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  1. Pharmacology. Glucagon is a polypeptide hormone that stimulates the formation of adenyl cyclase, which in turn increases the intracellular concentration of cyclic adenosine monophosphate (cAMP). This results in enhanced glycogenolysis and an elevated serum glucose concentration, vascular smooth-muscle relaxation, and positive inotropic, chronotropic, and dromotropic effects. These effects occur independently of beta-adrenergic stimulation (glucagon has a separate receptor on the myocardium) and seem to be most effective at increasing the heart rate. Glucagon may also increase arachidonic acid levels in cardiac tissue via an active metabolite, mini-glucagon. Arachidonic acid improves cardiac contractility owing to its effects on calcium. Glucagon is destroyed in the GI tract and must be given parenterally. After intravenous administration, effects are seen within 1–2 minutes and persist for 10–20 minutes. The serum half-life is about 3–10 minutes. Note: Glucagon usually is not considered first-line therapy for hypoglycemia because of its slow onset of action and reliance on glycogen stores. Instead, use glucose (See Glucose) if it is available.

  2. Indications

    1. Hypotension, bradycardia, or conduction impairment caused by beta-adrenergic blocker intoxication (See Beta-Adrenergic Blockers). Also consider in patients with hypotension associated with anaphylactic or anaphylactoid reactions who may be on beta-adrenergic–blocking agents.

    2. Possibly effective for severe cardiac depression caused by intoxication with calcium antagonists, tricyclic antidepressants, quinidine, or other types la and lc antiarrhythmic drugs. Because of the benign side-effect profile of glucagon, consider its early empiric use in any patient with myocardial depression (bradycardia, hypotension, or low cardiac output) who does not respond rapidly to usual measures.

    3. To facilitate passage of obstructed gastric foreign bodies (eg, drug packets) through the pylorus into the intestine (based on a case report).

  3. Contraindications. Known hypersensitivity to the drug (rare) or pheochromocytoma (stimulates the release of catecholamines and may result in severe hypertension) or insulinoma (indirectly stimulates release of insulin and may result in hypoglycemia).

  4. Adverse effects

    1. Hyperglycemia (usually transient), hypokalemia.

    2. Nausea and vomiting are dose-dependent (especially if >1 mg is administered) and caused by delayed gastric emptying and hypotonicity.

    3. Use in pregnancy. FDA Category B. Fetal harm is extremely unlikely (See Introduction in Section III).

  5. Drug or laboratory interactions. Concurrent administration of epinephrine potentiates and prolongs the hyperglycemic and cardiovascular effects of glucagon. It is unknown if glucagon interferes with the effectiveness of insulin and glucose therapy for severe calcium antagonist poisoning. Note that glucagon stimulates endogenous insulin secretion.

  6. Dosage and method of administration.

    1. Initial dose. Give 3–10 mg IV (may also titrate with 0.05-mg/kg boluses) over 1–2 minutes and repeat every 3–5 minutes until response (usually a cumulative total of 10 mg, but up to 30 mg has been given).

    2. Maintenance infusion. Infuse 1–5 mg/h (children: 0.15 mg/kg IV, or titrate with 0.05 mg/kg every 3 minutes, followed by 0.05–0.1 mg/kg/h). Alternatively, determine the total dose required to achieve the initial response and give this amount every hour. Infusions of up to 10 mg/h have been used for adults. Note: Tachyphylaxis may occur with prolonged infusions (case report with infusion duration >24 hours).

    3. For ...

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