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Vasoactive medication help

Hey all. I just finished up a shift last night with a pretty sick patient. Turns out he actually coded and u fortunately didn't make it on the dayshift.

Some background on the patient.... this was a 70 something year old man who presented to the ed and ultimately the icu for a vtach arrest while en route to the hospital.

Labs showed a a bumped troponin precode... and a stat echo showed ef of 15%. There was third spaced fluid on his extremities and definitely some pulmonary edema (wet audible cough). He was started on amio after a bolus and heparin.

Sometime in the night he went into a 7 minute tun of vtach with a pulse. During this time the physician was called to bedside. In this time I bolused 150 amio and gave two stat pushes of lidocaine. Ultimately the patient was started on a lidocaine drip.

He later converted and was "doing better."

Pressures began to become labile sometime later and he went into respiratory failure. We couldn't give lasiks per the physician because of the low pressures.

He was intubated and sedated to end my night.

As the story goes...on day shift... His pressures dropped into the 60s and levophed was started. He later went into vtach witjout a pulse and did not survive the code.

My question is this... seemingly as though the patient was presenting with chf exacerbation and perhaps some underlying pneumonia.... what would you guys have ordered when he became hypoyensive?

I don't understand the levophed choice because it will raise the pressures for sure...but wouldn't it make an already flogging heart have to work harder to push against the increased afterload? Furthermore, wouldn't it constrict the coronaries and further cause myocardial ischemia? Please let me know what you all think.

I have made the conscious effort to study my pressors and vasoactives tenfold because I want to understand even more than I have before.

Thank you

In any cardio-genic emergency, the first priority is getting blood down the coronary arteries. Any medicine that increases vasomotor tone, among the other beneficial effects, will increase aortic root pressure and therefore, coronary arterial flow. It is why vasopressin was once (and still should be) on the acls protocol.

If blood isn't flowing down the CA's, nothing else matters.

This is a very good, and very tricky question. I'm going to give some scattered thoughts:

In undifferentiated cariogenic shock, norepi has been found to be an OK choice until the the cardiac process is identified.

A few questions first - did the patient have systolic or diastolic dysfunction? If the EF was 15% clearly there was a good bit of systolic dysfunction, as EF is preserved in isolated diastolic dysfunction (ie. the name HFPEF). Though this can happen with someone with diastolic dysfunction who has an MI or very late-stage, and can have management implications.

SO the objective of someone with systolic dysfunction GENERALLY is to reduce afterload and increase contractility. Dobutamine up to 5 mcg/kg/min does this nicely (at doses >5 you will increase afterload). Milrinone is also a good choice. Lower doses of epi can also achieve this. However you must be mindful that increasing HR will increase myocardial O2 consumption and decrease diastolic filling time (which is when your coronaries are perfused). That said, a heart rate of 80-100 is typically ideal in these situations with a drastically low EF.

HOWEVER, if your pressure is in the toilet (ie cardiogenic shock), you have to do what needs doing to increase your MAP or you won't perfuse your coronaries and will end up right back in Vtach arrest. It's a tricky predicament and I sympathize with you and your doc. Norepi in this case makes some sense because you will increase your vascular tone (aka SVR, aka afterload) to help perfuse your coronaries and will also give you some positive inotropy. Dopamine can also achieve this, and has the added benefit of increasing UO but is a much weaker drug than norepi or epi.

It is hard to justify giving lasix if someones pressure is in the toilet. I have seen people do it and augment BP with more vasopressors. There isn't any real evidence to support that, though. Also don't forget that lasix does have some (albeit minor) vasodilatory effects.

Some things that definitely help in these post-arrest very low EF patients:

1. Maintain NSR (treat afib, pace, amio, whatever you gotta do! Afib can precipitate another arrest)

2. Increase inotropy (basically any pressor EXCEPT phenylephrine will do this)

3. IABP, impellas seem to help

4. Target SpO2 about 90-92% (high O2 levels have been shown to decrease coronary blood flow at rates that thwart any myocardial benefit of having Spo2 of 100%)

NB: Vasopressors, by increasing diastolic pressure (and thus coronary perfusion pressure) tend to increase coronary blood flow)

Sorry this is so scattered!

Edited by Georgia SRNA

I agree with Georgia that an IABP would probably have been ideal!

Thank you for the feedback. It truly was a lesson in futility. However the learning I will take with me will be long lasting.

I will say that we opted out of dopamine because it potentially would have exacerbated the frequent arrhythmias. Furthermore, I went back and asked the physician if dobutamine would have sufficed and he said yes.

Of note, The guy was tachycardic with heart rate into the 110s so we opted against an epic drip being that it would do as you said... place further strain and increase myocardial oxygen demands.

I can see Levo now in that we were increasing the driving force and Ohms law (P=Q/R) states that perfusion (Q) is affected by the driving force of pressure (P) over Resistance ®. We were augmenting the driving force with the pressors.

I just wanna say I think it's wonderful to see how your reply and the first persons reply finally make sense to me.

Levo restored aortic root pressure for the coronaries and you saw that dobut and an IABP were truly the only tx modalities.


Has 5 years experience.

I can see Levo now in that we were increasing the driving force and Ohms law (P=Q/R) states that perfusion (Q) is affected by the driving force of pressure (P) over Resistance ®. We were augmenting the driving force with the pressors.

I think you got some of your variables switched around.

Ohms law is actually V=IR. Voltage = current x resistance.

The analogue to this in terms of fluid dynamics is: deltaP=QR

Or the pressure difference from point A to point B is equal flow times resistance.

In terms of hemodynamics of the human body we kinda simplify this to BP = CO x SVR.

Or (MAP-CVP) = HR x SV x SVR


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