Ic contractile force. Pressure/frequency curves were drawn after stimulation fromIc contractile force. Pressure/frequency curves were

Ic contractile force. Pressure/frequency curves were drawn after stimulation from
Ic 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. 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 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. Conclusions: 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.Introduction Mechanical ventilation is a lifesaving technique and a leading treatment of acute respiratory failure in the intensive care unit (ICU). In the earliest stages of acute respiratory failure, maintaining respiratory muscles at rest, in* Correspondence: [email protected] 1 Intensive Care Unit, Department of Anaesthesia and Critical Care, Saint Eloi Teaching Hospital and Institut National de la Sant?et de la Recherche M icale Unit 1046 (INSERM U-1046), Universit?Montpellier 1, 34295 Montpellier, France Full list of author information is available at the end of the articleparticular the diaphragm, is frequently performed, the better to synchronize the patient and the ventilator. The ventilator settings often use a totally controlled mode and are combined with deep sedation to avoid spontaneous ventilator cycles. One of the consequences of resting respiratory muscles is the occurrence of ventilator-induced diaphragmatic dysfunction (VIDD) [1-3], largely described in animal models and more sparsely, but recently, in human studies [4-8]. ZM241385 web Another complication of mechanical ventilation is the occurrence of ventilator-induced lung?2013 Jung et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Jung et al. Critical Care 2013, 17:R15 http://ccforum.com/content/17/1/RPage 2 ofinjury (VILI), which is magnified when high alveolar pressures and volumes are applied [9], even in healthy lungs [10,11]. As a consequence, the historic goal of mechanical ventilation, normalizing the gas exchange, has evolved PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25636517 toward preventing lung injury by reducing alveolar pressure and lung volume, at the cost of reduced gas exchange. This concept, labeled protective ventilation, may lead to a permissive hypercapnic acidosis, which is well tolerated when not so severe (pH > 7.20 with PaCO2 < 60 to 65 mm Hg) [12]. Furthermore, some studies have shown a potential beneficial effect of moderate and prolonged hypercapnic acidosis per se on lung inflammation in animal models of experimental pneumonia [13], and it may prevent hypoxia-induced oxydative stress in the lungs [14] and NF-B activation in pulmonary endothelial cells exposed to lipopolysaccharide [15]. Hypercapnic acidosis may also inhibit endogenous xanthine oxidase activity.