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Discussion

ETT Epi

I have a random question about the physiology of ETT epi, and I'm wondering if you lovely folks (especially the providers) can help me out. I meant to ask in my NRP renewal last week but forgot...

The goal of transition is to decrease pulmonary vascular resistance and increase systemic vascular resistance. Epi is a profound vasoconstrictor. I understand that, theoretically, ETT epi should be absorbed into systemic circulation; however, if your kid is so sick in the DR that they need compressions and epi, they're going to be at very high risk for PPHN. It seems like the last thing you'd want to do to a high-risk PPHN kid during transition is to sprinkle their lungs with a vasoconstrictor... Especially when the actual treatment for severe PPHN is inhaled nitric as a selective pulmonary vasodilator and systemic pressors (up to and including epi) for systemic vasoconstriction in order to compete with and overcome super high PVR... ETT epi is the literal exact opposite of that.

I understand that ETT epi is relatively ineffective, that absorption can be hit-or-miss, and that we only give it as a last-ditch effort while we're trying to establish IV access. In theory, I get the idea that 'some epi is better than no epi' when you're profoundly bradycardic, and that you're in dire straits if you're giving ETT epi at all. However, physiologically, putting epi in the pulmonary vascular bed during transition seems like it would make the problem so much worse instead of making it better. Isn't ETT epi just going to throw fuel onto the dumpster fire that is PPHN?

Thoughts?

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    NRP instructor here.

    A few things-

    Yes, it's a vasoconstrictor and no it's not good for anyone with PPHN to have in the lungs. NRP does not really recommend it anymore- putting in a low lying UVC can be pretty quick (1-2 minutes), but it probably doesn't feel quick to the team or the provider and it's tempting to want to just DO something in the interim. Keep in mind that epinephrine has an extremely short half life- about 2 minutes, which is why it is often given as a continuous infusion in the NICU. So even if if you did shut down the pulmonary beds, the effects wouldn't theoretically last long. I also don't know the data, but I suspect most of the epinephrine being given is to tiny preemies for which PPHN is less of a problem than a term kiddo (might not based on pure numbers that there are more preemies than term kids but I wonder if the % of epi given is skewed towards preemies proportionally).

    It should be extremely rare to give epinephrine during a birth resuscitation. And chest compressions too for that matter. Establishing an airway is the most important thing which is why later editions of NRP have focused on MRSOPA. By correcting ventilation nearly all your problems go away.

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    Ahh, @babyNP., I'm so glad you responded!! (I almost tagged you in the initial post so you'd see it, but I thought that might be too pushy...)

    What you're saying makes so much sense. It does make me wonder if we'll ever get to a point where ETT epi is no longer recommended.

    My thought is that even if most kids don't develop PPHN, the kids who are sick enough to actually require epi and compressions in the DR are probably quite acidotic and (initially) poorly ventilated, which sets you up for PPHN (i.e. the HIE cooling kids). It seems like ETT epi could help push them over the edge to PPHN, and even if the epi 'wears off' that doesn't necessarily mean that the pulmonary vascular bed will stop 'clamping down' right away.

    I agree that there should be a much bigger emphasis on ensuring effective ventilation before jumping to compressions, especially in the DR. My current institution seems like they're pushing to try to start compressions sooner rather than later, which seems like it isn't exactly well-aligned with NRP. Part of the challenge is that we're a large Children's Hospital with kids who stay for months and months, so the providers are trying to figure out when and how to incorporate PALS for codes in older kids (not in the delivery room). PALS begins chest compressions and epi pretty much immediately; however, ETT epi doesn't even exist in PALS (I tried to explain ETT epi to my old PICU coworkers, and they thought I was nuts). I feel like sometimes the providers draw from little bits and pieces of NRP and PALS, and it doesn't make for the most unified code.

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