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.
