Patient self-inflicted lung injury associated pneumothorax/pneumomediastinum is a risk factor for worse outcomes of severe COVID-19: a case-control study.

We aimed to determine the clinical characteristics of patient self-inflicted lung injury (P-SILI)-associated pneumothorax/pneumomediastinum, to reveal its risk factors, and to assess its impact on severe COVID-19 cases. In total, 229 patients were included in this case-control study. They were randomly divided into either the case group or the control group as per the inclusion and exclusion criteria. The two groups were further analyzed to reveal the risk factors of spontaneous pneumothorax/pneumomediastinum (SP/P). Finally, risk factors for death were analyzed in the case group and the relationship between death and SP/P was also analyzed among all patients. The mean age of patients was 59.69 ± 17.01 years, most of them were male (74.2%), and 62.0% of them had comorbidities upon admission. A respiratory rate higher than 30 BPM was a risk factor for SP/P (OR 7.186, 95% CI 2.414-21.391, P < 0.001). Patients with delayed intubation due to early application of HFNC or NIV had a higher mortality rate when they developed SP/P (P < 0.05). Additionally, advanced age increased the risk of death (P < 0.05). Finally, SP/P may be a risk factor for death among patients with severe COVID-19 (OR 2.047). P-SILI occurs in severe COVID-19 with acute respiratory failure. It is necessary to identify the risk factors of P-SILI, the indicators of severe P-SILI, and the preventive measures.

State of the art: Monitoring of the respiratory system during veno-venous extracorporeal membrane oxygenation.

Monitoring the patient receiving veno-venous extracorporeal membrane oxygenation (VV ECMO) is challenging due to the complex physiological interplay between native and membrane lung. Understanding these interactions is essential to understand the utility and limitations of different approaches to respiratory monitoring during ECMO. We present a summary of the underlying physiology of native and membrane lung gas exchange and describe different tools for titrating and monitoring gas exchange during ECMO. However, the most important role of VV ECMO in severe respiratory failure is as a means of avoiding further ergotrauma. Although optimal respiratory management during ECMO has not been defined, over the last decade there have been advances in multimodal respiratory assessment which have the potential to guide care. We describe a combination of imaging, ventilator-derived or invasive lung mechanic assessments as a means to individualise management during ECMO.

Effect of high flow nasal oxygen on inspiratory effort of patients with acute hypoxic respiratory failure and do not intubate orders.

High flow nasal oxygen (HFNO) is recommended as a first-line respiratory support during acute hypoxic respiratory failure (AHRF) and represents a proportionate treatment option for patients with do not intubate (DNI) orders. The aim of the study is to assess the effect of HFNO on inspiratory effort as assessed by esophageal manometry in a population of DNI patients suffering from AHRF. Patients with AHRF and DNI orders admitted to Respiratory intermediate Care Unit between January 1st, 2018 and May 31st, 2023 to receive HFNO and subjected to esophageal manometry were enrolled. Esophageal pressure swing (ΔPes), clinical variables before and after 2 h of HFNO and clinical outcome (including HFNO failure) were collected and compared as appropriate. The change in physiological and clinical parameters according to the intensity of baseline breathing effort was assessed and the correlation between baseline ΔPes values and the relative change in breathing effort and clinical variables after 2 h of HFNO was explored. Eighty-two consecutive patients were enrolled according to sample size calculation. Two hours after HFNO start, patients presented significant improvement in ΔPes (12 VS 16 cmH2O, p < 0.0001), respiratory rate (RR) (22 VS 28 bpm, p < 0.0001), PaO2/FiO2 (133 VS 126 mmHg, p < 0.0001), Heart rate, Acidosis, Consciousness, Oxygenation and respiratory rate (HACOR) score, (4 VS 6, p < 0.0001), Respiratory rate Oxygenation (ROX) index (8.5 VS 6.1, p < 0.0001) and BORG (1 VS 4, p < 000.1). Patients with baseline ΔPes below 20 cmH2O where those who improved all the explored variables, while patients with baseline ΔPes above 30 cmH2O did not report significant changes in physiological or clinical features. A significant correlation was found between baseline ΔPes values and after 2 h of HFNO (R2 = 0.9, p < 0.0001). ΔPes change 2 h after HFNO significantly correlated with change in BORG (p < 0.0001), ROX index (p < 0.0001), HACOR score (p < 0.001) and RR (p < 0.001). In DNI patients with AHRF, HFNO was effective in reducing breathing effort and improving respiratory and clinical variables only for those patients with not excessive inspiratory effort.

Influence of different noninvasive oxygenation support devices on tidal volume.

BACKGROUND: Multiple devices are available for noninvasive oxygenation support, including non-rebreather oxygen mask (O2-mask), high-flow oxygen through nasal cannula (HFNC), continuous positive airway pressure (CPAP), mask noninvasive ventilation (Mask-NIV) and helmet NIV (Helmet-NIV). As tidal volume is a key determinant of efficacy and safety during ventilatory support, we assessed whether it was influenced by the type of noninvasive oxygenation device. METHODS: A bench study using a manikin with a realistic face connected to a lung simulator was performed. Six conditions were assessed: no device, O2-mask, HFNC, CPAP, Mask-NIV and Helmet-NIV. Three respiratory mechanics were simulated (normal, obstructive, restrictive), at three simulated efforts (low, moderate, respiratory distress). Flow was recorded at the lung simulator inlet and mouth pressure into the manikin mouth. The same devices were evaluated on healthy volunteers with tidal volume assessed by electrical impedance tomography (EIT). RESULTS: Tidal volume was significantly influenced by oxygenation devices in bench model. As compared to O2-mask, HFNC and CPAP delivered significantly lower tidal volumes (440 ± 352 mL, 414 ± 333 mL and 377 ± 297 mL, respectively), while Mask-NIV or Helmet-NIV were associated with significantly higher tidal volumes (690 ± 321 mL and 652 ± 366 mL, respectively). Tidal volume was strongly correlated with the specific effect of each device on mouth pressure during inspiration: HFNC and CPAP were characterized by a negative PTPmouth (- 0.3 [- 0.8 to - 0.2] and - 0.7 [- 2.2 to - 0.5] cmH2O.sec/cycle, respectively), while Helmet-NIV and Mask-NIV were associated with a positive PTPmouth (4.5 [4.1-4.6] and 6.1 [5.9-7.1] cmH2O.sec/cycle, respectively). Tidal volume was also significantly influenced by oxygenation devices in healthy volunteers, with similar tidal volumes between O2-mask and CPAP (644 [571-764] and 648 [586-770] mL) but higher with HFNC, Mask-NIV and Helmet-NIV (819 [609-918], 1110 [661-1305] and 1086 [833-1243] mL). CONCLUSIONS: Tidal volume is significantly influenced by noninvasive oxygenation support devices, with a strong correlation with the pressure variation generated into the mouth during inspiration. NIV was associated with the highest tidal volumes and CPAP with the lowest ones. Clinical studies are needed to clarify the clinical implications of these effects.

Effects of three spontaneous ventilation modes on respiratory drive and muscle effort in COVID-19 pneumonia patients.

BACKGROUND: High drive and high effort during spontaneous breathing can generate patient self-inflicted lung injury (P-SILI) due to uncontrolled high transpulmonary and transvascular pressures, with deterioration of respiratory failure. P-SILI has been demonstrated in experimental studies and supported in recent computational models. Different treatment strategies have been proposed according to the phenotype of elastance of the respiratory system (Ers) for patients with COVID-19. This study aimed to investigate the effect of three spontaneous ventilation modes on respiratory drive and muscle effort in clinical practice and their relationship with different phenotypes. This was achieved by obtaining the following respiratory signals: airway pressure (Paw), flow (V´) and volume (V) and calculating muscle pressure (Pmus). METHODS: A physiologic observational study of a series of cases in a university medical-surgical ICU involving 11 mechanically ventilated patients with COVID-19 pneumonia at the initiation of spontaneous breathing was conducted. Three spontaneous ventilation modes were evaluated in each of the patients: pressure support ventilation (PSV), airway pressure release ventilation (APRV), and BiLevel positive airway pressure ventilation (BIPAP). Pmus was calculated through the equation of motion. For this purpose, we acquired the signals of Paw, V´ and V directly from the data transmission protocol of the ventilator (Dräger). The main physiological measurements were calculation of the respiratory drive (P0.1), muscle effort through the ΔPmus, pressure‒time product (PTP/min) and work of breathing of the patient in joules multiplied by respiratory frequency (WOBp, J/min). RESULTS: Ten mechanically ventilated patients with COVID-19 pneumonia at the initiation of spontaneous breathing were evaluated. Our results showed similar high drive and muscle effort in each of the spontaneous ventilatory modes tested, without significant differences between them: median (IQR): P0.1 6.28 (4.92-7.44) cm H2O, ∆Pmus 13.48 (11.09-17.81) cm H2O, PTP 166.29 (124.02-253.33) cm H2O*sec/min, and WOBp 12.76 (7.46-18.04) J/min. High drive and effort were found in patients even with low Ers. There was a significant relationship between respiratory drive and WOBp and Ers, though the coefficient of variation widely varied. CONCLUSIONS: In our study, none of the spontaneous ventilatory methods tested succeeded in reducing high respiratory drive or muscle effort, regardless of the Ers, with subsequent risk of P-SILI.

Physiological effects of awake prone position in acute hypoxemic respiratory failure.

BACKGROUND: The effects of awake prone position on the breathing pattern of hypoxemic patients need to be better understood. We conducted a crossover trial to assess the physiological effects of awake prone position in patients with acute hypoxemic respiratory failure. METHODS: Fifteen patients with acute hypoxemic respiratory failure and PaO2/FiO2 < 200 mmHg underwent high-flow nasal oxygen for 1 h in supine position and 2 h in prone position, followed by a final 1-h supine phase. At the end of each study phase, the following parameters were measured: arterial blood gases, inspiratory effort (ΔPES), transpulmonary driving pressure (ΔPL), respiratory rate and esophageal pressure simplified pressure-time product per minute (sPTPES) by esophageal manometry, tidal volume (VT), end-expiratory lung impedance (EELI), lung compliance, airway resistance, time constant, dynamic strain (VT/EELI) and pendelluft extent through electrical impedance tomography. RESULTS: Compared to supine position, prone position increased PaO2/FiO2 (median [Interquartile range] 104 mmHg [76-129] vs. 74 [69-93], p < 0.001), reduced respiratory rate (24 breaths/min [22-26] vs. 27 [26-30], p = 0.05) and increased ΔPES (12 cmH2O [11-13] vs. 9 [8-12], p = 0.04) with similar sPTPES (131 [75-154] cmH2O s min-1 vs. 105 [81-129], p > 0.99) and ΔPL (9 [7-11] cmH2O vs. 8 [5-9], p = 0.17). Airway resistance and time constant were higher in prone vs. supine position (9 cmH2O s arbitrary units-3 [4-11] vs. 6 [4-9], p = 0.05; 0.53 s [0.32-61] vs. 0.40 [0.37-0.44], p = 0.03). Prone position increased EELI (3887 arbitrary units [3414-8547] vs. 1456 [959-2420], p = 0.002) and promoted VT distribution towards dorsal lung regions without affecting VT size and lung compliance: this generated lower dynamic strain (0.21 [0.16-0.24] vs. 0.38 [0.30-0.49], p = 0.004). The magnitude of pendelluft phenomenon was not different between study phases (55% [7-57] of VT in prone vs. 31% [14-55] in supine position, p > 0.99). CONCLUSIONS: Prone position improves oxygenation, increases EELI and promotes VT distribution towards dependent lung regions without affecting VT size, ΔPL, lung compliance and pendelluft magnitude. Prone position reduces respiratory rate and increases ΔPES because of positional increases in airway resistance and prolonged expiratory time. Because high ΔPES is the main mechanistic determinant of self-inflicted lung injury, caution may be needed in using awake prone position in patients exhibiting intense ΔPES. Clinical trail registeration: The study was registered on clinicaltrials.gov (NCT03095300) on March 29, 2017.

Long-term outcome of COVID-19 patients treated with helmet noninvasive ventilation vs. high-flow nasal oxygen: a randomized trial.

BACKGROUND: Long-term outcomes of patients treated with helmet noninvasive ventilation (NIV) are unknown: safety concerns regarding the risk of patient self-inflicted lung injury and delayed intubation exist when NIV is applied in hypoxemic patients. We assessed the 6-month outcome of patients who received helmet NIV or high-flow nasal oxygen for COVID-19 hypoxemic respiratory failure. METHODS: In this prespecified analysis of a randomized trial of helmet NIV versus high-flow nasal oxygen (HENIVOT), clinical status, physical performance (6-min-walking-test and 30-s chair stand test), respiratory function and quality of life (EuroQoL five dimensions five levels questionnaire, EuroQoL VAS, SF36 and Post-Traumatic Stress Disorder Checklist for the DSM) were evaluated 6 months after the enrollment. RESULTS: Among 80 patients who were alive, 71 (89%) completed the follow-up: 35 had received helmet NIV, 36 high-flow oxygen. There was no inter-group difference in any item concerning vital signs (N = 4), physical performance (N = 18), respiratory function (N = 27), quality of life (N = 21) and laboratory tests (N = 15). Arthralgia was significantly lower in the helmet group (16% vs. 55%, p = 0.002). Fifty-two percent of patients in helmet group vs. 63% of patients in high-flow group had diffusing capacity of the lungs for carbon monoxide < 80% of predicted (p = 0.44); 13% vs. 22% had forced vital capacity < 80% of predicted (p = 0.51). Both groups reported similar degree of pain (p = 0.81) and anxiety (p = 0.81) at the EQ-5D-5L test; the EQ-VAS score was similar in the two groups (p = 0.27). Compared to patients who successfully avoided invasive mechanical ventilation (54/71, 76%), intubated patients (17/71, 24%) had significantly worse pulmonary function (median diffusing capacity of the lungs for carbon monoxide 66% [Interquartile range: 47-77] of predicted vs. 80% [71-88], p = 0.005) and decreased quality of life (EQ-VAS: 70 [53-70] vs. 80 [70-83], p = 0.01). CONCLUSIONS: In patients with COVID-19 hypoxemic respiratory failure, treatment with helmet NIV or high-flow oxygen yielded similar quality of life and functional outcome at 6 months. The need for invasive mechanical ventilation was associated with worse outcomes. These data indicate that helmet NIV, as applied in the HENIVOT trial, can be safely used in hypoxemic patients. Trial registration Registered on clinicaltrials.gov NCT04502576 on August 6, 2020.

Patient Self-Inflicted Lung Injury-A Narrative Review of Pathophysiology, Early Recognition, and Management Options.

Patient self-inflicted lung injury (P-SILI) is a life-threatening condition arising from excessive respiratory effort and work of breathing in patients with lung injury. The pathophysiology of P-SILI involves factors related to the underlying lung pathology and vigorous respiratory effort. P-SILI might develop both during spontaneous breathing and mechanical ventilation with preserved spontaneous respiratory activity. In spontaneously breathing patients, clinical signs of increased work of breathing and scales developed for early detection of potentially harmful effort might help clinicians prevent unnecessary intubation, while, on the contrary, identifying patients who would benefit from early intubation. In mechanically ventilated patients, several simple non-invasive methods for assessing the inspiratory effort exerted by the respiratory muscles were correlated with respiratory muscle pressure. In patients with signs of injurious respiratory effort, therapy aimed to minimize this problem has been demonstrated to prevent aggravation of lung injury and, therefore, improve the outcome of such patients. In this narrative review, we accumulated the current information on pathophysiology and early detection of vigorous respiratory effort. In addition, we proposed a simple algorithm for prevention and treatment of P-SILI that is easily applicable in clinical practice.

The effects of flow settings during high-flow nasal cannula support for adult subjects: a systematic review.

BACKGROUND: During high-flow nasal cannula (HFNC) therapy, flow plays a crucial role in the physiological effects. However, there is no consensus on the initial flow settings and subsequent titration. Thus, we aimed to systematically synthesize the effects of flows during HFNC treatment. METHODS: In this systematic review, two investigators independently searched PubMed, Embase, Web of Science, Scopus, and Cochrane for in vitro and in vivo studies investigating the effects of flows in HFNC treatment published in English before July 10, 2022. We excluded studies that investigated the pediatric population (< 18 years) or used only one flow. Two investigators independently extracted the data and assessed the risk of bias. The study protocol was prospectively registered with PROSPERO, CRD42022345419. RESULTS: In total, 32,543 studies were identified, and 44 were included. In vitro studies evaluated the effects of flow settings on the fraction of inspired oxygen (FIO2), positive end-expiratory pressure, and carbon dioxide (CO2) washout. These effects are flow-dependent and are maximized when the flow exceeds the patient peak inspiratory flow, which varies between patients and disease conditions. In vivo studies report that higher flows result in improved oxygenation and dead space washout and can reduce work of breathing. Higher flows also lead to alveolar overdistention in non-dependent lung regions and patient discomfort. The impact of flows on different patients is largely heterogeneous. INTERPRETATION: Individualizing flow settings during HFNC treatment is necessary, and titrating flow based on clinical findings like oxygenation, respiratory rates, ROX index, and patient comfort is a pragmatic way forward.

Physiological adaptations during weaning from veno-venous extracorporeal membrane oxygenation.

Veno-venous extracorporeal membrane oxygenation (V-V ECMO) has an established evidence base in acute respiratory distress syndrome (ARDS) and has seen exponential growth in its use over the past decades. However, there is a paucity of evidence regarding the approach to weaning, with variation of practice and outcomes between centres. Preconditions for weaning, management of patients' sedation and mechanical ventilation during this phase, criteria defining success or failure, and the optimal duration of a trial prior to decannulation are all debated subjects. Moreover, there is no prospective evidence demonstrating the superiority of weaning the sweep gas flow (SGF), the extracorporeal blood flow (ECBF) or the fraction of oxygen of the SGF (FdO2), thereby a broad inter-centre variability exists in this regard. Accordingly, the aim of this review is to discuss the required physiological basis to interpret different weaning approaches: first, we will outline the physiological changes in blood gases which should be expected from manipulations of ECBF, SGF and FdO2. Subsequently, we will describe the resulting adaptation of patients' control of breathing, with special reference to the effects of weaning on respiratory effort. Finally, we will discuss pertinent elements of the monitoring and mechanical ventilation of passive and spontaneously breathing patients during a weaning trial. Indeed, to avoid lung injury, invasive monitoring is often required in patients making spontaneous effort, as pressures measured at the airway may not reflect the degree of lung strain. In the absence of evidence, our approach to weaning is driven largely by an understanding of physiology.

Pneumomediastinum as patient self-inflicted lung injury in patients with acute respiratory distress syndrome due to COVID-19: a case series.

Background: In patients with coronavirus disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 infection, pneumomediastinum has been increasingly reported in cases of noninvasive oxygen therapy, including high-flow nasal cannula, and invasive mechanical ventilation. However, its pathogenesis is still not understood. Case Presentation: We report two cases of pneumomediastinum in acute respiratory distress syndrome (ARDS) caused by COVID-19. In both cases, control of spontaneous breathing with neuromuscular blocking agents resulted in resolution of pneumoperitoneum. Conclusion: The improvement of pneumomediastinum with control of spontaneous breathing suggested patient self-inflicted lung injury as a possible mechanism in this case series. In ARDS cases with pneumomediastinum, in addition to controlling plateau pressure with conventional lung protective ventilation, spontaneous breathing should be controlled if the patient's inspiratory effort is suspected to be strong.

How to recognize patients at risk of self-inflicted lung injury.

INTRODUCTION: Patient self-inflicted lung injury (P-SILI) has been proposed as a form of lung injury caused by strong inspiratory efforts consequent to a high respiratory drive in patients with hypoxemic acute respiratory failure (hARF). Increased respiratory drive and effort may lead to variable combinations of deleterious phenomena, such as excessive transpulmonary pressure, pendelluft, intra-tidal recruitment, local lung volutrauma, and pulmonary edema. Gas exchange and respiratory mechanics derangements further increase respiratory drive and effort, thus inducing a vicious circle. Forms of partial ventilatory support may further add to the detrimental effects of P-SILI. Since P-SILI may worsen patient outcome, strategies aimed at identifying and preventing P-SILI would be of great importance. AREAS COVERED: We systematically searched Pubmed since inception until 15 April 2022 to review the patho-physiological mechanisms of P-SILI and the strategies to identify those patients at risk of P-SILI. EXPERT OPINION: Although the concept of P-SILI has been increasingly supported by experimental and clinical data, no study has insofar demonstrated the efficacy of any strategy to identify it in the clinical setting. Further research is thus needed to ascertain the detrimental effects of spontaneous breathing and identify patients with hARF at high risk of developing P-SILI.

Simulation to minimise patient self-inflicted lung injury: are we almost there?

Computational modelling has been used to enlighten pathophysiological issues in patients with acute respiratory distress syndrome (ARDS) using a sophisticated, integrated cardiopulmonary model. COVID-19 ARDS is a pathophysiologically distinct entity characterised by dissociation between impairment in gas exchange and respiratory system mechanics, especially in the early stages of ARDS. Weaver and colleagues used computational modelling to elucidate factors contributing to generation of patient self-inflicted lung injury, and evaluated the effects of various spontaneous respiratory efforts with different oxygenation and ventilatory support modes. Their findings indicate that mechanical forces generated in the lung parenchyma are only counterbalanced when the respiratory support mode reduces the intensity of respiratory efforts.

Optimising respiratory support for early COVID-19 pneumonia: a computational modelling study.

BACKGROUND: Optimal respiratory support in early COVID-19 pneumonia is controversial and remains unclear. Using computational modelling, we examined whether lung injury might be exacerbated in early COVID-19 by assessing the impact of conventional oxygen therapy (COT), high-flow nasal oxygen therapy (HFNOT), continuous positive airway pressure (CPAP), and noninvasive ventilation (NIV). METHODS: Using an established multi-compartmental cardiopulmonary simulator, we first modelled COT at a fixed FiO2 (0.6) with elevated respiratory effort for 30 min in 120 spontaneously breathing patients, before initiating HFNOT, CPAP, or NIV. Respiratory effort was then reduced progressively over 30-min intervals. Oxygenation, respiratory effort, and lung stress/strain were quantified. Lung-protective mechanical ventilation was also simulated in the same cohort. RESULTS: HFNOT, CPAP, and NIV improved oxygenation compared with conventional therapy, but also initially increased total lung stress and strain. Improved oxygenation with CPAP reduced respiratory effort but lung stress/strain remained elevated for CPAP >5 cm H2O. With reduced respiratory effort, HFNOT maintained better oxygenation and reduced total lung stress, with no increase in total lung strain. Compared with 10 cm H2O PEEP, 4 cm H2O PEEP in NIV reduced total lung stress, but high total lung strain persisted even with less respiratory effort. Lung-protective mechanical ventilation improved oxygenation while minimising lung injury. CONCLUSIONS: The failure of noninvasive ventilatory support to reduce respiratory effort may exacerbate pulmonary injury in patients with early COVID-19 pneumonia. HFNOT reduces lung strain and achieves similar oxygenation to CPAP/NIV. Invasive mechanical ventilation may be less injurious than noninvasive support in patients with high respiratory effort.

[Development of a giant bulla under spontaneous breathing by self-inflicted lung injury in a patient with COVID-19 pneumonia]. / Entwicklung einer Riesenbulla unter Spontanatmung durch "patient self-inflicted lung injury" bei COVID-19-Pneumonie.

The outbreak of SARS-CoV­2 and the associated COVID-19 pandemic pose major challenges to healthcare systems worldwide. New data on diagnosis, clinical presentation and treatment of the disease are published on a daily basis. This case report describes the fatal course of severe COVID-19 pneumonia in an 81-year-old patient with no previous pulmonary disease who developed a giant bulla during non-invasive high-flow oxygen therapy. Virus-induced diffuse destruction of alveolar tissue or patient self-inflicted lung injury (P-SILI) are discussed as possible pathomechanisms. Future studies must determine whether lung-protective mechanical ventilation with high levels of sedation and paralysis to suppress spontaneous respiratory drive and to reduce transpulmonary pressure can prevent structural lung damage induced both by the virus and P­SILI in COVID-19 patients with ARDS.

Spontaneous pneumomediastinum: A collaborative sequelae between COVID-19 and self-inflicted lung injury - A case report and literature review.

Spontaneous pneumomediastinum is an infrequent complication of COVID-19. The mechanism is still unknown and thought to be related to patient self-inflicted lung injury. Our patient is a 49-year-old male who presented with shortness of breath and cough. A COVID-19 Polymerase Chain Reaction was positive. He required a high-flow nasal cannula, but he did not demand mechanical ventilation. Computed tomography angiography scan of the chest revealed pneumomediastinum. He was managed conservatively, and a complete recovery was achieved. This case highlights the emerging association of COVID-19, patient self-inflicted lung injury, and pneumomediastinum. Furthermore, spontaneous pneumomediastinum should be suspected even in patients who were not mechanically ventilated.

Novel method of transpulmonary pressure measurement with an air-filled esophageal catheter.

BACKGROUND: There is a strong rationale for proposing transpulmonary pressure-guided protective ventilation in acute respiratory distress syndrome. The reference esophageal balloon catheter method requires complex in vivo calibration, expertise and specific material order. A simple, inexpensive, accurate and reproducible method of measuring esophageal pressure would greatly facilitate the measure of transpulmonary pressure to individualize protective ventilation in the intensive care unit. RESULTS: We propose an air-filled esophageal catheter method without balloon, using a disposable catheter that allows reproducible esophageal pressure measurements. We use a 49-cm-long 10 Fr thin suction catheter, positioned in the lower-third of the esophagus and connected to an air-filled disposable blood pressure transducer bound to the monitor and pressurized by an air-filled infusion bag. Only simple calibration by zeroing the transducer to atmospheric pressure and unit conversion from mmHg to cmH2O are required. We compared our method with the reference balloon catheter both ex vivo, using pressure chambers, and in vivo, in 15 consecutive mechanically ventilated patients. Esophageal-to-airway pressure change ratios during the dynamic occlusion test were close to one (1.03 ± 0.19 and 1.00 ± 0.16 in the controlled and assisted modes, respectively), validating the proper esophageal positioning. The Bland-Altman analysis revealed no bias of our method compared with the reference and good precision for inspiratory, expiratory and delta esophageal pressure measurements in both the controlled (largest bias -0.5 cmH2O [95% confidence interval: -0.9; -0.1] cmH2O; largest limits of agreement -3.5 to 2.5 cmH2O) and assisted modes (largest bias -0.3 [-2.6; 2.0] cmH2O). We observed a good repeatability (intra-observer, intraclass correlation coefficient, ICC: 0.89 [0.79; 0.96]) and reproducibility (inter-observer ICC: 0.89 [0.76; 0.96]) of esophageal measurements. The direct comparison with pleural pressure in two patients and spectral analysis by Fourier transform confirmed the reliability of the air-filled catheter-derived esophageal pressure as an accurate surrogate of pleural pressure. A calculator for transpulmonary pressures is available online. CONCLUSIONS: We propose a simple, minimally invasive, inexpensive and reproducible method for esophageal pressure monitoring with an air-filled esophageal catheter without balloon. It holds the promise of widespread bedside use of transpulmonary pressure-guided protective ventilation in ICU patients.

Patient-Self Inflicted Lung Injury: A Practical Review.

Patients with severe lung injury usually have a high respiratory drive, resulting in intense inspiratory effort that may even worsen lung damage by several mechanisms gathered under the name "patient-self inflicted lung injury" (P-SILI). Even though no clinical study has yet demonstrated that a ventilatory strategy to limit the risk of P-SILI can improve the outcome, the concept of P-SILI relies on sound physiological reasoning, an accumulation of clinical observations and some consistent experimental data. In this review, we detail the main pathophysiological mechanisms by which the patient's respiratory effort could become deleterious: excessive transpulmonary pressure resulting in over-distension; inhomogeneous distribution of transpulmonary pressure variations across the lung leading to cyclic opening/closing of nondependent regions and pendelluft phenomenon; increase in the transvascular pressure favoring the aggravation of pulmonary edema. We also describe potentially harmful patient-ventilator interactions. Finally, we discuss in a practical way how to detect in the clinical setting situations at risk for P-SILI and to what extent this recognition can help personalize the treatment strategy.

High risk of patient self-inflicted lung injury in COVID-19 with frequently encountered spontaneous breathing patterns: a computational modelling study.

BACKGROUND: There is on-going controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute hypoxaemic respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a computational simulator of cardiopulmonary pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator parameters were manually adjusted to generate a population of 10 patients that recapitulate clinical features exhibited by certain COVID-19 patients, i.e., severe hypoxaemia combined with relatively well-preserved lung mechanics, being treated with supplemental oxygen. RESULTS: Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 7/20, 7/30, 10/14, 10/20 and 10/30 ml/kg / breaths/min. While oxygenation improved with higher respiratory efforts, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 12.0 ± 0.3 cmH2O at baseline to 33.8 ± 0.4 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH2O at baseline to 17.9 ± 0.3 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Total lung strain increased from 0.29 ± 0.006 at baseline to 0.65 ± 0.016 at 10 ml/kg/30 breaths/min. Mechanical power increased from 1.6 ± 0.1 J/min at baseline to 12.9 ± 0.2 J/min at VT/RR of 7 ml/kg/30 breaths/min, and to 24.9 ± 0.3 J/min at 10 ml/kg/30 breaths/min. Driving pressure increased from 7.7 ± 0.2 cmH2O at baseline to 19.6 ± 0.2 cmH2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. CONCLUSIONS: Our results suggest that the forces generated by increased inspiratory effort commonly seen in COVID-19 acute hypoxaemic respiratory failure are comparable with those that have been associated with ventilator-induced lung injury during mechanical ventilation. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury.

Non-invasive ventilatory support and high-flow nasal oxygen as first-line treatment of acute hypoxemic respiratory failure and ARDS.

The role of non-invasive respiratory support (high-flow nasal oxygen and noninvasive ventilation) in the management of acute hypoxemic respiratory failure and acute respiratory distress syndrome is debated. The oxygenation improvement coupled with lung and diaphragm protection produced by non-invasive support may help to avoid endotracheal intubation, which prevents the complications of sedation and invasive mechanical ventilation. However, spontaneous breathing in patients with lung injury carries the risk that vigorous inspiratory effort, combined or not with mechanical increases in inspiratory airway pressure, produces high transpulmonary pressure swings and local lung overstretch. This ultimately results in additional lung damage (patient self-inflicted lung injury), so that patients intubated after a trial of noninvasive support are burdened by increased mortality. Reducing inspiratory effort by high-flow nasal oxygen or delivery of sustained positive end-expiratory pressure through the helmet interface may reduce these risks. In this physiology-to-bedside review, we provide an updated overview about the role of noninvasive respiratory support strategies as early treatment of hypoxemic respiratory failure in the intensive care unit. Noninvasive strategies appear safe and effective in mild-to-moderate hypoxemia (PaO2/FiO2 > 150 mmHg), while they can yield delayed intubation with increased mortality in a significant proportion of moderate-to-severe (PaO2/FiO2 ≤ 150 mmHg) cases. High-flow nasal oxygen and helmet noninvasive ventilation represent the most promising techniques for first-line treatment of severe patients. However, no conclusive evidence allows to recommend a single approach over the others in case of moderate-to-severe hypoxemia. During any treatment, strict physiological monitoring remains of paramount importance to promptly detect the need for endotracheal intubation and not delay protective ventilation.