I had a patient who came up from cath lab after having 2 stents placed to the circ and an IABP emergently placed (cath revelaed triple vessel disease). While in the field the patient went into pulseless VT three times, once in the cath lab and then 7 times while on my unit with one run of Toursades.
The patient came up on a dopamine gtt @ 30mcg/kg/min and levo @ 20mcg/min, in addition to Reopro, Heparin and Versed. The patient was hypotensive and was only augmenting in the 40's via the IABP. Obviously, the patient was circling the drain.
So thats the background. My question is, why did the doc want to switch the levo for neo? I understand levo is an alpha agonist with some beta effects and I realzie that neo is stictly an alpha agonist. Does levo increase myocardial oxygen demand more so than neo? This is the only thing I can think, however, I am just now begining to actually study things on a cellular level and would like to get some input from the people here.
By the way, this is my first post and this looks like a place I will be visiting much more often. Glad to be here.
Hi - and welcome!
I'm not sure about the answer to your question - maybe this could be moved to the CCU forum or ER forum.
Last edit by Spidey's mom on Jan 18, '10
Quote from GilaRN
You pretty much answered your own question. It is reasonable to consider an agent with less beta effects. However, the real question being, what is the cause of the hypotension? I would hope fluid volume and preload problems would have been considered?
Gosh, with all those pressors going, one would certainly hope so, LOL... Seriously, going from Levophed down to Neosynephrine may mildly save some cardiac work, but one has to consider that Neo isn't as powerful a pressor as Levo; so you're going two steps forward and one step back, IMHO.
The other question on my mind would be that someone with a augmented systolic of 40's doesn't sound too clinically hopeful. There wasn't any indication in the OP of what counterpulsation ratio was being used so I'm assuming it's already 1:1 since the pressure is so low. Since the stented lesions were in the Left Circumflex Artery (LCX) the other nagging question is why the severe impact on overall cardiac function. A possible explanation may be that it was LCX dominant heart to begin with, such that occlusion of the LCX impacted a much greater percentage of the left ventricle (LV). I'm guessing that this was an Acute Myocardial Infarction (AMI) with subsequent cardiogenic shock. We also don't know if there was any other pre-existing myocardial pathology; ie. this may have been a repeat event.
Given that they've already stented the patient and resolved the ischemia issue; it may be worthwhile to consider Dobutamine despite the increased cardiac oxygen consumption and work. I've been told that sometimes after surgery or cardiac arrest, a heart loses its ability to fully contract secondary to myocardial stunning; temporary use of a positive inotrope like Dobutamine may force the heart muscle into more effective action. Failing that, surgical implantation of a Ventricular Assist Device (VAD) may be another medical consideration worth discussion. At any rate, unfortunately, the clinical status described here is, like the OP noted (...circling the drain)
Oh, ...and a hearty welcome to the new member; glad to have ya here!
Last edit by Emergency RN on Jan 18, '10
Jan 18, '10
Many years ago, I heard and repeated a nickname for levophed: lethalphed.
Think about the vasoconstriction and its effect on vital organs such as kidneys, liver and other abdominal organs.
Think about the effect on afterload.
Last edit by erroridiot on Jan 18, '10
: Reason: addition