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Has been used as as a quick-relief bronchodilator for symptomatic treatment of acute symptoms and exacerbations of bronchial asthma and reversible bronchospasm associated with chronic bronchitis, emphysema, and other obstructive pulmonary diseases. However, generally should be used only when selective β2-agonists are not readily available, since excessive cardiac stimulation (e.g., increased heart rate, myocardial irritability, increased oxygen demand) can occur with nonselective agents, particularly at high doses.
Orally inhaled selective β2-agonists currently are recommended for prehospital management of asthma exacerbations (e.g., in emergency medicine facilities and/or ambulances) and for acute asthma management in emergency rooms and hospitals. Reserve sub-Q epinephrine for severe exacerbations when selective agents are not readily available or are ineffective. No proven advantage of systemically administered (e.g., sub-Q) epinephrine therapy over orally inhaled therapy for the acute management of asthma exacerbations. Parenteral epinephrine may be particularly useful in treating anaphylaxis and angioedema coexisting with asthma.
Nebulized bronchodilator therapy generally should be reserved for patients who are unable to coordinate inhalation via an MDI because of their age, agitation, or exacerbation severity.
Regular, daily use of a short-acting, inhaled β-agonist generally is no longer recommended for maintenance therapy of asthma. Current asthma guidelines emphasize long-term control with anti-inflammatory agents (e.g., corticosteroids), and concomitant anti-inflammatory therapy with an inhaled corticosteroid is recommended whenever inhaled β-agonist bronchodilators are used for maintenance.
Drug of choice in the emergency treatment of severe acute anaphylactic reactions, including anaphylactic shock, which can be profound and life-threatening.
May relieve anaphylactic symptoms (e.g., urticaria, pruritus, angioedema, wheezing, dyspnea, hypotension, swelling of the lips, eyelids, and tongue) caused by reactions to drugs, contrast media, sera, insect stings or bites, foods (e.g., milk, eggs, fish, shellfish, peanuts, tree nuts), latex, or other allergens as well as idiopathic or exercise-induced anaphylaxis.
Give to all patients with signs of shock, airway swelling, or definite breathing difficulty. Drug of choice for the treatment of both vasodilation/hypotension and cardiac arrest associated with anaphylaxis.
Parenteral administration (IM route favored) is preferred for the treatment of anaphylaxis. Administer IV if anaphylaxis appears to be severe with immediate life-threatening manifestations. Absorption and subsequent achievement of peak plasma concentrations after sub-Q injection is slower and may be substantially delayed in patients with shock.
High IV doses (i.e., rapid progression to high dose) should be used without hesitation in any patient in full cardiac arrest.
If necessary, institute other measures for management of cardiac arrhythmias, laryngeal edema, or bronchospasm. Once adequate ventilation is ensured, maintenance of BP in anaphylactic shock should be achieved with other pressor agents (e.g., norepinephrine, metaraminol).
Close monitoring critical; fatal overdose of epinephrine reported.
Risk of paradoxical response to epinephrine in patients receiving β-adrenergic blocking agents; consider glucagon and/or ipratropium for treatment of anaphylaxis in these patients. Increased incidence and severity of anaphylaxis in patients receiving β-adrenergic blocking agents.
Used for its α-adrenergic stimulatory effects to increase blood flow in ACLS during CPR. The principal beneficial effects in patients with cardiac arrest result from increases in aortic diastolic blood pressure and in myocardial and cerebral blood flow during resuscitation. The value and safety of the β-adrenergic effects are controversial because they may increase myocardial work and reduce subendocardial perfusion.
A drug of choice and a high priority for ACLS in cardiac arrest to facilitate return of spontaneous circulation (ROSC); generally used after failure of artificial ventilation, external or internal cardiac compression, and initial defibrillation to restore effective circulation.
Cardiac arrest: May be administered IV, intraosseously, or intracardially or by direct instillation into the tracheobronchial tree via an endotracheal tube to restore cardiac rhythm as an adjunct in the management of cardiac arrest.
Asystole: Restores cardiac electrical activity in asystole and, in some cases, restores myocardial contractility in electromechanical dissociation.
Impending pulseless electrical activity: May produce beneficial vasopressor effects in patients who are not in cardiac arrest but who have other indications for vasopressor therapy (e.g., in those with severe bradycardia and hypotension who are close to pulseless electrical activity or even asystole).
Bradycardia: Treatment of symptomatic bradycardia unresponsive to atropine, as a temporizing measure while awaiting availability of a pacemaker (e.g., out-of-hospital setting) or if pacing ineffective.
Drug-induced cardiovascular emergencies or altered vital signs: May consider use in bradycardia or shock associated with β-adrenergic or calcium-channel blocking agent or tricyclic antidepressant toxicity.
Anesthesia accidents: May be useful in treating cardiac arrest following anesthesia accidents, but should be used with extreme caution, if at all, in patients receiving cyclopropane or halogenated hydrocarbon general anesthetics. (See General Anesthetics under Interactions.)
Heart block: Has been used in the treatment of syncope and/or bradycardia resulting from AV nodal block, but has largely been replaced by isoproterenol. Electrical cardiac pacemakers have largely replaced drug therapy in third-degree AV nodal block (complete heart block).
Has been given intra-arterially† as an adjunct to radiographic contrast media in arteriography†.
Has been administered intra-arterially† via the celiac artery, inferior mesenteric artery, or superior mesenteric artery to control hemorrhage in patients with severe GI bleeding†.
Has been administered intra-arterially† via the renal artery to control hemorrhage in patients with renal arterial bleeding†.
Has been injected into a renal artery prior to and during irradiation of the abdominal area to protect the kidney from radiation nephritis†.
May be added to solutions of some local anesthetics to decrease the rate of their vascular absorption (to localize and prolong the duration of anesthesia and decrease the risk of systemic toxicity).
May be applied topically to control superficial bleeding from arterioles or capillaries in the skin, mucous membranes, or other tissues. Bleeding from larger vessels is not controllable by topical application.
Should not be used in cardiogenic shock (because it increases myocardial oxygen demand) or in hemorrhagic or traumatic shock.
Has been used to relax uterine musculature and inhibit uterine contractions in premature labor† (tocolysis); however, the cardiovascular and other adverse effects limit its usefulness. (See Pregnancy under Cautions.) Other β-agonists (e.g., terbutaline) preferred.
Has been used parenterally to correct hypoglycemia† in insulin shock; however, dextrose and/or glucagon is more effective.
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