Publications by authors named "John J Marini"

184 Publications

Role of total lung stress on the progression of early COVID-19 pneumonia.

Intensive Care Med 2021 Sep 16. Epub 2021 Sep 16.

Department of Anesthesiology, Medical University of Göttingen, University Medical Center Göttingen, Robert Koch Straße 40, 37075, Göttingen, Germany.

Purpose: We investigated if the stress applied to the lung during non-invasive respiratory support may contribute to the coronavirus disease 2019 (COVID-19) progression.

Methods: Single-center, prospective, cohort study of 140 consecutive COVID-19 pneumonia patients treated in high-dependency unit with continuous positive airway pressure (n = 131) or non-invasive ventilation (n = 9). We measured quantitative lung computed tomography, esophageal pressure swings and total lung stress.

Results: Patients were divided in five subgroups based on their baseline PaO/FiO (day 1): non-CARDS (median PaO/FiO 361 mmHg, IQR [323-379]), mild (224 mmHg [211-249]), mild-moderate (173 mmHg [164-185]), moderate-severe (126 mmHg [114-138]) and severe (88 mmHg [86-99], p < 0.001). Each subgroup had similar median lung weight: 1215 g [1083-1294], 1153 [888-1321], 968 [858-1253], 1060 [869-1269], and 1127 [937-1193] (p = 0.37). They also had similar non-aerated tissue fraction: 10.4% [5.9-13.7], 9.6 [7.1-15.8], 9.4 [5.8-16.7], 8.4 [6.7-12.3] and 9.4 [5.9-13.8], respectively (p = 0.85). Treatment failure of CPAP/NIV occurred in 34 patients (24.3%). Only three variables, at day one, distinguished patients with negative outcome: PaO/FiO ratio (OR 0.99 [0.98-0.99], p = 0.02), esophageal pressure swing (OR 1.13 [1.01-1.27], p = 0.032) and total stress (OR 1.17 [1.06-1.31], p = 0.004). When these three variables were evaluated together in a multivariate logistic regression analysis, only the total stress was independently associated with negative outcome (OR 1.16 [1.01-1.33], p = 0.032).

Conclusions: In early COVID-19 pneumonia, hypoxemia is not linked to computed tomography (CT) pathoanatomy, differently from typical ARDS. High lung stress was independently associated with the failure of non-invasive respiratory support.
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http://dx.doi.org/10.1007/s00134-021-06519-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8444534PMC
September 2021

The impact of fluid status and decremental PEEP strategy on cardiac function and lung and kidney damage in mild-moderate experimental acute respiratory distress syndrome.

Respir Res 2021 Jul 30;22(1):214. Epub 2021 Jul 30.

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Background: We evaluated the effects of abrupt versus gradual PEEP decrease, combined with standard versus high-volume fluid administration, on cardiac function, as well as lung and kidney damage in an established model of mild-moderate acute respiratory distress syndrome (ARDS).

Methods: Wistar rats received endotoxin intratracheally. After 24 h, they were treated with Ringer's lactate at standard (10 mL/kg/h) or high (30 mL/kg/h) dose. For 30 min, all animals were mechanically ventilated with tidal volume = 6 mL/kg and PEEP = 9 cmHO (to keep alveoli open), then randomized to undergo abrupt or gradual (0.2 cmHO/min for 30 min) PEEP decrease from 9 to 3 cmHO. Animals were then further ventilated for 10 min at PEEP = 3 cmHO, euthanized, and their lungs and kidneys removed for molecular biology analysis.

Results: At the end of the experiment, left and right ventricular end-diastolic areas were greater in animals treated with high compared to standard fluid administration, regardless of PEEP decrease rate. However, pulmonary arterial pressure, indicated by the pulmonary acceleration time (PAT)/pulmonary ejection time (PET) ratio, was higher in abrupt compared to gradual PEEP decrease, independent of fluid status. Animals treated with high fluids and abrupt PEEP decrease exhibited greater diffuse alveolar damage and higher expression of interleukin-6 (a pro-inflammatory marker) and vascular endothelial growth factor (a marker of endothelial cell damage) compared to the other groups. The combination of standard fluid administration and gradual PEEP decrease increased zonula occludens-1 expression, suggesting epithelial cell preservation. Expression of club cell-16 protein, an alveolar epithelial cell damage marker, was higher in abrupt compared to gradual PEEP decrease groups, regardless of fluid status. Acute kidney injury score and gene expression of kidney injury molecule-1 were higher in the high versus standard fluid administration groups, regardless of PEEP decrease rate.

Conclusion: In the ARDS model used herein, decreasing PEEP abruptly increased pulmonary arterial hypertension, independent of fluid status. The combination of abrupt PEEP decrease and high fluid administration led to greater lung and kidney damage. This information adds to the growing body of evidence that supports gradual transitioning of ventilatory patterns and warrants directing additional investigative effort into vascular and deflation issues that impact lung protection.
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http://dx.doi.org/10.1186/s12931-021-01811-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8323327PMC
July 2021

Improving lung compliance by external compression of the chest wall.

Crit Care 2021 07 28;25(1):264. Epub 2021 Jul 28.

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

As exemplified by prone positioning, regional variations of lung and chest wall properties provide possibilities for modifying transpulmonary pressures and suggest that clinical interventions related to the judicious application of external pressure may yield benefit. Recent observations made in late-phase patients with severe ARDS caused by COVID-19 (C-ARDS) have revealed unexpected mechanical responses to local chest wall compressions over the sternum and abdomen in the supine position that challenge the clinician's assumptions and conventional bedside approaches to lung protection. These findings appear to open avenues for mechanism-defining research investigation with possible therapeutic implications for all forms and stages of ARDS.
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http://dx.doi.org/10.1186/s13054-021-03700-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8318320PMC
July 2021

Personalized mechanical ventilation in acute respiratory distress syndrome.

Crit Care 2021 07 16;25(1):250. Epub 2021 Jul 16.

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

A personalized mechanical ventilation approach for patients with adult respiratory distress syndrome (ARDS) based on lung physiology and morphology, ARDS etiology, lung imaging, and biological phenotypes may improve ventilation practice and outcome. However, additional research is warranted before personalized mechanical ventilation strategies can be applied at the bedside. Ventilatory parameters should be titrated based on close monitoring of targeted physiologic variables and individualized goals. Although low tidal volume (V) is a standard of care, further individualization of V may necessitate the evaluation of lung volume reserve (e.g., inspiratory capacity). Low driving pressures provide a target for clinicians to adjust V and possibly to optimize positive end-expiratory pressure (PEEP), while maintaining plateau pressures below safety thresholds. Esophageal pressure monitoring allows estimation of transpulmonary pressure, but its use requires technical skill and correct physiologic interpretation for clinical application at the bedside. Mechanical power considers ventilatory parameters as a whole in the optimization of ventilation setting, but further studies are necessary to assess its clinical relevance. The identification of recruitability in patients with ARDS is essential to titrate and individualize PEEP. To define gas-exchange targets for individual patients, clinicians should consider issues related to oxygen transport and dead space. In this review, we discuss the rationale for personalized approaches to mechanical ventilation for patients with ARDS, the role of lung imaging, phenotype identification, physiologically based individualized approaches to ventilation, and a future research agenda.
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http://dx.doi.org/10.1186/s13054-021-03686-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8284184PMC
July 2021

Conceptual simplicity in pursuit of precision.

Intensive Care Med 2021 08 16;47(8):920-921. Epub 2021 Jun 16.

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

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http://dx.doi.org/10.1007/s00134-021-06424-zDOI Listing
August 2021

The 4DPRR Index and Mechanical Power: A Step Ahead or Four Steps Backward?

Am J Respir Crit Care Med 2021 08;204(4):491-492

University Medical Center Göttingen, Germany.

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http://dx.doi.org/10.1164/rccm.202104-0923LEDOI Listing
August 2021

The authors respond.

Respir Care 2021 05;66(5):887

Department of Surgery Regions Hospital St Paul, Minnesota.

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http://dx.doi.org/10.4187/respcare.08876DOI Listing
May 2021

Intra-cycle power: is the flow profile a neglected component of lung protection?

Intensive Care Med 2021 05 2;47(5):609-611. Epub 2021 Apr 2.

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

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http://dx.doi.org/10.1007/s00134-021-06375-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8017116PMC
May 2021

Can We Always Trust the Wisdom of the Body?

Authors:
John J Marini

Crit Care Med 2021 Mar 29. Epub 2021 Mar 29.

Divisions of Pulmonary and Critical Care, University of Minnesota, Regions Hospital, St. Paul, MN.

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http://dx.doi.org/10.1097/CCM.0000000000005022DOI Listing
March 2021

Prevalence and outcome of silent hypoxemia in COVID-19.

Minerva Anestesiol 2021 03;87(3):325-333

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

Background: In the early stages of COVID-19 pneumonia, hypoxemia has been described in absence of dyspnea ("silent" or "happy" hypoxemia). Our aim was to report its prevalence and outcome in a series of hypoxemic patients upon Emergency Department admission.

Methods: In this retrospective observational cohort study we enrolled a study population consisting of 213 COVID-19 patients with PaO2/FiO2 ratio <300 mmHg at hospital admission. Two groups (silent and dyspneic hypoxemia) were defined. Symptoms, blood gas analysis, chest X-ray (CXR) severity, need for intensive care and outcome were recorded.

Results: Silent hypoxemic patients (68-31.9%) compared to the dyspneic hypoxemic patients (145-68.1%) showed greater frequency of extra respiratory symptoms (myalgia, diarrhea and nausea) and lower plasmatic LDH. PaO2/FiO2 ratio was 225±68 mmHg and 192±78 mmHg in silent and dyspneic hypoxemia respectively (P=0.002). Eighteen percent of the patients with PaO2/FiO2 from 50 to 150 mmHg presented silent hypoxemia. Silent and dyspneic hypoxemic patients had similar PaCO2 (34.2±6.8 mmHg vs. 33.5±5.7 mmHg, P=0.47) but different respiratory rates (24.6±5.9 bpm vs. 28.6±11.3 bpm respectively, P=0.002). Even when CXR was severely abnormal, 25% of the population was silent hypoxemic. Twenty-six point five percent and 38.6% of silent and dyspneic patients were admitted to the ICU respectively (P=0.082). Mortality rate was 17.6% and 29.7% (log-rank P=0.083) in silent and dyspneic patients.

Conclusions: Silent hypoxemia is remarkably present in COVID-19. The presence of dyspnea is associated with a more severe clinical condition.
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http://dx.doi.org/10.23736/S0375-9393.21.15245-9DOI Listing
March 2021

Complexity and unanswered questions in the pathophysiology of COVID-19 ARDS.

Intensive Care Med 2021 04 1;47(4):495-496. Epub 2021 Feb 1.

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

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http://dx.doi.org/10.1007/s00134-021-06353-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7849962PMC
April 2021

Smoothing the Edges of Lung Protection.

Am J Respir Crit Care Med 2021 05;203(10):1212-1214

Department of Medicine Regions Hospital and University of Minnesota St. Paul, Minnesota.

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http://dx.doi.org/10.1164/rccm.202101-0111EDDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8456477PMC
May 2021

COVID-19 and ARDS: the baby lung size matters.

Intensive Care Med 2021 01 4;47(1):133-134. Epub 2020 Dec 4.

Department of Anesthesiology and Intensive Care, ASST Santi e Paolo Hospital, University of Milan, Milan, Italy.

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http://dx.doi.org/10.1007/s00134-020-06324-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7716792PMC
January 2021

Elastic Power of Mechanical Ventilation in Morbid Obesity and Severe Hypoxemia.

Respir Care 2021 Apr 1;66(4):626-634. Epub 2020 Dec 1.

Pulmonary, Allergy, Critical Care, and Sleep Medicine, University of Minnesota, Minneapolis, Minnesota.

Background: To minimize ventilator-induced lung injury, the primary clinical focus is currently expanding from measuring static indices of the individual tidal cycle (eg, plateau pressure and tidal volume) to more inclusive indicators of energy load, such as total power and its elastic components. Morbid obesity may influence these components. We characterized the relative values of elastic subcomponents of total power (ie, driving power and dynamic power) in subjects with severe hypoxemia, morbid obesity, or their combination.

Methods: We analyzed data from subjects receiving mechanical ventilation divided into 4 groups. [Formula: see text]/[Formula: see text] < 150 mm Hg (severe hypoxemia) indicated probable reduction of lung compliance while body mass index > 40 kg/m (morbid obesity) suggested a possible contribution to reduced respiratory system compliance from the chest wall. Group 1 included subjects with no expected abnormality of lung compliance or chest wall compliance; Group 2 included subjects with expected reduction of lung compliance on the basis of severe hypoxemia but with no morbid obesity; Group 3 included subjects with morbid obesity without severe hypoxemia; and Group 4 included subjects with morbid obesity and severe hypoxemia. All ventilator-induced lung injury predictors were compared among groups using mixed-effects linear models.

Results: Groups 1-4 included 61, 52, 49, and 51 subjects, respectively. Mean body mass index averaged 28.7 kg/m for nonobese subjects and 52.1 kg/m for morbidly obese subjects. Mean driving pressure, dynamic power, and driving power of Groups 2 and 3 exceeded the corresponding values of Group 1 but fell into similar ranges when compared with each other. These values were highest in Group 4 subjects. In Group 2, mean dynamic power and driving power values were comparable to those in Group 3.

Conclusions: In mechanically ventilated subjects, stress and energy-based ventilator-induced lung injury indicators are influenced by the relative contributions of chest wall and lung to overall respiratory mechanics. Numerical guidelines for ventilator-induced lung injury risk must strongly consider adjustment for these elastic characteristics in morbid obesity.
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http://dx.doi.org/10.4187/respcare.08234DOI Listing
April 2021

Pathophysiology of COVID-19-associated acute respiratory distress syndrome.

Lancet Respir Med 2021 01 13;9(1):e1. Epub 2020 Nov 13.

Pulmonary and Critical Care Medicine, Regions Hospital and University of Minnesota, St Paul, MN, USA.

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http://dx.doi.org/10.1016/S2213-2600(20)30505-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7837039PMC
January 2021

Prone position in ARDS patients: why, when, how and for whom.

Intensive Care Med 2020 12 10;46(12):2385-2396. Epub 2020 Nov 10.

Servei Medicina Intensiva, Hospital Universitari Sant Pau, Barcelona, Spain.

In ARDS patients, the change from supine to prone position generates a more even distribution of the gas-tissue ratios along the dependent-nondependent axis and a more homogeneous distribution of lung stress and strain. The change to prone position is generally accompanied by a marked improvement in arterial blood gases, which is mainly due to a better overall ventilation/perfusion matching. Improvement in oxygenation and reduction in mortality are the main reasons to implement prone position in patients with ARDS. The main reason explaining a decreased mortality is less overdistension in non-dependent lung regions and less cyclical opening and closing in dependent lung regions. The only absolute contraindication for implementing prone position is an unstable spinal fracture. The maneuver to change from supine to prone and vice versa requires a skilled team of 4-5 caregivers. The most frequent adverse events are pressure sores and facial edema. Recently, the use of prone position has been extended to non-intubated spontaneously breathing patients affected with COVID-19 ARDS. The effects of this intervention on outcomes are still uncertain.
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http://dx.doi.org/10.1007/s00134-020-06306-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7652705PMC
December 2020

Physiological and quantitative CT-scan characterization of COVID-19 and typical ARDS: a matched cohort study.

Intensive Care Med 2020 12 21;46(12):2187-2196. Epub 2020 Oct 21.

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Robert-Koch Straße 40, Göttingen, Germany.

Purpose: To investigate whether COVID-19-ARDS differs from all-cause ARDS.

Methods: Thirty-two consecutive, mechanically ventilated COVID-19-ARDS patients were compared to two historical ARDS sub-populations 1:1 matched for PaO/FiO or for compliance of the respiratory system. Gas exchange, hemodynamics and respiratory mechanics were recorded at 5 and 15 cmHO PEEP. CT scan variables were measured at 5 cmHO PEEP.

Results: Anthropometric characteristics were similar in COVID-19-ARDS, PaO/FiO-matched-ARDS and Compliance-matched-ARDS. The PaO/FiO-matched-ARDS and COVID-19-ARDS populations (both with PaO/FiO 106 ± 59 mmHg) had different respiratory system compliances (Crs) (39 ± 11 vs 49.9 ± 15.4 ml/cmHO, p = 0.03). The Compliance-matched-ARDS and COVID-19-ARDS had similar Crs (50.1 ± 15.7 and 49.9 ± 15.4 ml/cmHO, respectively) but significantly lower PaO/FiO for the same Crs (160 ± 62 vs 106.5 ± 59.6 mmHg, p < 0.001). The three populations had similar lung weights but COVID-19-ARDS had significantly higher lung gas volume (PaO/FiO-matched-ARDS 930 ± 644 ml, COVID-19-ARDS 1670 ± 791 ml and Compliance-matched-ARDS 1301 ± 627 ml, p < 0.05). The venous admixture was significantly related to the non-aerated tissue in PaO/FiO-matched-ARDS and Compliance-matched-ARDS (p < 0.001) but unrelated in COVID-19-ARDS (p = 0.75), suggesting that hypoxemia was not only due to the extent of non-aerated tissue. Increasing PEEP from 5 to 15 cmHO improved oxygenation in all groups. However, while lung mechanics and dead space improved in PaO/FiO-matched-ARDS, suggesting recruitment as primary mechanism, they remained unmodified or worsened in COVID-19-ARDS and Compliance-matched-ARDS, suggesting lower recruitment potential and/or blood flow redistribution.

Conclusions: COVID-19-ARDS is a subset of ARDS characterized overall by higher compliance and lung gas volume for a given PaO/FiO, at least when considered within the timeframe of our study.
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http://dx.doi.org/10.1007/s00134-020-06281-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7577365PMC
December 2020

COVID-19: scientific reasoning, pragmatism and emotional bias.

Ann Intensive Care 2020 Oct 12;10(1):134. Epub 2020 Oct 12.

Department of Adult Critical Care, Guy's and St Thomas' NHS Foundation Trust, King's Health Partners, and Division of Asthma, Allergy and Lung Biology, King's College London, London, UK.

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http://dx.doi.org/10.1186/s13613-020-00756-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549341PMC
October 2020

Hysteresis As an Indicator of Recruitment and Ventilator-Induced Lung Injury Risk.

Authors:
John J Marini

Crit Care Med 2020 10;48(10):1542-1543

Department of Pulmonary and Critical Care Medicine, Regions Hospital and University of Minnesota, Minneapolis/St. Paul, MN.

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http://dx.doi.org/10.1097/CCM.0000000000004533DOI Listing
October 2020

The Respiratory Drive: An Overlooked Tile of COVID-19 Pathophysiology.

Am J Respir Crit Care Med 2020 10;202(8):1079-1080

Department of Critical Care Guy's & St. Thomas NHS Foundation Trust London, United Kingdom.

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http://dx.doi.org/10.1164/rccm.202008-3142EDDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7560815PMC
October 2020

Integrating the evidence: confronting the COVID-19 elephant.

Intensive Care Med 2020 10 25;46(10):1904-1907. Epub 2020 Jul 25.

Division of Pulmonary, Allergy and Critical Care Medicine, Columbia University College of Physicians and Surgeons/New York-Presbyterian Hospital, New York, NY, USA.

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http://dx.doi.org/10.1007/s00134-020-06195-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7381417PMC
October 2020

Dealing With the CARDS of COVID-19.

Authors:
John J Marini

Crit Care Med 2020 08;48(8):1239-1241

Departments of Pulmonary and Critical Care Medicine, University of Minnesota and Regions Hospital, St. Paul, MN.

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http://dx.doi.org/10.1097/CCM.0000000000004427DOI Listing
August 2020

Time Course of Evolving Ventilator-Induced Lung Injury: The "Shrinking Baby Lung".

Crit Care Med 2020 08;48(8):1203-1209

Department of Anesthesiology, Intensive Care and Emergency Medicine, Medical University of Göttingen, Göttingen, Germany.

Objectives: To examine the potentially modifiable drivers that injure and heal the "baby lung" of acute respiratory distress syndrome and describe a rational clinical approach to favor benefit.

Data Sources: Published experimental studies and clinical papers that address varied aspects of ventilator-induced lung injury pathogenesis and its consequences.

Study Selection: Published information relevant to the novel hypothesis of progressive lung vulnerability and to the biophysical responses of lung injury and repair.

Data Extraction: None.

Data Synthesis: In acute respiratory distress syndrome, the reduced size and capacity for gas exchange of the functioning "baby lung" imply loss of ventilatory capability that dwindles in proportion to severity of lung injury. Concentrating the entire ventilation workload and increasing perfusion to these already overtaxed units accentuates their potential for progressive injury. Unlike static airspace pressures, which, in theory, apply universally to aerated structures of all dimensions, the components of tidal inflation that relate to power (which include frequency and flow) progressively intensify their tissue-stressing effects on parenchyma and microvasculature as the ventilated compartment shrinks further, especially during the first phase of the evolving injury. This "ventilator-induced lung injury vortex" of the shrinking baby lung is opposed by reactive, adaptive, and reparative processes. In this context, relatively little attention has been paid to the evolving interactions between lung injury and response and to the timing of interventions that worsen, limit or reverse a potentially accelerating ventilator-induced lung injury process. Although universal and modifiable drivers hold the potential to progressively injure the functional lung units of acute respiratory distress syndrome in a positive feedback cycle, measures can be taken to interrupt that process and encourage growth and healing of the "baby lung" of severe acute respiratory distress syndrome.
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http://dx.doi.org/10.1097/CCM.0000000000004416DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217130PMC
August 2020

Spontaneous breathing, transpulmonary pressure and mathematical trickery.

Ann Intensive Care 2020 Jul 8;10(1):88. Epub 2020 Jul 8.

Department of Adult Critical Care, Guy's and St Thomas' NHS Foundation Trust, and Centre of Human Applied Physiological Sciences, King's College London, London, UK.

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http://dx.doi.org/10.1186/s13613-020-00708-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7341701PMC
July 2020

COVID-19 phenotypes: leading or misleading?

Eur Respir J 2020 08 27;56(2). Epub 2020 Aug 27.

Regions Hospital and University of Minnesota, St Paul, MN, USA.

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http://dx.doi.org/10.1183/13993003.02195-2020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7331647PMC
August 2020

Estimating the Damaging Power of High-Stress Ventilation.

Respir Care 2020 Jul;65(7):1046-1052

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Redirection of our clinical attention from the pressures and volumes of the individual cycle to the broader and more inclusive considerations of energy load and power has untapped potential to reduce iatrogenic risk from ventilation (ie, ventilator-induced lung injury). Power is the product of breathing frequency and inflation energy per breath. Yet, while feasible to calculate at the bedside, measuring total power may not prove to be precise enough for accurate prediction of ventilator-induced lung injury, even if normalized to lung capacity (ie, specific power). The same power value can be reached by a multitude of frequency and tidal volume combinations, not all of which carry equal risk of damage. If some arbitrary level of alveolar pressure were accepted as a sharply defined hazard boundary, a rather straightforward geometric analysis theoretically would allow partitioning of overall tidal energy into components above and below a damage threshold. In this discussion, we introduce the concept of quantitative power partitioning and illustrate how tidal energy and power might be deconstructed into their key parts.
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http://dx.doi.org/10.4187/respcare.07860DOI Listing
July 2020

What have we learned from animal models of ventilator-induced lung injury?

Intensive Care Med 2020 12 4;46(12):2377-2380. Epub 2020 Jun 4.

University of Minnesota and Regions Hospital, Regions Hospital MS 11213 B, 640 Jackson St., St. Paul, 55101, MN, USA.

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http://dx.doi.org/10.1007/s00134-020-06143-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7270159PMC
December 2020

Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome.

Crit Care 2020 06 3;24(1):284. Epub 2020 Jun 3.

Department of Pulmonary and Critical Care, Regions Hospital, MS11203B, 640 Jackson St., St. Paul, MN, 55101, USA.

Background: We dissected total power into its primary components to resolve its relative contributions to tissue damage (VILI). We hypothesized that driving power or elastic (dynamic) power offers more precise VILI risk indicators than raw total power. The relative correlations of these three measures of power with VILI-induced histologic changes and injury biomarkers were determined using a rodent model of acute respiratory distress syndrome (ARDS). Herein, we have significantly extended the scope of our previous research.

Methods: Data analyses were performed in male Wistar rats that received endotoxin intratracheally to induce ARDS. After 24 h, they were randomized to 1 h of volume-controlled ventilation with low V = 6 ml/kg and different PEEP levels (3, 5.5, 7.5, 9.5, and 11 cmHO). Applied levels of driving power, dynamic power inclusive of PEEP, and total power were correlated with VILI indicators [lung histology and biological markers associated with inflammation (interleukin-6), alveolar stretch (amphiregulin), and epithelial (club cell protein (CC)-16) and endothelial (intercellular adhesion molecule-1) cell damage in lung tissue].

Results: Driving power was higher at PEEP-11 than other PEEP levels. Dynamic power and total power increased progressively from PEEP-5.5 and PEEP-7.5, respectively, to PEEP-11. Driving power, dynamic power, and total power each correlated with the majority of VILI indicators. However, when correlations were performed from PEEP-3 to PEEP-9.5, no relationships were observed between driving power and VILI indicators, whereas dynamic power and total power remained well correlated with CC-16 expression, alveolar collapse, and lung hyperinflation.

Conclusions: In this mild-moderate ARDS model, dynamic power, not driving power alone, emerged as the key promoter of VILI. Moreover, hazards from driving power were conditioned by the requirement to pass a tidal stress threshold. When estimating VILI hazard from repeated mechanical strains, PEEP must not be disregarded as a major target for modification.
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http://dx.doi.org/10.1186/s13054-020-03011-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7271482PMC
June 2020
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