Lung-protective Mechanical Ventilation Research Articles

Comparison of prone positioning and high-frequency oscillatory ventilation in patients with acute respiratory distress syndrome*

Both prone position and high-frequency oscillatory ventilation (HFOV) have the potential to facilitate lung recruitment, and their combined use could thus be synergetic on gas exchange. Keeping the lung open could also potentially be lung protective. The aim of this study was to compare physiologic and proinflammatory effects of HFOV, prone positioning, or their combination in severe acute respiratory distress syndrome (ARDS). : Prospective, comparative randomized study. A medical intensive care unit. Thirty-nine ARDS patients with a Pao2/Fio2 ratio <150 mm Hg at positive end-expiratory pressure > or =5 cm H2O. After 12 hrs on conventional lung-protective mechanical ventilation (tidal volume 6 mL/kg of ideal body weight, plateau pressure not exceeding the upper inflection point, and a maximum of 35 cm H2O; supine-CV), 39 patients were randomized to receive one of the following 12-hr periods: conventional lung-protective mechanical ventilation in prone position (prone-CV), HFOV in supine position (supine-HFOV), or HFOV in prone position (prone-HFOV). Prone-CV (from 138 +/- 58 mm Hg to 217 +/- 110 mm Hg, p < .0001) and prone-HFOV (from 126 +/- 40 mm Hg to 227 +/- 64 mm Hg, p < 0.0001) improved the Pao2/Fio2 ratio whereas supine-HFOV did not alter the Pao2/Fio2 ratio (from 134 +/- 57 mm Hg to 138 +/- 48 mm Hg). The oxygenation index ({mean airway pressure x Fio2 x 100}/Pao2) decreased in the prone-CV and prone-HFOV groups and was lower than in the supine-HFOV group. Interleukin-8 increased significantly in the bronchoalveolar lavage fluid (BALF) in supine-HFOV and prone-HFOV groups compared with prone-CV and supine-CV. Neutrophil counts were higher in the supine-HFOV group than in the prone-CV group. Although HFOV in the supine position does not improve oxygenation or lung inflammation, the prone position increases oxygenation and reduces lung inflammation in ARDS patients. Prone-HFOV produced similar improvement in oxygenation like prone-CV but was associated with higher BALF indexes of inflammation. In contrast, supine-HFOV did not improve gas exchange and was associated with enhanced lung inflammation.

Struggle for implementation of new strategies in intensive care medicine: anticoagulation, insulin, and lower tidal volumes

The management of intensive care patients have changed dramatically in the last years: from merely supportive care, it has moved to evidence-based strategies that have been demonstrated to reduce mortality of the severely ill patients. Clinical research have brought numerous positive clinical trials offering intensive care physicians specific therapies to improve outcome of intensive care patients. Among them were the trials that tested the infusion of activated protein C in patients with severe sepsis, tight glycemic control in surgical intensive care patients, and use of lung protective mechanical ventilation by using small tidal volumes in patients with acute lung injury. Although results of these trials were sufficiently strong to, at least, consider implementation of these strategies in critical care medicine, published and yet unpublished reports show that there is significant struggle with implementation of these therapies. This manuscript focuses on the potential reasons that underlie this problem.

Tidal Volume Reduction in Patients with Acute Lung Injury When Plateau Pressures Are Not High

Use of a volume- and pressure-limited mechanical ventilation strategy improves clinical outcomes of patients with acute lung injury and acute respiratory distress syndrome (ALI/ARDS). However, the extent to which tidal volumes and inspiratory airway pressures should be reduced to optimize clinical outcomes is a controversial topic. This article addresses the question, "Is there a safe upper limit to inspiratory plateau pressure in patients with ALI/ARDS?" We reviewed data from animal models with and without preexisting lung injury, studies of normal human respiratory system mechanics, and the results of five clinical trials of lung-protective mechanical ventilation strategies. We also present an original analysis of data from the largest of the five clinical trials. The available data from each of these assessments do not support the commonly held view that inspiratory plateau pressures of 30 to 35 cm H2O are safe. We could not identify a safe upper limit for plateau pressures in patients with ALI/ARDS.

Feedback and education improve physician compliance in use of lung-protective mechanical ventilation

Use of lung-protective mechanical ventilation (MV) by applying lower tidal volumes is recommended in patients suffering from acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Recent data suggest that lung-protective MV may benefit non-ALI/ARDS patients as well. This study analyzed tidal volume settings in three ICUs in The Netherlands to determine the effect of feedback and education concerning use of lung-protective MV. Observational study in one academic and two nonacademic "closed format" ICUs. Intubated mechanically ventilated subjects. Feedback and education concerning lung-protective MV with special attention to the importance of closely adjusting tidal volumes to predicted body weight (PBW). Tidal volumes declined significantly within 6 months after intervention (from 9.8+/-2.0 at baseline to 8.1+/-1.7 ml/kg PBW) as the percentage of undesirable ventilation data points, defined as tidal volumes greater than 8 ml/kg PBW (84% vs. 48%). There were no differences between patients meeting the international definition criteria for ALI/ARDS and those not. Only four patients received tidal volumes less than 6 ml/kg PBW. Lower tidal volumes were still used after 12 months. Tidal volumes in patients on mandatory MV and patients breathing on spontaneous modes were similar. Feedback and education improve physician compliance in use of lung-protective MV.

Lung protective mechanical ventilation in acute respiratory distress syndrome.

The evidence supports the idea that mechanical ventilation can potentially cause further lung injury. The only ventilator manipulation that so far has been shown definitively to reduce injury and improve mortality is the reduction of VT to 6 mL/kg PBW or lower and targeting Pplat to 30 cm H2O or lower. Much research is needed to provide further guidance in applying ventilatory support techniques.

Lung-protective ventilation strategies in acute lung injury.

To review the challenges of providing mechanical ventilatory support for respiratory failure while avoiding ventilator-associated lung injury in patients with acute lung injury. To review the results of several randomized clinical trials of lung-protective ventilation strategies using conventional mechanical ventilators. Published reports of clinical trials comparing clinical outcomes of patients with acute lung injury, randomized to mechanical ventilation with either a lung-protective or a control, conventional, standard, or traditional approach. Lung-protective mechanical ventilation strategies are designed to prevent injury from overdistention by using lower tidal volumes and lower inspiratory pressures (volume- and pressure-limited ventilation) or injury from ventilation with atelectasis and alveolar flooding at end-expiration (open-lung ventilation). In one trial, clinical outcomes were better in the study group that received combined volume- and pressure-limited and open-lung strategies compared with the study group that received a conventional approach. Of four trials focusing on volume- and pressure-limited ventilation alone, three did not demonstrate improvements in clinical outcomes, whereas one demonstrated a substantial reduction in mortality and an increase in ventilator-free days. The different results in these four trials may be attributable to differences in tidal volumes between the study groups, chance variation, or differences in the management of respiratory acidosis. Evidence supports the use of a volume- and pressure-limited approach to mechanical ventilation in patients with acute lung injury. It is not yet clear whether the open-lung approach will further reduce mortality in patients receiving volume- and pressure-limited ventilation support.

Long-term Assessment of Lung Function in Survivors of Severe ARDS

To investigate the long-term outcome of lung function in survivors of severe ARDS after modern treatment strategies including lung protective mechanical ventilation and prone positioning maneuvers. Follow-up cohort study. University hospital pulmonary division and level 1 trauma center. Sixteen survivors of severe ARDS (from 1992 to 1994) with a lung injury score > or = 2.5. The follow-up study (from 1995 to 1996) included interview, physical examination, chest radiographs, static and dynamic lung volumes, diffusion capacity of the lung for carbon monoxide (DLCO), blood gas analysis, and cardiopulmonary exercise testing (CPET). The mean +/- SD interval between hospital discharge and functional assessment was 29.5 +/- 8.7 months (range, 15.0 to 40.7 months). In approximately one half of the patients, mild abnormalities in static and dynamic lung volumes were found. In 25% (4 of 16 patients), lung function was obstructive; in 25% (4 of 16 patients), lung function was restrictive; and in 6.3% (1 of 16 patients), a combined obstructive-restrictive pattern was revealed. DLCO was impaired in 12.5% (2 of 16 patients); gas exchange during exercise was impaired in 45.5% (5 of 11 patients). Residual obstructive and restrictive defects as well as impaired pulmonary gas exchange remain common after severe ARDS. CPET is a very sensitive measure to evaluate residual impairment of lung function after ARDS. Using CPET, reduced pulmonary gas exchange can be detected in many patients with normal DLCO.

Kinetic and reversibility of mechanical ventilation-associated pulmonary and systemic inflammatory response in patients with acute lung injury.

To investigate the kinetic and reversibility of mechanical ventilation-associated pulmonary and systemic inflammatory response in patients with acute lung injury (ALI). Prospective observational cross-over study. Intensive care unit of a university hospital. Twelve mechanically ventilated patients with ALI. Mechanical ventilation was transiently changed from a lung protective setting with PEEP of 15 cmH(2)O and a V(T) of 5 ml/kg predicted body weight to a more conventional ventilatory setting with PEEP of 5 cmH(2)O and V(T) of 12 ml/kg predicted body weight for a period of 6 h. We examined the profile of interleukin (IL)-1beta, IL-1 receptor antagonist, IL-6, IL-10, and tumor necrosis factor in the plasma of all patients, and in the bronchoalveolar lavage (mini-BAL) fluid of six of these patients. Measurements were performed at baseline, 1 h, and 6 h after each change of the ventilatory setting. Switching to conventional mechanical ventilation was associated with a higher PaO(2) ( P < 0.05) and a marked increase ( P < 0.05) of measured plasma cytokines in patients with and without mini-BAL with a maximum after 1 h. Similarly, intraalveolar cytokine concentrations increased with conventional mechanical ventilation. While plasma cytokine levels returned to baseline values, intraalveolar cytokine concentrations further increased when lung protective mechanical ventilation was reestablished. In patients with ALI, initiation of low PEEP and high V(T) mechanical ventilation is associated with cytokine release into circulation which occurred within 1 h. It is independent from BAL procedures and can be reversed by reinstitution of lung protective mechanical ventilation.

Effect of cimetidine on upper gastrointestinal bleeding after renal transplantation.

<h3>BACKGROUND:</h3> A lung-protective mechanical ventilation strategy has become the hallmark of ventilation management for patients with acute respiratory failure. However, some patients progress to more severe forms of acute respiratory failure with refractory hypoxemia. In such circumstances, individualized titration of mechanical ventilation according to the patient9s specific respiratory and cardiovascular pathophysiology is desirable. A lung rescue team (LRT) was recently established at our institution to improve the medical care of patients with acute respiratory failure when conventional treatment fails. The aim of this report is to describe the consultation processes, the cardiopulmonary assessment, and the procedures of the LRT. <h3>METHODS:</h3> This was a retrospective review of the LRT management of patients with acute respiratory failure and refractory hypoxemia at Massachusetts General Hospital in Boston, Massachusetts. The LRT is composed of a critical care physician, the ICU respiratory therapist on duty, the ICU nurse on duty, and 2 critical care fellows. In the LRT approach, respiratory mechanics are evaluated through lung recruitment maneuvers and decremental PEEP trials by means of 3 tools: esophageal manometry, echocardiography, and electrical impedance tomography lung imaging. <h3>RESULTS:</h3> The LRT was consulted 89 times from 2014 to 2019 for evaluation and management of severely critically ill patients with acute respiratory failure and refractory hypoxemia on mechanical ventilation. The LRT was requested a median of 2 (interquartile range 1–6) d after intubation to optimize mechanical ventilation and to titrate PEEP in 77 (86%) subjects, to manage ventilation in 8 (9%) subjects on extracorporeal membrane oxygenation (ECMO), and to manage weaning strategy from mechanical ventilation in 4 (5%) subjects. The LRT found consolidations with atelectasis responsive to recruitment maneuvers in 79% (<i>n</i> = 70) of consultations. The LRT findings translated into a change of care in 81% (<i>n</i> = 72) of subjects. <h3>CONCLUSIONS:</h3> The LRT individualized the management of severe acute respiratory failure. The LRT consultations were shown to be effective, safe, and efficient, with an impact on decision-making in the ICU.

Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances.

Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances.