Faculty Bibliography

We analyzed the relationship of increases in oxygen delivery to changes in oxygen consumption in ten patients with hyperdynamic septic shock. Increases in oxygen delivery from 413 +/- 14 (SEM) to 535 +/- 19 ml/min X m2 (p less than .01) were associated with increases in oxygen consumption from 136 +/- 10 to 161 +/- 5 ml/min X m2 (p less than .05). Arterial lactate decreased from 4.6 +/- 1.6 to 2.1 +/- 0.3 mmol/L (p less than .05). These observations suggest that oxygen utilization is perfusion-limited in hyperdynamic septic shock

We prospectively studied 18 patients with septic shock prior to and during volume infusion in order to evaluate their hemodynamic response to fluid repletion. Fluid challenge increased left heart filling pressure from 7.7 +/- 0.5 to 15.4 +/- 0.6 mm Hg (P less than .01). The increases in left ventricular filling were associated with significant increases in stroke volume index from 25.4 +/- 2.5 to 35.7 +/- 2.5 ml/min/M2 and cardiac index from 2.49 +/- 0.19 to 3.32 +/- 0.16 L/min/M2. However, at the end of fluid challenge, the patients exhibited depressed left ventricular performance as evidenced by a left ventricular stroke work index of 29.5 +/- 2.6 g X m/M2. Over the next 24 hours of maintenance fluid infusion, the left ventricular stroke work index increased to 36.8 +/- 4.2 g X m/M2 (not significant). These data suggest that volume infusion restores ventricular filling in patients with sepsis. Although fluid repletion increases stroke and cardiac output, depressed left ventricular performance appears to be an early finding in septic shock

The effects of increasing oxygen delivery (DO2) on oxygen consumption (VO2) in eight patients with septic shock and five patients with hypovolemic shock were studied during fluid resuscitation. In the septic shock group, DO2 increased from 315 +/- 29 to 424 +/- 25 ml/min/m2 (p less than 0.01) and VO2 increased from 134 +/- 8 to 151 +/- 7 ml/min/m2 (p less than 0.01). In the hypovolemic shock group, DO2 increased from 239 +/- 26 to 386 +/- 48 ml/min/m2 (p less than 0.01) and VO2 increased from 96 +/- 9 to 135 +/- 6 ml/min/m2 (p less than 0.01). There was no significant difference in either the increase in DO2 or VO2 between the septic shock and hypovolemic shock patients. We conclude that increasing DO2 by fluid resuscitation increases VO2 during both hypovolemic and septic shock