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ABSTRACT: INTRODUCTION: Protective ventilation using limited airway pressures and ventilation may result in moderate and prolonged hypercapnic acidosis, as often observed in critically ill patients. Because allow of moderate and prolonged hypercapnia may be considered as a protective measure for the lungs, we hypothesized that moderate and prolonged hypercapnic acidosis may protect diaphragm against ventilator induced diaphragmatic dysfunction (VIDD). The aim of our study was to evaluate the effects of moderate and prolonged (72-h of mechanical ventilation) hypercapnic acidosis on in-vivo diaphragmatic function. METHODS: Two groups of anesthetized piglets were ventilated during a 72-h 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 mmHg) during the 72-h period of the study. Every 12h, we measured transdiaphragmatic pressure (Pdi) after bilateral, supramaximal trans-jugular stimulation of the two phrenic nerves to assess in vivo diaphragmatic contractile force. Pressure-frequency curves were drawn after stimulation from 20 to 120Hz of the phrenic nerves. The protocol was approved our institutional animal care committee's. RESULTS: Moderate 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 vs. 34.4+/-8.4 cm H2O; and at 120 Hz = 56.8+/-8.7 vs. 60.8+/-5.7 cm H2O, for Normocapnia and Hypercapnia groups respectively). After 72-h of ventilation, Pdi decreased by 25% of its baseline value in the normocapnia group, whereas Pdi did not decrease in the hypercapnia group. CONCLUSION: Moderate 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.
Critical care (London, England) 01/2013; 17(1):R15. · 4.61 Impact Factor
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Boris Jung,
Thomas Rimmele, Charlotte Le Goff,
Gérald Chanques,
Philippe Corne,
Olivier Jonquet,
Laurent Muller,
Jean-Yves Lefrant,
Christophe Guervilly,
Laurent Papazian,
Bernard Allaouchiche,
Samir Jaber
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ABSTRACT: In this study, we sought describe the incidence and outcomes of severe metabolic or mixed acidemia in critically ill patients as well as the use of sodium bicarbonate therapy to treat these illnesses.
We conducted a prospective, observational, multiple-center study. Consecutive patients who presented with severe acidemia, defined herein as plasma pH below 7.20, were screened. The incidence, sodium bicarbonate prescription and outcomes of either metabolic or mixed severe acidemia were analyzed.
Among 2, 550 critically ill patients, 200 (8%) presented with severe acidemia, and 155 (6% of the total admissions) met the inclusion criteria. Almost all patients needed mechanical ventilation and vasopressors during their ICU stay, and 20% of them required renal replacement therapy within the first 24 hours of their ICU stay. Severe metabolic or mixed acidemia was associated with a mortality rate of 57% in the ICU. Delay of acidemia recovery as opposed to initial pH value was associated with increased mortality in the ICU. The type of acidemia did not influence the decision to administer sodium bicarbonate.
The incidence of severe metabolic or mixed acidemia in critically ill patients was 6% in the present study, and it was associated with a 57% mortality rate in the ICU. In contradistinction with the initial acid-base parameters, the rapidity of acidemia recovery was an independent risk factor for mortality. Sodium bicarbonate prescription was very heterogeneous between ICUs. Further studies assessing specific treatments may be of interest in this population.
Critical care (London, England) 10/2011; 15(5):R238. · 4.61 Impact Factor
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Boris Jung,
Jean-Michel Constantin,
Nans Rossel, Charlotte Le Goff,
Mustapha Sebbane,
Yannael Coisel,
Gerald Chanques,
Emmanuel Futier,
Gerald Hugon,
Xavier Capdevila,
Basil Petrof,
Stefan Matecki,
Samir Jaber
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ABSTRACT: Contrary to adaptive support ventilation (ASV), prolonged totally controlled mechanical ventilation (CMV) results in the absence of diaphragm activity and causes ventilator-induced diaphragmatic dysfunction. Because maintaining respiratory muscles at rest is likely a major cause of ventilator-induced diaphragmatic dysfunction, ASV may prevent its occurrence in comparison with CMV. The aim of our study was to compare the effects of ASV with those of CMV on both in vivo and in vitro diaphragmatic properties.
Two groups of six anesthetized piglets were ventilated during a 72-h period. Piglets in the CMV group (n = 6) were ventilated without spontaneous ventilation, and piglets in the ASV group (n = 6) were ventilated with spontaneous breaths. Transdiaphragmatic pressure was measured after bilateral, supramaximal transjugular stimulation of the two phrenic nerves. A pressure-frequency curve was drawn after stimulation from 20 to 120 Hz of the phrenic nerves. Diaphragm fiber proportions and mean sectional area were evaluated.
After 72 h of ventilation, transdiaphragmatic pressure decreased by 30% of its baseline value in the CMV group, whereas it did not decrease in the ASV group. Although CMV was associated with an atrophy of the diaphragm (evaluated by mean cross-sectional area of both the slow and fast myosin chains), atrophy was not detected in the ASV group.
Maintaining diaphragmatic contractile activity by using the ASV mode may protect the diaphragm against the deleterious effect of prolonged CMV, as demonstrated both in vitro and in vivo, in healthy piglets.
Anesthesiology 06/2010; 112(6):1435-43. · 5.36 Impact Factor
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Boris Jung,
Jean-Michel Constantin,
Nans Rossel, Charlotte Le Goff,
Mustapha Sebbane,
Yannael Coisel,
Gerald Chanques,
Emmanuel Futier,
Gerald Hugon,
Xavier Capdevila,
Basil Petrof,
Stefan Matecki,
Samir Jaber
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ABSTRACT: Background: Contrary to adaptive support ventilation (ASV), prolonged totally controlled mechanical ventilation (CMV) results in the absence of diaphragm activity and causes ventilator-induced diaphragmatic dysfunction. Because main-taining respiratory muscles at rest is likely a major cause of ventilator-induced diaphragmatic dysfunction, ASV may prevent its occurrence in comparison with CMV. The aim of our study was to compare the effects of ASV with those of CMV on both in vivo and in vitro diaphragmatic properties.
Anesthesiology 05/2010; 112(6):1435-1443. · 5.36 Impact Factor
