The most utilized agents for push-dose pressors in the emergency department are currently phenylephrine as well as epinephrine, which both have rapid onset and short-lived effects. Prehospital EMS administration (which has been on the rise recently) To keep in your pocket “just in case” during transport of critical patients (e.g. Temporizing perfusion of critical organs (heart, brain, kidneys) while aggressive fluid and blood product replacement is taking time to effect peri-intubation)Īs a bridge prior to the initiation of a vasopressor drip (while the drip is being mixed, a central line is being placed, etc.) Push-doses of these pressors are useful in a number of given situations, including:Īn anticipated transient drop in blood pressure (e.g. Push-dose pressors are simply small intravenous bolus doses (“pushes”) of vasopressors & inotropes that can serve as a great temporizing measure in patients who are severely hypotensive, in order to rapidly increase cardiac and brain perfusion while other measures are being initiated.
#Levophed drip how to
Nevertheless, having a solid understanding of when & how to give push-dose vasopressors can be a vital (and practical) tidbit of ED resuscitation knowledge that can save your critically hypotensive patients from hemodynamic collapse if you have it in your arsenal. Anesthesiologists have been using bolus-doses of vasopressors for decades in the OR, but the concept has only recently penetrated into the ED/ICU resuscitation world the past few years, with very little EM-based literature published on the subject. I don’t think a lot of ED providers tend to consider push-dose pressors as a tool to keep in their back pockets during some of these split-second moments that they’re needed, but I also think not many providers may be familiar enough with them to be comfortable mixing & administering them during these high-stress situations. Some of my all-time favorites are obviously the ultrasound machine, Bi-Pap, the Glidescope, etc., etc.… But another favorite of mine is a tool that works within seconds and is a great temporizing measure in patients with dangerously low perfusion when you need an immediate increase in blood pressure, STAT. In the resuscitation bay, there are a handful life-saving tools we regularly keep within an arm’s reach during each resuscitation – tools for some of those critical moments that could prevent your crashing patient from coding if you quickly employ them when needed. Say 90kg patient i'd give 2 (20ml/kg that is 3.6L total) bolus if refractory still, I may do 1 more if no pul edema and then go for the presssor.Written by Dr. So OP patient is refractory to fluid bolus, granted 1L is low, but it should not be 12L by any means. The initial vasopressor (UG) dopamine is not recommended To decrease norepinephrine dose but should not be used as To either raise mean arterial pressure to target or Pressure (2B) vasopressin (0.03 U/min) can be added to norepinephrine When an additional agent is needed to maintain adequate blood Maintain mean arterial pressure ≥ 65 mm Hg (1B) epinephrine (UG) norepinephrine as the first-choice vasopressor to Improvement, as based on either dynamic or static variables (1C) fluid challenge technique continued as long as hemodynamic Minimum of 30 mL/kg of crystalloids (more rapid administrationĪnd greater amounts of fluid may be needed in some patients) Tissue hypoperfusion and suspicion of hypovolemia to achieve a (1C) initial fluid challenge in patients with sepsis-induced Generally it was a combination of pressors, while keeping an eye on end organ perfusion, pH, lactate, pyruvate, etc.
The last thing ill add (in this post anyway) is that septic patients are a balancing act, and I rarely managed them with only a single pressor. This is why in many protocols, norepi is first line for SERIOUS sepsis, but can be preceded by dopamine in early stage or even moderate sepsis. Remember, pH is logarithmic, so even a slight move has magnitudes of effect on h+ concentration.Īll this is to say, in my experience, norepi was a better drug in profound sepsis, and I believe it has to do with the acidosis we find many septic patients in. In acidic conditions, the pathway it takes to convert to norepi and epi will not proceed as effectively as it would when conditions are a homeostatic 7.4. Most septic patients we are dealing with are acidic.Īlso, dopamine is a precursor of epi and norepi.
I am reaching back to biochem class here.I seem to remember that norepinephrine has the lowest pKa of the four pressors we commonly use (epi, norepi, dopamine, dobutamine.) this in and of itself doesn't mean anything spectacular, other than the fact that the higher the pKa of the drug, the less effective it will be in an acidic environment. We would use norepinephrine for our sepsis protocol back when I was doing CC transport.
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