays of NTG. Our lead medical director, when explaining the amount of NTG we should be giving to our suspected cardiac related chest pain patients, uses the phrase "copious amounts". I put my faith and trust in all of my medical directors and the other 6 area medical directors that are all pro NTG. As I stated before, someone will always question that decision during one of our Audit and Review sessions. The MD's response is to just be prepared. Have an i.v. and watch for changes in their b/p.  As a side note, we also give "copious amounts" of NTG for patients with severe CHF. Please go through and correct my grammar after you are done explaining how I'm wrong again. Thanks for the discussion.


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## DESERTDOC (Sep 1, 2011)

In the region I am in NTG has no maximum dose.  It is titrated and stopped at a systolic of 90mmhg.  Absence of an IV does not preclude the use provided the criteria above is met.


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## usafmedic45 (Sep 1, 2011)

> i love it when folks such as yourself have these type of discussions with our area medical directors. always entertaining.



Actually, I'd take usalfyre's word over your own any day of the week.  He's a bit abrasive at times but generally knows his stuff.  Even as bright as I am, he'd still not be someone I would pick an argument with unless I was REALLY sure of what I was talking about.

You're in Indy correct?  I know most of the medical directors here and have to say that they aren't exactly the best I have ever seen. Not bad, but not great or progressive by any stretch.  USALFYRE's right...it's the fact that they don't trust EMS providers and the expectation is to run everyone into the hospital ASAP rather than intervening in the field.  Works great right up until the traffic sucks....


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## usalsfyre (Sep 1, 2011)

epipusher said:


> I worked for a previous service where we never gave NTG for RVI. Then I moved and started working for my current service, of which I consider a progressive service,


I consider my service fairly progressive as well.



epipusher said:


> and my partners would look at me funny when I stated I was going to withhold NTG with this particular finding. This would be followed by looks of confusion, followed by them wishing me luck when I explained to the er docs why I withheld nitrates.


Just because your partners look
at you funny is NOT a good reason to base a treatment off of. I make partners look at me funny on a regular basis, doesn't mean it's not good medicine, it means the treatment doesn't fit their paradigm. 



epipusher said:


> Keep in mind that when we have cardiac patients, we go above and beyond the usual standard of 3 sprays of NTG. Our lead medical director, when explaining the amount of NTG we should be giving to our suspected cardiac related chest pain patients, uses the phrase "copious amounts".


We follow up our SL NTG with an infusion up to 200mcg/min. So I know a bit about "copious amounts". But it's only appropriate in certain settings. It's also interesting your medical direction team puts so much faith in a treatment that's never been shown to reduce morbidity or mortality in AMI.



epipusher said:


> I put my faith and trust in all of my medical directors and the other 6 area medical directors that are all pro NTG.


I put my faith in science, physiologic understanding of the med I'm giving and consensus standard of what constitutes good care. I've had a lot of protocols that sucked that were written by paramedics, physicians practicing old medicine or physicians who did not trust their medics.



epipusher said:


> As I stated before, someone will always question that decision during one of our Audit and Review sessions. The MD's response is to just be prepared. Have an i.v. and watch for changes in their b/p.


Or...just avoid iatrogenic cardiogenic shock by withholding a the med in certain settings.



epipusher said:


> As a side note, we also give "copious amounts" of NTG for patients with severe CHF. Please go through and correct my grammar after you are done explaining how I'm wrong again. Thanks for the discussion.


My severe CHF patients tend to get one SL dose of 1.2mgs, a CPAP mask and an infusion at 75-100mcg/min. So it's not a med I'm uncomfortable with, I give without a line all the time, ect.

Several sound physiologic and consensus arguments have been presented here as to why NTG is a bad idea in the setting of RVI. You've failed to present anything more convincing than "my medical director said". Sell it to us, convince us we're wrong.


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## systemet (Sep 1, 2011)

epipusher said:


> Please go through and correct my grammar after you are done explaining how I'm wrong again. Thanks for the discussion.



Ok.

So, as I see it, you're saying you give NTG in RVI.  And when asked why, your response is basically:

(1) My medical directors recommend this.
(2) They're very smart people.
(3) They tell you to have an IV first, and "be prepared" for the pressure to drop.
(4) You feel that giving more than 3 nitro is going "above and beyond"
(5) You also do this in CHF (implied, so it's good in ACS /MI)

Is that fair?

I'm sure (1-3) and (5) are correct.  I'm sure your medical directors are very smart.  Most physicians are.  Including the numerous physicians and PhDs (and MD/PhDs) who sit on ILCOR.  Your local physician group would be going against the consensus opinion of the major governing body that establishes guidelines that ultimately translate into AHA / CHSF / ERC / etc. guidelines.  This has already been pointed out, quite politely.

Are they wrong?  Perhaps.  I think so.  But I'm sure they don't care about my opinion.  No one's suggesting that you should decide not to follow your protocols.  It is however being suggested that your protocols aren't in line with currently-accepted international guidelines.  

With regard to (3) it's fine to be prepared for hypotension.  Are you prepared for a sudden VF arrest?  Because that's how rapidly your hypotension may develop.  What do you think hypotension will do to coronary blood flow?  If the blood supply to the myocardium is further compromised, do you think the infarct will extend more rapidly?  Aren't we hoping to improve the oxygen supply/demand balance?

As to (4), and (5), I can't say that I think giving > 3 NTG in a chest pain patient is "going above and beyond".  I also think that CHF, i..e. LV failure, is a different clinical entity to RVI.

The question has been asked "Why do you do this?".  Why do you think it's a good idea to give NTG to an RVI?  What effect are you aiming for?  How do you think it benefits your patients?  What are you hoping to achieve?


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## epipusher (Sep 1, 2011)

Gentlemen, I'm not trying to sell you on anything. I'm not even saying you are wrong. I agree with everything you are saying, and for my first 4 years as a medic, this was how I operated. For the last 5 years I have worked for a  different service that follows a completely different path. I am not the type to confront these ER physicians as well as the cardiologists I have heard confirm this way of treatment at various local EMS seminars. "Because my medical director said so", is the only reason I need. Sorry fellas, I'm not trolling.


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## epipusher (Sep 1, 2011)

Two more after this and I can enter chat!


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## MrBrown (Sep 1, 2011)

epipusher said:


> "Because my medical director said so", is the only reason I need. Sorry fellas, I'm not trolling.



Come on mate, thats pretty poor.  What that says to the rest of us is "I am unable to think for myself".

3 doses of sublingual GTN is nothing to be impressed about, repeated GTN is inappropriate unless clearly associated with improvement, so if the patient improves with each dose of GTN why stop at 3? It sounds like you have been working in places where your delegated authority does not include more than three doses of GTN.

Remind Brown again why we even give some bloke with STEMI GTN? :unsure:

GTN is an anti-anginal agent, does it really have a role in STEMI?


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## DESERTDOC (Sep 1, 2011)

epipusher said:


> Gentlemen, I'm not trying to sell you on anything. I'm not even saying you are wrong. I agree with everything you are saying, and for my first 4 years as a medic, this was how I operated. For the last 5 years I have worked for a  different service that follows a completely different path. I am not the type to confront these ER physicians as well as the cardiologists I have heard confirm this way of treatment at various local EMS seminars. "Because my medical director said so", is the only reason I need. Sorry fellas, I'm not trolling.



Confrontation is not needed.  But educated conversation with the medical community is.  ED physicians and medical directors are not dictators.  Most physicains I encounter are more than happy to explain XYZ item or issue.  But I will be damned if I will blindly follow anyone just because they say so. In my world, physicians do not walk on water.  Most are cool dudes with real lives away from medicine.  Talk to them about anything but medicine and start building professional relationships.

If a lot of my posts center on people and behaviors it is because my degree is in Sociology.


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## systemet (Sep 2, 2011)

epipusher said:


> "Because my medical director said so", is the only reason I need. Sorry fellas, I'm not trolling.



Fair enough.

I like to discuss to physiology and pharmacology because they interest me, and I have a fair bit of education in these areas.  While this is probably an unpopular opinion, I think that doing so has made me a better paramedic.  But we're all in the same boat here.  I can't deliver a therapy that's not available on my ambulance.  And while I may have been able to move outside of the medical control guidelines from time-to-time, I can't just decide they're wrong and outright violate them without good cause.  I don't think anyone is suggesting that you should either.

Granted the topic of this thread has drifted far away from amiodarone maintenance infusions, but at some point we started discussing the pharmacology of nitroglycerin.  Feel free to contribute to that discussion, if you'd like.

If we steer this thread back to the original topic -- I'd always wondered why we use maintenance infusions with an antiarrhythmic like amiodarone that has such a long t1/2.  It seems like if we get high enough plasma concentrations to convert / suppress an arrhythmia, that if we're waiting 50 days for he concentration to half, there's not going to be a pressing need to administer more in the next couple of hours (days?).  

Then I looked at some research, and saw that amiodarone rapidly redistributes to the adipose tissue from the bloodstream.  So I think that after a bolus injection, we see a rapid movement of amiodarone from the bloodstream to the adipose tissue compartment.  So in the initial period following IV administration, the plasma concentration actually falls much much more rapidly.  The apparent half-life during this period is much shorter.  One the amiodarone has redistributed, and the vascular and adipose compartments are in equilibrium, the longer 50 day half-life is seen.  So I think the maintenance infusion may be designed to ensure that plasma [amiodarone] stays higher than it would otherwise.

I've got to say though -- given amiodarone's multiple complex, and perhaps not fully understood actions, I think it's surprising that we use a drug with such a long half-life.  Once it's in, we're stuck with relatively high levels for a couple of months.  Seems like that might present some potential for drug interactions and proarrhythmic effects.


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## ekgpress (Sep 2, 2011)

systemet said:


> Fair enough.
> 
> I like to discuss to physiology and pharmacology because they interest me, and I have a fair bit of education in these areas.  While this is probably an unpopular opinion, I think that doing so has made me a better paramedic.  But we're all in the same boat here.  I can't deliver a therapy that's not available on my ambulance.  And while I may have been able to move outside of the medical control guidelines from time-to-time, I can't just decide they're wrong and outright violate them without good cause.  I don't think anyone is suggesting that you should either.
> 
> ...


------------------------------------------------------
Wow- It's difficult for a newcomer to follow the energized flow of EMTLIFE conversation . . . .  Re Amio - my impression is that the 30-90 day half-life following oral loading is as you say different from initial IV loading which has more rapid redistribution - so there is a rationale for IV bolus and initial IV maintenance infusion on those occasions with potential life-threatening arrhythmias (when it is indicated).  I think we are on the same page as to "IF" amio infusion is indicated - with KEY to this decision being whether it was the IV amio bolus that converted the patient - and whether there may be other underlying/contributing factors to having caused the VT/V Fib in the first place. Amio IV infusion is not necessarily indicated in all cases, esp. if something "fixable" is found and corrected after conversion to sinus rhythm.

As to Nitro - I'd summarize what I'm getting as the "gist" of your conversation flow by adding the following thoughts/comments:
i) the physiologic effects of IV nitro differ from nitro given by any other route in that there clearly is more arterial vasodilatation with IV NTG (vs predominant venous/preload effect when NTG is given by other routes).  This is why IV NTG has been a drug of choice for acute pulmonary edema (great afterload reduction effect in this situation). IV NTG also offers the advantage of immediately "turn on/turn off" effect for hospitalized patients with acute ischemic chest pain.
ii) NTG given by any formulation may lower BP. Caution (at the least) if not contraindication is advised if your starting BP is very low.  How low is "very low" may be a matter of judgement depending on the situation.  When one is dealing with a volume dependent situation like acute RV MI - my tendency had been not to use NTG (because of the expected potentially dangerous BP drop you anticipate).  Whether to say NTG can "never" be tried in such situations is a difficult call since one rarely has "pure" RV MI (it is usually associated with inferior LV MI also - and how much RV vs LV involvement effect is operating may be difficult to determine . . . ). 
iii) The problem of course with sublingual administration of NTG is that IF you do get a big BP drop - you "can't take the sublingual pill back . . . " - vs a more controlled situation with cautious initiation of a low-dose IV drip that can be much more rapidly titrated (which obviously is NOT something EMS will be able to do in the field . . . ).
iv) I agree that even if you as EMS personnel are working in a situation where you are compelled to "follow protocols" - that it is still good to think about "Why?".  Hopefully the situation will allow some conversation with the Medical Director (at least at some point . . . ). Your input should (in a good system) be heard and at least considered . . .
v) My impression (if memory serves me - since it has been a while ... ) - the big ISIS-4 study on use of IV NTG did not show benefit for acute ACS patients - BUT that huge study was FLAWED since it did not control for the use of sublingual NTG prior to administration of IV NTG in the study . . . ergo despite wide publicity in cardiology circles - I don't know that it has truly ever been established as to whether there may be some positive effect of NTG in ACS. Physiologically - it makes sense to me that there may be, if ischemia is a contributing mechanism - but I don't know that this is known for sure.  So like almost everything else in medicine - the question of whether or not to use NTG (sublingual and/or IV, depending on circumstance) is a "balance" depending on specific circumstances of the case at hand plus baseline BP and clinical status - without any rigid "yes" or "no" answers.  I personally loved the drug when I was in practice - but I had a healthy respect for potential adverse effects of its use . . . 
HOPE the above sheds some light from the perspective of this MD - : ) Ken


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