Dataset Information

High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in ARDS with Class III Obesity.

ABSTRACT: Rationale: Obesity is characterized by elevated pleural pressure (P_PL) and worsening atelectasis during mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). Objectives: To determine the effects of lung recruitment maneuver (LRM) in the presence of elevated P_PL on hemodynamics, left and right ventricular pressures and pulmonary vascular resistance. We hypothesized that elevated P_PL protects the cardiovascular system against high airway pressures and prevents lung overdistension. Methods: First, an interventional crossover trial in adult subjects with ARDS and BMI ≥35 kg/m² (n=21) was performed to explore the hemodynamic consequences of LRM. Second, cardiovascular function was studied during low/high PEEPs in a model of swine with ARDS and high P_PL (n=9) versus healthy swine with normal P_PL (n=6). Measurements and Main Results: Subjects with ARDS and obesity (BMI=57±12 kg/m²), following LRM, required an increase in PEEP of 8[7, 10] cmH₂O above traditional ARDSnet settings to improve lung function, oxygenation and ventilation/perfusion matching, without impairment of hemodynamics or right heart function. ARDS swine with high P_PL demonstrated unchanged transmural left ventricle pressure and systemic blood pressure after LRM protocol. Pulmonary artery hypertension decreased 8[13, 4] mmHg, as did vascular resistance 1.5[2.2, 0.9] WU, and transmural right ventricle pressure 10[15, 6] mmHg during exhalation. LRM and PEEP decreased pulmonary vascular resistance and normalized ventilation/perfusion ratio. Conclusions: High airway pressure is required to recruit lung atelectasis in patients with ARDS and class III obesity but causes minimal overdistension. Additionally, patients with ARDS and class III obesity tolerate hemodynamically LRM with high airway pressure.

SUBMITTER: De Santis Santiago R

PROVIDER: S-EPMC7924574 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in Acute Respiratory Distress Syndrome with Class III Obesity. A Clinical Trial.

De Santis Santiago Roberta R Teggia Droghi Maddalena M Fumagalli Jacopo J Marrazzo Francesco F Florio Gaetano G Grassi Luigi G LG Gomes Susimeire S Morais Caio C A CCA Ramos Ozires P S OPS Bottiroli Maurizio M Pinciroli Riccardo R Imber David A DA Bagchi Aranya A Shelton Kenneth K Sonny Abraham A Bittner Edward A EA Amato Marcelo B P MBP Kacmarek Robert M RM Berra Lorenzo L

American journal of respiratory and critical care medicine 20210301 5

<b>Rationale:</b> Obesity is characterized by elevated pleural pressure (Ppl) and worsening atelectasis during mechanical ventilation in patients with acute respiratory distress syndrome (ARDS).<b>Objectives:</b> To determine the effects of a lung recruitment maneuver (LRM) in the presence of elevated Ppl on hemodynamics, left and right ventricular pressure, and pulmonary vascular resistance. We hypothesized that elevated Ppl protects the cardiovascular system against high airway pressure and pr ...[more]

PMID: 32876469

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Project description:BackgroundAmong the challenges for personalizing the management of mechanically ventilated patients with coronavirus disease (COVID-19)-associated acute respiratory distress syndrome (ARDS) are the effects of different positive end-expiratory pressure (PEEP) levels and body positions in regional lung mechanics. Right-left lung aeration asymmetry and poorly recruitable lungs with increased recruitability with alternating body position between supine and prone have been reported. However, real-time effects of changing body position and PEEP on regional overdistension and collapse, in individual patients, remain largely unknown and not timely monitored. The aim of this study was to individualize PEEP and body positioning in order to reduce the mechanisms of ventilator-induced lung injury: collapse and overdistension.MethodsWe here report a series of five consecutive mechanically ventilated patients with COVID-19-associated ARDS in which sixteen decremental PEEP titrations were performed in the first days of mechanical ventilation (8 titration pairs: supine position immediately followed by 30° targeted lateral position). The choice of lateral tilt was based on X-Ray. This targeted lateral position strategy was defined by selecting the less aerated lung to be positioned up and the more aerated lung to be positioned down. For each PEEP level, global and regional collapse and overdistension maps and percentages were measured by electrical impedance tomography. Additionally, we present the incidence of lateral asymmetry in a cohort of forty-four patients.ResultsThe targeted lateral position strategy resulted in significantly smaller amounts of overdistension and collapse when compared with the supine one: less collapse along the PEEP titration was found within the left lung in targeted lateral (P = 0.014); and less overdistension along the PEEP titration was found within the right lung in targeted lateral (P = 0.005). Regarding collapse within the right lung and overdistension within the left lung: no differences were found for position. In the cohort of forty-four patients, ventilation inequality of > 65/35% was observed in 15% of cases.ConclusionsTargeted lateral positioning with bedside personalized PEEP provided a selective attenuation of overdistension and collapse in mechanically ventilated patients with COVID-19-associated ARDS and right-left lung aeration/ventilation asymmetry.Trial registrationTrial registration number: NCT04460859.

Project description:BackgroundThe superimposed pressure is the primary determinant of the pleural pressure gradient. Obesity is associated with elevated end-expiratory esophageal pressure, regardless of lung disease severity, and the superimposed pressure might not be the only determinant of the pleural pressure gradient. The study aims to measure partitioned respiratory mechanics and superimposed pressure in a cohort of patients admitted to the ICU with and without class III obesity (BMI ≥ 40 kg/m2), and to quantify the amount of thoracic adipose tissue and muscle through advanced imaging techniques.MethodsThis is a single-center observational study including ICU-admitted patients with acute respiratory failure who underwent a chest computed tomography scan within three days before/after esophageal manometry. The superimposed pressure was calculated from lung density and height of the largest axial lung slice. Automated deep-learning pipelines segmented lung parenchyma and quantified thoracic adipose tissue and skeletal muscle.ResultsN = 18 participants (50% female, age 60 [30-66] years), with 9 having BMI < 30 and 9 ≥ 40 kg/m2. Groups showed no significant differences in age, sex, clinical severity scores, or mortality. Patients with BMI ≥ 40 exhibited higher esophageal pressure (15.8 ± 2.6 vs. 8.3 ± 4.9 cmH2O, p = 0.001), higher pleural pressure gradient (11.1 ± 4.5 vs. 6.3 ± 4.9 cmH2O, p = 0.04), while superimposed pressure did not differ (6.8 ± 1.1 vs. 6.5 ± 1.5 cmH2O, p = 0.59). Subcutaneous and intrathoracic adipose tissue were significantly higher in subjects with BMI ≥ 40 and correlated positively with esophageal pressure and pleural pressure gradient (p < 0.05). Muscle areas did not differ between groups.ConclusionsIn patients with class III obesity, the superimposed pressure does not approximate the pleural pressure gradient, which is higher than in patients with lower BMI. The quantity and distribution of subcutaneous and intrathoracic adiposity also contribute to increased pleural pressure gradients in individuals with BMI ≥ 40. This study introduces a novel physiological concept that provides a solid rationale for tailoring mechanical ventilation in patients with high BMI, where specific guidelines recommendations are lacking.

Project description:BackgroundHemodynamic response to prone position (PP) has never been studied in a large series of patients with acute respiratory distress syndrome (ARDS). The primary aim of this study was to estimate the rate of PP sessions associated with cardiac index improvement. Secondary objective was to describe hemodynamic response to PP and during the shift from PP to supine position.MethodsThe study was a single-center retrospective observational study, performed on ARDS patients, undergoing at least one PP session under monitoring by transpulmonary thermodilution. PP sessions performed more than 10 days after ARDS onset, or with any missing cardiac index measurements before (T1), at the end (T3), and after the PP session (T4) were excluded. Changes in hemodynamic parameters during PP were tested after statistical adjustment for volume of fluid challenges, vasopressor and dobutamine dose at each time point to take into account therapeutic changes during PP sessions.ResultsIn total, 107 patients fulfilled the inclusion criteria, totalizing 197 PP sessions. Changes in cardiac index between T1 and T2 (early response to PP) and between T1 and T3 (late response to PP) were significantly correlated (R2 = 0.42, p < 0.001) with a concordance rate amounting to 85%. Cardiac index increased significantly between T1 and T3 in 49 sessions (25% [95% confidence interval (CI95%) 18-32%]), decreased significantly in 46 (23% [CI95% 16-31%]), and remained stable in 102 (52% [CI95% 45-59%]). Global end-diastolic volume index (GEDVI) increased slightly but significantly from 719 ± 193 mL m-2 at T1 to 757 ± 209 mL m-2 at T3 and returned to baseline values at T4. Cardiac index and oxygen delivery decreased slightly but significantly from T3 to T4, without detectable increase in lactate level. Patients who increased their cardiac index during PP had significantly lower CI, GEDVI, global ejection fraction at T1, and received significantly more fluids than patients who did not.ConclusionPP is associated with an increase in cardiac index in 18% to 32% of all PP sessions and a sustained increase in GEDVI reversible after return to supine position. Return from prone to supine position is associated with a slight hemodynamic impairment.

Project description:Background: Hemodynamic forces exert a profound influence on endothelial cell signaling and, when abnormal, contribute centrally to human vascular disease. Pulmonary arterial hypertension (PAH) is characterized by both hemodynamic derangement and pulmonary arterial endothelial cell (PAEC) dysfunction. Despite importance in disease initiation and progression, the combined effects of shear and pressure forces on PAEC biology remain incompletely understood, particularly in the context of PAH. Methods: PAECs obtained at explant from controls and from patients with idiopathic or congenital heart disease-associated PAH (CHD-PAH) were cultured in a custom resistor-coupled microfluidic platform and exposed to static, low (3 dyne/cm²), or high (20 dyne/cm²) shear stress under either low or elevated (60 mmHg) pressure. After 24 hours, we assessed cellular morphology and performed systems-level transcriptomic analysis via bulk RNA sequencing, incorporating analyses of PAH subtype and donor sex. Results: PAECs (n=18 donors) aligned with flow under high, but not low, shear, and alignment was not significantly altered by disease state or pressure. Shear stress fundamentally reorganized the PAEC transcriptome and the “dose-response” to increasing shear differed across biological pathways in six statistically significant patterns. Increasing shear led to divergence in transcription between control and PAH cells, particularly in pathways involved in immune activation, stress signaling, and vascular remodeling, with subtype differences also observed. Pressure alone had modest effects on transcription, though CHD-PAH PAECs especially displayed pressure-induced stress and inflammatory signaling. We identified sexual dimorphism in the endothelial shear response, noting male cells under shear enriched for pathways involved in proliferation and inflammation and female cells enriched for lipid metabolism and stress responses. Conclusions: Shear and pressure forces profoundly influence PAEC transcription, with responses shaped by disease state, PAH subtype, and sex. These findings highlight the need for further investigation into mechanosensitive pathways in PAH as potential targets for novel therapies.

Dataset Information

High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in ARDS with Class III Obesity.

Publications

High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in Acute Respiratory Distress Syndrome with Class III Obesity. A Clinical Trial.

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