STEMI and Dopamine

[MikeyBSN]

I just wanted to make sure that I haven't been out of school that long. I had a situation the other day where I thought we should have given a pt dopamine (so did the other nurses). We had an acute MI who was very unstable. We were working the pt up and trying to get the pt to the cath lab. The BP was 40/20 and HR was 50-60. There were several people working on the pt so I went to get dopamine. When I came back with the dopamine, the attending, a doc who was fairly new to our hospital, ordered us not to give dopamine. She didn't was the pt "to go into a-fib." She wouldn't order epi or atropine. She was more concerned with crushing ASA and plavix (which the pt was already on) and cramming to down the OG tube. Naturally, the pt with an untreated systolic BP of 40 eventually went into cardiac arrest. Perhaps some people with a little more experience could help me out, and explain to me why giving a pt the plavix they were already taking was more important than anything else, and what difference it makes if the pt might go into A-fib when they don't have a blood pressure. Thanks

[glasgow3]

Pump problem? Cardiac output issue? Balloon pump? Rate problem? Gezzzzzzzzzzz--------the patient has a B/P of 40/20!!! The dysrhythmia (s)this ED doc SHOULD have been worried about was v-fib or asystole.

In this case we already have been told that the cause of this shock was cardiac secondary to an acute MI........so the main overall priority should have been to deliver a live patient for revascularization as soon as possible. Key word here "live".

Unless the patient was in full blown pulmonary edema I see no reason not to try small fluid challenges (250cc at a time) to insure adequate preload/cardiac output. There is also no reason to avoid Dopamine or Levophed......Yea sure dopamine can cause tachyarrhythmias particularly at certain doses which in turn may cause increased workload and O2 consumption blah blah. But THIS patient had a rate of only 50 to begin with. And the LAST thing I'd be concerned with is the possibilty of a-fib due to dopamine like this ED doc .

Now other "nice" things while waiting might have been getting in a central line in to monitor CVP/Fluids, getting the patient intubated etc etc, but to ignore a crashing patient's B/P and rate in favor of giving additional ASA and Plavix seems like a recipe for disaster. And apparently it was.

In all fairness, this patient's chances were pretty ominous under the best of circumstances....but geeeezzz. Worrying about a-fib?

[GilaRRT]

Pump problem? Cardiac output issue? Balloon pump? Rate problem? Gezzzzzzzzzzz--------the patient has a B/P of 40/20!!! The dysrhythmia (s)this ED doc SHOULD have been worried about was v-fib or asystole.

In this case we already have been told that the cause of this shock was cardiac secondary to an acute MI........so the main overall priority should have been to deliver a live patient for revascularization as soon as possible. Key word here "live".

Unless the patient was in full blown pulmonary edema I see no reason not to try small fluid challenges (250cc at a time) to insure adequate preload/cardiac output. There is also no reason to avoid Dopamine or Levophed......Yea sure dopamine can cause tachyarrhythmias particularly at certain doses which in turn may cause increased workload and O2 consumption blah blah. But THIS patient had a rate of only 50 to begin with. And the LAST thing I'd be concerned with is the possibilty of a-fib due to dopamine like this ED doc .

Now other "nice" things while waiting might have been getting in a central line in to monitor CVP/Fluids, getting the patient intubated etc etc, but to ignore a crashing patient's B/P and rate in favor of giving additional ASA and Plavix seems like a recipe for disaster. And apparently it was.

In all fairness, this patient's chances were pretty ominous under the best of circumstances....but geeeezzz. Worrying about a-fib?

I cannot disagree with the fact that the patient requires interventions other than PO meds; however, let us look at the possible physiology behind this patients condition.

If we are in fact talking about an inferior wall MI with RV infarct, how will dopamine as a primary intervention help this patient? Remember, the left ventricle actually has to have blood to pump otherwise pressors are simply not effective. This is why pressors are not used as primary interventions in the hypovolemic trauma patient.

[hypocaffeinemia, BSN, RN]

I cannot disagree with the fact that the patient requires interventions other than PO meds; however, let us look at the possible physiology behind this patients condition.

If we are in fact talking about an inferior wall MI with RV infarct, how will dopamine as a primary intervention help this patient? Remember, the left ventricle actually has to have blood to pump otherwise pressors are simply not effective. This is why pressors are not used as primary interventions in the hypovolemic trauma patient.

If it's a right pump failure, wouldn't there be some clinical signs like peripheral edema or (+)JVD to go off (not to mention an increased CVP)? In the field (I'm only a nursing student but have been an EMT for years), if the lungs were clear we'd run fluid wide open and push pressors. Something--anything to get that pressure up and establish adequate organ perfusion.

[time4meRN]

ditto

[GilaRRT]

If it's a right pump failure, wouldn't there be some clinical signs like peripheral edema or (+)JVD to go off (not to mention an increased CVP)? In the field (I'm only a nursing student but have been an EMT for years), if the lungs were clear we'd run fluid wide open and push pressors. Something--anything to get that pressure up and establish adequate organ perfusion.

Peripheral edema may not be appreciated in the acute setting of right ventricular failure. JVD may be appreciated; however, with all of the other things going on, it would be an easy sign to miss. CVP measurements would be impossible without a central line. From the information in the OP, I suspect things were happening so fast, a central line was not placed and transduced.

Look at the presenting signs:

Bradycardia: The nodes are perfused from arteries that stem from the RCA. (Inferior wall)

Hypotension: Very common in the setting of Inferior wall MI with RV infarct. Remember the whole preload concept.

These two findings are well known in people who experience an inferior wall MI with RV infarct. However, a standard 12 lead will not look at the right ventricular wall. We need right sided leads for this, the V4R is highly specific and sensitive when looking for RV infarct.

I think this is a good thing to talk about because people tend to simply look at B/P and want to give pressors without actually considering the cause of the B/P problem and the consequences of their actions. I simply want people to stop for a minute and critically think about what may be going on with the patient.

[glasgow3]

I cannot disagree with the fact that the patient requires interventions other than PO meds; however, let us look at the possible physiology behind this patients condition.

If we are in fact talking about an inferior wall MI with RV infarct, how will dopamine as a primary intervention help this patient? Remember, the left ventricle actually has to have blood to pump otherwise pressors are simply not effective. This is why pressors are not used as primary interventions in the hypovolemic trauma patient.

Did you miss what I said about small, repeated fluid challenges to effect, getting a line in to facilitate infusion and monitor CVP etc etc?

Catacholomines used to improve cardiac performance/contractility does have its drawbacks some possibly detrimental (dopamine in particular) but this patient was extremely shocky..... yes appropriate/adequaten fluids are important. Did I imply otherwise?

[GilaRRT]

Did you miss what I said about small, repeated fluid challenges to effect, getting a line in to facilitate infusion and monitor CVP etc etc?

Catacholomines used to improve cardiac performance/contractility does have its drawbacks some possibly detrimental (dopamine in particular) but this patient was extremely shocky..... yes appropriate/adequaten fluids are important. Did I imply otherwise?

No, I read your post; however, I want to emphasize that starting pressors prior to preload augmentation could exacerbate the situation.

[ibnathan]

It may be a inferior wall MI with RV infarct. But all in all we need a pressure, the patient needs perfusing pressure.

A. Start Levophed or Dopamine as well a a 250cc bolus of albumin or NS

B. Watch patients pressure and heart rate and any funky arrythmias

C. Call Cath Lab team Stat!

B. Insert IABP stat and I qoute, " The goal of the IAB in such a disease stat (such as cardiogenic shock) is to decrease or "optimize" preload by ensuring a filling pressure high enough to obtain the highest CO on the Starling curve but not so high as to cause pulmonary congestion." (Counterpulsation Applied, An introduction to Intra-Aortic Balloon Pumping).

Again the importance is to agressively treat BP and HR stabilize patient for cath lab. The patient also needs an A-line, and a Swan-Ganz for hemodynamics.

Oh I forgot he needs to pray.