TISSUE PLASMINOGEN ACTIVATOR IN CARDIAC ARREST SECONDARY TO MASSIVE PULMONARY EMBOLUS

Abstract

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Cardiac arrest secondary to massive pulmonary embolism carries a poor prognosis. In most cases, the diagnosis is made post-mortem. CASE PRESENTATION: 64-year-old lady with past medical history of DVT and pulmonary embolus (PE) not on anticoagulation, type 2 diabetes, hypertension, coronary artery disease presented with sudden onset shortness of breath and mild chest pain of less than 1 day duration. Upon presentation, she was hypotensive, tachycardic, and tachypneic. Initial EKG showed ST-elevation in leads 3 and V1 with deep S wave in lead 1. CTA chest showed extensive bilateral pulmonary emboli and RV to LV ratio greater than 2. Shortly after returning from CT, she became hypoxia and bradycardia followed by asystole. CPR was started and she attained ROSC after 1 cycle of CPR. She was given 50 mg IV tPA bolus followed by continuous infusion of 50 mg over 1 hour. Blood pressure improved after administration of tPA and she was intubated thereafter for airway protection. She had cardiac arrest again after intubation and attained ROSC after 1 cycle of CPR. She was transferred to the ICU and started on heparin drip and vasopressors. Her condition continued to improve and she was extubated the next day. She was ultimately discharged in stable condition on direct-acting oral anticoagulant. DISCUSSION: The diagnosis of PE during an in-hospital cardiac arrest can be difficult. In most cases, thrombolytic therapy is given based on high clinical suspicion, often due to the presence of echocardiogram changes on point-of-care ultrasound. “McConnell sign,” which is a specific pattern of RV dysfunction is observed in massive PE and is characterized by akinesis of the mid free wall and normal contractility of the apical wall. It is approximately 77% sensitive and 94% specific [3]. However in clinical practice, McConnell sign can be difficult to recognize. tPA may also be underutilized due to concern for major bleeding. However, there is literature to suggest that administration of tPA during cardiac arrest is not associated with increased risk of bleeding and often leads to decreased time to return of spontaneous circulation [1]. The optimal timing of tPA administration has yet to be determined. In retrospective studies, tPA is either given as a single 50 mg bolus, 50 mg bolus followed by a second 50 mg bolus, or as 50 mg bolus followed by 85 mg over 90 minutes [2]. However, there are no trials that compare the utility and efficacy of these protocols against each other. CONCLUSIONS: There is general consensus that tPA should be administered during cardiac arrest in patients with high suspicion of PE, however the optimal dose and timing of tPA administration is yet to be determined. In our patient, a dose of 50mg IV bolus followed by 50mg infusion over 1 hour had resulted in a favorable outcome. Reference #1: Yousuf T, Brinton T, Ahmed K, et al. Tissue Plasminogen Activator Use in Cardiac Arrest Secondary to Fulminant Pulmonary Embolism. J Clin Med Res. 2016;8(3):190-5. Reference #2: Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535. Reference #3: Borloz, Matthew P., William J. Frohna, Carolyn A. Phillips, and Michael S. Antonis. "Emergency Department Focused Bedside Echocardiography In Massive Pulmonary Embolism.” The Journal of Emergency Medicine 41, no. 6 (2011): 658-60. https://doi.org/10.1016/j.jemermed.2011.05.044. DISCLOSURES: No relevant relationships by basma al-bast, source=Web Response No relevant relationships by Mirza Ali, source=Web Response No relevant relationships by Abdisamad Ibrahim, source=Web Response No relevant relationships by Thamer Sartawi, source=Web Response No relevant relationships by Tareq Zaza, source=Web Response