This is a tangent from the now-closed epi-pen thread (I had another version of this all typed up, but I lost it as the admin closed the thread while i was typing..oops!). I'm do not want to have any part in that fight - the thread just inspired a couple of thoughts/questions for those of you who know more than I, and which I think are clinically relevant.
Admin: Hopefully this doesn't break the rules about closed threads. Sorry if I seem like I'm trying to cheat. If that’s the case you’ll hear no objection from me if you remove this thread for the time being. .
Short story long- My thought was that Sub-Q or IM EPI injection (ie through an epi-pen, whether you hit muscle or fatty tissue) would be at least somewhat effective because the vasodilatation caused by anaphylaxis would provide good perfusion to the peripheral or muscular areas of the body - although the heart may be moving that blood in-efficiently due to the hypovolemic effect of such profound dilation, somewhat negating this effect.
Further, the stress of anaphylaxis should cause a catecholamine release which would then cause skeletal vasodilatation (due mostly to NE release) as well as visceral and peripheral vasoconstriction (due to EPI primarily, the cause of observed nausea, paleness) – which, assuming the epi-pen needle reaches muscle as intended, would both overcome the problem of poor circulation due to hypovolemia (due tothe pressor effects on the viscera and the periphery) and increase the rate of distribution of the EPI from the epi-pen due to the increased perfusion of musculature.
Yes? No? I could certainly see this being a slow route of administration - but certainly faster than, for instance, eip-pen administration during cardiac arrest, where the full pressor effect of NE, EPI, Vasopressin, and angiotensin have caused vasoconstriction in the viscera, skeletal muscles, and the periphery. Clearly this is not the best route of administration, but it seems like it could be feasible.
Second: just to throw a monkey-wrench in the whole thing I just said. Vasodilatation caused by anaphylaxis may well cause hypovolemic shock - however, the hypovolemia, and resulting hypotension, would be detected by cardiac and arterial barorecepors, respectively, causing a cascade of catecholamine responses (NE, EPI, ANG, VP) which would, in the absence of the anaphylaxis, cause systemic vasoconstriction. Because this response includes release of angiotensin and vasopressin, unlike the stress response mentioned above, skeletal vasoconstriction would be present as well (the pressor effect of angiotensin is much more powerful than the dilatory effect of NE on the blood vessels supplying the muscles).I honestly have no idea what the resolution of this would be - as there are now two body systems in competition, one attempting to cause vasoconstriction and one attempting to cause vasodilatation. Anyone happen to know which one wins? In other words - is hypovolemia or hypotension (caused by systemic vasodilatation) empirically present in anaphylaxis, or is it compensated for by sympathetic mechanisms? How about visceral, skeletal, and peripheral vasodilatation or constriction?
Admin: Hopefully this doesn't break the rules about closed threads. Sorry if I seem like I'm trying to cheat. If that’s the case you’ll hear no objection from me if you remove this thread for the time being. .
Short story long- My thought was that Sub-Q or IM EPI injection (ie through an epi-pen, whether you hit muscle or fatty tissue) would be at least somewhat effective because the vasodilatation caused by anaphylaxis would provide good perfusion to the peripheral or muscular areas of the body - although the heart may be moving that blood in-efficiently due to the hypovolemic effect of such profound dilation, somewhat negating this effect.
Further, the stress of anaphylaxis should cause a catecholamine release which would then cause skeletal vasodilatation (due mostly to NE release) as well as visceral and peripheral vasoconstriction (due to EPI primarily, the cause of observed nausea, paleness) – which, assuming the epi-pen needle reaches muscle as intended, would both overcome the problem of poor circulation due to hypovolemia (due tothe pressor effects on the viscera and the periphery) and increase the rate of distribution of the EPI from the epi-pen due to the increased perfusion of musculature.
Yes? No? I could certainly see this being a slow route of administration - but certainly faster than, for instance, eip-pen administration during cardiac arrest, where the full pressor effect of NE, EPI, Vasopressin, and angiotensin have caused vasoconstriction in the viscera, skeletal muscles, and the periphery. Clearly this is not the best route of administration, but it seems like it could be feasible.
Second: just to throw a monkey-wrench in the whole thing I just said. Vasodilatation caused by anaphylaxis may well cause hypovolemic shock - however, the hypovolemia, and resulting hypotension, would be detected by cardiac and arterial barorecepors, respectively, causing a cascade of catecholamine responses (NE, EPI, ANG, VP) which would, in the absence of the anaphylaxis, cause systemic vasoconstriction. Because this response includes release of angiotensin and vasopressin, unlike the stress response mentioned above, skeletal vasoconstriction would be present as well (the pressor effect of angiotensin is much more powerful than the dilatory effect of NE on the blood vessels supplying the muscles).I honestly have no idea what the resolution of this would be - as there are now two body systems in competition, one attempting to cause vasoconstriction and one attempting to cause vasodilatation. Anyone happen to know which one wins? In other words - is hypovolemia or hypotension (caused by systemic vasodilatation) empirically present in anaphylaxis, or is it compensated for by sympathetic mechanisms? How about visceral, skeletal, and peripheral vasodilatation or constriction?