Pharmacology · Adrenergic Pharmacology

Catecholamine Agonists

Epinephrine · Norepinephrine · Dopamine · Dobutamine

Epinephrine is the most broadly acting catecholamine — it activates all adrenergic receptor subtypes; at therapeutic doses, beta-2 bronchodilation and cardiac stimulation predominate, while at very high doses alpha-1 vasoconstriction takes over; intramuscular injection into the lateral thigh is the route of choice for anaphylaxis, achieving faster and more reliable absorption than subcutaneous.
Norepinephrine's receptor profile (alpha-1 dominant + beta-1, minimal beta-2) makes it the preferred vasopressor in septic shock — the SOAP II trial showed superior outcomes versus dopamine, with less arrhythmia; it must be given via central access because extravasation causes tissue necrosis (treat with phentolamine infiltration).
Dobutamine selectively stimulates beta-1 receptors to increase contractility and cardiac output, with mild beta-2 vasodilation reducing afterload — it is combined with norepinephrine in cardiogenic shock to address both inotropy and pressure; the FIRST trial showed long-term continuous dobutamine increases mortality, so it should not be used chronically.
The most dangerous catecholamine interaction is with MAO inhibitors — irreversible MAO-A blockade prevents catecholamine degradation, causing accumulation and hypertensive crisis; this interaction persists for 2 weeks after MAOI discontinuation; phenylephrine (alpha-1 only, not a MAO substrate in the same way) is the safer vasopressor alternative when MAOIs are on board.
Beta-blockers create a paradoxical problem in anaphylaxis — by blocking beta-2, they allow unopposed alpha-1 vasoconstriction from epinephrine while preventing bronchodilation; glucagon (1–2 mg intravenously) bypasses the blocked receptors by directly activating Gs via its own GPCR, restoring cardiac output independent of adrenergic signaling.

Interacting Drug	Risk Level	Mechanism and Effect	Management
Monoamine oxidase inhibitors	Dangerous	Irreversible enzyme inhibition → catecholamine accumulation → hypertensive crisis. Effect persists 2 weeks after stopping.	Avoid catecholamines for 2 weeks. Use phenylephrine if vasopressor required.
Tricyclic antidepressants	Caution	Norepinephrine transporter blockade → prolonged catecholamine effect. Indirect agents less effective.	Reduce direct catecholamine doses; monitor closely.
Non-selective beta-blockers (anaphylaxis)	Dangerous	Beta-2 blockade → unopposed alpha-1 → paradoxical hypertension + persistent bronchospasm despite epinephrine.	Glucagon 1–2 mg intravenous (bypasses blocked receptors via Gs). Add ipratropium.
Cocaine intoxication	Dangerous	Norepinephrine transporter blockade → catecholamine excess. Additional sympathomimetics risk crisis. Beta-blockers contraindicated (unopposed alpha-1).	Benzodiazepines; phentolamine for hypertension; nitrates. No beta-blockers.

Suggested References

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