Evidence map›Paper›PMID 35341424›Full record

ReviewExpert review of respiratory medicine2022

Understanding the pathophysiology of typical acute respiratory distress syndrome and severe COVID-19.

Lorenzo Ball, Pedro Leme Silva, Daniele Roberto Giacobbe, Matteo Bassetti, Gustavo R Zubieta-Calleja, Patricia R M Rocco, Paolo Pelosi

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of respiratory medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  7. Respiratory Support in COVID-19-Related Respiratory Failure: Lessons Learnt.Advances in experimental medicine and biology · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Lorenzo BallDepartment of Surgical Sciences and Integrated Diagnostics (DISC), University of Genoa, Genoa, Italy.
Pedro Leme SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Brazil.
Daniele Roberto GiacobbeDepartment of Health Sciences (DISSAL), University of Genoa, Genoa, Italy.ORCID 0000-0003-2385-1759
Matteo BassettiDepartment of Health Sciences (DISSAL), University of Genoa, Genoa, Italy.
Gustavo R Zubieta-CallejaHigh Altitude Pulmonary and Pathology Institute (Happi-hippa), La Paz, Bolivia.
Patricia R M RoccoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Brazil.ORCID 0000-0003-1412-7136
Paolo PelosiDepartment of Surgical Sciences and Integrated Diagnostics (DISC), University of Genoa, Genoa, Italy.ORCID 0000-0002-8459-2730
Ospedale Policlinico San Martino · ITUniversidade Federal do Rio de Janeiro · BRInstituto Boliviano de Ciencia y Tecnología Nuclear · BO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTypical acute respiratory distress syndrome (ARDS) and severe coronavirus-19 (COVID-19) pneumonia share complex pathophysiology, a high mortality rate, and an unmet need for efficient therapeutics. AREAS COVERED: This review discusses the current advances in understanding the pathophysiologic mechanisms underlying typical ARDS and severe COVID-19 pneumonia, highlighting specific aspects of COVID-19-related acute hypoxemic respiratory failure that require attention. Two models have been proposed to describe the mechanisms of respiratory failure associated with typical ARDS and severe COVID-19 pneumonia. EXPERT OPINION: ARDS is defined as a syndrome rather than a distinct pathologic entity. There is great heterogeneity regarding the pathophysiologic, clinical, radiologic, and biological phenotypes in patients with ARDS, challenging clinicians, and scientists to discover new therapies. COVID-19 has been described as a cause of pulmonary ARDS and has reopened many questions regarding the pathophysiology of ARDS itself. COVID-19 lung injury involves direct viral epithelial cell damage and thrombotic and inflammatory reactions. There are some differences between ARDS and COVID-19 lung injury in aspects of aeration distribution, perfusion, and pulmonary vascular responses.

Indexed as

COVID-19Lung InjuryRespiratory Distress SyndromeRespiratory InsufficiencyHumansLungSARS-CoV-2ARDSCOVID-19pathophysiologyperfusionrespiratory failure

Identifiers

PMID35341424
PMCPMC9115784
OpenAlexW4220774258

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.