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• W3033978030 abstract "HomeCirculationVol. 141, No. 23A Chief Complaint of “I Am Going to Die!” Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessCase ReportPDF/EPUBA Chief Complaint of “I Am Going to Die!” Stephen C. Infanger, MD and G. Neal Kay, MD Stephen C. InfangerStephen C. Infanger Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham. Search for more papers by this author and G. Neal KayG. Neal Kay G. Neal Kay, MD, 930 Faculty Office Tower, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294. Email E-mail Address: [email protected] https://orcid.org/0000-0003-0421-2214 Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham. Search for more papers by this author Originally published8 Jun 2020https://doi.org/10.1161/CIRCULATIONAHA.120.046659Circulation. 2020;141:1927–1929ECG ChallengeA 57-year-old man with diabetes mellitus transiently lost consciousness at a gas station. Paramedics found him hypotensive, hypoxemic, and intermittently conscious. He denied chest pain, but he was dyspneic and gasped, “I am going to die.” Physical examination showed an acutely ill, diaphoretic man breathing with his accessory muscles with a respiratory rate of 35 breaths/min and systolic blood pressure of 60 mm Hg. The precordium was hyperdynamic with a right ventricular heave without murmurs and clear lungs on auscultation. There was bilateral lower extremity edema. The serum lactate was 6.8 mmol/L, creatinine 1.6 mg/dL, and troponin 68 ng/mL (normal ≤20). Arterial blood gases were pH 7.32, Pco2 26, and Po2 86 on 100% inspired oxygen. The initial ECG is shown in Figure 1. What is the most likely diagnosis and the next step in treatment?Download figureDownload PowerPointFigure 1. ECG on admission to the emergency department.Please turn the page to read the diagnosis.Response to ECG ChallengeThe ECG demonstrated ST-segment elevation in V1 and V2 with ST-segment depression in leads I, II, III, AVF, and V3 through V6. There was ST-segment elevation in aVR with an S1Q3T3 pattern and P pulmonale. The differential diagnosis of this ECG includes anteroseptal myocardial injury or an acute pulmonary thromboembolus (PTE). This patient received intravenous heparin, ticagrelor, and aspirin along with vasopressors and endotracheal intubation. The D-dimer was >20 000 ng/mL. Emergency coronary angiography showed nonobstructive disease. Pulmonary artery angiography demonstrated bilateral pulmonary thromboemboli with complete occlusion of the left pulmonary artery and near-complete occlusion of the right (Figure 2). Mechanical maceration with a pigtail catheter and stiff guidewire was unsuccessful in recannulating the pulmonary arteries. Because of continued severe hypotension, extracorporeal membrane oxygenation and alteplase were initiated. Computed tomographic angiography 24 hours later demonstrated persistent bilateral PTE (Figure 3), and surgical embolectomy was performed. The postoperative ECG showed resolution of the acute ECG findings (Figure 4), and the patient was discharged after a 6-week hospital course. An extensive evaluation for hereditary causes of hypercoagulability was negative as was screening for malignancy.Download figureDownload PowerPointFigure 2. Pulmonary angiogram (anteroposterior view) demonstrating complete occlusion of the left main pulmonary artery and nearly complete occlusion of the right pulmonary artery. Note the large filling defects in the main pulmonary artery, and both pulmonary arteries, as well.Download figureDownload PowerPointFigure 3. Computed tomographic angiogram performed after failed direct attempt to mechanically lyse pulmonary thromboemboli and intravenous alteplase. Large filling defects are seen in the main pulmonary artery, and the right and left pulmonary arteries, as well, with complete absence of flow in the left lung and minimal flow in the right lung. After stabilization with extracorporeal membrane oxygenation, the patient underwent surgical thrombectomy.Download figureDownload PowerPointFigure 4. ECG after surgical thrombectomy. Note that the large S waves in lead I and the Q wave in lead III have resolved with normalization of the ST segments in leads AVR, V1, and V2. T-wave inversion persists in the lateral leads.The initial ECG showed ST-segment elevation in leads V1 and V2 and aVR, an S1Q3T3, and ST-segment depression in the lateral and inferior leads. Combined with physical examination findings of right ventricular pressure overload, the clinical presentation strongly suggested PTE. An acute ST-segment elevation injury pattern is associated with increased in-hospital complications (odds ratio, 4.2) and mortality (odds ratio, 6.3) in PTE.1 The absence of ischemic ECG changes in patients with PTE is associated with a favorable prognosis (odds ratio of 0.13 compared with the presence of ischemic changes).1 Other ECG indicators of PTE include a QR in V1, QRS fragmentation, ST-segment elevation in leads III, V1, and aVR.2 A meta-analysis of the ECG in PTE identified ST-segment elevation in lead V1 (odds ratio, 5.14) and aVR (odds ratio, 3.3) as predictors of in-hospital complications.3 Furthermore, the odds ratio of clinical deterioration was 16.8 when T-wave inversion was present in ≥7 leads.3 An elevated troponin level also predicts mortality in PTE.1 This case demonstrates that ischemic ECG changes are strongly correlated with clinical deterioration in acute PTE and should prompt consideration of more aggressive therapies.DisclosuresNone.Footnoteshttps://www.ahajournals.org/journal/circG. Neal Kay, MD, 930 Faculty Office Tower, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294. Email [email protected]comReferences1. Kukla P, McIntyre WF, Fijorek K, Krupa E, Mirek-Bryniarska E, Jastrzębski M, Bryniarski KL, Zajchowski W, Bryniarski L, Baranchuk A. Use of ischemic ECG patterns for risk stratification in intermediate-risk patients with acute PE.Am J Emerg Med. 2014; 32:1248–1252. doi: 10.1016/j.ajem.2014.07.029CrossrefMedlineGoogle Scholar2. Digby GC, Kukla P, Zhan ZQ, Pastore CA, Piotrowicz R, Schapachnik E, Zareba W, Bayés de Luna A, Pruszczyk P, Baranchuk AM. The value of electrocardiographic abnormalities in the prognosis of pulmonary embolism: a consensus paper.Ann Noninvasive Electrocardiol. 2015; 20:207–223. doi: 10.1111/anec.12278CrossrefMedlineGoogle Scholar3. Qaddoura A, Digby GC, Kabali C, Kukla P, Zhan ZQ, Baranchuk AM. The value of electrocardiography in prognosticating clinical deterioration and mortality in acute pulmonary embolism: a systematic review and meta-analysis.Clin Cardiol. 2017; 40:814–824. doi: 10.1002/clc.22742CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails June 9, 2020Vol 141, Issue 23Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.120.046659PMID: 32511003 Originally publishedJune 8, 2020 PDF download Advertisement SubjectsCardiopulmonary Resuscitation and Emergency Cardiac Care" @default.
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