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• Tissue oxygenation - oriented Approach to patients with ARDS
  Mohamad Abdelsalam Abdelkader
  Published on: 22 January 2004

• Published on: 22 January 2004

  Tissue oxygenation - oriented Approach to patients with ARDS

  • Mohamad Abdelsalam Abdelkader, King Fahd Hospital in Hofuf

  Dear Editor

  Despite the great advances in critical care medicine, the mortality of ARDS is still high. Protective ventilatory strstegy - utilizing lower tidal volumes and PEEP levels to prevent atelectatic trauma regardless of arterial oxygenation - has been used in an attempt to reduce the mortality of ARDS. Both conventional and protective ventialtory strategies concenterate more on achieving satisfactory arteria...

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  Dear Editor

  Despite the great advances in critical care medicine, the mortality of ARDS is still high. Protective ventilatory strstegy - utilizing lower tidal volumes and PEEP levels to prevent atelectatic trauma regardless of arterial oxygenation - has been used in an attempt to reduce the mortality of ARDS. Both conventional and protective ventialtory strategies concenterate more on achieving satisfactory arterial oxygenation rather than tissue oxygenation . In order to do so, FIO ₂, PEEP and I:E ratio are usually adjusted to maintain arterial O₂ saturation- SPO₂- not less than 90% even at the expense of pulmonary O₂ toxicity - due to high FIO₂ - and barotrauma including more and more lung injury - form hihger PEEP and inverse-ratio ventilation with the potential of Auto-PEEP.According to protective strategy, PEEP is used - even with acceptable SPO₂ - to prevent atelectato-trauma. When SPO₂ is low, PEEP is usually set at higher level to improve arterial oxygenation. In the clinical setting of ARDS, the severely-injured lungs may be particularlly more vulnerable to damage from high FIO₂ and PEEP than would be otherwise expected. It may be more appropriate to concenterate on the tissue oxygenation when dealing with ARDS patients not only the arterial oxygenation. The tissue oxygenation can be monitored either directly by measuring the whole-body O₂ uptake by calorimetery or indirectly by calculating the Oxygen extraction ratio ( 0₂ ER = Sao₂-Sao₂/Sao₂ ) where Sao₂ is the arterial O₂ saturation and Svo₂ is the mixed venous O₂ saturation taken from the pulmonary artery with Swan- Ganz catheter.Other parameters of tissue oxygenation include gasteric mucosal pH - mainly representetive of GIT - and arterial blood lactate - which lack specificity. The tissue oxygenation can be improved and the tissue hypoxia prevented by increasing the oxygen delivery to the tissues - DO₂ - and decreasing the oxygen uptake - VO₂. The Oxygen delivery can be increased not only by improving the arterial O2 saturation but also by optimizing the hemoglobin level and improving the cardiac output - QT . DO2 = 1.34 x Sao₂ x Hb x QT. According to the previous equation, it can be concluded than DO₂ (O₂ delivery) can be maintained - at least theoretically - by supra-normal QT (cardiac output) if Sao₂ (arterial O₂ saturation) is relatively low. The cardiac output may be increased to supra-normal levels by various inotropic agents - that only minimally increase the whole-body O₂ uptake - such as dobutamine and milrinone. To achieve supra-normal QT, in addition to the inotropics, volume expantion - by colloids rather than crystalloids - and vasodilator agents such as prostacyclin may be used. Prostacyclin is a systemic and pulmonary vasodilator that can increase the cardiac output and counteract the expected vasospastic effect of the hypoxemia on the pulmonary vasculature. Using this tissue oxygenation-oriented approach to ARDS patients, we may be able to use more protective ventilatory settings - lower levels of FIO2,PEEP and I:E ratio - and to accept lower levels of arterial O₂ saturation as long as the parameters of tissue oxygenation are acceptable, a method that may be called "permissive hypoxemia". In conclusion, i hypothesize that maintaining adequate tissue oxygenation - by supranormal cardiac output - may enable us to use lower levels of PEEP, FIO₂ and I:E ratio and to accept lower levels of SPO2 with the aim of reducing the risk of pulmonary O₂ toxicity, barotrauma and lund injury that may be particularlly difficult to diagnose in the clinical setting of ARDS.

  Reference

  HR Smith and DG Sinclair Severe pulmonary dysfunction following acute respiratory distress syndrome Postgrad Med J 1996; 72: 555-556

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  Conflict of Interest:
  None declared.

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