Ventilación soporte elevada y ventilación mécanica inducen disfunción y atrofia del diafragma
Both high level pressure support ventilation and controlled mechanical ventilation induce diaphragm dysfunction and atrophy.
Hudson MB, Smuder AJ, Nelson WB, Bruells CS, Levine S, Powers SK.
Crit Care Med. 2012 Apr;40(4):1254-60. doi: 10.1097/CCM.0b013e31823c8cc9.
Abstract
OBJECTIVES: Previous workers have demonstrated that controlled mechanical ventilation results in diaphragm inactivity and elicits a rapid development of diaphragm weakness as a result of both contractile dysfunction and fiber atrophy. Limited data exist regarding the impact of pressure support ventilation, a commonly used mode of mechanical ventilation-that permits partial mechanical activity of the diaphragm-on diaphragm structure and function. We carried out the present study to test the hypothesis that high-level pressure support ventilation decreases the diaphragm pathology associated with CMV. METHODS:Sprague-Dawley rats were randomly assigned to one of the following five groups:1) control (no mechanical ventilation); 2) 12 hrs of controlled mechanical ventilation (12CMV); 3) 18 hrs of controlled mechanical ventilation (18CMV); 4) 12 hrs of pressure support ventilation (12PSV); or 5) 18 hrs of pressure support ventilation (18PSV). MEASUREMENTS AND MAIN RESULTS:We carried out the following measurements on diaphragm specimens: 4-hydroxynonenal-a marker of oxidative stress, active caspase-3 (casp-3), active calpain-1 (calp-1), fiber type cross-sectional area, and specific force (sp F). Compared with the control, both 12PSV and 18PSV promoted a significant decrement in diaphragmatic specific force production, but to a lesser degree than 12CMV and 18CMV. Furthermore, 12CMV, 18PSV, and 18CMV resulted in significant atrophy in all diaphragm fiber types as well as significant increases in a biomarker of oxidative stress (4-hydroxynonenal) and increased proteolytic activity (20S proteasome, calpain-1, and caspase-3). Furthermore, although no inspiratory effort occurs during controlled mechanical ventilation, it was observed that pressure support ventilation resulted in large decrement, approximately 96%, in inspiratory effort compared with spontaneously breathing animals. CONCLUSIONS: High levels of prolonged pressure support ventilation promote diaphragmatic atrophy and contractile dysfunction. Furthermore, similar to controlled mechanical ventilation, pressure support ventilation-induced diaphragmatic atrophy and weakness are associated with both diaphragmatic oxidative stress and protease activation.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3308123/pdf/nihms338236.pdf
Efectos de la administración aguda de corticoides durante la ventilación mecánica sobre el diafragma de la rata
Effects of acute administration of corticosteroids during mechanical ventilation on rat diaphragm.
Maes K, Testelmans D, Cadot P, Deruisseau K, Powers SK, Decramer M, Gayan-Ramirez G.
Am J Respir Crit Care Med. 2008 Dec 15;178(12):1219-26. doi: 10.1164/rccm.200702-296OC. Epub 2008 Oct 10.
Abstract
RATIONALE: Mechanical ventilation is known to induce ventilator-induced diaphragm dysfunction. Patients submitted to mechanical ventilation often receive massive doses of corticosteroids that may cause further deterioration of diaphragm function. OBJECTIVES: To examine whether the combination of 24 hours of controlled mechanical ventilation with corticosteroid administration would exacerbate ventilator-induced diaphragm dysfunction. METHODS: Rats were randomly assigned to a group submitted to 24 hours of controlled mechanical ventilation receiving an intramuscular injection of saline or 80 mg/kg methylprednisolone, a group submitted to 24 hours of spontaneous breathing receiving saline, or methylprednisolone and a control group. MEASUREMENTS AND MAIN RESULTS: The diaphragm force-frequency curve was shifted downward in the mechanical ventilation group, but this deleterious effect was prevented when corticosteroids were administered. Diaphragm cross-sectional area of type I fibers was similarly decreased in both mechanical ventilation groups while atrophy of type IIx/b fibers was attenuated after corticosteroid administration. The mechanical ventilation-induced reduction in diaphragm MyoD and myogenin protein expression was attenuated after corticosteroids. Plasma cytokine levels were unchanged while diaphragm lipid hydroperoxides were similarly increased in both mechanical ventilation groups. Diaphragmatic calpain activity was significantly increased in the mechanical ventilation group, but calpain activation was abated with corticosteroid administration. Inverse correlations were found between calpain activity and diaphragm force. CONCLUSIONS:A single high dose of methylprednisolone combined with controlled mechanical ventilation protected diaphragm function from the deleterious effects of controlled mechanical ventilation. Inhibition of the calpain system is most likely the mechanism by which corticosteroids inducethis protective effect.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266049/pdf/AJRCCM178121219.pdf
La ventilación mecánica prolongada altera la estructura y función diafragmática
Prolonged mechanical ventilation alters diaphragmatic structure and function.
Powers SK, Kavazis AN, Levine S.
Crit Care Med. 2009 Oct;37(10 Suppl):S347-53. doi: 10.1097/CCM.0b013e3181b6e760.
Abstract
OBJECTIVE:To review current knowledge about the impact of prolonged mechanical ventilation on diaphragmatic function and biology. MEASUREMENTS:Systematic literature review.CONCLUSIONS:Prolonged mechanical ventilation can promote diaphragmatic atrophy and contractile dysfunction. As few as 18 hrs of mechanical ventilation results in diaphragmatic atrophy in both laboratory animals and humans. Prolonged mechanical ventilation is also associated with diaphragmatic contractile dysfunction. Studies using animal models revealed that mechanical ventilation-induced diaphragmatic atrophy is due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, and the ubiquitin-proteasome system as key proteases that contribute to mechanical ventilation-induced diaphragmatic proteolysis. The scientific challenge for the future is to delineate the mechanical ventilation-induced signaling pathways that activate these proteases and depress protein synthesis in thediaphragm. Future investigations that define the signaling mechanisms responsible for mechanical ventilation-induced diaphragmatic weakness will provide the knowledge required for the development of new medicines that can maintain diaphragmatic mass and function during prolongedmechanical ventilation.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909674/pdf/nihms218840.pdf
Atentamente
Dr. Juan C. Flores-Carrillo
Anestesiología y Medicina del Dolor
www.anestesia-dolor.org
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