Antiarrhythmic confusion.........

[Smash]

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.

 

[Melclin]

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.

 

[Trevor]

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

 

[hyperlyeman1]

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.

 

[Smash]

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.

 

[hyperlyeman1]

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

 

[usafmedic45]

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

 

[Smash]

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.

 

[usalsfyre]

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.

 

[Hunter]

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?

 

[usalsfyre]

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:?

 

[Hunter]

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?

 

[usalsfyre]

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.

 

[Hunter]

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...

 

[MrBrown]

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.

 

[Melclin]

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.

 

[Melclin]

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.

 

[usalsfyre]

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
bradycardia (less than 50 beats per minute [bpm]),
tachycardia (more than 100 bpm), or suspected RV
infarction. (Level of Evidence: C) [bolding mine]

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.

 

[silver]

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.

 

[ekgpress]

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