therealqert.blogg.se - Levophed drip

In order to prove that high doses of norepinephrine are truly required, it would be ideal to perform ongoing, repeated dose-titration. Everyone in this universe concludes that the high dose of norepinephrine caused her blood pressure to improve. By the end of the hour, the norepinephrine has been increased to a dose of 200 mcg/min and the patient’s blood pressure finally improves. For the hour that the patient is hypotensive, norepinephrine is continually up-titrated. Universe B: Everyone in this universe believes that there is no maximal dose of norepinephrine.Everyone in this universe concludes that the patient simply needed some time to recover. The patient will be hypotensive for one hour on 30 mcg/min norepinephrine, then her blood pressure will improve.

Consequently, the norepinephrine will be titrated up to 30 mcg/min, but no higher. Universe A: Everyone in this universe believes that the maximal dose of norepinephrine is 30 mcg/min.Let’s imagine how this case could play out in two parallel universes: This will happen regardless of vasopressor dose – she simply needs an hour to respond to resuscitation. Imagine that we have a patient who is going to be hypotensive for one hour, and then her blood pressure will improve.Any infusion above 30 mcg/min has exactly the same efficacy as 30 mcg/min. Imagine that there is a maximal effective dose of norepinephrine, let’s say 30 mcg/min.One way to appreciate this is through the following thought experiments. Before considering the evidence, we must respect its limitations. Unfortunately, all available evidence consists of retrospective case series. Methodology pitfalls: Self-fulfilling prophecies & circular logic someone with cardiogenic shock) might be required to keep another patient alive (e.g.

The same dose of norepinephrine that would kill one patient (e.g. Thus, there might not exist any specific norepinephrine dose which would be expected to be detrimental for every patient. The norepinephrine dose at which this occurs would reflect several competing factors: cardiac function, volume status, and underlying vasoplagia. Specifically, excessive afterload could threaten to choke off cardiac output (thereby generating an iatrogenic state of vasopressor-induced shock). However, excessive norepinephrine doses could be dangerous within the context of an individual patient’s physiology. This suggests that commonly used clinical doses aren’t close to saturating all the alpha-receptors. Dose-titration in rats shows that norepinephrine has a nearly linear effect up to a dose of 1.35 mcg/kg/min ( Pang 1986). However, it also implies that higher doses of vasopressor aren’t dangerous (they are merely futile, since all the receptors at this point are fully saturated).ĭose-response curves don’t exist for humans due to ethical concerns. This would suggest that a maximal effective dose of vasopressor ought to exist. Such curves indicate that above a certain dose, additional drug will have little effect. Theory: What is the maximum effective dose of vasopressors ?Īny drug ought to have a dose-response curve.

Failure of the patient to respond to “maximal” doses may be interpreted as meaning that the patient is moribund, with any further therapy being futile.

Clinicians may be afraid to titrate above their hospital’s “maximum” dose, lest they run afoul of institutional policy.

The maximum dose of vasopressors is important for a few reasons: Every hospital and pharmacopeia have their own “maximum dose” of vasopressors. Maximal doses used in clinical studies have ranged between 0.2-5 mcg/kg/min ( Dopp-Zemel 2013). What is your hospital’s “maximum dose” of vasopressor? Within a few hours we were down-titrating the vasopressors. His blood pressure steadily improved over the next 15 minutes. Meanwhile, we up-titrated his vasopressors to 80 mcg/min norepinephrine and 40 mcg/min epinephrine. We told his family that things were looking dire, and they did come into the room for what we all anticipated was a last encounter. It was suggested that he was dying and we should call his family in from the waiting room to say goodbye. His blood pressure was 60/30 on a femoral arterial line. He was on the maximal dose of three agents according to institutional guidelines (30 mcg/min norepinephrine, 10 mcg/min epinephrine, 0.04 U/min vasopressin), meanwhile phenylephrine was being up-titrated. Soon after arriving in the unit his blood pressure dropped, so vasopressors were started and lines were inserted.Ī few hours later, I was called to his bedside due to refractory hypotension. We admitted him to the ICU despite a normal blood pressure because he looked toxic. Once upon a time at Genius General Hospital, an elderly man was admitted to the ICU with rapidly progressive cellulitis and tachypnea (1).