Role of Oxygen Debt in the Development of Organ Failure Sepsis, and Death in High-Risk Surgical Patients (4)
The patients were allocated (a) to a control group (29 patients) maintained at normal hemodynamic and oxygen transport values, or (b) to a protocol group (27 patients) maintained at supranormal values of Cl greater than 4.5 L/min*m2, oxygen delivery (DoJ greater than 600 ml/min-m2, and Vo2 greater than 170 ml/min-m2; these therapeutic goals were empirically determined as the median values of critically ill survivors of high-risk surgery.
Role of Oxygen Debt in the Development of Organ Failure Sepsis, and Death in High-Risk Surgical Patients (3)
The second aim was to study the capacity of supranormal cardiac index (Cl), Do2, and Vo2 to reduce tissue oxygen debt and subsequent organ failures as part of a prospective randomized clinical trial of high-risk surgical patients. In this study, a control group was maintained at normal circulatory values, while a protocol group was maintained at supranormal values that were empirically observed in critically ill survivors.
Role of Oxygen Debt in the Development of Organ Failure Sepsis, and Death in High-Risk Surgical Patients (2)
Subsequently, increased cardiac output and Vo2 values were reported in patients with various surgical illnesses,’ but these studies primarily involved Vo2 measurements in the postoperative period after the hemodynamic crisis. When temporal patterns of Vo2 were observed throughout the perioperative course by frequent serial Vo2 measurements, an early reduction in Vo2 was observed at or prior to the initial hypotensive crisis and was followed by compensatory increases in cardiac output and Vo2.n 15 These increases were greater in the survivors. Increased Vo2 was also reported by other investigators in septic, traumatic, and postoperative patients, especially in the patients given fluid therapy. Moreover, prospective trials have shown improved survival when Vo2 was increased by fluids and inotropic therapy.
Role of Oxygen Debt in the Development of Organ Failure Sepsis, and Death in High-Risk Surgical Patients (1)
In 1922, Blalock defined shock as a failure of tissue perfusion and in experimental shock demonstrated reduced renal and splanchnic oxygen consumption as a measure of perfusion. Subsequent studies on lethal hemorrhagic shock in dogs confirmed the early reduced rate of oxygen consumption (Vo2).’ When the survivors of experimental hemorrhagic shock were followed over an appropriate time period, there were later increases in Vo2.