Dead space in acute respiratory distress syndrome: more than a feeling!
نویسندگان
چکیده
Why clinicians are slow to implement advances in diagnosis and treatment from well-designed clinical trials is a continuously debated question in critical care. For instance, prone positioning significantly improves mortality in patients with severe acute respiratory distress syndrome (ARDS), but the usefulness of recruitment measures in this population is still under debate. Nevertheless, a recent observational study in intensive care units in 50 countries found that prone positioning was used in only 16.3 % of patients with severe ARDS, whereas recruitment maneuvers were used in 32.7 % [1]. Similarly, despite the established usefulness of measuring physiologic variables such as dead space in mechanically ventilated ARDS patients, this practice is not widely employed. Dead space refers to lung areas that are ventilated but not perfused. Dead space comprises two separate components: airway dead space (the volume of areas that do not contribute to gas exchange) and alveolar dead space (the volume of well-ventilated alveoli that receive minimal blood flow). The physiologic ventilatory dead space fraction (VD/VTphys) is usually defined as the fraction of tidal volume (VT) that does not participate in gas exchange [2, 3]. Currently, dead space is measured at the bedside by volumetric capnography, which reports expired CO2 elimination as a function of expired VT, and VD/VTphys is calculated using the Enghoff ’s modification of Bohr’s original equation: VD/VTphys = (PaCO2 – PECO2)/PaCO2, where PaCO2 is the arterial partial pressure of CO2 obtained by arterial blood sampling and PECO2 is an estimate of mixed expired partial pressure of CO2 obtained from the mid-portion of phase III of the volumetric capnogram [2, 3]. Modern volumetric capnographs incorporate this physiologic approach, enabling intensivists to measure VD/VTphys at the bedside. However, if data generated breath-by-breath by capnographs are not integrated and analyzed together with data coming from other physiologic monitors and lung image analysis, their clinical meaning could be incomplete and even misleading. Over 40 years ago, Suter et al. [4] pointed out that increasing positive end-expiratory pressure (PEEP) in ARDS augments blood oxygenation and decreases shunt. Although they used the maximum level of oxygen transport to determine the optimum levels of PEEP, they showed that maximizing total compliance and minimizing physiologic dead space (VD/VTphys) yielded the best results. Interestingly, the decrease in VD/VTphys occurred with no significant change in anatomic dead space. The authors state that “this observation supports the concept of the recruitment of previously atelectatic lung areas leading to an increase in compliance and a decrease in alveolar dead space, whereas overdistension of alveoli decreases compliance and increases alveolar dead space” [4]. This is, in a nutshell, exactly what intensivists strive for at the bedside: to recruit the lung without doing harm. Unfortunately, in critical care practice dead space is not routinely measured at the bedside. Factors that explain this reluctance to monitor dead space at the bedside include difficulties in understanding physiologically derived information and in interpreting capnograms, together with the lack of integration of CO2 waveforms and derived data with other respiratory measurements. There are several reasons why dead space is an attractive parameter that should be routinely monitored in critical care. First, dead space has important prognostic implications. In ARDS, alveolar and endothelial cell injuries result in alterations of the pulmonary microcirculation in all lung compartments with high and low * Correspondence: [email protected] Critical Care Center, Hospital de Sabadell, Corporació Sanitària Universitària ParcTaulí, Universitat Autònoma de Barcelona, c. ParcTaulí 1, 08208 Sabadell, Spain CIBER de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain Full list of author information is available at the end of the article
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Alveolar Dead Space Fraction Discriminates Mortality in Pediatric Acute Respiratory Distress Syndrome.
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