The purpose of these Rounds is to illustrate how bedside echocardiography allows the clinician to rapidly determine the mechanism of hemodynamic instability, which may be multifactorial in patients presenting with loss of consciousness. Consent to publish the accompanying images was obtained from the Research Ethics Board of the Montreal Heart Institute. A young Caucasian woman was transferred to the emergency department after she was found unconscious in her car. Her medical history was unremarkable with no illicit drug use, and her initial blood pressure was 80/60 mmHg with a heart rate of 100 beats min. Cardiopulmonary auscultation revealed bilateral crackles, and her oxygen saturation was 90% on room air. Since she was unable to protect her airway, the woman’s trachea was rapidly intubated. The chest radiograph showed pulmonary edema (Fig. 1a), and the end-tidal CO2 after tracheal intubation was 20 mmHg. The initial electrocardiogram demonstrated normal sinus rhythm, inverted T waves, and ST segment depression in leads II, III, and AVF. Mild elevation of troponin I was also noted. Brain computed tomography showed evidence of diffuse subarachnoid hemorrhage (SAH) (Fig. 1b), and cerebral angiography showed an aneurysm at the bifurcation of the right internal carotid artery. The patient was transferred to the operating room for aneurysm clipping. Due to persistent hypotension despite increasing doses of vasopressors, a pulmonary artery catheter was inserted and her pulmonary artery pressure was elevated (Fig. 2 and Video #1, available as Electronic Supplementary Material). Upon opening of the dura mater, severe swelling was noted. After stabilization, the neurosurgeons successfully clipped the aneurysm and the patient was then transferred to the intensive care unit (ICU). In ICU, because of the patient’s persistently high vasopressor requirements, a transesophageal echocardiographic exam (TEE) was performed to assess her cardiac function, which showed preserved left ventricular basal function but mid-ventricular hypokinesia with apical systolic ballooning (Fig. 3 and Video #2, available as Electronic Supplementary Material) and apical right ventricular involvement (Video #3, available as Electronic Supplementary Material). No left ventricular outflow tract (LVOT) obstruction was observed. The patient’s diastolic function was also abnormal (Fig. 4). This scenario is typical of Tako-Tsubo syndrome, a stressrelated cardiomyopathy. Following supportive therapy, the patient’s cardiac function recovered completely one week after her ICU admission. She was discharged with only mild cognitive deficits. Up to 10% of patients with SAH present with pulmonary edema. This was formerly known as ‘‘neurogenic pulmonary edema’’, suggesting a non-cardiogenic origin and Electronic supplementary material The online version of this article (doi:10.1007/s12630-009-9218-3) contains supplementary material, which is available to authorized users.