Initial ventilator settings for critically ill patients

Purpose of ReviewTo summarize pathophysiology, key conflicts, and therapeutic approaches in managing concomitant severe acute brain injury (SABI) and acute respiratory distress syndrome (ARDS).Recent FindingsARDS is common in SABI and independently associated with worse outcomes in all SABI subtypes. Most landmark ARDS trials excluded patients with SABI, and evidence to guide decisions is limited in this population. Potential areas of conflict in the management of patients with both SABI and ARDS are (1) risk of intracranial pressure (ICP) elevation with high levels of positive end-expiratory pressure (PEEP), permissive hypercapnia due to lung protective ventilation (LPV), or prone ventilation; (2) balancing a conservative fluid management strategy with ensuring adequate cerebral perfusion, particularly in patients with symptomatic vasospasm or impaired cerebrovascular blood flow; and (3) uncertainty about the benefit and harm of corticosteroids in this population, with a mortality benefit in ARDS, increased mortality shown in TBI, and conflicting data in other SABI subtypes. Also, the widely adapted partial pressure of oxygen (PaO2) target of > 55 mmHg for ARDS may exacerbate secondary brain injury, and recent guidelines recommend higher goals of 80–120 mmHg in SABI. Distinct pathophysiology and trajectories among different SABI subtypes need to be considered.SummaryThe management of SABI with ARDS is highly complex, and conventional ARDS management strategies may result in increased ICP and decreased cerebral perfusion. A crucial aspect of concurrent management is to recognize the risk of secondary brain injury in the individual patient, monitor with vigilance, and adjust management during critical time windows. The care of these patients requires meticulous attention to oxygenation and ventilation, hemodynamics, temperature management, and the neurological exam. LPV and prone ventilation should be utilized, and supplemented with invasive ICP monitoring if there is concern for cerebral edema and increased ICP. PEEP titration should be deliberate, involving measures of hemodynamic, pulmonary, and brain physiology. Serial volume status assessments should be performed in SABI and ARDS, and fluid management should be individualized based on measures of brain perfusion, the neurological exam, and cardiopulmonary status. More research is needed to define risks and benefits in corticosteroids in this population.

To the Editor Management of patient sedation and analgesia to alleviate anxiety and pain and facilitate mechanical ventilation is one of the key roles of every intensivist. During the coronavirus disease 2019 (COVID-19) pandemic, unprecedented numbers of patients require sedation in intensive care units (ICUs) and other hospital locations due to their ventilator dependence. However, pharmacologic sedation in mechanically ventilated patients with COVID-19 has thus far received very little attention in the critical care literature, with minimal mention in the Society of Critical Care Medicine's COVID-19 guidelines or clinical reviews.1,2 We propose that sedation of mechanically ventilated patients with COVID-19 poses unique challenges and has multiple important implications that we would like to briefly outline: Unusually high sedation requirements in a large proportion of COVID-19 patients are observed in current clinical experience. These high sedation requirements are likely related to younger age and good health of many patients before the onset of COVID-19, high respiratory drive, and intense inflammatory responses previously linked to tolerance.3 This translates into the need to administer combinations of multiple agents (eg, propofol, ketamine, hydromorphone, dexmedetomidine, and midazolam), increasing potential risks of side effects (eg, QT interval prolongation, hypertriglyceridemia, hypotension, and delirium) and requiring vigilance of the ICU staff. When these are administered in combinations, the typical requirements to ensure patient comfort and ventilator synchrony in adult patients range between 25 and 50 µg/kg/min for propofol, 10 and 20 µg/kg/min for ketamine, 2 and 4 mg/h for hydromorphone, and 2 and 5 mg/h for midazolam. There are currently no sedation guidelines specific for this patient population requiring high doses and prolonged drug administrations. Deeper sedation levels may be required to facilitate ventilator synchrony in patients with severe acute respiratory distress syndrome (ARDS) and may also be favored by ICU staff to reduce risk of patient self-extubation, which is particularly problematic in this population given the need for emergent reintubation and risk of exposure to coronavirus. Subsequent tolerance to sedatives (eg, dexmedetomidine) from their use early in the course of illness and high doses will also limit the effectiveness of these drugs during ventilator weaning. Intermittent administration of certain drugs (eg, narcotics) tailored to individual needs of each patient may not always be feasible in situations of overwhelmed health care systems (eg, when one nurse is required to attend to multiple critically ill patients). In these situations, continuous infusions of sedative drugs are favored for their practicality, but this practice further increases the risks of side effects. A subset of patients with severe ARDS is likely to require prolonged sedation (often >2 weeks)4 to facilitate lung-protective mechanical ventilation or extracorporeal membrane oxygenation (ECMO) therapy and subsequent weaning. These prolonged periods of time may lead to drug accumulation (midazolam), tolerance and tachyphylaxis (dexmedetomidine), hypertriglyceridemia (propofol), QT interval prolongation (haloperidol), psychomimetic effects (ketamine), hyperalgesia or opioid dependence (fentanyl and/or hydromorphone), and delirium (midazolam). Increased precision in monitoring the depth of sedation (eg, processed electroencephalogram [EEG]) is required in patients with high sedation requirements who also require neuromuscular blockade to improve respiratory system compliance. While these neuromonitoring technologies exist,5 they may not be widely available given the number of patients who would benefit. Patient awareness under these conditions (eg, paralysis or prone position) may result in significant psychological trauma. Prolonged infusions of opioids that are often required to facilitate strict lung-protective ventilation are known to result in gut hypomotility, leading to intolerance to feeding, interruptions in feeding, and malnutrition during prolonged ICU stay. These gastrointestinal side effects of opioids may also result in abdominal distension, which can impair ventilation and/or contribute to nausea/vomiting, increasing the risk of aspiration. High doses of opioids, sometimes required to facilitate lung-protective ventilation in patients with ventilator dyssynchrony, may paradoxically complicate ventilation management by inducing breathing patterns with large tidal volumes that may further injure lungs. Prolonged infusions of high doses of sedatives and analgesics in large numbers of patients have already resulted in drug shortages at hospital, regional, and state levels. In these situations, providing sedation with less commonly used agents (barbiturates, methadone, clonidine, chlorpromazine, and propranolol) may need to be considered. The use of inhalational anesthetics (eg, isoflurane), at least in locations with appropriately designed scavenging systems, such as operating rooms converted to ICUs, may be a rational alternative that is supported by their documented safety6 and potential anti-inflammatory and lung-protective effects. Attention must be paid to the potential interaction between sedative drugs and other agents administered as part of clinical trials (there are >300 clinical COVID-19 trials currently ongoing worldwide). For instance, significant QT prolongations may result from combinations of hydroxychloroquine and haloperidol. Administration of barbiturates may increase metabolism of hydroxychloroquine. In patients with high fevers, dexmedetomidine may need to be discontinued to help delineate the cause of the fever. In summary, management of sedation in ICU patients with COVID-19 needs to reflect individual properties and side effect profiles of agents, unique patient characteristics (prolonged intubation and virus shedding), and health care system limitations (large numbers of patients, ICU patients in emergency rooms and operating rooms, and drug shortages). Potential for interactions with investigational drugs used in clinical trials (some blinded to ICU staff) needs to be considered. The collective clinical experience from the United States and from other highly affected areas around the world should be quickly leveraged to formulate recommendations and guidelines to increase patient safety and provider awareness of these unique challenges. Dusan Hanidziar, MD, PhDEdward A. Bittner, MD, PhDDepartment of Anesthesia, Critical Care and Pain MedicineMassachusetts General HospitalBoston, Massachusetts[email protected]

COVID-19 acute respiratory distress syndrome: intriguing haemodynamics of an intriguing syndrome.

Division of Surgical Intensive Care, Department of Anesthesiology, Pharmacology, and Surgical Intensive Care (APSIC), University Hospital of Geneva, Geneva, Switzerland. peter.suter@hcuge.chACUTE lung injury (ALI) and adult respiratory distress syndrome (ARDS) are characterized by the tendency of peripheral air spaces to collapse, particularly in dependent lung areas. The application of a positive end-expiratory pressure (PEEP) and an appropriate tidal volume (VT) is thought to prevent and reverse the collapse of airways and respiratory units in such patients. Other means to recruit alveoli include frequent position changes, e.g . from supine to prone. The introduction of specific inflation maneuvers, using either an intermittent high-tidal volume, or an elevated inspiratory (plateau) pressure, allows significant increases in end-inspiratory and end-expiratory lung volume, and an associated improvement in gas exchange. Clinical results obtained with such recruitment strategies are reported in the current issue of Anesthesiology by two groups of well-known clinical investigators. 1,2Both articles describe the effects of lung inflation in patients with ARDS, studied in the early or late phases of their disease. The advent of ventilatory techniques using lower VTto decrease ventilator-induced lung injury and improve outcome in ALI and ARDS 3,4has renewed interest in the requirement for, and the potential benefit of, periodic inflation maneuvers. It has indeed been shown that VTparticipates to a significant extent in the opening of collapsed or hypoventilated areas in such patients. 5Therefore, it is not surprising that with the new low VTapproach, an old intermittent inflation method, called sigh, 6would regain some credibility in ventilatory management. In the first of the two studies discussed here, Salvatore Grasso et al . reports the effects of a continuous 40-cm H2O inflation pressure applied for 3–5 s in 22 patients undergoing controlled mechanical ventilation (MV) with a VTof 6 ml/kg and a mean PEEP of 9 cm H2O. Pulmonary gas exchange, respiratory mechanics, and hemodynamics were assessed. The investigation was done at two different times during the evolution of ARDS, i.e. in early (1 to 2 days after beginning MV) or later phases (5–10 days after onset of MV). The results are clearcut: only in the early phase of the disease was a marked positive response in the Pao2/ Fio2ratio observed. Patients in the later phases of ARDS had smaller increases in oxygenation, which were associated with a significant decrease in cardiac output during the inflation maneuver. This difference may simply be related to respiratory mechanics; in the early phase of ARDS, the elastance of the lung and chest wall were lower, which means higher compliance values, and hence, larger increases in volume for a given change in distending pressure.In the second study, 2Nicolo Patroniti et al. describes thirteen ARDS patients intubated and breathing spontaneously, assisted by an inspiratory pressure support of 12 cm H2O and a PEEP of 11 cm H2O, resulting in a VTof 420 ml. A majority of these patients can be considered to be in an early phase of the disease. The recruitment maneuver applied was similar to that used by Patroniti et al. ; airway pressure was increased to a mean of 38 cm H2O for 3.6 s, resulting in a VTof 1,150 ml. This sigh produced marked improvements in gas exchange and expiratory lung volume and a decrease in respiratory drive. What can we learn from these two elegant investigations? First, the findings confirm that sustained inflation using a pressure of 30 to 45 cm H2O results in a marked improvement in arterial oxygenation and has no significant side effects. 7Second, the reader will not be surprised to see that in early ARDS, functional respiratory units can be inflated and recruited more easily than in later phases of the disease, and that the gain in arterial oxygenation is more impressive. Similar results have been shown for prone positioning where improvement in gas exchange is greater in patients with pulmonary edema or with early ARDS, as compared with late ARDS or pulmonary fibrosis. 8Third, it should not be forgotten that alveolar recruitment and pulmonary gas exchange depend largely on the level of PEEP applied during protective ventilatory strategies. 9In conclusion, the two articles on recruitment maneuvers published in this issue add important information for the clinician; however, a number of questions remain. For instance, further studies should explore which single or combined therapy, including higher PEEP levels, regular position changes, and intermittent inflation strategies achieves the greatest sustained improvement in lung function. In addition, the effects on outcome in ARDS patients, including end-points such as duration of mechanical ventilation, duration of stay in the intensive care unit, and hospital mortality, must be assessed. It seems likely that understanding the role of factors such as the underlying morphologic features of lung injury, the stage of ARDS, hemodynamic status, and tolerance to increased intrapulmonary pressure will be essential to determining optimal treatment strategies for individual patients.

IntroductionWe compared the effects of mechanical ventilation with a lower tidal volume (VT) strategy versus those of greater VT in patients with or without acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) on the use of opioids and sedatives.MethodsThis is a secondary analysis of a previously conducted before/after intervention study, which consisting of feedback and education on lung protective mechanical ventilation using lower VT. We evaluated the effects of this intervention on medication prescriptions from days 0 to 28 after admission to our multidisciplinary intensive care unit.ResultsMedication prescriptions in 23 patients before and 38 patients after intervention were studied. Of these patients, 10 (44%) and 15 (40%) suffered from ALI/ARDS. The VT of ALI/ARDS patients declined from 9.7 ml/kg predicted body weight (PBW) before to 7.8 ml/kg PBW after the intervention (P = 0.007). For patients who did not have ALI/ARDS there was a trend toward a decline from 10.2 ml/kg PBW to 8.6 ml/kg PBW (P = 0.073). Arterial carbon dioxide tension was significantly greater after the intervention in ALI/ARDS patients. Neither the proportion of patients receiving opioids or sedatives, or prescriptions at individual time points differed between pre-intervention and post-intervention. Also, there were no statistically significant differences in doses of sedatives and opioids. Findings were no different between non-ALI/ARDS patients and ALI/ARDS patients.ConclusionConcerns regarding sedation requirements with use of lower VT are unfounded and should not preclude its use in patients with ALI/ARDS.

BackgroundPreventing ventilator-associated lung injury (VALI) has become pivotal in mechanical ventilation of patients with acute lung injury (ALI) or its more severe form, acute respiratory distress syndrome (ARDS). In the present study we investigated whether plasma levels of lung-specific biological markers can be used to evaluate lung injury in patients with ALI/ARDS and patients without lung injury at onset of mechanical ventilation.MethodsPlasma levels of surfactant protein D (SP-D), Clara Cell protein (CC16), KL-6 and soluble receptor for advanced glycation end-products (sRAGE) were measured in plasma samples obtained from 36 patients - 16 patients who were intubated and mechanically ventilated because of ALI/ARDS and 20 patients without lung injury at the onset of mechanical ventilation and during conduct of the study. Patients were ventilated with either a lung-protective strategy using lower tidal volumes or a potentially injurious strategy using conventional tidal volumes. Levels of biological markers were measured retrospectively at baseline and after 2 days of mechanical ventilation.ResultsPlasma levels of CC16 and KL-6 were higher in ALI/ARDS patients at baseline as compared to patients without lung injury. SP-D and sRAGE levels were not significantly different between these patients. In ALI/ARDS patients, SP-D and KL-6 levels increased over time, which was attenuated by lung-protective mechanical ventilation using lower tidal volumes (P = 0.02 for both biological markers). In these patients, with either ventilation strategy no changes over time were observed for plasma levels of CC16 and sRAGE. In patients without lung injury, no changes of plasma levels of any of the measured biological markers were observed.ConclusionPlasma levels of SP-D and KL-6 rise with potentially injurious ventilator settings, and thus may serve as biological markers of VALI in patients with ALI/ARDS.

ObjectivesThis study aims to demonstrate the positive effects on oxygenation of flow-controlled ventilation compared to conventionally ventilated patients in patients suffering from Acute respiratory distress syndrome (ARDS) associated with COVID-19.We define ARDS according to the “Berlin” definition integrating the oxygenation index (P/F ratio), the level of Positive End Expiratory Pressure (PEEP), radiological and clinical findings.Trial designThis is a prospective, randomized (1:1 ratio), parallel group feasibility study in adult patients with proven COVID-19 associated ARDS.ParticipantsAll adult patients admitted to the ICU of Hamad Medical Corporation facilities in Qatar because of COVID-19 infection who develop moderate to severe ARDS are eligible. The inclusion criteria are above 18 years of age, proven COVID-19 infection, respiratory failure necessitating intubation and mechanical ventilation, ARDS with a P/F ratio of at least 200mmHg or less and a minimum PEEP 5cmH2O, BMI less 30 kg/ m2. The following exclusion criteria: no written consent, chronic respiratory disease, acute or chronic cardiovascular disease, pregnancy or need for special therapy (prone position and/or Extracorporeal membrane oxygenation).Intervention and comparatorAfter randomisation, the group A patients will be ventilated with the test-device for 48 hours. The settings will be started with the pre-existing-PEEP. The upper pressure will be determined to achieve a tidal volume of 6 ml/kg lean body mass, while the respiratory rate will be set to maintain an arterial pH above 7.2.In group B, the ventilator settings will be adjusted by the attending ICU team in accordance with lung-protective ventilation strategy.All other treatment will be unchanged and according to our local policies/guidelines.Main outcomesThe primary end point is PaO2. As this is a dynamic parameter, we will record it every 6-8 hours and analyse it sequentially.RandomisationThe study team screens the ventilated patients who fulfil the inclusion criteria and randomise using a 1:1 allocation ratio after consenting using a closed envelope method. The latter were prepared and sealed in advance by an independent person.Blinding (masking)Due to the technical nature of the study (use of a specific ventilator) blinding is only possible for the data-analysts and the patients.Numbers to be randomised (sample size)The sample size calculation based on the assumption of an effect size (change in PaO2) of 1.5 SDS in the primary endpoint (PaO2), an intended power of 80%, an alpha error of 5% and an equal sample ratio results in n=7 patients needed to treat. However, to compensate for dropouts we will include 10 patients in each group, which means in total 20 patients.Trial StatusThe local registration number is MRC-05-018 with the protocol version number 3. The date of approval is 14th April 2020. Recruitment began 28th May 2020 and is expected to end in September 2020.Trial registrationThe protocol was registered before starting subject recruitment under the title: “Flow controlled ventilation in ARDS associated with COVID-19” in ClinicalTrials.org with the registration number: NCT04399317. Registered on 22 May 2020.Full protocolThe full protocol is attached as an additional file, accessible from the Trials website (Additional file 1). In the interest in expediting dissemination of this material, the familiar formatting has been eliminated; this Letter serves as a summary of the key elements of the full protocol.

Rebuttal From Dr Hall

Clinicians' current practice patterns in the management of acute respiratory distress syndrome (ARDS) and refractory hypoxemia are not well described. To describe mechanical ventilation strategies and treatment adjuncts for adults with ARDS, including refractory hypoxemia. This was a prospective cohort study (March 2014-February 2015) of mechanically ventilated adults with moderate-to-severe ARDS requiring an FiO2 of 0.50 or greater in 24 intensive care units. We enrolled 664 patients: 222 (33%) with moderate and 442 (67%) with severe ARDS. On Study Day 1, mean Vt was 7.5 (SD = 2.1) ml/kg predicted body weight (n = 625); 80% (n = 501) received Vt greater than 6 ml/kg. Mean positive end-expiratory pressure (PEEP) was 10.5 (3.7) cm H2O (n = 653); 568 patients (87%) received PEEP less than 15 cm H2O. Treatment adjuncts were common (n = 440, 66%): neuromuscular blockers (n = 276, 42%), pulmonary vasodilators (n = 118, 18%), prone positioning (n = 67, 10%), extracorporeal life support (n = 29, 4%), and high-frequency oscillatory ventilation (n = 29, 4%). Refractory hypoxemia, defined as PaO2 less than 60 mm Hg on FiO2 of 1.0, occurred in 138 (21%) patients. At onset of refractory hypoxemia, mean Vt was 7.1 (SD = 2.0) ml/kg (n = 124); 95 patients (77%) received Vt greater than 6 ml/kg. Mean PEEP was 12.1 (SD = 4.4) cm H2O (n = 133); 99 patients (74%) received PEEP less than 15 cm H2O. Among patients with refractory hypoxemia, 91% received treatment adjuncts (126/138), with increased use of neuromuscular blockers (n = 87, 63%), pulmonary vasodilators (n = 57, 41%), and prone positioning (n = 32, 23%). Patients with moderate-to-severe ARDS receive treatment adjuncts frequently, especially with refractory hypoxemia. Paradoxically, therapies with less evidence supporting their use (e.g., pulmonary vasodilators) were over-used, whereas those with more evidence (e.g., prone positioning, neuromuscular blockade) were under-used. Patients received higher Vts and lower PEEP than would be suggested by the evidence.

BackgroundPostoperative delirium (POD) is a frequent complication in elderly patients, usually occurring within a few days after surgery. This study investigated the effect of lung-protective ventilation (LPV) on POD in elderly patients undergoing spinal surgery and the mechanism by which LPV suppresses POD.Material/MethodsSeventy-one patients aged ≥65 years were randomized to receive LPV or conventional mechanical ventilation (MV), consisting of intermittent positive pressure ventilation following induction of anesthesia. The tidal volume in patients who received MV was 8 ml/kg predicted body weight (PBW), and the ventilation frequency was 12 times/min. The tidal volume in patients who received LPV was 6 ml/kg PBW, the positive end-expiratory pressure was 5 cmH2O, and the ventilation frequency was 15 times/min, with a lung recruitment maneuver performed every 30 min. Blood samples were collected immediately before anesthesia induction (T0), 10 min (T1) and 60 min (T2) after turning over, immediately after the operation (T3), and 15 min after extubation (T4) for blood gas analysis. Simultaneous cerebral oxygen saturation (rSO2) and cerebral desaturation were recorded. Preoperative and postoperative serum concentrations of interleukin (IL)-6, IL-10 and glial fibrillary acidic protein (GFAP) were measured by ELISA. POD was assessed by nursing delirium screening score.ResultsCompared with the MV group, pH was lower and PaCO2 higher in the LPV group at T2. In addition PaO2, SaO2, and PaO2/FiO2 were higher at T1, and T4, and rSO2 was higher at T3, and T4 in the LPV than in the MV group (P<0.05 each). Postoperative serum GFAP and IL-6 were lower and IL-10 higher in the LPV group. The incidences of cerebral desaturation and POD were significantly lower in the LPV group (P<0.05).ConclusionsLPV may reduce POD in elderly patients undergoing spinal surgery by inhibiting inflammation and improving cerebral oxygen metabolism.

Peripartum use of Extracorporeal Membrane Oxygenation (ECMO) in a Patient Suffering from COVID-19 Severe Acute Respiratory Distress Syndrome (ARDS): A Case Report

Background: Lung-protective ventilation (LPV) strategies have been beneficial in patients with acute respiratory distress syndrome (ARDS). As a vital part of LPV, positive end-expiratory pressure (PEEP) can enhance oxygenation. However, randomized clinical trials of different PEEP strategies seem to show no advantages in clinical outcomes in patients with ARDS. A potential reason is that diverse etiologies and phenotypes in patients with ARDS may account for different PEEP responses, resulting in variations in mortality. We consider hospital mortality to be associated with a more specific classification of ARDS, such as sepsis induced or not, and pulmonary or extrapulmonary one. Our study aimed to compare clinical outcomes in various patients with ARDS by etiologies using the China Critical Care Sepsis Trial (CCCST) database. This was a retrospective analysis of a prospective cohort of 2,138 patients with ARDS in the CCCST database. According to ARDS induced by sepsis or not and medical history, patients were stratified into different four groups. Differences among groups were assessed in hospital mortality, ventilation-free days, and other clinical features.Results: A total of 2,138 patients with ARDS were identified in the database, including 647 patients with sepsis-induced pulmonary ARDS (30.3%), 396 patients with sepsis-induced extrapulmonary ARDS (18.5%), 536 patients with non-sepsis pulmonary ARDS (25.1%), and 559 patients with non-sepsis extrapulmonary ARDS (26.1%). The pulmonary ARDS group had higher mortality compared with the extrapulmonary group (45.9 vs. 23.0%, p < 0.01), longer intensive care unit (ICU) and hospital stays (9 vs. 6 days, p < 0.01, 20 vs. 18 days, p = 0.01, respectively), and fewer ventilation-free days (5 vs. 9 days) in the presence of sepsis. However, the mortality in ARDS without sepsis was inverted compared with extrapulmonary ARDS (pulmonary 23.5% vs. extrapulmonary 29.2%, p = 0.04). After adjusting for the Acute Physiology and Chronic Health Evaluation II and sequential organ failure assessment scores and other clinical features, the sepsis-induced pulmonary condition was still a risk factor for death in patients with ARDS (hazard ratio 0.66, 95% CI, 0.54–0.82, p < 0.01) compared with sepsis-induced extrapulmonary ARDS and other subphenotypes.Conclusions: In the presence of sepsis, hospital mortality in pulmonary ARDS is higher compared with extrapulmonary ARDS; however, mortality is inverted in ARDS without sepsis. Sepsis-induced pulmonary ARDS should attract more attention from ICU physicians and be cautiously treated.Trial registration: ChiCTR-ECH-13003934. Registered August 3, 2013, http://www.chictr.org.cn.

Despite the breadth of life-sustaining interventions available, mortality in patients with acute respiratory distress syndrome (ARDS) remains high. A greater appreciation of the potential iatrogenic injury associated with the use of mechanical ventilation has led clinicians and researchers to seek alternatives. Extracorporeal life support (ECLS) may be used to rescue patients with severely impaired gas exchange and provide time for injured lungs to recover while treating the underlying disease. In patients with ARDS, venovenous (VV) ECLS is commonly used, where venous blood is drained into a circuit that passes through a membrane lung, which provides gas exchange, and then returned to the venous system. VV-ECLS can be configured as a system that uses higher blood flows with extracorporeal membrane oxygenation (VV-ECMO) or as one that uses lower blood flows for extracorporeal carbon dioxide removal (VV-ECCO2R). Recent studies support the use of VV-ECMO in patients with severe ARDS who present with refractory gas exchange despite the use of lung-protective mechanical ventilation, positive end-expiratory pressure optimization, neuromuscular blockade, and prone positioning. The optimal management of patients during ECLS (i.e., anticoagulation, transfusions, mechanical ventilation) and the role of ECCO2R in the management of ARDS remain to be determined.

High versus low PEEP in non-recruitable collapsed lung tissue: possible implications for patients with COVID-19

Lung protective ventilation (LPV) characterized by small tidal volume ventilation can improve the prognosis of acute respiratory distress syndrome (ARDS) through a variety of mechanisms, which makes LPV gradually become the basic concept of mechanical ventilation.In some patients, PaCO2 is significantly elevated after receiving LPV, which is permissive hypercapnia.Initially permissive hypercapnia was considered to be benign or even lung protective, but in recent years it has become increasingly recognized that PaCO2 elevated has significant physiological effects and may be detrimental.This article reviews the physiological and clinical effects of permissive hypercapnia in ARDS ventilation. Key words: Respiratory distress syndrome, adult; Permissive hypercapnia; Mechanical ventilation