Cardiac / BP

Endogenous catecholamine, α + β agonist

α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.

Endogenous catecholamine, α1 > β1 agonist

Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.

Synthetic α1-agonist

Pure α1 agonist → vasoconstriction. No β activity.

Selective α2-adrenergic agonist

α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.

Antidiuretic hormone analog / V1 vasoconstrictor

Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.

Ultra-short-acting cardioselective β1 antagonist

Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.

Divalent cation / NMDA antagonist / calcium-channel modulator

Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).

Class III antiarrhythmic (multichannel: K, Na, Ca, β-blocker)

Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.

Dihydropyridine calcium channel blocker (vascular-selective)

Selective L-type voltage-gated calcium channel blocker, dihydropyridine class (vascular >> cardiac selectivity). Vascular smooth muscle relaxation → arterial vasodilation → afterload reduction. Minimal direct cardiac inotropic or chronotropic effect at clinical doses (vs verapamil/diltiazem which are non-selective).

Indirect + direct mixed alpha + beta sympathomimetic

Indirect-acting sympathomimetic — promotes release of stored norepinephrine from presynaptic vesicles AND has direct alpha + beta receptor agonism. Mixed action → increases HR (β1) + contractility (β1) + SVR (α1). Tachyphylaxis develops with repeated dosing (depleted NE stores).

Combined alpha-1 + non-selective beta antagonist (β:α ratio ~7:1 IV)

Combined alpha-1 + beta-1 + beta-2 antagonist. Alpha-1 blockade → vasodilation; beta blockade → reduces HR + contractility + reflex tachycardia from alpha blockade. Gives smooth BP reduction without reflex tachycardia (both alpha + beta covered) — a double-acting agent.

Organic nitrate / nitric oxide donor / vasodilator

Metabolized to nitric oxide (NO) in vascular smooth muscle → activates guanylyl cyclase → ↑cGMP → smooth muscle relaxation. PREFERENTIAL VENOUS dilation (low doses) → reduces preload (decreases LV wall stress, ↓myocardial O₂ demand). Higher doses → arterial dilation, including coronary arteries (↑coronary perfusion in non-stenotic vessels).

Phosphodiesterase-3 inhibitor (inodilator)

Selective PDE3 inhibitor in cardiac + vascular smooth muscle. Increases intracellular cAMP → ↑contractility (positive inotropy) + ↓SVR + ↓PVR (vasodilation). 'INODILATOR' — distinct from pure inotropes (dobutamine) and pure vasodilators. Particularly effective for RV failure and pulmonary hypertension.

Beta-1-selective synthetic catecholamine

Synthetic catecholamine with PREDOMINANT β1 activity (also β2, mild α1). Pure inotrope — increases contractility + heart rate (β1) with mild vasodilation (β2 + α1 balance). Does NOT release endogenous norepinephrine (unlike ephedrine).

Antifibrinolytic / synthetic lysine analog

Synthetic lysine analog. Competitively binds plasminogen LYSINE binding sites, preventing plasminogen activation to plasmin. Inhibits fibrinolysis without inducing hypercoagulability per se.

Non-competitive irreversible alpha-1 + alpha-2 antagonist

IRREVERSIBLE non-competitive antagonist at alpha-1 + alpha-2 adrenergic receptors. Covalently binds + permanently inactivates receptors — duration of action depends on receptor RESYNTHESIS (24-48 h after each dose). Distinguishes from competitive antagonists (phentolamine) where catecholamine surge can overcome blockade.