Antiarrhythmic confusion.........

[Sharktooth]

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?

 

[Smash]

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.

 

[Sharktooth]

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

 

[Smash]

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.

 

[Handsome Robb]

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

 

[squrt29batt12]

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

 

[Smash]

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.

 

[Smash]

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

 

[Handsome Robb]

I'm still trying to process all of it.

 

[Smash]

I'm still trying to process all of it.

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

 

[MrBrown]

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

 

[Aprz]

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

 

[fma08]

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

 

[abckidsmom]

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

Agreed. Thanks!

 

[Smash]

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!

 

[Melbourne MICA]

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

 

[Trevor]

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!

 

[Smash]

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.

 

[ah2388]

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

 

[Trevor]

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?