ArticleCritical care (London, England)2013
Moderate and prolonged hypercapnic acidosis may protect against ventilator-induced diaphragmatic dysfunction in healthy piglet: an in vivo study.
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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Who cites it
10 citing papers in PubMed.
- The role of hypercapnia in acute respiratory failure.Intensive care medicine experimental · 2019Review
- Ventilator-induced diaphragm dysfunction: translational mechanisms lead to therapeutical alternatives in the critically ill.Intensive care medicine experimental · 2019Review
- Effects of hypercapnia in acute respiratory distress syndrome.Annals of translational medicine · 2018Review
- Critical illness-associated diaphragm weakness.Intensive care medicine · 2017Review
- Kinetics of ventilation-induced changes in diaphragmatic metabolism by bilateral phrenic pacing in a piglet model.Scientific reports · 2016Article
- Dysfunction of respiratory muscles in critically ill patients on the intensive care unit.Journal of cachexia, sarcopenia and muscle · 2016Review
- Hypercapnia attenuates ventilator-induced diaphragm atrophy and modulates dysfunction.Critical care (London, England) · 2014Article
- [Ventilator-induced diaphragm dysfunction : clinically relevant problem].Der Anaesthesist · 2014Review
- Hypercapnia: is it protective in lung injury?Medical gas research · 2013Article
- Hypercapnia and ventilator-induced diaphragmatic dysfunction.Critical care (London, England) · 2013Article
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9 authors.
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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.
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