Dataset Information

Cardiac contractile reserve parameters are related to prognosis in septic shock.

ABSTRACT:

Introduction

Cardiac reserve could be defined as the spontaneous magnitude from basal to maximal cardiac power under stress conditions. The aim of this study was to evaluate the prognostic value of cardiac reserve parameters in resuscitated septic shock patients.

Methods

Seventy patients with septic shock were included in a prospective and observational study. Prior to inclusion, patients were resuscitated to reach a mean arterial pressure of 65-75?mmHg with an euvolemic status. General, hemodynamic, and cardiac reserve-related parameters (cardiac index, double product, and cardiac power index) were collected at inclusion and at day 1.

Results

Seventy patients were included with 28-day mortality at 38.5%. Ten of the 70 patients died during the first day. In multivariate analysis, independent predictors of death were SAPS II ? 58 (OR: 3.36 [1.11-10.17]; P = 0.032), a high double product at inclusion (OR [95% IC]: 1.20 [1.00-1.45] per 10(3)?mmHg · min; P = 0.047), and at day 1, a decrease in cardiac index (1.30 [1.08-1.56] per 0.5 L/min/m(2); P = 0.007) or cardiac power index (1.84 [1.18-2.87] per 0.1 W/m(2), P = 0.008).

Conclusion

In the first 24?hours, parameters related to cardiac reserve, such as double product and cardiac index evolution, provide crucial and easy to achieve hemodynamic physiological information, which may impact the outcome.

SUBMITTER: Kimmoun A

PROVIDER: S-EPMC3730160 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Publications

Cardiac contractile reserve parameters are related to prognosis in septic shock.

Kimmoun Antoine A Ducrocq Nicolas N Mory Sébastien S Delfosse Remi R Muller Laura L Perez Pierre P Fay Renaud R Levy Bruno B

BioMed research international 20130717

<h4>Introduction</h4>Cardiac reserve could be defined as the spontaneous magnitude from basal to maximal cardiac power under stress conditions. The aim of this study was to evaluate the prognostic value of cardiac reserve parameters in resuscitated septic shock patients.<h4>Methods</h4>Seventy patients with septic shock were included in a prospective and observational study. Prior to inclusion, patients were resuscitated to reach a mean arterial pressure of 65-75 mmHg with an euvolemic status. G ...[more]

PMID: 23957012

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Project description:BackgroundAssessment of tissue hypoxia at the bedside has yet to be translated into daily clinical practice in septic shock patients. Perfusion markers are surrogates of deeper physiological phenomena. Lactate-to-pyruvate ratio (LPR) and the ratio between veno-arterial PCO2 difference and Ca-vO2 (ΔPCO2/Ca-vO2) have been proposed as markers of tissue hypoxia, but they have not been compared in the clinical scenario. We studied acute septic shock patients under resuscitation. We wanted to evaluate the relationship of these hypoxia markers with clinical and biochemical markers of hypoperfusion during septic shock resuscitation.MethodsSecondary analysis of a randomized controlled trial. Septic shock patients were randomized to fluid resuscitation directed to normalization of capillary refill time (CRT) versus normalization or significant lowering of lactate. Multimodal assessment of perfusion was performed at 0, 2, 6 and 24 hours, and included macrohemodynamic and metabolic perfusion variables, CRT, regional flow and hypoxia markers. Patients who attained their pre-specified endpoint at 2-hours were compared to those who did not.ResultsForty-two patients were recruited, median APACHE-II score was 23 [15-31] and 28-day mortality 23%. LPR and ΔPCO2/Ca-vO2 ratio did not correlate during early resuscitation (0-2 h) and the whole study period (24-hours). ΔPCO2/Ca-vO2 ratio derangements were more prevalent than LPR ones, either in the whole cohort (52% vs. 23%), and in association with other perfusion abnormalities. In patients who reached their resuscitation endpoints, the proportion of patients with altered ΔPCO2/Ca-vO2 ratio decreased significantly (66% to 33%, P=0.045), while LPR did not (14% vs. 25%, P=0.34).ConclusionsHypoxia markers did not exhibit correlation during resuscitation in septic shock patients. They probably interrogate different pathophysiological processes and mechanisms of dysoxia during early septic shock. Future studies should better elucidate the interaction and clinical role of hypoxia markers during septic shock resuscitation.

Project description:Septic shock is the leading cause of cardiovascular failure in the intensive care unit (ICU). Cardiac output is a primary component of global oxygen delivery to organs and a sensitive parameter of cardiovascular failure. Any mismatch between oxygen delivery and rapidly varying metabolic demand may result in tissue dysoxia, hence organ dysfunction. Since the intricate alterations of both vascular and cardiac function may rapidly and widely change over time, cardiac output should be measured repeatedly to characterize the type of shock, select the appropriate therapeutic intervention, and evaluate patient's response to therapy. Among the numerous techniques commercially available for measuring cardiac output, transpulmonary thermodilution (TPT) provides a continuous monitoring with external calibration capability, whereas critical care echocardiography (CCE) offers serial hemodynamic assessments. CCE allows early identification of potential sources of inaccuracy of TPT, including right ventricular failure, severe tricuspid or left-sided regurgitations, intracardiac shunt, very low flow states, or dynamic left ventricular outflow tract obstruction. In addition, CCE has the unique advantage of depicting the distinct components generating left ventricular stroke volume (large cavity size vs. preserved contractility), providing information on left ventricular diastolic properties and filling pressures, and assessing pulmonary artery pressure. Since inotropes may have deleterious effects if misused, their initiation should be based on the documentation of a cardiac dysfunction at the origin of the low flow state by CCE. Experts widely advocate using CCE as a first-line modality to initially evaluate the hemodynamic profile associated with shock, as opposed to more invasive techniques. Repeated assessments of both the efficacy (amplitude of the positive response) and tolerance (absence of side-effect) of therapeutic interventions are required to best guide patient management. Overall, TPT allowing continuous tracking of cardiac output variations and CCE appear complementary rather than mutually exclusive in patients with septic shock who require advanced hemodynamic monitoring.

Project description:Objective: Septic shock is the severe complication of sepsis, with a high mortality. The inflammatory response regulates the immune status and mediates the progression of septic shock. In this study, we aim to identify the key immune-related genes (IRGs) of septic shock and explore their potential mechanism. Methods: Gene expression profiles of septic shock blood samples and normal whole blood samples were retrieved from the Gene Expression Omnibus (GEO) and Genotype-Tissue Expression Portal (GTEx). The differential expression genes (DEGs) and septic shock-specific immune-related genes (SSSIRGs) were evaluated and identified, along with the immune components by "cell type identification by estimating relative subsets of RNA transcripts (CIBERSORT, version x)" algorithm. Additionally, in order to explore the key regulatory network, the relationship among SSSIRGs, upstream transcription factors (TFs), and downstream signaling pathways were also identified by Gene Set Variation Analysis (GSVA) and co-expression analysis. Moreover, the Connectivity Map (CMap) analysis was applied to find bioactive small molecules against the members of regulation network while Chromatin Immunoprecipitation sequencing (ChIP-seq) and Assay for Targeting Accessible-Chromatin with high-throughput sequencing (ATAC-seq) data were used to validate the regulation mechanism of the network. Results: A total of 14,843 DEGs were found between 63 septic shock blood samples and 337 normal whole blood samples. Then, we identified septic shock-specific 839 IRGs as the intersection of DEGs and IRGs. Moreover, we uncovered the regulatory networks based on co-expression analysis and found 28 co-expression interaction pairs. In the regulation network, protein phosphatase 3, catalytic subunit, alpha isozyme (PPP3CA) may regulate late estrogen response, glycolysis and TNFα signaling via NFκB and HLA; Kirsten rat sarcoma viral oncogene homolog (KRAS) may be related to late estrogen response and HLA; and Toll-like receptor 8 (TLR8) may be associated with TNFα signaling via NFκB. And the regulation mechanisms between TFs and IRGs (TLR8, PPP3CA, and KRAS) were validated by ChIP-seq and ATAC-seq. Conclusion: Our data identify three SSSIRGs (TLR8, PPP3CA, and KRAS) as candidate therapeutic targets for septic shock and provide constructed regulatory networks in septic shock to explore its potential mechanism.

Dataset Information

Cardiac contractile reserve parameters are related to prognosis in septic shock.

Introduction

Methods

Results

Conclusion

Publications

Cardiac contractile reserve parameters are related to prognosis in septic shock.

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