Introduction:Cocaine is a widely abused substance globally. It effects on the pulmonary system can range from bronchospasm to pulmonary vasoconstriction. We present a case of cocaine induced pulmonary vasoconstriction mimicking pulmonary embolism on ventilation-perfusion scan. Case summary:A 65 male with a past medical history of hypertension, diabetes, renal call carcinoma status-post nephrectomy and chronic kidney disease stage IV presents to the emergency department with sudden chest pain and shortness of breath. Denies any fever, chills or prior episodes. Social history was significant 20-year pack smoking history, intravenous drug abuse. Vitals were blood pressure 160/95 mmhg, pulse 90 beats per minutes, respiratory rate 18 breaths per minute and temperature 37.8 C. Physical exam was significant for a non-obese male in acute distress and chest wall tenderness on palpation. A 12 lead electrocardiogram obtained revealed no ischemic findings. Laboratory findings revealed creatinine of 4.3 mg/dL with baseline 3.0-4.5. Other labs including troponin, brain natriuretic peptide were normal. Ventilationperfusion (V/Q) scan obtained to revealed a filing defects in the inferior lingual, posterior inferior upper lobe and posterior inferior lower lobe characteristic for pulmonary embolism (PE). Follow up transthoracic echocardiogram revealed no evidence of ventricular strain. The patient was started on heparin drip and admitted for further management. He remained stable throughout admission, was successfully bridged to warfarin and home in stable condition, international normalized ratio (INR) at that time was 2.3. Two weeks later, he presented to the emergency department with similar complains. Vitals were unremarkable and physical examination was unchanged from prior. Significant laboratory findings were INR 1.12. Patient reports non adherence to warfarin. Due to concern for recurrent PE V/Q scan was ordered, however it revealed no filling defects and lower extremity doppler ultrasound revealed no clot. D-dimers was also normal. Urine drug screen obtained was positive for cocaine. With the help of the radiologist we compared both V/Q scans, it was deemed that the filling defect initially identified was due to vasospasm of the pulmonary vessels, likely secondary to cocaine. Warfarin was discontinued, cocaine cessation was advised and his chest pain was managed as a musculoskeletal pain. He was later discharged home in stable condition. Discussion:While ventilation-perfusion scan is a safe screening tool to evaluated for pulmonary embolism, it lacks specificity. Other causes of ventilation or perfusion defects should be considered. In this case it was due to cocaine inhalation.