Way back in episode 1 of EMCrit, I introduced the term SCAPE and discussed this unique clinical presentation. Today, I want to discuss a case of resistant SCAPE posted on twitter. SCAPE is Sympathetic, Crashing Acute Pulmonary Edema. It is a vicious cycle of increased afterload causing LV failure, edema in the lungs, an endogenous catecholamine surge, which worsens afterload and so on… What do you do when the normal treatment for SCAPE, nitroglycerin and NIPPV are not working.
The Case…
https://twitter.com/MikePallaci/status/1646988627073802249?s=20
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Editor-in-Chief, at EMCrit.org
An ED Intensivist from NY.
Professor
Nassau University Medical Center
No conflicts of interest (coi).
Professor
Nassau University Medical Center
No conflicts of interest (coi).
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Any experience with using Phentolamine? Alpha blockade just like for phaeochromocytomas?
Since the pathophysiology is a catecholamine surge, it would make sense to directly block the catecholamine (alpha) effect rather than indirectly vasodilator using CCBs or nitro. Phentolamine is also short acting.
I want to hear more about the logistics of the 60 second art line. I know I can put it in that quickly, but there always seems to be a scavenger hunt for the nursing supplies as well as a nurse that knows how to do it.
A bit off topic: I’m just a young doctor (IM PGY4 at the present time) and recently got to know that the evidence supporting NIV in acute pulmonary edema is not that good as I previously thought, specially after the provoking results of the 3CPO trial.
Any thoughts on that? If you, Josh Farkas or other already discussed it on a previous post, I’d be willing to read/listen.
Thanks!
Hey there, M4 soon to be PGY-1 EM. Was listening to the podcast and it was very briefly mentioned how IPAP may not necessarily be helping patients and could actually be doing harm (unless I misunderstood). Im trying to understand why pressure support (with BiPAP) is not really helpful, while EPAP is really the only important part. At baseline, I understand that EPAP helps reduce dynamic airway collapse and aid in reabsorption of pulmonary edema, but I don’t understand why IPAP is not helpful if not potentially deleterious (which is why we could just use CPAP instead of BiPAP in… Read more »
I have never seen this SCAPE phenomenon but I have limited ED experience.
Has anyone seen this beast in its natural state?
I imagine a large diabetic smoker at the peak of a meth binge could present this way. But maybe that’s agitated delirium…
Unfortunately, my ED experience is too limited to have ever witnessed the SCAPE phenomenon. Since a surge of catecholamines plays a role in the pathophysiology, it seems logical to target the catecholamine (alpha) action instead of the vasodilator effects of CCBs or nitro eggy car. Phentolamine has a similarly brief half-life.
Hey there, know this comment is a little however, just wanted to give a little insight about Clevidipine from clinical practice. While not as big of a problem with these resistant scape patients but something to watch out for. The concentration of Clevidipine is 0.5mg/ml so the starting dose is usually running approximately 2 to 4 ml/hr. Since the medication can be titrated so quickly and the slow infusion rate I originally noticed patient experiencing over correction of blood pressure. The solution, and likely reason was that by the time the medication had traveled through the IV extension tubing (aka… Read more »
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Resistant SCAPE (Sympathetic Crashing Acute Pulmonary Edema) demands quick, precise intervention. I find that using https://www.almaaftercare.com/ non-invasive ventilation alongside aggressive vasodilation is crucial in managing these challenging cases. Staying updated on advanced treatment strategies ensures better outcomes, especially when standard approaches fall short in rapidly stabilizing patients with resistant SCAPE.