Introduction: The mechanism for carbamate toxicity is reversible cholinesterase inhibition, which leads to accumulation of acetylcholine at the neuromuscular junction.1 The cardiac manifestations of carbamate toxicity are rare. We report a case of carbamate toxicity with atrial fibrillation as the cardiac manifestation. Case presentation: A 28-year-old patient, previously healthy, presented to the ED complaining of diplopia, dizziness, palpitation, and one episode of vomiting. The symptoms began two hours before when he was spraying pesticide at a farm. According to the patient he sprayed 9 liters of pesticide over a short period of two hours. The patient was not using any personal protective equipment. The pesticide used was later identified as Lannate, which contain Methomyl (carbamate). On examination, a chemical odor was noted. His initial vital signs were normal except heart rate of 134/min. The patient was decontaminated in the decontamination room to avoid further exposure. He had constricted pupils of 2 mm. There were no other signs of organophosphate or carbamate toxicity. His initial ECG showed atrial fibrillation (AF) with fast ventricular response rate. The pseudo-cholinesterase level was. The toxicology service was consulted, and they advised not to start antidote treatment only for the AF, as other signs and symptoms were absent. The cardiology on call assessed the patient and started amiodarone infusion presuming new onset of AF. The patient's rhythm reverted back to sinus 12-hour post-presentation. He was discharged next day with a diagnosis of paroxysmal AF secondary to carbamate poisoning. Discussion: AF in carbamate toxicity is rare and only few cases have been reported in the literature.2,3 It is postulated that, enhanced nicotinic activity stimulates postganglionic sympathetic terminals and produces a dramatic release of norepinephrine.4 Norepinephrine mediates its arrhythmogenic effects by increasing automaticity of cardiac cells and by decreasing the cardiac muscle fibrillatory threshold.5