Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study

Abstract Background Preservation of spontaneous breathing (SB) is sometimes debated because it has potentially both negative and positive effects on lung injury in comparison with fully controlled mechanical ventilation (CMV). We wanted (1) to verify in mechanically ventilated patients if the change in transpulmonary pressure was similar between pressure support ventilation (PSV) and CMV for a similar tidal volume, (2) to estimate the influence of SB on alveolar pressure (Palv), and (3) to determine whether a reliable plateau pressure could be measured during pressure support ventilation (PSV). Methods We studied ten patients equipped with esophageal catheters undergoing three levels of PSV followed by a phase of CMV. For each condition, we calculated the maximal and mean transpulmonary (ΔPL) swings and Palv. Results Overall, ΔPL was similar between CMV and PSV, but only loosely correlated. The differences in ΔPL between CMV and PSV were explained largely by different inspiratory flows, indicating that the resistive pressure drop caused this difference. By contrast, the Palv profile was very different between CMV and SB; SB led to progressively more negative Palv during inspiration, and Palv became lower than the set positive end-expiratory pressure in nine of ten patients at low PSV. Finally, inspiratory occlusion holds performed during PSV led to plateau and Δ PL pressures comparable with those measured during CMV. Conclusions Under similar conditions of flow and volume, transpulmonary pressure change is similar between CMV and PSV. SB during mechanical ventilation can cause remarkably negative swings in Palv, a mechanism by which SB might potentially induce lung injury

Reliability of plateau pressure during patient-triggered assisted ventilation. Analysis of a multicentre database

Purpose: An inspiratory hold during patient-triggered assisted ventilation potentially allows to measure driving pressure and inspiratory effort. However, muscular activity can make this measurement unreliable. We aim to define the criteria for inspiratory holds reliability during patient-triggered breaths. Material and methods: Flow, airway and esophageal pressure recordings during patient-triggered breaths from a multicentre observational study (BEARDS, NCT03447288) were evaluated by six independent raters, to determine plateau pressure readability. Features of “readable” and “unreadable” holds were compared. Muscle pressure estimate from the hold was validated against other measures of inspiratory effort. Results: Ninety-two percent of the recordings were consistently judged as readable or unreadable by at least four raters. Plateau measurement showed a high consistency among raters. A short time from airway peak to plateau pressure and a stable and longer plateau characterized readable holds. Unreadable plateaus were associated with higher indexes of inspiratory effort. Muscular pressure computed from the hold showed a strong correlation with independent indexes of inspiratory effort. Conclusion: The definition of objective parameters of plateau reliability during assisted-breath provides the clinician with a tool to target a safer assisted-ventilation and to detect the presence of high inspiratory effort

Individual response in patient’s effort and driving pressure to variations in assistance during pressure support ventilation

Abstract Background During Pressure Support Ventilation (PSV) an inspiratory hold allows to measure plateau pressure (Pplat), driving pressure (∆P), respiratory system compliance (Crs) and pressure-muscle-index (PMI), an index of inspiratory effort. This study aims [1] to assess systematically how patient’s effort (estimated with PMI), ∆P and tidal volume (Vt) change in response to variations in PSV and [2] to confirm the robustness of Crs measurement during PSV. Methods 18 patients recovering from acute respiratory failure and ventilated by PSV were cross-randomized to four steps of assistance above (+ 3 and + 6 cmH2O) and below (-3 and -6 cmH2O) clinically set PS. Inspiratory and expiratory holds were performed to measure Pplat, PMI, ∆P, Vt, Crs, P0.1 and occluded inspiratory airway pressure (Pocc). Electromyography of respiratory muscles was monitored noninvasively from body surface (sEMG). Results As PSV was decreased, Pplat (from 20.5 ± 3.3 cmH2O to 16.7 ± 2.9, P < 0.001) and ∆P (from 12.5 ± 2.3 to 8.6 ± 2.3 cmH2O, P < 0.001) decreased much less than peak airway pressure did (from 21.7 ± 3.8 to 9.7 ± 3.8 cmH2O, P < 0.001), given the progressive increase of patient’s effort (PMI from -1.2 ± 2.3 to 6.4 ± 3.2 cmH2O) in line with sEMG of the diaphragm (r = 0.614; P < 0.001). As ∆P increased linearly with Vt, Crs did not change through steps (P = 0.119). Conclusion Patients react to a decrease in PSV by increasing inspiratory effort—as estimated by PMI—keeping Vt and ∆P on a desired value, therefore, limiting the clinician’s ability to modulate them. PMI appears a valuable index to assess the point of ventilatory overassistance when patients lose control over Vt like in a pressure-control mode. The measurement of Crs in PSV is constant—likely suggesting reliability—independently from the level of assistance and patient’s effort

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

Rationale: Obesity is characterized by elevated pleural pressure (Ppl) and worsening atelectasis during mechanical ventilation in patients with acute respiratory distress syndrome (ARDS).Objectives: 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 prevents lung overdistension.Methods: First, an interventional crossover trial in adult subjects with ARDS and a body mass index ≥ 35 kg/m2 (n = 21) was performed to explore the hemodynamic consequences of the LRM. Second, cardiovascular function was studied during low and high positive end-expiratory pressure (PEEP) in a model of swine with ARDS and high Ppl (n = 9) versus healthy swine with normal Ppl (n = 6).Measurements and Main Results: Subjects with ARDS and obesity (body mass index = 57 ± 12 kg/m2) after LRM required an increase in PEEP of 8 (95% confidence interval [95% CI], 7-10) cm H2O above traditional ARDS Network settings to improve lung function, oxygenation and [Formula: see text]/[Formula: see text] matching, without impairment of hemodynamics or right heart function. ARDS swine with high Ppl demonstrated unchanged transmural left ventricular pressure and systemic blood pressure after the LRM protocol. Pulmonary arterial hypertension decreased (8 [95% CI, 13-4] mm Hg), as did vascular resistance (1.5 [95% CI, 2.2-0.9] Wood units) and transmural right ventricular pressure (10 [95% CI, 15-6] mm Hg) during exhalation. LRM and PEEP decreased pulmonary vascular resistance and normalized the [Formula: see text]/[Formula: see text] ratio.Conclusions: High airway pressure is required to recruit lung atelectasis in patients with ARDS and class III obesity but causes minimal overdistension. In addition, patients with ARDS and class III obesity hemodynamically tolerate LRM with high airway pressure.Clinical trial registered with www.clinicaltrials.gov (NCT02503241)

A lung rescue team improves survival in obesity with acute respiratory distress syndrome.

BackgroundLimited data exist regarding ventilation in patients with class III obesity [body mass index (BMI) &gt; 40 kg/m2] and acute respiratory distress syndrome (ARDS). The aim of the present study was to determine whether an individualized titration of mechanical ventilation according to cardiopulmonary physiology reduces the mortality in patients with class III obesity and ARDS.MethodsIn this retrospective study, we enrolled adults admitted to the ICU from 2012 to 2017 who had class III obesity and ARDS and received mechanical ventilation for &gt; 48 h. Enrolled patients were divided in two cohorts: one cohort (2012-2014) had ventilator settings determined by the ARDSnet table for lower positive end-expiratory pressure/higher inspiratory fraction of oxygen (standard protocol-based cohort); the other cohort (2015-2017) had ventilator settings determined by an individualized protocol established by a lung rescue team (lung rescue team cohort). The lung rescue team used lung recruitment maneuvers, esophageal manometry, and hemodynamic monitoring.ResultsThe standard protocol-based cohort included 70 patients (BMI = 49 ± 9 kg/m2), and the lung rescue team cohort included 50 patients (BMI = 54 ± 13 kg/m2). Patients in the standard protocol-based cohort compared to lung rescue team cohort had almost double the risk of dying at 28 days [31% versus 16%, P = 0.012; hazard ratio (HR) 0.32; 95% confidence interval (CI95%) 0.13-0.78] and 3&nbsp;months (41% versus 22%, P = 0.006; HR 0.35; CI95% 0.16-0.74), and this effect persisted at 6&nbsp;months and 1&nbsp;year (incidence of death unchanged 41% versus 22%, P = 0.006; HR 0.35; CI95% 0.16-0.74).ConclusionIndividualized titration of mechanical ventilation by a lung rescue team was associated with decreased mortality compared to use of an ARDSnet table