Mechanism of Action

Anticholinergic (parasympatholytic) that competitively blocks acetylcholine at muscarinic receptors on the SA and AV nodes. The vagus nerve normally slows the heart by releasing acetylcholine; atropine removes that vagal 'brake,' letting intrinsic sympathetic tone raise the rate. This makes it first-line for symptomatic bradycardia at the nodal level — sinus bradycardia and AV blocks above the node. It is ineffective in infranodal blocks (Mobitz Type II, wide-QRS third-degree block) because those occur below where vagal tone has influence. Atropine also dries secretions (preoperative use) and is the antidote for organophosphate/nerve-agent poisoning, where cholinergic excess produces the SLUDGE picture.

Common Medications

atropinePrototype

single high-yield agent; no class suffix

Indications

symptomatic sinus bradycardia

first-line per ACLS

symptomatic nodal AV block

blocks at or above the AV node

organophosphate poisoning

antidote for cholinergic excess (SLUDGE)

nerve agent poisoning

preoperative secretion reduction

Side Effects

dry mouth

expected anticholinergic effect, not an adverse reaction

urinary retention

blurred vision

mydriasis / cycloplegia

photophobia

constipation

flushed dry skin

decreased sweating

anhidrosis raises hyperthermia risk

Contraindications & Interactions

Contraindications

Mobitz Type II block

infranodal — atropine ineffective; use pacing or epinephrine/dopamine

wide-QRS third-degree block

infranodal complete block — atropine ineffective

narrow-angle glaucoma

mydriasis raises intraocular pressure

benign prostatic hyperplasia

worsens urinary retention

Interactions

other anticholinergics

additive antimuscarinic effects / toxicity

Administration & Monitoring

give 1 mg IV push1 mg IV q3–5 min, max 3 mg

current AHA ACLS dose for symptomatic bradycardia

never give less than 0.5 mg IVHold≥ 0.5 mg per dose

sub-0.5 mg risks paradoxical bradycardia

continuous cardiac monitoring

watch for rate response and tachydysrhythmias

prepare transcutaneous pacing

backup for atropine-refractory bradycardia

monitor blood pressure and perfusion

reassess LOC, lactate, urine output — rate alone is not the goal

assess urinary output

anticholinergic retention

Patient Teaching

expect dry mouth

sip water, sugar-free hard candy

report palpitations

report difficulty urinating

rise slowly

dizziness can occur

avoid overheating

reduced sweating impairs cooling

report blurred vision or eye pain

eye pain may signal acute glaucoma

Report Nowescalate immediately

tachydysrhythmias Hallmark

anticholinergic toxicity — excessive vagolysis driving tachycardia

paradoxical bradycardiadose < 0.5 mg IV

sub-therapeutic dosing partially stimulates the central vagal nucleus — classic NCLEX trap

anticholinergic toxicity

'hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter'

acute confusion

delirium/agitation, especially in older adults

hyperthermia

impaired sweating impairs heat loss

Clinical Pearl

Atropine lifts the vagal foot off the brake — it doesn't press the gas. No vagus, no atropine: if the block is below the node (Mobitz II, wide-QRS complete block), pace instead. And never push less than 0.5 mg — too little speeds the heart the wrong way.

Atropine

Mechanism of Action

Common Medications

Indications

Side Effects

Contraindications & Interactions

Administration & Monitoring

Patient Teaching

The patient's heart rate is 38 and they're pale and diaphoretic. The first drug you reach for isn't a cardiac stimulant — it's a blocker. Understanding why is the key to atropine.

Key Distinctions

Clinical Pearl

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