Effect of hyperoxia on VO2 under pathological conditions

(Condition of oxygen-supply dependence)

In the healthy individual at rest, VO2 is kept constant and not confined by oxygen delivery. However, under certain pathological conditions, DO2 falls below a critical value and induces a concomitant decline of VO2 which characterizes the period of pathological oxygen supply dependence, and which has been reported in various disease states such as sepsis syndrome, haemorrhage or multi-system organ failure36. Even if DO2 is above the critical threshold, a dependence of VO2 on DO2 has been shown, and used as a prognostic outcome index in critically ill patients37.

Although an increased inspiratory fraction of oxygen (FiO2) is widely used in clinical practice to improve tissue oxygenation, only a few investigations deal with the impact of hyperoxia on VO2. An investigation in 20 critically ill (11 septic, 9 non-septic) patients38 showed a reversible decrease of oxygen consumption by 10%, and maintenance of cardiac index with increasing FiO2 from 0.4 to 1.0. To the authors, the decrease of VO2 without decrease of DO2 was a sign of maldistribution of blood flow and functional oxygen shunting as protection against normobaric hyperoxia.

There is rare data about the effect of hyperbaric hyperoxia on oxygen consumption. Mathieu39 studied the VO2-DO2 relationship in eight critically ill patients undergoing HBO therapy at 253.2kPa (2.5ata) for 90 minutes by indirect calorimetry and by the reverse Fick method. The study aimed at evaluating whether VO2 would be modified by HBO, and whether the effect of the increase of DO2 by HBO would be comparable to that of an increased DO2 by a standardized volume challenge. The fluid loading led to a rise in DO2 without concomitant increase of VO2. Hyperbaric oxygen did not induce a rise in VO2 despite a rise of DO2.

Cerebral oxygen consumption has been investigated in 37 severely brain injured patients40. A maximum of seven treatments per patient had been applied at 151.9kPa (1.5ata) for 60 minutes. Patients were divided into the three categories of reduced, normal or increased pre-session cerebral blood flow. Cerebral blood flow, arterial/venous oxygen content difference, cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid lactate and intracranial pressure values were assessed one hour before, and one and six hours after HBO therapy. CMRO2 increased and lactate levels decreased after treatment, which suggested an improvement of aerobic cerebral metabolism and showed a prolonged effect of HBO, which did not last, however, until the next hyperbaric session. The authors concluded that more frequent sessions might be beneficial in severely brain-injured patients.

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