Chest
-
Randomized Controlled Trial Clinical Trial
Elevation of cardiac output and oxygen delivery improves outcome in septic shock.
Septic shock is characterized by hypoperfusion and tissue energy defects. We prospectively evaluated the therapeutic benefit of augmenting cardiac output and therefore oxygen delivery (DO2) on mortality in patients with septic shock. Twenty-five patients were randomized to a normal treatment (NT) group and 26 patients were randomized to an optimal treatment (OT) group. ⋯ Since some of the NT patients were spontaneously hyperdynamic and some of the OT patients did not achieve their desired end point, patients were arbitrarily subsetted using a midpoint CI of 4.5 L/min/m2. The NT less than 4.5 group had a CI of 3.1 +/- 0.2 L/min/m2 and DO2 of 10.9 +/- 1.0 ml/min/kg while the OT group greater than 4.5 L/min/m2 had a CI of 5.7 +/- 0.2 L/min/m2 and a DO2 of 13.8 +/- 0.7 ml/min/kg (p less than 0.01). Mortality in the NT less than 4.5 group was 74 percent as compared with 40 percent in the OT greater than 4.5 group (p less than 0.05).
-
Randomized Controlled Trial Clinical Trial
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 (VO2) at frequent intervals before, during, and immediately after surgical operations and calculated the rate of VO2 deficit from the measured VO2 minus the VO2 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 VO2 deficit averaged 33.2 +/- 4.0 L/m2 (+/- SEM) at its maximum, which occurred 17.8 +/- 2.2 h after surgery. ⋯ 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 less than 0.05), fewer organ failures, and lower mortality (4 percent vs 33 percent; p less than 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 VO2 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.