A meta-analysis of three randomized controlled trials (RCTs) concluded that PCV was not superior to VCV, with a relative risk of hospital and ICU mortality for PCV versus VCV of 0.83 (95 % CI 0.67–1.02 p = 0.08) and 0.84 (95 % CI 0.71–0.99 p = 0.04), respectively. Whether pressure-controlled ventilation (PCV) can reduce ventilator-associated lung injury (VALI) compared to volume-controlled (VCV) ventilation is a matter of debate. Therefore a target for conservative arterial oxygenation is recommended (PaO 2 = 65–75 mmHg, SaO 2 = 90–95 %), which should be bundled in a general “organ failure prevention” strategy. However an individualized, organ-specific approach for monitoring of hypoxemia is currently not available. In summary, “simple” and global parameters (PaO 2, SaO 2, SvO 2, lactate) are imprecise surrogates for hypoxia in ARDS patients. It remains to be evaluated in further studies whether selected biomarkers may help identify tissue hypoxia in the individual patient. Since inadequate tissue oxygenation as well as excessive oxygen administration (with expression of oxygen reactive species) can both be harmful, a careful balance based on precise control of arterial oxygenation including the acceptance of a “safe” threshold may avoid deleterious hypoxia as well as hyperoxia-associated injury. In clinical practice the definition of “hypoxemia” is often based on one or more of these global values, and currently no parameter for the precise assessment of tissue hypoxia in the individual patient is available. ![]() Hypoxemia and tissue hypoxia could be detected by PaO 2, SaO 2, serum lactate, and central venous oxygen saturation (SvO 2), which are global measurements, and the extent to which these flow/volume-average-weighted measurements reflect organ hypoxia remains unknown. Furthermore, in a retrospective analysis of ARDS patients, lower PaO 2 during mechanical ventilation (median < 72 mmHg) was associated with a higher incidence of long-term cognitive impairment and psychiatric disorders compared with higher PaO 2 (median 86 mmHg, p < 0.02). ![]() A recent Cochrane review failed to identify any relevant studies evaluating hypoxemia versus normoxemia in ventilated patients with ARDS. Of note the “classical” concept of oxygen delivery/consumption dependency is controversial. In recent years a strategy of permissive hypoxemia (SaO 2 82–88 %) in patients with severe ARDS was proposed aimed at minimizing the harmful effects of high inspiratory oxygen concentrations by accepting a low SaO 2 and optimizing cardiac output to maintain adequate oxygen delivery. 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.Ī clinical determination of hypoxemia varies, but typical values areĪrterial oxygenation (pulse oximetry ) < 88 %. 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. 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 ). 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. 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. Introduction: hypoxemia in ARDS: definition, monitoring, and pitfalls A negative fluid balance is associated with improved lung function and the use of hemofiltration might be indicated for specific indications. ![]() Neuromuscular blockage (Cisatracurium ≤ 48 hrs after onset of ARDS), as well as an adequate sedation strategy (score guided) is an important supportive therapy. An advanced infection management/control includes early diagnosis of bacterial, atypical, viral and fungal specimen (blood culture, bronchoalveolar lavage), and of infection sources by CT scan, followed by administration of broad-spectrum anti-infectives. Individual bedside methods to guide PEEP/recruitment (e.g., transpulmonary pressure) are not (yet) available. Typical clinical determinations are: arterial partial pressure of oxygen 12 cmH 2O), a recruitment manoeuvre in special situations, and a ‘balanced’ respiratory rate (20-30/min). A precise definition of life-threating hypoxemia is not identified.
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