Evidence map›Paper›PMID 23347872›Full record

ArticleCritical care (London, England)2013

Moderate and prolonged hypercapnic acidosis may protect against ventilator-induced diaphragmatic dysfunction in healthy piglet: an in vivo study.

Boris Jung, Mustapha Sebbane, Charlotte Le Goff, Nans Rossel, Gerald Chanques, Emmanuel Futier, Jean-Michel Constantin, Stefan Matecki, Samir Jaber

Abstract read
In one paragraph

Article in Critical care (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

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0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. The role of hypercapnia in acute respiratory failure.Intensive care medicine experimental · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Boris Jung
Mustapha Sebbane
Charlotte Le Goff
Nans Rossel
Gerald Chanques
Emmanuel Futier
Jean-Michel Constantin
Stefan Matecki
Samir Jaber

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionProtective ventilation by using limited airway pressures and ventilation may result in moderate and prolonged hypercapnic acidosis, as often observed in critically ill patients. Because allowing moderate and prolonged hypercapnia may be considered protective measure for the lungs, we hypothesized that moderate and prolonged hypercapnic acidosis may protect the diaphragm against ventilator-induced diaphragmatic dysfunction (VIDD). The aim of our study was to evaluate the effects of moderate and prolonged (72 hours of mechanical ventilation) hypercapnic acidosis on in vivo diaphragmatic function.

methodsTwo groups of anesthetized piglets were ventilated during a 72-hour period. Piglets were assigned to the Normocapnia group (n = 6), ventilated in normocapnia, or to the Hypercapnia group (n = 6), ventilated with moderate hypercapnic acidosis (PaCO₂ from 55 to 70 mm Hg) during the 72-hour period of the study. Every 12 hours, we measured transdiaphragmatic pressure (Pdi) after bilateral, supramaximal transjugular stimulation of the two phrenic nerves to assess in vivo diaphragmatic contractile force. Pressure/frequency curves were drawn after stimulation from 20 to 120 Hz of the phrenic nerves. The protocol was approved by our institutional animal-care committee.

resultsModerate and prolonged hypercapnic acidosis was well tolerated during the study period. The baseline pressure/frequency curves of the two groups were not significantly different (Pdi at 20 Hz, 32.7 ± 8.7 cm H₂O, versus 34.4 ± 8.4 cm H₂O; and at 120 Hz, 56.8 ± 8.7 cm H₂O versus 60.8 ± 5.7 cm H₂O, for Normocapnia and Hypercapnia groups, respectively). After 72 hours of ventilation, Pdi decreased by 25% of its baseline value in the Normocapnia group, whereas Pdi did not decrease in the Hypercapnia group.

conclusionsModerate and prolonged hypercapnic acidosis limited the occurrence of VIDD during controlled mechanical ventilation in a healthy piglet model. Consequences of moderate and prolonged hypercapnic acidosis should be better explored with further studies before being tested on patients.

Indexed as

Acidosis, RespiratoryAnimalsAnimals, NewbornDiaphragmHypercapniaMuscle ContractionRespiration, ArtificialSwine

Identifiers

PMID23347872
PMCPMC4056755

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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.