Vasopressors, inotropes, antihypertensives, antiarrhythmics
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.
Endogenous nucleoside antiarrhythmic (transient AV nodal block)
Activates A1 receptors → ↑ K⁺ efflux, ↓ Ca²⁺ current at the AV node → transient complete AV block. Terminates re-entrant SVT that uses the AV node.
Class IA antiarrhythmic (Na⁺-channel blocker)
Blocks fast Na⁺ channels (↓ conduction) + K⁺ channels (↑ refractoriness/QT). Slows conduction in accessory pathways.
Class III antiarrhythmic (K⁺-channel effect; also activates slow Na⁺ current)
Prolongs action potential/repolarization → chemical cardioversion of atrial fibrillation/flutter.
Non-dihydropyridine calcium channel blocker (class IV antiarrhythmic)
Blocks L-type Ca²⁺ channels — strong AV-nodal + myocardial effect (more cardiac than diltiazem), less vascular. Negative inotrope/chronotrope/dromotrope.
Non-dihydropyridine calcium channel blocker (class IV antiarrhythmic)
L-type Ca²⁺ blocker — AV-nodal slowing with less myocardial depression than verapamil; some vasodilation.
Ultra-short-acting dihydropyridine calcium channel blocker
Arterial-selective L-type Ca²⁺ blockade → ↓ SVR with little effect on venous capacitance/preload or myocardial contractility. Ester-metabolized (like esmolol/remifentanil).
Direct arterial vasodilator (antihypertensive)
Direct arteriolar smooth-muscle relaxation (afterload reduction), minimal venodilation. Reflex tachycardia is common.
Selective dopamine-1 (D1) receptor agonist — antihypertensive
D1 agonist → arterial + renal/splanchnic/coronary vasodilation. Increases renal blood flow, natriuresis, and diuresis while lowering BP.
Central alpha-2 adrenergic agonist (antihypertensive / analgesic adjunct)
Central α2 agonism → ↓ sympathetic outflow → ↓ HR/BP; also spinal α2 analgesia + sedation.
Endogenous catecholamine — dose-dependent inopressor
Dose-dependent receptor activation: low → dopaminergic (renal/splanchnic vasodilation); moderate → β1 (inotropy/chronotropy); high → α1 (vasoconstriction). Also releases norepinephrine.
Nonselective beta (β1 + β2) agonist
Pure β agonist → ↑ HR/contractility (β1) + vasodilation/bronchodilation (β2). No α activity → ↓ diastolic BP.
Synthetic vasopressor (renin-angiotensin system peptide)
Directly activates AT1 receptors → potent arterial + venous vasoconstriction; also aldosterone/ADH release. A vasopressor with a mechanism distinct from catecholamines/vasopressin.
Phosphodiesterase-3 inhibitor inodilator
Inhibits cardiac PDE3 → ↑ cAMP → inotropy + vasodilation (inodilator); mechanism identical to milrinone (milrinone has largely replaced it).
IV ACE inhibitor (antihypertensive)
Enalaprilat is the active de-esterified ACE inhibitor → blocks angiotensin I→II conversion → ↓ SVR without reflex tachycardia; the only IV ACE inhibitor.
Direct arterial + venous vasodilator (NO donor)
Spontaneously releases nitric oxide → ↑ cGMP → balanced arterial + venous dilation (↓ afterload AND preload). Each molecule contains 5 cyanide groups.
Cardiac glycoside (positive inotrope + AV-nodal blocker)
Inhibits the Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↑ Ca²⁺ via Na/Ca exchange → ↑ contractility. Also ↑ vagal tone → AV-nodal slowing (rate control).
Cardioselective β1-adrenergic antagonist
Selective β1 blockade → ↓ HR, contractility, AV conduction, and myocardial O₂ demand. Cardioselectivity is dose-dependent (lost at high dose).
Non-selective β (β1 + β2) antagonist
Non-selective β blockade + membrane-stabilizing (Na-channel) activity at high dose. Lipophilic → crosses BBB.
Class III antiarrhythmic with non-selective β-blockade
Combines K⁺-channel blockade (class III → ↑ QT/refractoriness) with non-selective β-blockade (class II).
Dihydropyridine calcium channel blocker (cerebroselective)
Lipophilic DHP CCB with CNS penetration → improves neurologic outcomes after aneurysmal SAH (mechanism beyond vasospasm — likely neuroprotective).
Phosphodiesterase-5 inhibitor (pulmonary vasodilator)
Inhibits PDE5 → ↑ cGMP in pulmonary vascular smooth muscle → pulmonary vasodilation. Used to treat pulmonary HTN and to ease weaning from inhaled NO.