Sepsis is defined as a dysregulated host response to an infection, leading to life-threatening organ dysfunction. While sepsis is most commonly the result of a bacterial infection, it may also be caused by viral pathogens. The aim of this study was to describe differences in organ dysfunction patterns and inflammatory markers between bacterial and viral sepsis. In this prospective multicenter cohort study, adults meeting SEPSIS-3 criteria were recruited from four Austrian ICUs between 1 August 2021 and 1 April 2024, excluding those who were immunocompromised within the preceding 12 months. Ninety patients were enrolled, of whom 57 had bacterial and 33 viral sepsis. Inflammatory markers, including IL-6 and PCT, were higher at ICU admission in bacterial sepsis. Adjusted linear regression confirmed bacterial etiology as the only significant predictor of higher 48 h peak IL-6 and PCT values. Patients with viral sepsis typically fulfilled SEPSIS-3 criteria through respiratory and cardiovascular SOFA components, while other organ dysfunctions were less frequent. Significant differences in the phenotype of bacterial and viral sepsis were observed, characterized by distinct inflammatory profiles and differing patterns of organ dysfunction. These findings may support the improved differentiation of bacterial and viral etiologies in sepsis.

Background: There is conflicting data about which ventilation strategy is better when performing external chest compressions with mechanical devices. During manual cardiopulmonary resuscitation, continuous ventilation is recommended when the airway is secured and a ventilation rate of 10/min is maintained. However, during mechanical cardiopulmonary resuscitation, some expert groups and various data have raised concerns about ineffective ventilation with continuous ventilation due to the high intrathoracic pressure generated by the devices without pauses for effective ventilation. This study compares the two possible ventilation strategies - continuous ventilation and 30:2 (30 compressions followed by 2 ventilations) - during mechanical cardiopulmonary resuscitation. We analysed the effects of the two resuscitation strategies on ventilatory parameters measured during cardiopulmonary resuscitation and compared mechanical with manual cardiopulmonary resuscitation with both ventilation strategies. Methods: 30 students of human medicine performed cardiopulmonary resuscitation on endotracheally intubated resuscitation training manikins. The chest compressions were performed manually or by using mechanical chest compression devices (LUCAS ^® , EASY PULSE ^® ). Tidal volume, respiratory minute ventilation volume, ventilation frequency, compression frequency, and chest compression depth were recorded by sensors built into the manikins. Cardiopulmonary resuscitation was performed with either continuous ventilation (ventilations every 6 s; 10/min) or 30:2 in two resuscitation runs of 3 min each. Results: Respiratory minute ventilation volume was significantly higher with continuous ventilation than with 30:2 cardiopulmonary resuscitation (4.8 l/min vs. 3.1 l/min, p <.001). Tidal volume was lower with continuous ventilation than with a 30:2 cardiopulmonary resuscitation (521 ml vs. 565 ml; p = .013). There were no significant differences between manual and mechanical cardiopulmonary resuscitation with both ventilation strategies. Conclusion: This study showed that ventilation during mechanical cardiopulmonary resuscitation using mechanical chest compression devices was efficient with both ventilation strategies. Interestingly, the respiratory minute ventilation volume was even higher with continuous ventilation than with 30:2 due to the higher respiratory rate. In addition, there was no significant difference in ventilation outcome between manual and mechanical chest compressions.