Does this have a technical name, not only have I never heard of it (which is extremely rare in trauma), but both a medscape and pubmed search brings up nothing.
opa or npa?
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Does this have a technical name, not only have I never heard of it (which is extremely rare in trauma), but both a medscape and pubmed search brings up nothing.
thisgirlisamedic
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Prils are gonna be the class of ace inhibiters aka hypertension meds.
I have heard captopril is being tried as a renal protective therapy in addition to erythropoietin in the ICU.
I haven't heard anything about its use in the EMS or emergent trauma setting.
thisgirlisamedic
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I don't think it'd a use as much as it a life threat, someone said something about since it works on the kidneys production of the receptors that it would cause the body to not be able to respond to shock? I'm trying to find information about this because I had a call that still bothers me and I think his meds, were part of the reason that he died
There is nothing simple about trauma
I think the idea behind using the ace inhibitor is to stop constriction of the afferent renal arterioloes.
In hypovolemia, renal arteriole constriction (starting with efferent) for maintaining GFR is a physiologic reaction. With a high enouugh level of stimulation can be pathologic by reducing or eliminating glomular blood flow.
If the mechanism is identified and treatment begun early enough, AKI is treatable. The kidney can actually last days in some cases.
I can see where in resuscitation, in the effort to mitigate catecholamine response and preserve renal blood flow, the ace inhibitor would be a logical choice.
It may (theorhetically) also have some residual effects in the pulmonay vascular circuit too, which may secondarily inhibit neutrophil activation in the lungs. (haven't found anything that states it actually works though)
The erythropoeitin is still in early research stages, but it is being shown to have an antiapoptotic effect in not only the kidney but on many other cells. (This would offer molecular support to the clinical observation that the loss of the kidneys plays a larger role in the development of MODS than just a single organ would suggest. Particularly with the availability of dialysis.)
Progesterone and pregnenolone are being shown to have antiapoptotic effects as well, particularly in TBI, but I have yet to figure out if it acts conjunctively, synergistically, or not at all with the erythro.
People on chronic medications present increased challenges in trauma care. Especially elderly patients who have not only physiologic and pathologic changes, but may be on multiple meds too. ( I once silenced a M&M meeting at a major hospital I was visiting when I suggested that perhaps resuscitating to the normal textbook respiratory end points of the elderly chronic smoker, post car vs. ped, whos death was attributed to respiratory failure by pathology, was probably a predictable outcome of the efforts.)
Recently I ran across some information on endorphins causing endocardial capilary constriction resulting in Q wave infarctions. (an MI while in hypovolemic shock would be bad) There is no reason to think that synthetic opioids would not have the same or potentiate the effect.
Additionally, several anesthesia studies show that overresuscitation increases mortality, particularly with over fuild resus. So not only does what you are doing, but how much.
did your dead person have an autopsy?
I think the idea behind using the ace inhibitor is to stop constriction of the afferent renal arterioloes.
In hypovolemia, renal arteriole constriction (starting with efferent) for maintaining GFR is a physiologic reaction. With a high enouugh level of stimulation can be pathologic by reducing or eliminating glomular blood flow.
If the mechanism is identified and treatment begun early enough, AKI is treatable. The kidney can actually last days in some cases.
I can see where in resuscitation, in the effort to mitigate catecholamine response and preserve renal blood flow, the ace inhibitor would be a logical choice.
It may (theorhetically) also have some residual effects in the pulmonay vascular circuit too, which may secondarily inhibit neutrophil activation in the lungs. (haven't found anything that states it actually works though)
The erythropoeitin is still in early research stages, but it is being shown to have an antiapoptotic effect in not only the kidney but on many other cells. (This would offer molecular support to the clinical observation that the loss of the kidneys plays a larger role in the development of MODS than just a single organ would suggest. Particularly with the availability of dialysis.)
Progesterone and pregnenolone are being shown to have antiapoptotic effects as well, particularly in TBI, but I have yet to figure out if it acts conjunctively, synergistically, or not at all with the erythro.
People on chronic medications present increased challenges in trauma care. Especially elderly patients who have not only physiologic and pathologic changes, but may be on multiple meds too. ( I once silenced a M&M meeting at a major hospital I was visiting when I suggested that perhaps resuscitating to the normal textbook respiratory end points of the elderly chronic smoker, post car vs. ped, whos death was attributed to respiratory failure by pathology, was probably a predictable outcome of the efforts.)
Recently I ran across some information on endorphins causing endocardial capilary constriction resulting in Q wave infarctions. (an MI while in hypovolemic shock would be bad) There is no reason to think that synthetic opioids would not have the same or potentiate the effect.
Additionally, several anesthesia studies show that overresuscitation increases mortality, particularly with over fuild resus. So not only does what you are doing, but how much.
did your dead person have an autopsy?
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