A triad of circulatory collapse, right ventricular dilatation, and large alveolar dead space is proposed for the rapid diagnosis and treatment of massive pulmonary embolism. A 17year-old female on oral contraceptives collapsed at home becoming incoherent with shallow breathing. Paramedics initiated mechanical chest compression and transported the patient to our emergency department, arriving minimally responsive with undetectable blood pressure but having positive corneal reflexes and bradycardia with wide QRS. The trachea was intubated and goal-directed echocardiography revealed marked right ventricular dilatation with septal flattening. The arterial PCO₂ was 40mmHg with an end-tidal PCO₂ of 8mmHg, revealing a large alveolar dead space. Persistent hypotension, bradycardia, and fading alertness despite epinephrine and norepinephrine infusions prompted resumption of chest compression. Intravenous alteplase (10mg bolus over 10min followed by 90mg over 110min) begun 125min after collapse improved hemodynamic function within 10min allowing discontinuation of chest compression. Five and a half hours after starting alteplase, the patient was hemodynamically stable and had normal end-tidal PCO₂. A CT-angiogram showed the pulmonary arteries free of emboli but a thrombus in the right common iliac vein. The patient recovered fully and was discharged home on warfarin 8days later. Based on this and other reports, we propose a triad of circulatory collapse, right ventricular dilatation, and large alveolar dead space for the rapid diagnosis and treatment of massive pulmonary embolism, with systemic fibrinolysis as the first-line intervention.