Editor’s Perspective What We Already Know about This Topic Higher driving pressure during controlled mechanical ventilation is known to be associated with increased mortality in patients with acute respiratory distress syndrome. Whereas patients with acute respiratory distress syndrome are initially managed with controlled mechanical ventilation, as they improve, they are transitioned to assisted ventilation. Whether higher driving pressure assessed during pressure support (assisted) ventilation can be reliably assessed and whether higher driving pressure is associated with worse outcomes in patients with acute respiratory distress syndrome has not been well studied. What This Article Tells Us That Is New This study shows that in the majority of adult patients with acute respiratory distress syndrome, both driving pressure and respiratory system compliance can be reliably measured during pressure support (assisted) ventilation. Higher driving pressure measured during pressure support (assisted) ventilation significantly associates with increased intensive care unit mortality, whereas peak inspiratory pressure does not. Lower respiratory system compliance also significantly associates with increased intensive care unit mortality. Background Driving pressure, the difference between plateau pressure and positive end-expiratory pressure (PEEP), is closely associated with increased mortality in patients with acute respiratory distress syndrome (ARDS). Although this relationship has been demonstrated during controlled mechanical ventilation, plateau pressure is often not measured during spontaneous breathing because of concerns about validity. The objective of the present study is to verify whether driving pressure and respiratory system compliance are independently associated with increased mortality during assisted ventilation ( i.e ., pressure support ventilation). Methods This is a retrospective cohort study conducted on 154 patients with ARDS in whom plateau pressure during the first three days of assisted ventilation was available. Associations between driving pressure, respiratory system compliance, and survival were assessed by univariable and multivariable analysis. In patients who underwent a computed tomography scan (n = 23) during the stage of assisted ventilation, the quantity of aerated lung was compared with respiratory system compliance measured on the same date. Results In contrast to controlled mechanical ventilation, plateau pressure during assisted ventilation was higher than the sum of PEEP and pressure support (peak pressure). Driving pressure was higher (11 [9–14] vs . 10 [8–11] cm H 2 O; P = 0.004); compliance was lower (40 [30–50] vs. 51 [42–61] ml · cm H 2 O -1 ; P < 0.001); and peak pressure was similar, in nonsurvivors versus survivors. Lower respiratory system compliance (odds ratio, 0.92 [0.88–0.96]) and higher driving pressure (odds ratio, 1.34 [1.12–1.61]) were each independently associated with increased risk of death. Respiratory system compliance was correlated with the aerated lung volume (n = 23, r = 0.69, P < 0.0001). Conclusions In patients with ARDS, plateau pressure, driving pressure, and respiratory system compliance can be measured during assisted ventilation, and both higher driving pressure and lower compliance are associated with increased mortality.

Editor’s Perspective What We Already Know about This Topic After pulmonary artery occlusion (mimicking a pulmonary embolism), perfusion is redistributed to the rest of the lung tissue, but the distribution of ventilation is uncertain. What This Article Tells Us That Is New Data from anesthetized pigs (uninjured lungs) indicate that the perfusion is redistributed as suspected. Similarly, ventilation is redistributed from nonperfused to perfused lung tissue. This limits the increase in dead space and is accompanied by less density in the occluded lung. Background Acute unilateral pulmonary arterial occlusion causes ventilation–perfusion mismatch of the affected lung area. A diversion of ventilation from nonperfused to perfused lung areas, limiting the increase in dead space, has been described. The hypothesis was that the occlusion of a distal branch of the pulmonary artery would cause local redistribution of ventilation and changes in regional lung densitometry as assessed with quantitative computed tomography. Methods In eight healthy, anesthetized pigs (18.5 ± 3.8 kg) ventilated with constant ventilatory settings, respiratory mechanics, arterial blood gases, and quantitative computed tomography scans were recorded at baseline and 30 min after the inflation of the balloon of a pulmonary artery catheter. Regional (left vs. right lung and perfused vs. nonperfused area) quantitative computed tomography was performed. Results The balloon always occluded a branch of the left pulmonary artery perfusing approximately 30% of lung tissue. Physiologic dead space increased (0.37 ± 0.17 vs. 0.43 ± 0.17, P = 0.005), causing an increase in Pa co 2 (39.8 [35.2 to 43.0] vs. 41.8 [37.5 to 47.1] mmHg, P = 0.008) and reduction in pH (7.46 [7.42 to 7.50] vs . 7.42 [7.38 to 7.47], P = 0.008). Respiratory system compliance was reduced (24.4 ± 4.2 vs. 22.8 ± 4.8 ml · cm H 2 O −1 , P = 0.028), and the reduction was more pronounced in the left hemithorax. Quantitative analysis of the nonperfused lung area revealed a significant reduction in lung density (−436 [−490 to −401] vs. −478 [−543 to −474] Hounsfield units, P = 0.016), due to a reduction in lung tissue (90 ± 23 vs. 81 ± 22 g, P < 0.001) and an increase in air volume (70 ± 22 vs. 82 ± 26 ml, P = 0.022). Conclusions Regional pulmonary vascular occlusion is associated with a diversion of ventilation from nonperfused to perfused lung areas. This compensatory mechanism effectively limits ventilation perfusion mismatch. Quantitative computed tomography documented acute changes in lung densitometry after pulmonary vascular occlusion. In particular, the nonperfused lung area showed an increase in air volume and reduction in tissue mass, resulting in a decreased lung density.

Respiratory function is fundamental in the practice of anesthesia. Knowledge of basic physiologic principles of respiration assists in the proper implementation of daily actions of induction and maintenance of general anesthesia, delivery of mechanical ventilation, discontinuation of mechanical and pharmacologic support, and return to the preoperative state. The current work provides a review of classic physiology and emphasizes features important to the anesthesiologist. The material is divided in two main sections, gas exchange and respiratory mechanics; each section presents the physiology as the basis of abnormal states. We review the path of oxygen from air to the artery and of carbon dioxide the opposite way, and we have the causes of hypoxemia and of hypercarbia based on these very footpaths. We present the actions of pressure, flow, and volume as the normal determinants of ventilation, and we review the resulting abnormalities in terms of changes of resistance and compliance.

Editor’s Perspective What We Already Know about This Topic Extracorporeal membrane oxygenation is used in severe acute respiratory distress syndrome; whereas the long-term complications among survivors of acute respiratory distress syndrome treated without extracorporeal membrane oxygenation are well described, the status of extracorporeal membrane oxygenation survivors is poorly understood What This Article Tells Us That Is New In a single-center cohort of acute respiratory distress syndrome survivors, management with ( vs . without) extracorporeal membrane oxygenation resulted in similar survival at 1 yr, pulmonary function, and computed tomography lung imaging, but less impairment in quality of life Background Survivors of acute respiratory distress syndrome (ARDS) have long-term impairment of pulmonary function and health-related quality of life, but little is known of outcomes of ARDS survivors treated with extracorporeal membrane oxygenation. The aim of this study was to compare long-term outcomes of ARDS patients treated with or without extracorporeal membrane oxygenation. Methods A prospective, observational study of adults with ARDS (January 2013 to December 2015) was conducted at a single center. One year after discharge, survivors underwent pulmonary function tests, computed tomography of the chest, and health-related quality-of-life questionnaires. Results Eighty-four patients (34 extracorporeal membrane oxygenation, 50 non–extracorporeal membrane oxygenation) were studied; both groups had similar characteristics at baseline, but comorbidity was more common in non–extracorporeal membrane oxygenation (23 of 50 vs . 4 of 34, 46% vs . 12%, P < 0.001), and severity of hypoxemia was greater in extracorporeal membrane oxygenation (median Pa o 2 / Fio 2 72 [interquartile range, 50 to 103] vs . 114 [87 to 133] mm Hg, P < 0.001) and respiratory compliance worse. At 1 yr, survival was similar (22/33 vs . 28/47, 66% vs. 59%; P = 0.52), and pulmonary function and computed tomography were almost normal in both groups. Non–extracorporeal membrane oxygenation patients had lower health-related quality-of-life scores and higher rates of posttraumatic stress disorder. Conclusions Despite more severe respiratory failure at admission, 1-yr survival of extracorporeal membrane oxygenation patients was not different from that of non–extracorporeal membrane oxygenation patients; each group had almost full recovery of lung function, but non–extracorporeal membrane oxygenation patients had greater impairment of health-related quality of life.

Editor’s Perspective What We Already Know about This Topic Hospital mortality in acute respiratory distress syndrome is approximately 40%, but mortality and trajectory in “mild” acute respiratory distress syndrome (classified only since 2012) are unknown, and many cases are not detected What This Article Tells Us That Is New Approximately 80% of cases of mild acute respiratory distress syndrome persist or worsen in the first week; in all cases, the mortality is substantial (30%) and is higher (37%) in those in whom the acute respiratory distress syndrome progresses Background Patients with initial mild acute respiratory distress syndrome are often underrecognized and mistakenly considered to have low disease severity and favorable outcomes. They represent a relatively poorly characterized population that was only classified as having acute respiratory distress syndrome in the most recent definition. Our primary objective was to describe the natural course and the factors associated with worsening and mortality in this population. Methods This study analyzed patients from the international prospective Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG SAFE) who had initial mild acute respiratory distress syndrome in the first day of inclusion. This study defined three groups based on the evolution of severity in the first week: “worsening” if moderate or severe acute respiratory distress syndrome criteria were met, “persisting” if mild acute respiratory distress syndrome criteria were the most severe category, and “improving” if patients did not fulfill acute respiratory distress syndrome criteria any more from day 2. Results Among 580 patients with initial mild acute respiratory distress syndrome, 18% (103 of 580) continuously improved, 36% (210 of 580) had persisting mild acute respiratory distress syndrome, and 46% (267 of 580) worsened in the first week after acute respiratory distress syndrome onset. Global in-hospital mortality was 30% (172 of 576; specifically 10% [10 of 101], 30% [63 of 210], and 37% [99 of 265] for patients with improving, persisting, and worsening acute respiratory distress syndrome, respectively), and the median (interquartile range) duration of mechanical ventilation was 7 (4, 14) days (specifically 3 [2, 5], 7 [4, 14], and 11 [6, 18] days for patients with improving, persisting, and worsening acute respiratory distress syndrome, respectively). Admissions for trauma or pneumonia, higher nonpulmonary sequential organ failure assessment score, lower partial pressure of alveolar oxygen/fraction of inspired oxygen, and higher peak inspiratory pressure were independently associated with worsening. Conclusions Most patients with initial mild acute respiratory distress syndrome continue to fulfill acute respiratory distress syndrome criteria in the first week, and nearly half worsen in severity. Their mortality is high, particularly in patients with worsening acute respiratory distress syndrome, emphasizing the need for close attention to this patient population.

Background The amount of extracorporeal carbon dioxide removal may influence respiratory drive in acute respiratory distress syndrome (ARDS) patients undergoing extracorporeal membrane oxygenation (ECMO). The authors evaluated the effects of different levels of extracorporeal carbon dioxide removal in patients recovering from severe ARDS undergoing pressure support ventilation (PSV) and neurally adjusted ventilatory assist (NAVA). Methods The authors conducted a prospective, randomized, crossover study on eight spontaneously breathing ARDS patients undergoing venovenous ECMO since 28 ± 20 days. To modulate carbon dioxide extraction, ECMO gas flow (GF) was decreased from baseline resting protective conditions ( i.e. , GF100%, set to obtain pressure generated in the first 100 ms of inspiration against an occluded airway less than 2 cm H 2 O, respiratory rate less than or equal to 25 bpm, tidal volume less than 6 ml/kg, and peak airway pressure less than 25 cm H 2 O) to GF50%-GF25%-GF0% during both PSV and NAVA (random order for ventilation mode). Continuous recordings of airway pressure and flow and esophageal pressure were obtained and analyzed during all study phases. Results At higher levels of extracorporeal carbon dioxide extraction, pressure generated in the first 100 ms of inspiration against an occluded airway decreased from 2.8 ± 2.7 cm H 2 O (PSV, GF0%) and 3.0 ± 2.1 cm H 2 O (NAVA, GF0%) to 0.9 ± 0.5 cm H 2 O (PSV, GF100%) and 1.0 ± 0.8 cm H 2 O (NAVA, GF100%; P < 0.001) and patients’ inspiratory muscle pressure passed from 8.5 ± 6.3 and 6.5 ± 5.5 cm H 2 O to 4.5 ± 3.1 and 4.2 ± 3.7 cm H 2 O ( P < 0.001). In time, decreased inspiratory drive and effort determined by higher carbon dioxide extraction led to reduction of tidal volume from 6.6 ± 0.9 and 7.5 ± 1.2 ml/kg to 4.9 ± 0.8 and 5.3 ± 1.3 ml/kg ( P < 0.001) and of peak airway pressure from 21 ± 3 and 25 ± 4 cm H 2 O to 21 ± 3 and 21 ± 5 cm H 2 O ( P < 0.001). Finally, transpulmonary pressure linearly decreased when the amount of carbon dioxide extracted by ECMO increased (R 2 = 0.823, P < 0.001). Conclusions In patients recovering from ARDS undergoing ECMO, the amount of carbon dioxide removed by the artificial lung may influence spontaneous breathing. The effects of carbon dioxide removal on spontaneous breathing during the earlier acute phases of ARDS remain to be elucidated. Abstract Patients recovering from severe acute respiratory distress syndrome on extracorporeal membrane oxygenation while receiving ventilator support developed lower tidal volume and transpulmonary pressure when extracorporeal carbon dioxide extraction was increased and Pa co 2 levels decreased. This suggests a mechanism for lessening lung injury in spontaneously breathing patients on extracorporeal membrane oxygenation.

Background The authors studied the effects on membrane lung carbon dioxide extraction (VCO 2 ML), spontaneous ventilation, and energy expenditure (EE) of an innovative extracorporeal carbon dioxide removal (ECCO 2 R) technique enhanced by acidification (acid load carbon dioxide removal [ALCO 2 R]) via lactic acid. Methods Six spontaneously breathing healthy ewes were connected to an extracorporeal circuit with blood flow 250 ml/min and gas flow 10 l/min. Sheep underwent two randomly ordered experimental sequences, each consisting of two 12-h alternating phases of ALCO 2 R and ECCO 2 R. During ALCO 2 R, lactic acid (1.5 mEq/min) was infused before the membrane lung. Caloric intake was not controlled, and animals were freely fed. VCO 2 ML, natural lung carbon dioxide extraction, total carbon dioxide production, and minute ventilation were recorded. Oxygen consumption and EE were calculated. Results ALCO 2 R enhanced VCO 2 ML by 48% relative to ECCO 2 R (55.3 ± 3.1 vs. 37.2 ± 3.2 ml/min; P less than 0.001). During ALCO 2 R, minute ventilation and natural lung carbon dioxide extraction were not affected (7.88 ± 2.00 vs. 7.51 ± 1.89 l/min, P = 0.146; 167.9 ± 41.6 vs. 159.6 ± 51.8 ml/min, P = 0.063), whereas total carbon dioxide production, oxygen consumption, and EE rose by 12% each (223.53 ± 42.68 vs. 196.64 ± 50.92 ml/min, 215.3 ± 96.9 vs. 189.1 ± 89.0 ml/min, 67.5 ± 24.0 vs. 60.3 ± 20.1 kcal/h; P less than 0.001). Conclusions ALCO 2 R was effective in enhancing VCO 2 ML. However, lactic acid caused a rise in EE that made ALCO 2 R no different from standard ECCO 2 R with respect to ventilation. The authors suggest coupling lactic acid–enhanced ALCO 2 R with active measures to control metabolism. Abstract In a study of six spontaneously breathing conscious sheep connected to a minimally invasive circuit, extracorporeal blood acidification with lactic acid (acid load carbon dioxide removal) increased extracorporeal carbon dioxide removal by 50% compared with standard extracorporeal carbon dioxide removal. Although lactic acid infusion increased overall energy expenditure, feasibility safety and efficiency of acid load carbon dioxide removal were proved. Supplemental Digital Content is available in the text.

Background: Auto-positive end-expiratory pressure (auto-PEEP) may substantially increase the inspiratory effort during assisted mechanical ventilation. Purpose of this study was to assess whether the electrical activity of the diaphragm (EAdi) signal can be reliably used to estimate auto-PEEP in patients undergoing pressure support ventilation and neurally adjusted ventilatory assist (NAVA) and whether NAVA was beneficial in comparison with pressure support ventilation in patients affected by auto-PEEP. Methods: In 10 patients with a clinical suspicion of auto-PEEP, the authors simultaneously recorded EAdi, airway, esophageal pressure, and flow during pressure support and NAVA, whereas external PEEP was increased from 2 to 14 cm H 2 O. Tracings were analyzed to measure apparent “dynamic” auto-PEEP (decrease in esophageal pressure to generate inspiratory flow), auto-EAdi (EAdi value at the onset of inspiratory flow), and ID EAdi (inspiratory delay between the onset of EAdi and the inspiratory flow). Results: The pressure necessary to overcome auto-PEEP, auto-EAdi, and ID EAdi was significantly lower in NAVA as compared with pressure support ventilation, decreased with increase in external PEEP, although the effect of external PEEP was less pronounced in NAVA. Both auto-EAdi and ID EAdi were tightly correlated with auto-PEEP ( r 2 = 0.94 and r 2 = 0.75, respectively). In the presence of auto-PEEP at lower external PEEP levels, NAVA was characterized by a characteristic shape of the airway pressure. Conclusions: In patients with auto-PEEP, NAVA, compared with pressure support ventilation, led to a decrease in the pressure necessary to overcome auto-PEEP, which could be reliably monitored by the electrical activity of the diaphragm before inspiratory flow onset (auto-EAdi).

Background: Extracorporeal carbon dioxide removal has been proposed to achieve protective ventilation in patients at risk for ventilator-induced lung injury. In an acute study, the authors previously described an extracorporeal carbon dioxide removal technique enhanced by regional extracorporeal blood acidification. The current study evaluates efficacy and feasibility of such technology applied for 48 h. Methods: Ten pigs were connected to a low-flow veno-venous extracorporeal circuit (blood flow rate, 0.25 l/min) including a membrane lung. Blood acidification was achieved in eight pigs by continuous infusion of 2.5 mEq/min of lactic acid at the membrane lung inlet. The acid infusion was interrupted for 1 h at the 24 and 48 h. Two control pigs did not receive acidification. At baseline and every 8 h thereafter, the authors measured blood lactate, gases, chemistry, and the amount of carbon dioxide removed by the membrane lung (VCO 2 ML). The authors also measured erythrocyte metabolites and selected cytokines. Histological and metalloproteinases analyses were performed on selected organs. Results: Blood acidification consistently increased VCO 2 ML by 62 to 78%, from 79 ± 13 to 128 ± 22 ml/min at baseline, from 60 ± 8 to 101 ± 16 ml/min at 24 h, and from 54 ± 6 to 96 ± 16 ml/min at 48 h. During regional acidification, arterial pH decreased slightly (average reduction, 0.04), whereas arterial lactate remained lower than 4 mEq/l. No sign of organ and erythrocyte damage was recorded. Conclusion: Infusion of lactic acid at the membrane lung inlet consistently increased VCO 2 ML providing a safe removal of carbon dioxide from only 250 ml/min extracorporeal blood flow in amounts equivalent to 50% production of an adult man.

Background: Mechanical ventilation is necessary during acute respiratory distress syndrome, but it promotes lung injury because of the excessive stretch applied to the aerated parenchyma. The authors’ hypothesis was that after a regional lung injury, the noxious effect of mechanical ventilation on the remaining aerated parenchyma would be more pronounced. Methods: Mice, instilled with hydrochloric acid (HCl) in the right lung, was assigned to one of the following groups: mechanical ventilation with tidal volumes (V T ) 25 ml/kg (HCl-VILI 25 , n = 12), or V T 15 ml/kg (HCl-VILI 15 , n = 9), or spontaneous breathing (HCl-SB, n = 14). Healthy mice were ventilated with V T 25 ml/kg (VILI 25 , n = 11). Arterial oxygenation, lung compliance, bronchoalveolar lavage inflammatory cells, albumin, and cytokines concentration were measured. Results: After 7 h, oxygenation and lung compliance resulted lower in HCl-VILI 25 than in VILI 25 ( P < 0.05, 210 ± 54 vs . 479 ± 83 mmHg, and 32 ± 3.5 vs . 45 ± 4.1 µl/cm H 2 O, mean ± SD, respectively). After right lung injury, the left lung of HCl-VILI 25 group received a greater fraction of the V T than the VILI 25 group, despite an identical global V T . The number of total and polymorphonuclear cells in bronchoalveolar lavage resulted significantly higher in HCl-VILI 25, compared with the other groups, in not only the right lung, but also in the left lung. The albumin content in the left lung resulted higher in HCl-VILI 25 than in VILI 25 (224 ± 85 vs . 33 ± 6 µg/ml; P < 0.05). Cytokines levels did not differ between groups. Conclusion: Aggressive mechanical ventilation aggravates the preexisting lung injury, which is noxious for the contralateral, not previously injured lung, possibly because of a regional redistribution of V T .

Background The aim of this study was to test the hypothesis that, during weaning from mechanical ventilation, when the pressure support level is reduced, oxygen consumption increases more in patients unable to sustain the decrease in ventilatory assistance (weaning failure). Methods Patients judged eligible for weaning were enrolled. Starting from 20 cm H2O, pressure support was decreased in 4-cm H2O steps, lasting 10 min each, until 0 cm H2O; this level was kept for 1 h. The average oxygen consumption from the last 3 min of each step, along with other ventilatory variables, was measured by indirect calorimetry (M-CAiOVX "metabolic module," Engstrom Carestation; GE Healthcare, Madison, WI) and recorded. Patients were defined as belonging to the failure group if, at any moment, they developed signs of respiratory distress according to standard criteria, or to the success group otherwise. Results Twenty-eight patients were studied. In most patients, the minimum oxygen consumption was not recorded at the highest pressure support applied. Sixteen patients were able to complete the weaning trial successfully, whereas 12 failed it; the success group had a minimum oxygen consumption lower than failure group (mean +/- SD: 174 +/- 44 vs. 215 +/- 53 ml/min, P < 0.05). Moreover, although respiratory drive (assessed by P0.1) increased more in the failure group, this group had a lower increase in oxygen consumption, contradicting our hypothesis. Conclusions Patients failing a decremental pressure support trial, in comparison with those who succeed, had an higher baseline oxygen consumption and were not able to increase their oxygen consumption in response to an increased demand.

Background Acid aspiration is a complication of general anesthesia. Most animal models developed to define its pathophysiology have focused on the acute (< or =24 h) phase of the injury. The authors describe a model of acid aspiration allowing the study of this type of lung injury over time. Methods The authors instilled hydrochloric acid (0.1 m, 1.5 ml/kg) or normal saline in the right bronchus of mice. Lung injury was evaluated at 6 h, 12 h, 24 h, and 2 weeks by assessing arterial blood gases, respiratory system compliance, lung wet weight normalized by body weight, lung myeloperoxidase activity, and histology. Twelve hours and 2 weeks after injury, a computed tomography scan was obtained. Results In the hydrochloric acid group, arterial oxygen tension decreased (P < 0.05) at 12 and 24 h, whereas it recovered at 2 weeks; respiratory system compliance was lower both at 24 h and 2 weeks (P < 0.05). Lung weight increased at 12 and 24 h (P < 0.05). Myeloperoxidase activity peaked between 6 and 12 h. Computed tomography at 12 h showed that almost 30% of the injured lung was abnormally aerated. Although reduced, the abnormalities were still present at 2 weeks as confirmed by a fibrotic scar well evident at histologic examination. Conclusion The authors characterized a murine model of regional acid aspiration allowing long-term survival. Despite a partial recovery, at 2 weeks the injury persisted, with evidence of fibrosis and lung compliance reduction. This long-term, low-mortality model seems suitable for assessment of the effects of different therapies on lung injury and repair.

Background Measuring the work of breathing of patients undergoing spontaneous assisted ventilation can be useful to monitor and titrate ventilatory support. The aim of this study was to obtain measurements of the pressure generated by the respiratory muscles (PMUSC) and the derived pressure-time product (PTP; a good indicator of the metabolic work of breathing), performing the rapid interrupter technique with a commercial ventilator. Methods A Draeger Evita 4 ventilator (Draeger Medical, Lubeck, Germany) was controlled by a personal computer to rapidly interrupt the airway flow at different times and volumes of the respiratory cycle during pressure-support ventilation. From the airway pressure tracing after the occlusion, the authors estimated the alveolar pressure and PMUSC; the integration of PMUSC values over the inspiratory time yields the measurement of PTP. Esophageal pressure measurements were used as a reference. After a bench study of the valves' performance, the authors performed 11 measurement sequences in eight patients. Results The closure times for the inspiratory and expiratory valves were 74 +/- 10 and 61 +/- 13 ms, respectively. The interrupter technique provided a reliable estimate of PMUSC (PMUSC, occl = 1.00 . PMUSC, pes + 0.19; r = 0.88; 95% confidence interval for agreement, +5.49/-5.32 cm H2O). PTPoccl tightly correlated with PTPpes (PTPoccl = 0.95 . PTPpes + 0.13; r = 0.96; 95% confidence interval, 1.94/-1.61 cm H2O . s). Conclusion The rapid interrupter technique can be performed by means of a commercial ventilator, providing reliable measurement of PMUSC and PTP.

Background The aim of our study was to assess the effect of periodic hyperinflations (sighs) during pressure support ventilation (PSV) on lung volume, gas exchange, and respiratory pattern in patients with early acute respiratory distress syndrome (ARDS). Methods Thirteen patients undergoing PSV were enrolled. The study comprised 3 steps: baseline 1, sigh, and baseline 2, of 1 h each. During baseline 1 and baseline 2, patients underwent PSV. Sighs were administered once per minute by adding to baseline PSV a 3- to 5-s continuous positive airway pressure (CPAP) period, set at a level 20% higher than the peak airway pressure of the PSV breaths or at least 35 cm H2O. Mean airway pressure was kept constant by reducing the positive end-expiratory pressure (PEEP) during the sigh period as required. At the end of each study period, arterial blood gas tensions, air flow and pressures traces, end-expiratory lung volume (EELV), compliance of respiratory system (Crs), and ventilatory parameters were recorded. Results Pao2 improved (P < 0.001) from baseline 1 (91.4 +/- 27.4 mmHg) to sigh (133 +/- 42.5 mmHg), without changes of Paco2. EELV increased (P < 0.01) from baseline 1 (1,242 +/- 507 ml) to sigh (1,377 +/- 484 ml). Crs improved (P < 0.01) from baseline 1 (40.2 +/- 12.5 ml/cm H2O) to sigh (45.1 +/- 15.3 ml/cm H2O). Tidal volume of pressure-supported breaths and the airway occlusion pressure (P0.1) decreased (P < 0.01) during the sigh period. There were no significant differences between baselines 1 and 2 for all parameters. Conclusions The addition of 1 sigh per minute during PSV in patients with early ARDS improved gas exchange and lung volume and decreased the respiratory drive.