STEPTRACKERPHARMACOLOGY | AUTONOMIC | HIGH-YIELD REVIEW

Sympathomimetics

Catecholamines and their relatives differ only in which adrenergic receptors they prefer — predict heart rate, blood pressure and vascular resistance from the receptor profile.

FOCUS ON

Direct agonists: epinephrine (α1, α2, β1, β2; low dose β > α): anaphylaxis, cardiac arrest, with local anesthetics; norepinephrine (α1 > β1, little β2): septic shock — ↑ BP with reflex bradycardia; dopamine (D1 → β1 → α1 as dose rises); dobutamine (β1 > β2): cardiogenic shock, stress echo; isoproterenol (β1 = β2): bradyarrhythmia, torsades; phenylephrine (α1): hypotension, decongestant, mydriasis; midodrine (α1): orthostatic hypotension; albuterol/salmeterol (β2): asthma; terbutaline: tocolysis; mirabegron (β3): bladder. Indirect: amphetamine (release + reverse NET), cocaine (block reuptake; local anesthetic; vasospasm), ephedrine (mixed, tachyphylaxis). Avoid β-blockers alone in cocaine toxicity (unopposed α).

DRUG

RECEPTORS

HEMODYNAMICS

USE

Epinephrine

α1, α2, β1, β2 (low dose β-selective)

↑ HR, ↑ contractility, ↑ SBP; low dose ↓ DBP (β2)

Anaphylaxis (IM), cardiac arrest, open-angle glaucoma, prolongs local anesthetics

Norepinephrine

α1 > α2 > β1 (minimal β2)

↑↑ SBP and DBP, ↑ SVR, reflex ↓ HR

First-line vasopressor in septic shock

Dopamine

Low D1 · medium β1 · high α1

Dose-dependent: renal vasodilation → inotropy → vasoconstriction

Bradycardia, shock (less favored now)

Dobutamine

β1 > β2, α

↑ contractility and CO; little change or ↓ BP

Cardiogenic shock, acute decompensated HF, pharmacologic stress test

Isoproterenol

β1 = β2

↑ HR, ↓ DBP (vasodilation)

Bradyarrhythmia, torsades (shortens QT by speeding HR)

Phenylephrine

α1 > α2

↑ BP, reflex ↓ HR

Hypotension (anesthesia), nasal decongestant, mydriasis without cycloplegia

Midodrine

α1 (prodrug)

↑ BP

Orthostatic hypotension · supine hypertension

Albuterol · salmeterol · formoterol

β2

Bronchodilation; mild tachycardia, tremor, ↓ K⁺

Asthma, COPD (LABA never alone in asthma)

Terbutaline · ritodrine

β2

Uterine relaxation

Short-term tocolysis

Mirabegron

β3

Detrusor relaxation

Overactive bladder; may ↑ BP

Amphetamine · methylphenidate

Indirect: release NE/DA, reverse or block reuptake

↑ HR, ↑ BP, CNS stimulation

ADHD, narcolepsy · ↓ appetite, insomnia

Cocaine

Indirect: blocks NE, DA, 5-HT reuptake; Na⁺-channel block

Vasoconstriction, ↑ HR, ↑ BP

MI from coronary vasospasm · treat with benzodiazepines

Ephedrine · pseudoephedrine

Mixed direct + releaser

↑ HR, ↑ BP

Decongestant, hypotension in anesthesia · tachyphylaxis

Mechanism — norepinephrine's reflex bradycardia

α1 vasoconstriction↑ SVR, ↑ MAP

→

Baroreceptors fireCarotid sinus

→

↑ Vagal toneOverrides direct β1 effect → HR falls

Phenylephrine does the same. Atropine abolishes the reflex and unmasks the β1 tachycardia.

Choosing a pressor

SHOCK

FIRST CHOICE

WHY

Septic

Norepinephrine

Restores SVR

Cardiogenic

Dobutamine (± NE)

↑ contractility

Anaphylactic

Epinephrine IM

α1 + β2 + mast cell stabilization

Neurogenic

Phenylephrine / NE

Replace lost tone

How it's tested

COMMON CONFUSIONLow-dose epinephrine lowers diastolic pressure (β2 vasodilation) while raising systolic; high dose raises both (α1).

THE TRAPEpinephrine's effect after an α-blocker: BP falls ("epinephrine reversal") because only β2 vasodilation is left.

YOUR APPROACHWrite the receptor profile → predict SBP, DBP, HR, SVR → check for baroreflex.

If you see… think…

Anaphylaxis → IM epinephrine

Septic shock after fluids → norepinephrine

BP up, heart rate down after a pressor → α1 agonist with baroreflex

Cardiogenic shock with low output → dobutamine

Pharmacologic stress echo → dobutamine

Orthostatic hypotension (oral) → midodrine

Chest pain in a young cocaine user → coronary vasospasm → benzodiazepines, avoid β-blocker alone

BP falls after epinephrine given with phenoxybenzamine → epinephrine reversal

Tremor and hypokalemia on albuterol → β2 effects

Nasal spray rebound congestion → α1 agonist overuse