Article

Adaptive Support Ventilation Prevents Ventilator-induced Diaphragmatic Dysfunction in Piglet: An In Vivo and In Vitro Study

Department of Anesthesiology and Critical Care, Intensive Care Unit, Saint Eloi Teaching Hospital, Equipe soutenue par la Région et l'Institut National de la Santé et de la Recherche Médicale 25, Centre Hospitalier Universitaire Montpellier, Montpellier, France.
Anesthesiology (Impact Factor: 5.88). 06/2010; 112(6):1435-43. DOI: 10.1097/ALN.0b013e3181d7b036
Source: PubMed

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.

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    • "VIDD related to totally controlled mechanical ventilation has been well described, both in several animal studies [17,21,22,24-29] and recently in humans [4-8]. Maintaining diaphragm at rest in the present study (Normocapnia group) effectively promoted VIDD (Figure 1). "
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    ABSTRACT: Introduction Protective 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. Methods Two 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. 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.
    Full-text · Article · Jan 2013 · Critical care (London, England)

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    ABSTRACT: La sédation existe dès lors que la VM invasive est instaurée. L’arrêt de la VM qui est l’objectif de la réanimation, passe par une optimisation préalable du couplage sédation-ventilation: sédation la moins profonde possible allant de paire avec des réglages du ventilateur adaptés au patient. Il est donc nécessaire de diminuer l’adaptation du patient au ventilateur (la sédation) et d’optimiser l’adaptation du ventilateur au patient (la ventilation). De même que la sédation doit être comprise comme une analgésie-sédation à la carte allant vers une prise en charge détaillée de l’ensemble des troubles neurologiques et psychologiques chez le patient critique agressé par une réanimation invasive, l’adaptation du ventilateur au patient s’étend à l’adaptation de l’environnement de réanimation au patient allant vers une réanimation minimale invasive, et la moins iatrogénique possible. Le dépistage du prérequis à l’arrêt de la sédation et l’arrêt de la sédation proprement dit sont le préalable indispensable à l’arrêt de la VM qui passe par la recherche quotidienne du prérequis à l’épreuve de ventilation sur pièce en T et sa réalisation. Le couplage sédation-ventilation évoluera probablement vers la période postextubation, avec le développement des techniques de ventilation non invasive, et le recours à un protocole d’analgésie-sédation pour certains patients, comme en VM contrôlée (34).
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