Selected article for: "ARDS respiratory distress syndrome and hemoglobin level"

Author: Bein, Thomas; Grasso, Salvatore; Moerer, Onnen; Quintel, Michael; Guerin, Claude; Deja, Maria; Brondani, Anita; Mehta, Sangeeta
Title: The standard of care of patients with ARDS: ventilatory settings and rescue therapies for refractory hypoxemia
  • Document date: 2016_4_4
  • ID: krpg9u1u_1
    Snippet: The acute respiratory distress syndrome (ARDS) is characterized by life-threatening impairment of pulmonary gas exchange, resulting in hypoxemia, hypercapnia, and respiratory acidosis and requiring acute rescue measures. Oxygen delivery to the tissues is necessary for all aerobic life, and tissue hypoxia will result in various deleterious effects including altered vascular reactivity, inflammation, cell apoptosis, and organ dysfunction or failure.....
    Document: The acute respiratory distress syndrome (ARDS) is characterized by life-threatening impairment of pulmonary gas exchange, resulting in hypoxemia, hypercapnia, and respiratory acidosis and requiring acute rescue measures. Oxygen delivery to the tissues is necessary for all aerobic life, and tissue hypoxia will result in various deleterious effects including altered vascular reactivity, inflammation, cell apoptosis, and organ dysfunction or failure [1] . Tissue hypoxia is the result of hypoxemia, and hypoxemia is a consequence of insufficient support of the respiratory system and/or of the oxygen delivery system (cardiac output, hemoglobin level [2] ). Unfortunately, a precise and "simple" limit area to hypoxemia has not been identified and a "critical" level at which harm appears might vary between organs and patients. Furthermore, it is not known whether critically ill patients have the same spectrum of compensatory mechanisms to hypoxemia as the "normal" human body, and the rapidity of onset ("acclimatization effect"), severity, and duration of hypoxemia may determine the induction of tissue hypoxia.

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