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Anaphylactic Shock - #MEDSHED

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🐼 Anaphylactic Shock Pharmacologic Agents - #MEDSHED



🥜You’d actually be surprised how many people die each year from bee stings and peanuts. Anaphylactic shock is derived from mast cells, basophils, and histamanergic-mediated acute onset of hypersensitivity and inflammation.



💣This will progress to profuse vasodilation, decreased venous return/CO, and eventual shock. Around 90% of patients will present with angioedema, which is inflammation of the throat, tongue, and lips. If left untreated, patients can rapidly progress to acute cardiopulmonary arrest.



🐍Epinephrine agonizes alpha and beta receptors, leading to bronchodilation, increased inotropy, and vasoconstriction.



🐲Give 0.3 to 0.5 mg IM q 5 min up to three doses, then transition to IV epinephrine for refractory shock. Thigh is preferable given the vasculature provides a faster onset compared to the deltoid. Consider glucagon when patients are on beta blockers. Glucagon is indicated given it will promote inotropy/chronotropy via increased cAMP and bybassing adrenergic receptors.



🤽Everything we give is considered to be symptomatic and only given after epinephrine has been given (when indicated). Diphehydramine (H1-antihistamine) addresses symptomatic control of urticuria. Famotidine (H2 receptor antagonist) has minimal acute effect given H2 receptors are primarily in gut. Steroids have limited acute benefit since their onset is 4 to 6 hours their biphasics prevention is questionable.



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