Background:Hemodynamic instability in pediatric trauma is traditionally defined using reference values derived from healthy children rather than...

Excellence in Hemodynamic Management

The neonatal cardiovascular system is dynamic and influenced by multiple factors, which makes neonatal shock a challenging early clinical diagnosis. Real-time monitoring has been limited to indirect measurements of hemodynamic well-being, such as heart rate, blood pressure, capillary refill time, and biochemical markers of adequate oxygen delivery and oxygen consumption. Bedside diagnostic ultrasound to guide decision-making has become increasingly integrated into modern neonatal care. It allows...

Background Microcirculatory dysfunction may persist despite restoration of conventional macrocirculatory targets in sepsis, reflecting loss of hemodynamic coherence. This review synthesizes current microcirculatory monitoring approaches according to the physiological information they provide and examines how complementary modalities may be integrated to characterize persistent or regional tissue hypoperfusion. Main body A narrative review of PubMed-indexed literature was conducted, with emphasis on bedside peripheral perfusion assessment, tissue oxygenation and superficial perfusion imaging, direct microvascular visualization, and organ- or tissue-specific monitoring. Recent studies were prioritized together with landmark methodological and validation studies. Available techniques interrogate distinct but overlapping components of the circulation. Bedside peripheral measures provide rapid information on skin reperfusion and vascular tone; spectroscopic and optical techniques characterize tissue oxygenation, reactivity, and spatial perfusion heterogeneity; direct microvascular imaging enables assessment of microvascular density and flow; and organ-specific approaches provide information on renal, cerebral, or retinal perfusion and oxygenation. Discordance between these domains may persist despite improvement in blood pressure or cardiac output, supporting serial multimodal rather than single-variable interpretation. However, substantial heterogeneity in acquisition protocols, measurement sites, devices, analytical methods, and proposed thresholds limits comparability and clinical implementation. Conclusion Microcirculatory monitoring should currently be viewed as a complementary framework for identifying persistent or heterogeneous tissue hypoperfusion beyond conventional macrocirculatory targets. Its integration into individualized resuscitation remains promising but requires standardized methodology, external validation, and prospective interventional evidence before any single modality or multimodal strategy can be adopted as a validated resuscitation endpoint.

Background Supraventricular arrhythmias are frequent in critically ill patients and landiolol, an ultra-short-acting, highly β1-selective adrenergic blocker, is increasingly used for their management. Its efficacy and dosing have been described, but its early hemodynamic tolerance at the bedside — when intolerance occurs, how it presents, and which patients are at risk — remains poorly characterized, particularly in vasopressor-dependent patients under-represented in existing cohorts. We aimed to describe the hemodynamic tolerance of landiolol and to identify bedside predictors of poor tolerance. Methods We conducted a retrospective single-center study in patients admitted to the intensive care unit who received landiolol for supraventricular arrhythmia between January 2021 and February 2023. Hemodynamic variables, including pulse pressure, were recorded at baseline (H0) and at H1, H2, H4, H6 and H24. A hemodynamic adverse event was defined as a composite of mean arterial pressure below 64 mmHg, bradycardia below 50 bpm, or a more than 50% increase in vasopressor dose, counted only while landiolol was infused. Predictors of poor tolerance were identified by multivariable logistic regression. Results Among 133 patients (median age 68 years; SAPS II 51; sepsis 54.9%; vasopressors 49.6%), a hemodynamic adverse event occurred in 27 (20.3%), mostly within the first six hours. Events consisted of hypotension or vasopressor escalation; no patient developed bradycardia below 50 bpm. A lower diastolic pressure (adjusted OR 1.05 per 1-mmHg decrease, 95% CI 1.01–1.10) and vasopressor use at initiation (adjusted OR 3.00, 95% CI 1.14–7.91) were independently associated with poor tolerance. Heart rate control was achieved without deterioration of arterial pressure, pulse pressure, ventricular function, or tissue perfusion. Conversion to sinus rhythm was more frequent in new-onset than in pre-existing atrial fibrillation (54.4% vs. 27.9%; p = 0.004). Conclusion In critically ill patients, hemodynamic intolerance to landiolol occurred in one-fifth of cases, arose early, and took the form of hypotension or increased vasopressor requirements rather than bradycardia. A low diastolic pressure and vasopressor dependence identified patients at risk, supporting cautious, individualized use with close monitoring during early titration.

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This single-center cohort study sought to evaluate the association between Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Angina with Non-Obstructive Coronary Arteries (ANOCA), by det...

This single-center cohort study sought to evaluate the association between Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Angina with Non-Obstructive Coronary Arteries (ANOCA), by determining the observed frequency of ME/CFS among patients with ANOCA diagnosed by coronary function testing (CFT). Additionally, we performed an exploratory analysis of the diagnostic utility of invasive cardiopulmonary exercise testing (iCPET) in ME/CFS patients with CFT-confirmed ANOCA, with the aim of identifying the predominant physiological mechanism responsible for exertional limitation in this population. Systematic medical record review of 261 patients with CFT-confirmed ANOCA was performed using standardized diagnostic criteria to identify concurrent ME/CFS diagnosis. ME/CFS was identified in 47 patients, representing an observed frequency of 18%. The only statistically significant difference between ANOCA patients with and without ME/CFS was a higher frequency of connective tissue disease in the ME/CFS group (p = 0.0221). In a separate cohort of 27 patients with ME/CFS who underwent iCPET, 24 patients (89%) had CFT-confirmed ANOCA. The diagnosis of ANOCA by CFT prompted a change in medical management in 81% of patients in this cohort. iCPET revealed a primary peripheral limitation to exercise, characterized by impaired peak systemic oxygen extraction despite normal peak oxygen delivery. This study demonstrates a clinically significant association between ME/CFS and ANOCA. These findings underscore the clinical value of CFT in patients with ME/CFS and exertional chest pain and highlight iCPET as a complementary tool for hemodynamic phenotyping in this population. Prospective studies incorporating simultaneous CFT and iCPET with molecular phenotyping are warranted.