• K M Kelly.
• Surgical Intensive Care Unit, Morristown Memorial Hospital, New Jersey, USA.
• Crit Care Clin. 1996 Jul 1; 12 (3): 635-44.

AbstractIncreasing DO2 to supranormal levels, spontaneously or therapeutically, correlates with better survival in the critically ill patient, but not all patients who attain a DO2I greater than 600 mL/min/m2 survive. Conversely, there is often a 50% or greater survival rate in patients who do not reach normal DO2I values. No investigator has been able to show an incremental increase in survival with increasing DO2I; but studies have shown improved survival rates with increasing SVO2. The observations support the idea that absolute values for DO2I are not as important as the ability to normalize SVO2 when SVO2 is low. Therapeutic interventions may be most effective in those patients demonstrating increased peripheral oxygen extraction (SVO2 = 40% to 60%). These "type A" patients are mounting an appropriate response to increased needs. Several authors have noted increased mortality rates for patients unable to increase a low VO2 despite increased DO2. This is McClave's "type B" physiologic response. Flow dependency is not correlated with mortality. In fact, it is the patient who can raise VO2 when DO2 is increased who tends to survive. Dantzker, Giunta, and Hotchkiss propose that the flow dependency of VO2 may be a normal physiologic response. Clinical outcomes continue to support the necessity of maintaining an optimal DO2 in critically ill patients. The question of what is optimal DO2 has yet to be answered. Vincent nicely summaries the present "state of the art" in treating the critically ill: "Rather than aim at achieving arbitrary target values in all patients, we believe that this process should be based on a careful clinical evaluation of the individual patient, complemented by measurements of cardiac output, determinations of mixed venous oxygen saturation (or the oxygen-extraction ratio), and other measurements of tissue perfusion, such as the base deficit, blood lactate level, or gastric intramucosal pH." In addition, the type or stage of physiologic response should be identified. Independent markers of tissue ischemia should be sought and abnormalities corrected by increasing DO2. SVO2 should be normalized when low, again by increasing DO2. Data continue to support clinical interventions aimed at optimizing DO2. Does increasing DO2 increase the survival rates of critically ill patients? Sometimes.

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