Sepsis is a systemic inflammatory response syndrome of suspected or confirmed infectious origin, which frequently culminates in multiorgan failure, including cardiac involvement. Septic cardiomyopathy (SCM) remains a poorly defined clinical entity, lacking a formal or consensus definition and representing a significant knowledge gap in critical care medicine. It is an often-underdiagnosed complication of sepsis. The only widely accepted aspect of its definition is that SCM is a transient myocardial dysfunction occurring in patients with sepsis, which cannot be attributed to ischemia or pre-existing cardiac disease. The pathogenesis of SCM appears to be multifactorial, involving inflammatory cytokines, overproduction of nitric oxide, mitochondrial dysfunction, calcium homeostasis dysregulation, autonomic imbalance, and myocardial edema. Diagnosis primarily relies on echocardiography, with advanced tools such as tissue Doppler imaging (TDI) and global longitudinal strain (GLS) providing greater sensitivity for detecting subclinical dysfunction and guiding therapeutic decisions. Traditional echocardiographic findings, such as left ventricular ejection fraction measured by 2D echocardiography, often reflect systemic vasoplegia rather than intrinsic myocardial dysfunction, complicating accurate diagnosis. Right ventricular (RV) dysfunction, identified as a critical component of SCM in many studies, has multifactorial pathophysiology. Factors including septic cardiomyopathy itself, mechanical ventilation, hypoxemia, and hypercapnia—particularly in cases complicated by acute respiratory distress syndrome (ARDS)—increase RV afterload and exacerbate RV dysfunction. The prognostic value of cardiac biomarkers, such as troponins and natriuretic peptides, remains uncertain, as these markers primarily reflect illness severity rather than being specific to SCM. Treatment focuses on the early recognition of sepsis, hemodynamic optimization, and etiological interventions, as no targeted therapies currently exist. Emerging therapies, such as levosimendan and VA-ECMO, show potential in severe SCM cases, though further validation is needed. The lack of standardized diagnostic criteria, combined with the heterogeneity of sepsis presentations, poses significant challenges to the effective management of SCM. Future research should focus on developing cluster-based classification systems for septic shock patients by integrating biomarkers, echocardiographic findings, and clinical parameters. These advancements could clarify the underlying pathophysiology and enable tailored therapeutic strategies to improve outcomes for SCM patients.

Background/Objectives: Critically ill patients admitted to the intensive care unit (ICU) frequently develop new-onset atrial fibrillation (NOAF) due to numerous risk factors. While NOAF has been associated with increased mortality, it remains unclear whether it serves merely as a marker of illness severity or directly contributes to adverse outcome. This study aimed to determine the incidence and risk factors for NOAF in a homogenized population of mechanically ventilated patients at ICU admission, excluding well-established predisposing factors. Additionally, we examined the impact of NOAF on mortality in this context. Methods: We prospectively studied consecutive patients over a 3-year period to identify triggers for NOAF. Factors associated with 30-day mortality during the ICU stay were recorded. Demographic data, medical history, laboratory findings, and the severity of illness at admission were compared between patients who developed NOAF and those remaining in sinus rhythm. In NOAF patients, the course of atrial fibrillation (resolution, persistence, or recurrence) was evaluated during the 30-day ICU stay. Results: Of the 1330 patients screened, 685 were eligible for analysis, with 110 (16.1%) developing NOAF. Septic episodes occurred more frequently in the NOAF group compared to the no-NOAF group (92.7% vs. 58.1%, p < 0.001). Notably, 80% of NOAF patients developed a septic episode concurrently with the atrial fibrillation, often stemming from secondary infections, and 85.3% presented with septic shock. When focusing on patients with at least one septic episode during the 30-day ICU stay, 23.4% of them developed NOAF. Additionally, patients with NOAF were older and had a higher prevalence of hypertension; disease severity at admission was not a triggering factor. Mainly sepsis, but also advanced age, and a history of hypertension remained independent factors associated with its occurrence. Sepsis, primarily, along with advanced age and a history of hypertension, was identified as independent factors associated with the occurrence of NOAF. Mortality was higher in the NOAF group compared to the control group (39 patients (35.5%) vs. 138 patients (24%), p = 0.01). NOAF occurrence, sepsis, disease severity at admission, and age were associated with increased ICU mortality; however, NOAF was not found to be an independent predictor of ICU mortality in multivariate analysis. Instead, sepsis, age, and disease severity at admission remained independent predictors of 30-day mortality. Sinus rhythm was restored in 60.9% of NOAF patients within 48 h, with the improvement or stabilization of sepsis being crucial for rhythm restoration. Conclusions: NOAF is a common complication in intubated ICU patients and is independently associated with sepsis, advanced age, and hypertension. While NOAF is linked to increased ICU mortality, it is more likely a marker of disease severity than a direct cause of death. Sepsis improvement appears critical for restoring and maintaining sinus rhythm.

Sepsis is a life-threatening organ dysfunction, and septic cardiomyopathy (SCM) may complicate the course of the disease. Infection with multidrug-resistant (MDR) pathogens has been linked with worse outcomes. This study aims to evaluate SCM in patients with infections caused by different antimicrobial-resistant phenotypes. This retrospective study included patients with sepsis/septic shock, hospitalized, and intubated in the intensive care unit of the University Hospital of Larissa between January 2022 and September 2023 with echocardiographic data during the first two days after infection onset. The patients were divided into two groups: non-MDR-SCM group and MDR-SCM group. The cardiac function was compared between the two groups. A total of 62 patients were included in the study. Forty-four patients comprised the MDR-SCM and 18 the non-MDR-SCM group. Twenty-six patients (41.9%) presented with left ventricular (LV) systolic dysfunction, and ≤35% right ventricular fractional area change (RVFAC) was present in 56.4%. LV systolic function was more severely impaired in the non-MDR-SCM group (left ventricular ejection fraction, 35.8% ±4.9% vs. 45.6%±2.4%, P=0.049; LV outflow tract velocity time integral, [10.1±1.4] cm vs. [15.3±0.74] cm, P=0.001; LV-Strain, –9.02%±0.9% vs. –14.02%±0.7%, P=0.001). The MDR-SCM group presented with more severe right ventricular (RV) dilatation (right ventricular end-diastolic area/left ventricular end-diastolic area, 0.81±0.03 vs. 0.7±0.05, P=0.042) and worse RV systolic function (RVFAC, 32.3%±1.9% vs. 39.6%±2.7%, P=0.035; tricuspid annular plane systolic excursion, [15.9±0.9] mm vs. [18.1±0.9] mm, P=0.165; systolic tissue Doppler velocity measured at the lateral tricuspid annulus, [9.9±0.5] cm/s vs. [13.1±0.8] cm/s, P=0.002; RV-strain, –11.1%±0.7% vs. –15.1%±0.9%, P=0.002). SCM related to MDR infection presents with RV systolic dysfunction predominance, while non-MDR-SCM is mainly depicted with LV systolic dysfunction impairment.

OBJECTIVES: To evaluate the effects of positive end-expiratory pressure (PEEP) on pulse pressure variation (PPV) in patients with moderate/severe acute respiratory distress syndrome (ARDS). DESIGN: Prospective interventional self-controlled study. SETTING: University Hospital of Larissa. PATIENTS: ARDS patients admitted intubated in the ICU (from August 2020 to March 2022). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: PPV and inferior vena cava (IVC) respiratory variability were evaluated at two PEEP levels (first value mainly based on PEEP/Fio ₂ and second value based on respiratory system compliance). Additionally, respiratory mechanics, hemodynamics, and echocardiographic indices assessing right ventricular (RV) size (RV end-diastolic area/left ventricular end-diastolic area [RVEDA/LVEDA]), RV systolic function, and RV afterload (pulmonary artery systolic pressure [PASP] and PASP/left ventricular outflow tract velocity time integral [PASP/VTI_LVOT]) were recorded. Ninety-five patients were evaluated. PPV decreased after PEEP reduction (11.7 ± 0.2 to 7.9% ± 0.2%), whereas IVC respiratory variability increased (9.1 ± 0.9 to 14.6% ± 0.1%) and central venous pressure decreased (all p < 0.0001). RV afterload indices decreased (p < 0.0001), simultaneously with RV size (< 0.0001) and systolic function indices’ improvements (< 0.05); shock warranted less noradrenaline doses. The change in PPV correlated significantly to respiratory variability in IVC diameter distensibility (p < 0.0001) and moderately to changes in RV size and systolic function (change in RVEDA/change in LVEDA, change in tricuspid annular plane systolic excursion); RV afterload (change in PASP [ΔPASP], ΔPASP/VTI_LVOT); and change in Paco ₂ (all p < 0.05). CONCLUSIONS: PPV alteration with PEEP decrease, associated with IVC distensibility increases, may indicate the presence of RV dysfunction and increased pulmonary vascular resistances. Whether the patients are in need for fluid loading, fluid responsiveness assessment may be further warranted.