SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Modafinil is a psychostimulant medication that is approved for shift work disorder, narcolepsy, and other sleep disorders. While studies have shown modafinil raises blood pressure and heart rate, little is known of its effects on the respiratory drive. Here we present a patient who had primary hyperventilation suspected to be secondary to modafinil use. CASE PRESENTATION: A 36 year-old female with a history of mild asthma (as needed albuterol inhaler), anxiety, and shift work sleep disorder presented to the emergency department in acute respiratory distress. One week prior to presentation she had a prodrome of cough and congestion while returning from a road trip. Her home medications include albuterol and modafinil as needed. She took modafinil prior to presentation for her long drive. On physical exam, she was tachypneic with a respiratory rate of 30-50 breaths/min and in obvious distress. She was sitting leaning forward in tripod position with accessory muscle use and inability to complete full sentences. Of note, she had bilateral breath sounds with good air entry and no wheezes, rales, or rhonchi. Laboratory values at time of examination included pH 7.52, pCO2 15, pO2 156 on 4L oxygen, chemistry bicarbonate is 9, potassium 2.9, lactic acid 7.2 with no other derangements. Chest radiograph and computed tomography angiogram of chest were unremarkable. She was placed on bilevel positive airway pressure (BIPAP) to assist her work of breathing but she remained tachypneic. Respiratory viral panel and echocardiogram were within normal limits. Dexmedetomidine was initiated with significant improvement in her work of breathing and resolution of tachypnea. A repeat arterial blood gas showed pH 7.37, pCO2 35, pO2 67% on 35%. She was weaned off BIPAP to room air. DISCUSSION: Modafinil acts upon the arousal state of the brain via the dopaminergic and sympathetic nervous system pathways. The theory of its effect, as seen in our patient, is through the brainstem respiratory system, resulting in its stimulation. The end pharmacologic result is increased wakefulness and increased respiratory drive. Taneja et al demonstrated that modafinil causes a strong central adrenergic response, resulting in increased catecholamines and an increase in respiratory drive. Dexmedetomidine is a centrally acting sympatholytic agent that was used in our patient for respiratory drive suppression with great success and resolution of symptoms. Modafinil use likely stimulated our patient’s sympathetic drive resulting in hyperventilation causing respiratory alkalosis and lactic acidosis. CONCLUSIONS: Early recognition and targeting treatment of central hyperventilation is crucial to treat secondary metabolic derangements. While there is a need for more research regarding modafinil’s effects on the ventilatory drive, It is prudent that clinicians are aware of the side effects of this medication as seen in our patient. Reference #1: Taneja I, Haman K, Shelton RC, Robertson D (2007). A randomized, double-blind, crossover trial of modafinil on mood. J Clin Psychopharmacol 27: 76–78. DISCLOSURES: No relevant relationships by Thomas Blair, source=Web Response No relevant relationships by Lakshmi Kallur, source=Web Response No relevant relationships by Poorvi King, source=Web Response No relevant relationships by JENNIFER Stahl, source=Web Response