Atropine's effect on heart rate is biphasic and dose-dependent:

1. Low doses (typical clinical doses, ~0.4-0.6 mg IM/IV) A brief, modest bradycardia can occur first (heart rate drops by roughly 4-8 beats/min), with no change in blood pressure or cardiac output. This paradoxical slowing happens because atropine blocks presynaptic M1 muscarinic receptors on parasympathetic postganglionic nerve terminals in the SA node - normally these M1 receptors act as an inhibitory feedback loop that limits ACh release, so blocking them transiently increases vagal ACh release. This effect is usually absent after a rapid IV bolus - Goodman & Gilman's Pharmacological Basis of Therapeutics.

2. Higher/progressive doses As the dose increases, atropine blocks the postsynaptic M2 muscarinic receptors on the sinoatrial (SA) node pacemaker cells directly, antagonizing vagal tone to the heart. This produces a progressive, dose-dependent tachycardia - the dominant clinical effect. In young men given 2 mg IM, resting heart rate rises by about 35-40 beats/min. Atropine does not raise the maximal heart rate achieved during exercise, and its effect is most noticeable in healthy young adults (less so in infants and the elderly, who have lower resting vagal tone) - Goodman & Gilman's; Lippincott Illustrated Reviews: Pharmacology.

Clinical relevance: This is why atropine is used to treat symptomatic sinus bradycardia (e.g., from vagal stimulation, peritoneal traction during surgery, or high spinal/epidural anesthesia) - it reliably increases heart rate at clinical doses used for that purpose (Barash, Cullen, and Stoelting's Clinical Anesthesia). It's also why, during reversal of neuromuscular blockade with neostigmine (which is pro-vagal), atropine is co-administered to prevent bradycardia/arrhythmias.