The use of atropine in cardiovascular disorders is mainly in the management of patients with bradycardia. Atropine increases the heart rate and improves the atrioventricular conduction by blocking the parasympathetic influences on the heart. Recent observations that atropine in low doses results in paradoxical effects at the sinoatrial node (vagotonic) and the atrioventricular node (vagolytic) have lead to a concern for its safety in patients with acute myocardial infarction and bradycardia. This review discusses the basic cardiovascular pharmacology of the atropine, explores the mechanisms responsible for its paradoxical effects and discusses the clinical implications of these observations.