Pressure Positive End-expiratory Pressure Research Articles

Real-Time Effort Driven Ventilator Management: A Pilot Study.

Mechanical ventilation of patients with acute respiratory distress syndrome should balance lung and diaphragm protective principles, which may be difficult to achieve in routine clinical practice. Through a Phase I clinical trial, we sought to determine whether a computerized decision support-based protocol (real-time effort-driven ventilator management) is feasible to implement, results in improved acceptance for lung and diaphragm protective ventilation, and improves clinical outcomes over historical controls. Interventional nonblinded pilot study. PICU. Mechanically ventilated children with acute respiratory distress syndrome. A computerized decision support tool was tested which prioritized lung-protective management of peak inspiratory pressure-positive end-expiratory pressure, positive end-expiratory pressure/FIO2, and ventilatory rate. Esophageal manometry was used to maintain patient effort in a physiologic range. Protocol acceptance was reported, and enrolled patients were matched 4:1 with respect to age, initial oxygenation index, and percentage of immune compromise to historical control patients for outcome analysis. Thirty-two patients were included. Acceptance of protocol recommendations was over 75%. One-hundred twenty-eight matched historical controls were used for analysis. Compared with historical controls, patients treated with real-time effort-driven ventilator management received lower peak inspiratory pressure-positive end-expiratory pressure and tidal volume, and higher positive end-expiratory pressure when FIO2 was greater than 0.60. Real-time effort-driven ventilator management was associated with 6 more ventilator-free days, shorter duration until the first spontaneous breathing trial and 3 fewer days on mechanical ventilation among survivors (all p ≤ 0.05) in comparison with historical controls, while maintaining no difference in the rate of reintubation. A computerized decision support-based protocol prioritizing lung-protective ventilation balanced with reduction of controlled ventilation to maintain physiologic levels of patient effort can be implemented and may be associated with shorter duration of ventilation.

Driving Pressure during Thoracic Surgery: A Randomized Clinical Trial.

Driving pressure (plateau minus end-expiratory airway pressure) is a target in patients with acute respiratory distress syndrome, and is proposed as a target during general anesthesia for patients with normal lungs. It has not been reported for thoracic anesthesia where isolated, inflated lungs may be especially at risk. In a double-blinded, randomized trial (292 patients), minimized driving pressure compared with standard protective ventilation was associated with less postoperative pneumonia or acute respiratory distress syndrome. Recently, several retrospective studies have suggested that pulmonary complication is related with driving pressure more than any other ventilatory parameter. Thus, the authors compared driving pressure-guided ventilation with conventional protective ventilation in thoracic surgery, where lung protection is of the utmost importance. The authors hypothesized that driving pressure-guided ventilation decreases postoperative pulmonary complications more than conventional protective ventilation. In this double-blind, randomized, controlled study, 292 patients scheduled for elective thoracic surgery were included in the analysis. The protective ventilation group (n = 147) received conventional protective ventilation during one-lung ventilation: tidal volume 6 ml/kg of ideal body weight, positive end-expiratory pressure (PEEP) 5 cm H2O, and recruitment maneuver. The driving pressure group (n = 145) received the same tidal volume and recruitment, but with individualized PEEP which produces the lowest driving pressure (plateau pressure-PEEP) during one-lung ventilation. The primary outcome was postoperative pulmonary complications based on the Melbourne Group Scale (at least 4) until postoperative day 3. Melbourne Group Scale of at least 4 occurred in 8 of 145 patients (5.5%) in the driving pressure group, as compared with 18 of 147 (12.2%) in the protective ventilation group (P = 0.047, odds ratio 0.42; 95% CI, 0.18 to 0.99). The number of patients who developed pneumonia or acute respiratory distress syndrome was less in the driving pressure group than in the protective ventilation group (10/145 [6.9%] vs. 22/147 [15.0%], P = 0.028, odds ratio 0.42; 95% CI, 0.19 to 0.92). Application of driving pressure-guided ventilation during one-lung ventilation was associated with a lower incidence of postoperative pulmonary complications compared with conventional protective ventilation in thoracic surgery.

Impact of the driving pressure on mortality in obese and non-obese ARDS patients: a retrospective study of 362 cases.

The relation between driving pressure (plateau pressure-positive end-expiratory pressure) and mortality has never been studied in obese ARDS patients. The main objective of this study was to evaluate the relationship between 90-day mortality and driving pressure in an ARDS population ventilated in the intensive care unit (ICU) according to obesity status. We conducted a retrospective single-center study of prospectively collected data of all ARDS patients admitted consecutively to a mixed medical-surgical adult ICU from January 2009 to May 2017. Plateau pressure, compliance of the respiratory system (Crs) and driving pressure of the respiratory system within 24h of ARDS diagnosis were compared between survivors and non-survivors at day 90 and between obese (body mass index ≥ 30kg/m2) and non-obese patients. Cox proportional hazard modeling was used for mortality at day 90. Three hundred sixty-two ARDS patients were included, 262 (72%) non-obese and 100 (28%) obese patients. Mortality rate at day 90 was respectively 47% (95% CI, 40-53) in the non-obese and 46% (95% CI, 36-56) in the obese patients. Driving pressure at day 1 in the non-obese patients was significantly lower in survivors at day 90 (11.9 ± 4.2cmH2O) than in non-survivors (15.2 ± 5.2cmH2O, p < 0.001). Contrarily, in obese patients, driving pressure at day1 was not significantly different between survivors (13.7 ± 4.5cmH2O) and non-survivors (13.2 ± 5.1cmH2O, p = 0.41) at day 90. After three multivariate Cox analyses, plateau pressure [HR = 1.04 (95% CI 1.01-1.07) for each point of increase], Crs [HR = 0.97 (95% CI 0.96-0.99) for each point of increase] and driving pressure [HR = 1.07 (95% CI 1.04-1.10) for each point of increase], respectively, were independently associated with 90-day mortality in non-obese patients, but not in obese patients. Contrary to non-obese ARDS patients, driving pressure was not associated with mortality in obese ARDS patients.

Bedside Adjustment of Proportional Assist Ventilation to Target a Predefined Range of Respiratory Effort*

During proportional assist ventilation with load-adjustable gain factors, peak respiratory muscle pressure can be estimated from the peak airway pressure and the percentage of assistance (gain). Adjusting the gain can, therefore, target a given level of respiratory effort. This study assessed the clinical feasibility of titrating proportional assist ventilation with load-adjustable gain factors with the goal of targeting a predefined range of respiratory effort. Prospective, multicenter, clinical observational study. Intensive care departments at five university hospitals. Patients were included after meeting simple criteria for assisted mechanical ventilation. Patients were ventilated in proportional assist ventilation with load-adjustable gain factors. The peak respiratory muscle pressure, estimated in cm H2O as (peak airway pressure-positive end-expiratory pressure)×[(100-gain)/gain], was calculated from a grid at the bedside. The gain adjustment algorithm was defined to target a peak respiratory muscle pressure between 5 and 10 cm H2O. Additional recommendations were available in case of hypoventilation or hyperventilation. Fifty-three patients were enrolled. Median time spent under proportional assist ventilation with load-adjustable gain factors was 3 days (interquartile range, 1-5). Gain was adjusted 1.0 (0.7-1.8) times per day, according to the peak respiratory muscle pressure target range in 91% of cases and because of hypoventilation or hyperventilation in 9%. Thirty-four patients were ventilated with proportional assist ventilation with load-adjustable gain factors until extubation, which was successful in 32. Eighteen patients required volume assist-controlled reventilation because of clinical worsening and need for continuous sedation. One patient was intolerant to proportional assist ventilation with load-adjustable gain factors. This first study assessing the clinical feasibility of titrating proportional assist ventilation with load-adjustable gain factors in an attempt to target a predefined range of effort showed that adjusting the level of assistance to maintain a predefined boundary of respiratory muscle pressure is feasible, simple, and often sufficient to ventilate patients until extubation.

Manoeuvres to elevate mean airway pressure, effects on blood gases and lung function in children with and without pulmonary pathology.

During mechanical ventilation, mean airway pressure (MAP) can be increased by a variety of manoeuvres, for example increasing inspiratory time or elevating the positive end expiratory pressure (PEEP). It seemed likely that the effect on blood gases and lung function of a particular manoeuvre to increase MAP would be influenced by the presence of respiratory pathology and thus the manoeuvre best at improving respiratory status in children with an abnormal chest radiograph appearance would differ from that most efficacious in children without such a problem. The aim of this study was to test that hypothesis. Twenty-two children, median age 15 months (range 2.5 weeks-10 years) were examined. Group 1 (n = 10) had no chest radiograph abnormalities and group 2 (n = 12) lobar collapse and/or consolidation. The patients were studied at baseline settings and at an elevated MAP resulting from (in random order) an increase in inspiratory time (T1), pressure PEEP or peak inspiratory pressure (PIP). In group 1, elevating PIP improved oxygenation and carbon dioxide elimination (P < 0.01) and prolonging T1 improved oxygenation (P < 0.05). In group 2, only raising PEEP significantly improved oxygenation (P < 0.01), but this was associated with carbon dioxide retention (P < 0.01). The presence of lung pathology does influence which manoeuvre should be used to elevate MAP to improve blood gases in the paediatric population.

Neither Dopamine nor Dobutamine Reverses the Depression in Mesenteric Blood Flow Caused by Positive End-Expiratory Pressure

Positive end-expiratory pressure (PEEP) has been shown to cause a depression of mesenteric blood flow (MBF) and redistribution of blood flow away from the mesenteric vascular bed. We sought to determine whether two commonly used vasoactive agents, dopamine, a known mesenteric vasodilator and inotrope, and dobutamine, with its inotropic properties, would correct the MBF depression caused by PEEP. DESIGN, MATERIAL, AND METHODS: Sprague-Dawley rats, 180 to 250 g, were treated with mechanical ventilation and either no PEEP (control group) or increasing levels (0, 10, 15, and 20 cm of H2O pressure) of PEEP (PEEP group). Also, we evaluated PEEP's effect on MBF and cardiac output (CO) under the influence of a continuous infusion of 2.5 or 12.5 microgram/kg/min of dopamine or 2.5 or 12.5 microgram/kg/min of dobutamine. Cardiac output and, using in vivo videomicroscopy, mesenteric A1, A2, and A3 arteriolar intraluminal radii and A1 arteriolar optical Doppler velocities were measured. After 20 cm of H2O pressure PEEP was attained, two boluses of 2 mL of 0.9 normal saline were given. The MBF was calculated from vessel radius and red blood cell velocity. There were no significant changes from baseline in mean arterial pressure or A2 or A3 diameters in any of the groups. Both MBF and CO were unchanged over time in the control group. The MBF was reduced 78% (p < 0.05) and the CO was reduced 31% (p < 0.05) from baseline at 20 cm of H2O pressure PEEP. After 4 mL of normal saline, the MBF was still 53% below baseline (p < 0.05), while the CO had returned to baseline in the PEEP group. Low-dose dopamine partially ameliorated both the decrease in CO and MBF caused by PEEP, but 4 mL of normal saline was required in addition to the low-dose dopamine to return MBF to baseline levels while on 20 cm of H2O pressure PEEP. High-dose dopamine with the addition of 4 mL of normal saline returned CO to baseline on 20 cm of H2O pressure PEEP, but MBF remained approximately 46% below baseline despite fluid boluses. Neither low-dose nor high-dose dobutamine, with or without fluid boluses, had an appreciable positive effect on CO or MBF. It is clear that inotropes are not a replacement for adequate fluid loading to correct the depression in cardiac output and mesenteric blood flow associated with the use of mechanical ventilation and PEEP. Low-dose dopamine may serve as an adjunct to adequate fluid resuscitation to improve MBF.

Positive End-Expiratory Pressure Decreases Mesenteric Blood Flow despite Normalization of Cardiac Output

Positive end-expiratory pressure (PEEP) is a commonly used adjunct to mechanical ventilation and is known to have deleterious effects on cardiac output (CO). Its effects on regional blood flow are not well known. We evaluated the effect of PEEP on the mesenteric microcirculation and CO. Sprague-Dawley rats were treated with mechanical ventilation and either no PEEP (Control) or increasing levels of PEEP (PEEP). Using in vivo video-microscopy, mesenteric A1 arteriolar optical Doppler velocities and A1 and A3 (the first- and third-order arterioles branching off the feeding mesenteric arcade) intraluminal diameters were measured (n = 6/group). In a separate set of experimental animals, CO was determined by thermodilution technique (n = 5/group). Additionally, after the PEEP group attained a PEEP level of 20-cm H2O PEEP, two boluses of 2 mL 0.9 normal saline (NS) were given intravenously. The Control groups had the same determinations performed over the same time course as the PEEP group but were not exposed to any PEEP. Mesenteric blood flow (MBF) was calculated from vessel diameter and red blood cell velocity. The MBF and CO fell progressively as PEEP was increased from 10- to 15- to 20-cm H2O pressure. MBF was reduced 75% (p < 0.05) and the CO was reduced 31% (p < 0.05) from baseline at 20-cm H2O pressure PEEP. After 4 mL normal saline, the MBF was still 45% below baseline (p < 0.05) while the CO had returned to baseline. In conclusion, both MBF and CO are decreased significantly with increasing PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)