BackgroundSepsis is a common condition encountered by emergency and critical care physicians, with significant costs, both economic and human. Myocardial dysfunction in sepsis is a well-recognized but poorly understood phenomenon. There is an extensive body of literature on this subject, yet results are conflicting and no objective definition of septic cardiomyopathy exists, representing a critical knowledge gap.ObjectivesIn this article, we review the pathophysiology of septic cardiomyopathy, covering the effects of key inflammatory mediators on both the heart and the peripheral vasculature, highlighting the interconnectedness of these two systems. We focus on the extant literature on echocardiographic and laboratory assessment of the heart in sepsis, highlighting gaps therein and suggesting avenues for future research. Implications for treatment are briefly discussed.ConclusionsAs a result of conflicting data, echocardiographic measures of left ventricular (systolic or diastolic) or right ventricular function cannot currently provide reliable prognostic information in patients with sepsis. Natriuretic peptides and cardiac troponins are of similarly unclear utility. Heterogeneous classification of illness, treatment variability, and lack of formal diagnostic criteria for septic cardiomyopathy contribute to the conflicting results. Development of formal diagnostic criteria, and use thereof in future studies, may help elucidate the link between cardiac performance and outcomes in patients with sepsis.

Objectives: The primary goal of this study was to determine accuracy for diagnosing acutely decompensated heart failure (ADHF) in the undifferentiated dyspneic emergency department (ED) patient using a lung and cardiac ultrasound (LuCUS) protocol. Secondary objectives were to determine if US findings acutely change management and if findings are more accurate than clinical gestalt.Methods: This was a prospective, observational study of adult patients presenting to the ED with undifferentiated dyspnea. The intervention consisted of a 12-view LuCUS protocol performed by experienced emergency physician sonographers. The primary objective was measured by comparing US findings to the final diagnosis independently determined by two physicians blinded to the LuCUS result. Acute treatment changes based on US findings were tracked in real time through a standardized data collection form.Results: Data on 99 patients were analyzed; ADHF was the final diagnosis in 36%. The LuCUS protocol had sensitivity of 83% (95% confidence interval [CI] = 67% to 93%), specificity of 83% (95% CI = 70% to 91%), positive likelihood ratio of 4.8 (95% CI = 2.7 to 8.3), and negative likelihood ratio of 0.20 (95% CI = 0.09 to 0.42). Forty-seven percent of patients had changes in acute management, and 42% had changes in acute treatment. Observed agreement for the LuCUS protocol was 93% between coinvestigators. Overall, accuracy improved by 20% (83% vs. 63%, 95% CI = 8% to 31% for the difference) over clinical gestalt alone. Conclusions:The LuCUS protocol may accurately identify ADHF and may improve acute clinical management in dyspneic ED patients. This protocol has improved diagnostic accuracy over clinical gestalt alone.ACADEMIC EMERGENCY MEDICINE 2015;22:182-191

Introduction: Severe sepsis is a leading cause of non-coronary death in hospitals across the United States. Early identification and risk stratification in the emergency department (ED) is difficult because there is limited ability to predict escalation of care. In this study we evaluated if a sustained shock index (SI) elevation in the ED was a predictor of short-term cardiovascular collapse, defined as vasopressor dependence within 72 hours of initial presentation.Methods: Retrospective dual-centered cross-sectional study using patients identified in the Yale-New Haven Hospital Emergency Medicine sepsis registry.Results: We included 295 patients in the study with 47.5% (n=140) having a sustained SI elevation in the ED. Among patients with a sustained SI elevation, 38.6% (54 of 140) required vasopressors within 72 hours of ED admission contrasted to 11.6% (18 of 155) without a sustained SI elevation (p=0.0001; multivariate modeling OR 4.42 with 95% confidence intervals 2.28–8.55) . In the SI elevation group the mean number of organ failures was 4.0 ± 2.1 contrasted to 3.2 ± 1.6 in the non-SI elevation group (p=0.0001).Conclusion: ED patients with severe sepsis and a sustained SI elevation appear to have higher rates of short-term vasopressor use, and a greater number of organ failures contrasted to patients without a sustained SI elevation. An elevated SI may be a useful modality to identify patients with severe sepsis at risk for disease escalation and cardiovascular collapse.