Dataset Information

Relationship between Driving Pressure and Mortality in Ventilated Patients with Heart Failure: A Cohort Study.

ABSTRACT:

Background

Heart failure (HF) is a leading cause of mortality and morbidity worldwide, with an increasing incidence. Invasive ventilation is considered to be essential for patients with HF. Previous studies have shown that driving pressure is associated with mortality in acute respiratory distress syndrome (ARDS). However, the relationship between driving pressure and mortality has not yet been examined in ventilated patients with HF. We assessed the association of driving pressure and mortality in patients with HF.

Methods

We conducted a retrospective cohort study of invasive ventilated adult patients with HF from the Medical Information Mart for Intensive Care-III database. We used multivariable logistic regression models, a generalized additive model, and a two-piecewise linear regression model to show the effect of the average driving pressure within 24 h of intensive care unit admission on in-hospital mortality.

Results

Six hundred and thirty-two invasive ventilated patients with HF were enrolled. Driving pressure was independently associated with in-hospital mortality (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.06-1.18; P < 0.001) after adjusted potential confounders. A nonlinear relationship was found between driving pressure and in-hospital mortality, which had a threshold around 14.27 cmH₂O. The effect sizes and CIs below and above the threshold were 0.89 (0.75 to 1.05) and 1.17 (1.07 to 1.30), respectively.

Conclusions

There was a nonlinear relationship between driving pressure and mortality in patients with HF who were ventilated for more than 48 h, and this relationship was associated with increased in-hospital mortality when the driving pressure was more than 14.27 cmH₂O.

SUBMITTER: Yang Q

PROVIDER: S-EPMC8648448 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundIt is commonly observed that a higher target of mean arterial pressure (MAP) is in previous studies. This study assessed the association of MAP with short-term mortality in heart failure (HF) patients.MethodsA retrospective cohort study was conducted by using data from Hospitalized patients with heart failure: integrating electronic healthcare records and external outcome database (v1.2 ). The characteristic of patients was described by 3 groups of MAP: below 80 mmHg, 80-100 mmHg, and above 100 mmHg. Univariate and multivariate logistic regression analyses were used to assess the relevance between MAP and all-cause mortality within 28 days and 6 months. For assessing the effect of multiple variables on patient survival time, 28-day and 6-month, Kaplan-Meier survival analysis and Forest plot were performed.ResultsThe overall cohort comprised 2008 patients divided by MAP into 3 groups, each group had 344 (17.1%), 938 (46.7%), and 726 (36.2%) patients. Patients in MAP < 80 mmHg group had higher mortality than MAP 80-100 mmHg and MAP ≥ 100 mmHg in 28 days(3.8% versus 1.6% versus 1.2%) and in 6 months (4.9% versus 2.5% versus 2.3%). Univariate analysis showed that MAP as a continuous variate was associated with 28-day (OR was 0.98, 95% CIs: 0.96-0.99, P = 0.011) and 6-month mortality (OR was 0.98, 95% CIs: 0.97-1, P = 0.021) in HF patients. Model 4 put into multivariate logistic regression analyses showed MAP 80-100 mmHg (OR was 0.13, 95% CIs: 0.02-0.8, P = 0.027) stably associated with 28-day and 6-month mortality after adjusted covariable. Kaplan-Meier survival curves revealed a higher survival rate in the MAP ≥ 80 mmHg group than in the MAP < 80 mmHg group. The forest plot showed the stable effect of MAP ≥ 80 mmHg compared with MAP < 80 mmHg, the interaction analysis had no statistical significance effect between the two groups of MAP and multi-variable.ConclusionIt is indicated that MAP was independently associated with 28-day, 6-month all-cause mortality of HF patients, and compared with MAP < 80 mmHg, MAP ≥ 80 mmHg had a lower risk of 28-day, 6-month all-cause mortality of patients with HF.

Project description:BackgroundDuring control mechanical ventilation (CMV), the driving pressure of the respiratory system (ΔPrs) serves as a surrogate of transpulmonary driving pressure (ΔPlung). Expiratory muscle activity that decreases end-expiratory lung volume may impair the validity of ΔPrs to reflect ΔPlung. This prospective observational study in patients with acute respiratory distress syndrome (ARDS) ventilated with proportional assist ventilation (PAV+), aimed to investigate: (1) the prevalence of elevated ΔPlung, (2) the ΔPrs-ΔPlung relationship, and (3) whether dynamic transpulmonary pressure (Plungsw) and effort indices (transdiaphragmatic and respiratory muscle pressure swings) remain within safe limits.MethodsThirty-one patients instrumented with esophageal and gastric catheters (n = 22) were switched from CMV to PAV+ and respiratory variables were recorded, over a maximum of 24 h. To decrease the contribution of random breaths with irregular characteristics, a 7-breath moving average technique was applied. In each patient, measurements were also analyzed per deciles of increasing lung elastance (Elung). Patients were divided into Group A, if end-inspiratory transpulmonary pressure (PLEI) increased as Elung increased, and Group B, which showed a decrease or no change in PLEI with Elung increase.ResultsIn 44,836 occluded breaths, ΔPlung ≥ 12 cmH2O was infrequently observed [0.0% (0.0-16.9%) of measurements]. End-expiratory lung volume decrease, due to active expiration, was associated with underestimation of ΔPlung by ΔPrs, as suggested by a negative linear relationship between transpulmonary pressure at end-expiration (PLEE) and ΔPlung/ΔPrs. Group A included 17 and Group B 14 patients. As Elung increased, ΔPlung increased mainly due to PLEI increase in Group A, and PLEE decrease in Group B. Although ΔPrs had an area receiver operating characteristic curve (AUC) of 0.87 (95% confidence intervals 0.82-0.92, P < 0.001) for ΔPlung ≥ 12 cmH2O, this was due exclusively to Group A [0.91 (0.86-0.95), P < 0.001]. In Group B, ΔPrs showed no predictive capacity for detecting ΔPlung ≥ 12 cmH2O [0.65 (0.52-0.78), P > 0.05]. Most of the time Plungsw and effort indices remained within safe range.ConclusionIn patients with ARDS ventilated with PAV+, injurious tidal lung stress and effort were infrequent. In the presence of expiratory muscle activity, ΔPrs underestimated ΔPlung. This phenomenon limits the usefulness of ΔPrs as a surrogate of tidal lung stress, regardless of the mode of support.