PIP: A case report is presented of supraventricular tachycardia (SVT) associated with metoclopramide administration in the early postpartum period in a 37-year-old woman. The patient was scheduled for elective laparoscopic tubal ligation 4 hours after an uncomplicated spontaneous vaginal delivery. The preoperative evaluation revealed that the patient's only significant past medical history was a total of 4 spontaneous vaginal deliveries. A review of systems was noncontributory, and the patient denied any untoward effects from drugs. Metoclopramide, 10 mg, was administered intravenously to facilitate gastric emptying and as an anti-emetic. Within 1 minute, the heart rate rose to 170 bpm. She was in no distress, being unaware of any change in her status. Arterial blood pressure remained in the 130-140 mmHg (systolic) range throughout the ensuing period. Various approaches, i.e., valsalva, carotid sinus massage, ocular pressure, were used to increase vagal tone without a decrease in the heart rate. After determining that the PR interval was grossly normal, she received 2 boluses of verapamil (10 mg intravenously) over a 10-minute period without change in heart rate. She then was given alphaprodine and droperidol for sedation. The patient then was administered Digoxin approximately 20 minutes after the administration of metoclopramide. This was followed by a gradual decrease in her heart rate to 130 bpm over the next 5 minutes. The patient was transferred to a telemetry unit for a 24-hour period, where her arterial blood pressure remained stable and her heart rate was noted to be in the 90-110 range. 12-lead EKG revealed sinus tachycardia with "nonspecific" ST changes. PR, QRS, and QTC intervals were within normal limits. Chest radiograph was without pathology. The patient was reinterviewed on several occasions and continued to deny a history of SVT, palpitations, syncope, or any other cardiac symptomatology. 2 days following the initial episode, she underwent successful laparoscopic tubal ligation under spinal anesthesia and sedation. In sum, a stable postpartum patient without history of SVT or evidence of structural heart disorder developed SVT immediately following metoclopramide administration. This may be because of the cardioactive properties of metoclopramide or to an underlying predisposition from her peripartum state, or a combination of factors.