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aCRNAhopeful specializes in CVICU.

aCRNAhopeful's Latest Activity

  1. aCRNAhopeful

    Fluid bolus by gravity or pump?

    We are talking about different things. You are saying that if you give a medication through a central line it will reach its target tissue faster than if you had given that same medication via a PIV. No one would question that. The thread was about giving a fluid bolus. Therefore flow rate is the key issue. A PIV has a faster flow rate than a triple lumen. Also I would disagree that a medication given given through a PIV would have a "profound" difference on the speed it reaches the lungs. It would be delayed by a matter of seconds but thats it. It definitely would not have an effect on metabolism unless you're talking about adenosine or something that is metabolized in seconds. Even a medication like succs which is heavily metabolized before ever reaching its target tissue at the neuromuscular junction doesnt require a dosage adjustment based on PIV vs central line. With that said, if I have a patient in the OR with a central line and a large bore IV i will use the PIV for my volume resuscitation and mantenance fluid line and I will use the central line to to push drugs that I want to work immediately because it works a little bit faster than the peripheral. So yes I agree with that part
  2. aCRNAhopeful

    Fluid bolus by gravity or pump?

    I dont think anyone would deny that a central line is closer to the heart than a PIV but thats not the point. The most effective way to get volume into a patient fast is a large bore peripheral IV hung by gravity (or pressure bag). Hang the same bag of LR to a 18cm triple lumen and the flow rate will be significantly less than the large bore IV. It's simple physics. Now if your talking about a cordis with a huge inner radius and shorter length then maybe it'll give the 16g PIV a run for it's money. Volume flow rate = pressure gradient * radius^4/ 8 * viscosity * length
  3. aCRNAhopeful

    Fluid bolus by gravity or pump?

    See Poiseuille's law in the post above. In other words you can increase flow rate by decreasing length of the catheter, increasing the pressure on the IV bag, decreasing viscosity of the fluid, and most of all increasing radius of the catheter (increases flow rate by the increased radius to the fourth power!). In most instances gravity is much faster than the IV pump as long as you have optimized all the factors I listed above
  4. aCRNAhopeful

    Cause of uneven pulse/ox wave form

    Not a PICU nurse but I had a couple thoughts. I am an anesthesia student with experience mostly in adult CVICU and now anesthesia FYI but I think the concept is relevant in pediatrics as well. I agree with the previous poster regarding the pulsus paradoxus. To go a little further you will see it anytime positive intrathoracic pressure causes significant decrease in venous return. If the pt is intubated the decrease in the pulse ox waveform or art line tracing will occur during inspiration and if spontaneously breathing it will occur during expiration due to positive pressure collapsing the vena cava and thus decreasing venous return/pre-load, thus decreasing stroke volume and blood pressure for those brief periods. With adults (and for the life of me I cant think why it wouldnt be the same for peds) this is a sign that someone is VOLUME responsive. Is the patient hypotensive with significant variability in the aline and/or pulse ox waveform with risk factors for hypovolemia: the BP will likely respond to a fluid challenge. This is the concept that the vigileo/flowtrack monitors use to calculate stroke volume variance (SVV). Other terms are systolic pressure variation, pulse pressure variation, SVV and they all refer to this phenomenon. So all the other causes like superior vena cava syndrome, tamponade, etc are all things you have to think about but I would say that the most common cause for this (at least in adults and surgical patients) is hypovolemia. Final caveat: seeing this on the monitor is not necessarily a bad thing, if everything else checks out OK then just note it and move on, maybe patient is just a tad on the dry side but still perfusing well, if so just leave it alone.
  5. aCRNAhopeful


    That's incredibly stupid. If you really insisted that the patients hemodynamics dictated both drips with overlapping mechanisms of action then why wouldn't you infuse both separately so you could tailor the ratio based on changes in the patients condition and hemodynamic state? There's simply no benefit to mixing them together.
  6. aCRNAhopeful

    Triple Lumen Cath anatomy

    They are separate lumens each with their own size. The brown port is typically the largest and best for volume
  7. aCRNAhopeful

    Leaving Phenylephrine on with an Epi Drip?

    I agree but the point is you can still use neo with epi. It does work even if epi may have a stronger affinity for alpha1 receptors. So in my opinion it is reasonable in circumstances where you want more vascular tone without the increased myocardial o2 demand of epi. Of course preload should be optimized in preference to vasopressors though i agree with you there
  8. aCRNAhopeful

    Leaving Phenylephrine on with an Epi Drip?

    I wouldnt be so sure that everyone knows what receptors they work on... Yes there are situations where it is useful to have both drugs on. Unless the doses of epi were so high that they have saturated all the alpha 1 receptors then neo is still going to have an effect. For example, a post CABG pt is on neo and an epi gtt. Currently the CI is 2.8, MAP is 55, and SVR is 680. You can titrate up on the neo and achieve the desired effect of increasing vascular tone and SVR and it will certainly work. If your goal at the time is increasing SVR but you dont need inotropic or chronotropic effects of epi then use neo.
  9. aCRNAhopeful

    Leaving Phenylephrine on with an Epi Drip?

    When i worked in CVICU it was not uncommon to have both going at once but not for the rationale you're stating. First of all even if epi and neo are structurally similar they are night and day different as far as pressors go. Epi is a powerful Beta1, beta 2, and alpha1 agonist while phenylephrine is a pure alpha 1 agonist. The reason why you would put someone on neo is for hypotension with low SVR and adequate cardiac output. Neo can DECREASE HR and CO secondary to reflex baroreceptor stimulation and increased afterload respectively. Epi obviously doesnt do either of those things as it is a powerful inotrope, chronotrope, and vasopressor. Maybe you already know this stuff but your post made it seem like you did not so i just wanted to clarify this. Now we would often receive pts from CVOR on epi and neo but it was guided by CCO from a swan and such. The scenario when you would not want neo and epi is if you were starting epi for cardiogenic shock, neo in that situation would mostly serve to increase afterload and SVR and fight against your goal of increasing CO. Other times it may be reasonable to continue both depending on the particular hemodynamic status of the patient.
  10. aCRNAhopeful

    Leveling art line to tragus for cpp???

    I dont have any evidence to support the practice of leveling to the tragus but it makes sense. The perfusion pressure of any organ is going to be equal to the MAP minus the highest force opposing the map. In the brain it could be ICP or CVP if that is higher. Most organs perfusion pressure is going to be MAP minus the venous pressure. The point is the closer you can approximate the arterial pressure directly entering the organ of interest the closer you are going to be to the actual perfusion pressure of that organ. The physics just make more sense that way than leveling the art line to the heart and calling it good enough.
  11. aCRNAhopeful

    Stroke volume variance

    Regarding SVR - you have the basic idea but just remember you're not treating the actual SVR number. You're treating the hypotension or low cardiac output state or whatever. So yes if pt is hypotensive and has a low svr (sepsis for example) then a pressor like norepi would be a good choice. If the SVR abnormal but the BP and CI are normal you would not be treating the number just to make it normal. Regarding CO/CI - cardiac output is the amt of blood pumped by the heart/min and the CI is CO divided by BSA to account for body size. CO/CI tell you how well the heart is pumping. If the CI is low and PA/CVP/PAOP pressures are high (or if the SVV is low indicating pt is not fluid responsive) then an inotrope would be used to get the weakened heart pumping adequately again. I suppose maybe the swan may provide a more specific picture in some ways but it can also muddy the waters and incorrect use of the data can be harmful to the patient. SVV may be a better way to determine fluid responsiveness than a clinician guessing what PA pressures are too low for that particular patient. Visit pacep.org for more info on hemodynamics, its free and a great resource for ICU nurses ESPECIALLY if you are studying for CCRN
  12. aCRNAhopeful

    Stroke volume variance

    Other than the SVV they should want to know things like the CO/CI (or SV/SVI same concept) and the SVR/SVRI. Just like with a swan the goal being try to figure out how to fix a hemodynamic problem (fluids, pressors, inotropes). As far as which numbers correllate: On a swan you have your CVP, PA, and PAOP pressures which are essentially measures of preload (volume). On a flowtrack you use SVV to determine your preload.Contractility is measured on a swan with CO/CI, both of these are available on the flow track vigileo system. Afterload is determined by numbers like SVR, this info is available with both swans and the flow track.
  13. aCRNAhopeful

    CPR question

    Thats because there isn't one. The patients brain is literally dying rapidly during a code so trying to limit the blood pressure and perfusion is just silly. I can see not being over the top aggressive with compressions but anything else doesnt make sense
  14. aCRNAhopeful


    Your pharmacy probably has a policy as far as "max" doses for pressors which should give you an idea of what high doses are. The typical dose ranges are just memorization info you can find anywhere. There is no rule to know if it is too high or too low, it is determined by the clinical picture, ie - BP, HR, UO, other signs of perfusion.. Basically it doesn't really matter because you are titrating to effect.
  15. aCRNAhopeful


    if the infusion is running in mcg/kg/min you could multiply mcg by kg to get mcg/min. Not sure what that would do for you though? Some hospitals run certain gtts like epi, levo, or neo in mcg/kg/min and others do mcg/min. The therapeutic dose is the one that achieves the target hemodynamic parameters so there is no magic number. Let me know if that isn't what you were looking for.
  16. aCRNAhopeful

    IABP Mean Greater than Systolic?

    I cant say for sure as I dont have experience with ECMO but yes the augmentation pressure is accounted for in the MAP. I have seen the MAP > assisted systolic before with severe cardiogenic shock. The patient's own pulse pressure was so terribly low that the only good pressure being generated was from the augmentation pressure of the balloon. So assisted systolic/diastolic would have been something along the lines of 50/40 with the augmentation pressure of 100 and a MAP somewhere around 60 (just an approximate guess with the actual numbers). So now that I'm thinking about it, why would one need a balloon pump while on ECMO? (no ecmo experience remember so forgive the basic question). Wouldnt the ECMO pump provide all the perfusion just as is the case while someones on bypass intraop? If I understand correctly the patients CO would be determined by the pump flows and whatnot and the MAP could be adjusted with pressors to maintain enough SVR for adequate organ perfusion while on ECMO/CBP. Is there something beneficial about the pulsation generated by the IABP? Thanks