Debate Pro/Contra. ¿Debe el PaCO2 ser estrictamente controlado en todos los pacientes con lesiones cerebrales agudas?
Pro/con debate: should PaCO2 be tightly controlled in all patients with acute brain injuries?
Go SL, Singh JM.
Crit Care. 2013 Jan 29;17(1):202. doi: 10.1186/cc11389.
Abstract
You are the attending intensivist in a neurointensive care unit caring for a woman five days post-rupture of a cerebral aneurysm (World Federation of Neurological Surgeons Grade 4 and Fisher Grade 3). She is intubated for airway protection and mild hypoxemia related to an aspiration event at the time of aneurysm rupture, but is breathing spontaneously on the ventilator. Your patient is spontaneously hyperventilating with high tidal volumes despite minimal support and has developed significant hypocapnia. She has not yet developed the acute respiratory distress syndrome. You debate whether to tightly control her partial pressure of arterial carbon dioxide, weighing the known risks of acute hypocapnia in other forms of brain injury against the potential loss of clinical neuromonitoring associated with deep sedation and neuromuscular blockade in this patient who is at high risk of delayed ischemia from vasospasm. You are also aware of the potential implications of tidal volume control if this patient were to develop the acute respiratory distress syndrome and the effect of permissive hypercapnia on her intracranial pressure. In this paper we provide a detailed and balanced examination of the issues pertaining to this clinical scenario, including suggestions for clinical management of ventilation, sedation and neuromonitoring. Until more definitive clinical trial evidence is available to guide practice, clinicians are forced to carefully weigh the potential benefits of tight carbon dioxide control against the potential risks in each individual patient based on the clinical issues at hand.
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Hipercapnia. Un ambiente no permisivo para el pulmón.
Hypercapnia: a nonpermissive environment for the lung.
Vadász I, Hubmayr RD, Nin N, Sporn PH, Sznajder JI.
Am J Respir Cell Mol Biol. 2012 Apr;46(4):417-21. doi: 10.1165/rcmb.2011-0395PS. Epub 2012 Jan 12.
Abstract
Patients with severe acute and chronic lung diseases develop derangements in gas exchange that may result in increased levels of CO(2) (hypercapnia), the effects of which on human health are incompletely understood. It has been proposed that hypercapnia may have beneficial effects in patients with acute lung injury, and the concepts of "permissive" and even "therapeutic" hypercapnia have emerged. However, recent work suggests that CO(2) can act as a signaling molecule via pH-independent mechanisms, resulting in deleterious effects in the lung. Here we review recent research on how elevated CO(2) is sensed by cells in the lung and the potential harmful effects of hypercapnia on epithelial and endothelial barrier, lung edema clearance, innate immunity, and host defense. In view of these findings, we raise concerns about the potentially deleterious effects hypercapnia may have in patients with acute and chronic lung diseases.
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Investigación a la clínica. La acidosis hipercápnica en la lesión pulmonar - de permisiva a terapéutica.
Bench-to-bedside review: hypercapnic acidosis in lung injury--from 'permissive' to 'therapeutic'.
Ijland MM, Heunks LM, van der Hoeven JG.
Crit Care. 2010;14(6):237. doi: 10.1186/cc9238. Epub 2010 Nov 3.
Abstract
Modern ventilation strategies for patients with acute lung injury and acute respiratory distress syndrome frequently result in hypercapnic acidosis (HCA), which is regarded as an acceptable side effect ('permissive hypercapnia'). Multiple experimental studies have demonstrated advantageous effects of HCA in several lung injury models. To date, however, human trials studying the effect of carbon dioxide per se on outcome in patients with lung injury have not been performed. While significant concerns regarding HCA remain, in particular the possible unfavorable effects on bacterial killing and the inhibition of pulmonary epithelial wound repair, the potential for HCA in attenuating lung injury is promising. The underlying mechanisms by which HCA exerts its protective effects are complex, but dampening of the inflammatory response seems to play a pivotal role. After briefly summarizing the physiological effects of HCA, a critical analysis of the available evidence on the potential beneficial effects of therapeutic HCA from in vitro, ex vivo and in vivo lung injury models and from human studies will be reviewed. In addition, the potential concerns in the clinical setting will be outlined.
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