Guido Tavazzi, MD; Gabriele Via, MD; Antonio Braschi, MD; Susanna Price, MD, PhD

Chest. 2016;150(1):e9-e11. doi:10.1016/j.chest.2016.02.687

An 82-year-old woman presented to the ED with severe dyspnea and hypertension (200/133/100 mm Hg). Her medical history included chronic obstructive pulmonary disease and a recent admission for heart failure that was treated with furosemide and a calcium channel blocker. Her ECG was known to show left bundle branch block. Chest auscultation revealed bilateral bibasal crackles. Her oxygen saturation was 92% using helmet CPAP (Fio₂, 60%; positive end-expiratory pressure, 10 cm of water). Arterial blood gas analysis revealed a pH of 7.30, Pao₂ of 66 mm Hg, Paco₂ of 54 mm Hg, a hemoglobin value of 15.9 g/dL, and a lactate level of 1.8 mg/dL. The brain natriuretic peptide level was 350 ng/dL and both 3-h and 6-h troponin I (TnI) assays were negative (0.04 ng/mL). The creatinine level was 1.72 mg/dL and the BUN level was 75 mg/dL. The ECG showed sinus rhythm (85 beats/min), complete left bundle branch block, QS in V₁-V₂ with no new changes on the ECG suggestive of cardiac ischemia. Lung ultrasonography (LUS) revealed bilateral pleural effusions and features consistent with pulmonary interstitial syndrome. Focused cardiac ultrasonography (FoCUS) demonstrated mild left ventricular (LV) dilatation with moderate to severe LV systolic dysfunction (ejection fraction [EF], 35%) with no other abnormalities. Chest radiography confirmed the LUS findings (Video 1). Acute coronary syndrome was ruled out, and the diagnosis of acute decompensation of chronic hypertensive heart disease was made. She was treated with intravenous urapidil and furosemide, with substantial improvement allowing transfer to the general medical ward.

From http://journal.publications.chestnet.org/article.aspx?articleid=2531944&resultClick=1#appsec1