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Antipyretic and analgesic; exact mechanism unknown — believed to raise pain threshold. Mild anti-inflammatory effects. Rapidly absorbed through GI tract.

Stimulates β1, α1, and β2-adrenergic receptors — relaxes bronchial smooth muscle, increases cardiac output (↑myocardial O2 consumption), dilates skeletal muscle vasculature. Large doses cause vasoconstriction.

Class I/II/III/IV antidysrhythmic. Blocks sodium channels; lengthens cardiac action potential. Slows AV node conduction. Antisympathetic and negative inotropic effects. Used for VT/VF and some atrial arrhythmias.

Irreversibly inhibits COX-1/COX-2; inactivates cyclooxygenase, interfering with Thromboxane A2 production in platelets. Thromboxane A2 also causes arterial constriction. Reduces morbidity/mortality in AMI.

Parasympatholytic; blocks acetylcholine at parasympathetic sites in smooth muscle, secretory glands and CNS. Results in increased cardiac output and dried secretions.

Slows conduction through AV node, interrupting re-entry pathways and restoring normal sinus rhythm. Also causes coronary vasodilation and increases blood flow in normal coronary arteries.

Selective β2-adrenergic agonist; relaxes bronchial smooth muscle by action on β2-receptors with little effect on heart rate.

Anticholinergic; inhibits muscarinic receptors in bronchial smooth muscle, reducing bronchoconstriction

Venous and arterial vasodilator via release of nitric oxide. Reduces preload; dilates coronary arteries and improves collateral flow. In smooth muscle, nitric oxide activates smooth muscle relaxation.

Competitive narcotic antagonist. Displaces narcotics bound to opiate receptor sites (mu, kappa, delta), reversing their effects including respiratory depression and sedation.

Carbohydrate; exogenous glucose that replenishes blood glucose levels, reversing hypoglycemia. Metabolized to carbon dioxide and water.

Stimulates adenylate cyclase to produce increased cyclic AMP, promoting hepatic glycolysis and gluconeogenesis, resulting in a rise in blood glucose levels.

Binds to opiate receptors in the CNS causing inhibition of ascending pain pathways, altering the perception of and response to pain. Produces generalized CNS depression.

Binds to opioid mu-receptors in the CNS causing inhibition of ascending pain pathways, altering the perception of and response to pain. Produces CNS depression, respiratory depression, and can cause apnea. Can cause muscle rigidity with rapid IV injection.

NMDA receptor antagonist; dissociative anesthesia, analgesia, bronchodilation, and sympathomimetic effects

Binds to stereospecific benzodiazepine receptors on the post-synaptic GABA neuron at several CNS sites. Enhances inhibitory effect of GABA on neural excitability by increasing membrane permeability to chloride ions.

Enhances GABA-A receptor activity; produces anxiolysis, sedation, and anticonvulsant effects

GABA-A positive allosteric modulator; anticonvulsant, anxiolytic, muscle relaxant, and sedative

Competes with histamine at H1-receptor sites on effector cells in GI tract, blood vessels and respiratory tract. Anticholinergic and sedative effects.

Selective 5-HT3 receptor antagonist; blocks the action of serotonin (5-HT3) peripherally on vagal nerve terminals and centrally on the chemoreceptor trigger zone.

Competes with histamine for H1-receptor sites on effector cells in GI tract, blood vessels and respiratory tract. Blocks chemoreceptor trigger zone, diminishes vestibular stimulation, and depresses function through central anticholinergic activity.

Non-selective COX inhibitor; blocks prostaglandin formation, thereby decreasing nociceptor stimulation. Provides analgesia, anti-inflammatory, and antipyretic effects.

Inhibits COX-2, decreasing synthesis of prostaglandins involved in mediating inflammation, pain, fever and swelling. Antipyretic effects via action on hypothalamus, increasing peripheral blood flow and heat dissipation.

Binds to mu-opioid receptors in the CNS causing inhibition of ascending pain pathways, altering the perception of and response to pain. Produces generalized CNS depression.

Class 1b antiarrhythmic. Suppresses automaticity of conductive tissue by increasing the electrical stimulus threshold. Blocks initiation and conduction of nerve impulses by decreasing neural membrane permeability to Na+ ions.

Potent glucocorticoid with minimal mineralocorticoid activity. Binds to glucocorticoid receptors inhibiting release of pro-inflammatory cytokines, resulting in decreased edema, fibrin deposition, capillary leakage and migration of inflammatory cells.

Short-acting glucocorticoid and mineralocorticoid; when used in adrenal crisis replaces/mimics cortisol which regulates glucose, regulates the immune system, and supports the cardiovascular system during stress.

Inhibits acetylcholine activity on smooth muscles and structures innervated by postganglionic nerves. Causes bronchodilation, decreased gastric secretions, and controls excessive pharyngeal, tracheal and bronchial secretions. Also has antimuscarinic properties.

Butyrophenone antipsychotic. Mechanism not fully understood — possible effect through central dopamine, adrenergic, cholinergic and histaminergic receptors.

Promotes uterine contractions by increasing intracellular calcium levels. Greatest effect during labor at term due to increased oxytocin receptor concentrations in uterine myometrial tissue.

Non-selective beta-blocker and alpha-1 blocker; reduces BP and HR without reflex tachycardia

Provides calcium ions; stabilizes cardiac membrane, reverses hypocalcemia effects, antagonizes hyperkalemia cardiac effects. Calcium protects the myocardium from deleterious effects of hyperkalemia.

Provides bicarbonate ions to buffer metabolic acidosis; reverses sodium channel blockade in TCA overdose

Physiologic calcium antagonist; stabilizes cardiac membrane, inhibits neuromuscular transmission, bronchodilator

Depolarizing NMB; mimics acetylcholine at NMJ, causing fasciculations then paralysis

Non-depolarizing NMB; competitive antagonist at nicotinic acetylcholine receptors at the NMJ

V1 receptor agonist causing vasoconstriction; V2 receptor agonist increasing water reabsorption

Primarily alpha-1 agonist with some beta-1 activity; potent vasoconstriction increases SVR and MAP

Stimulates both adrenergic and dopaminergic receptors. Low doses: dopaminergic — renal/mesenteric vasodilation. Medium doses: β1-adrenergic — cardiac stimulation. High doses: α-adrenergic — vasoconstriction. 25% converted to norepinephrine.