Background: Pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of a pulmonary artery or one of its branches. The intricate relationship between substance abuse and thromboembolic events has emerged as a significant concern in clinical medicine. Cocaine, a potent vasoconstrictor, has been associated with both arterial and venous thrombotic events due to its prothrombotic effects on the coagulation cascade and its impact on the vascular endothelium. We present a case of a 42-year-old male with a history of cocaine abuse who presented with a life-threatening PE. Case Presentation: A 42-year-old male with a past medical history of cocaine abuse presented after a syncopal episode. He described the episode as passing out from a standing position and regaining consciousness quickly on the ground. He endorsed a 3 day history of worsening dyspnea and lightheadedness. On examination, the patient was experiencing mild respiratory distress and was found to be tachycardic. ECG revealed sinus tachycardia with evidence concerning for right heart strain. Laboratory findings were significant for elevated troponin and pro-BNP. A ventilation/perfusion lung scan was ordered which showed a high probability of PE. A subsequent CT angiography of the chest was performed which confirmed acute bilateral pulmonary emboli with moderate-large clot burden and evidence of right heart strain with a right ventricle to left ventricle size ratio of 1.35. Lower extremity doppler ultrasound was positive for deep vein thrombosis in the right popliteal vein. The patient was evaluated by the interventional cardiology team and was taken for mechanical thrombectomy of the pulmonary emboli. Pre-intervention right heart catheterization was significant for a mean pulmonary artery pressure of 47 mmHg and a pulmonary capillary wedge pressure of 23 mmHg. The clot burden was reduced by greater than 90% and excellent filling with a good venous phase of all pulmonary arteries was noted. The patient improved symptomatically after the procedure. Discussion: Cocaine's prothrombotic properties are multifaceted, involving the activation of the coagulation process and the secretion of von Willebrand factor (VWF), among other factors, which collectively contribute to thrombus formation. The presence of adulterants in cocaine, such as levamisole, further complicates its pathophysiological impact, potentially exacerbating pulmonary damage and fibrosis, thus predisposing individuals to thromboembolic events. The reported case emphasizes the need for a high index of suspicion for cocaine-induced PE in patients with a history of substance abuse presenting with symptoms suggestive of thromboembolic events.