Role of Oxygen Debt in the Development of Organ Failure Sepsis, and Death in High-Risk Surgical Patients

In a series of 253 high-risk surgical patients, we measured the oxygen consumption ( ${\dot{\text{V}}\text{o}}_2$) at frequent intervals before, during, and immediately after surgical operations and calculated the rate of ${\dot{\text{V}}\text{o}}_2$ deficit from the measured ${\dot{\text{V}}\text{o}}_2$ minus the ${\dot{\text{V}}\text{o}}_2$ need estimated from the patient's own resting preoperative control values corrected for both temperature and anesthesia. The calculated oxygen deficit was related to multiple organ failure, complications, and outcome. The 64 patients who died all had organ failure; their cumulative ${\dot{\text{V}}\text{o}}_2$ deficit averaged 33.2 ± 4.0 L/m² (± SEM) at its maximum, which occurred 17.8 ± 2.2 h after surgery. In the 31 survivors with organ failure, the cumulative ${\dot{\text{V}}\text{o}}_2$ deficit averaged 21.6 ± 3.7 L/m² at its maximum, which occurred 10.1 ± 2.7 h after surgery (p<0.05). In the 158 survivors without organ failure or major complications, the maximum cumulative ${\dot{\text{V}}\text{o}}_2$ deficit averaged 9.2 ± 1.3 L/m² at 4.1 ± 0.6 h after surgery (p<0.05). In a prospective randomized clinical trial, a protocol group maintained at supranormal hemodynamic and oxygen transport values had significantly reduced oxygen debt (7.6 ± 3.4 L/m² vs 17.3 ± 6.8 L/m²; p<0.05), fewer organ failures, and lower mortality (4 percent vs 33 percent; p<0.05) compared with a control group maintained at normal hemodynamic values. The data demonstrate a strong relationship between the magnitude and duration of the ${\dot{\text{V}}\text{o}}_2$ deficit in the intraoperative and early postoperative period and the subsequent appearance of organ failure and death. The latter may be reduced when oxygen debts were prevented or minimized by augmenting naturally occurring compensations that increased oxygen delivery. (Chest 1992; 102:208–15)