Oxygen consumption and central hemodynamics in septic shock treated with antibiotics, fluid infusions, and corticosteroids.
The multidimensional pathophysiology of septic shock is poorly understood and treatment modalities are controversial. The present study evaluates the relative importance of three therapeutic measures: antibiotics (trimethoprim and sulphamethoxazole [TS]); fluid infusions (lactated Ringer's solution [RL] and 3% albumin [ Alb]), and pharmacologic doses of corticosteroids (CS) (dexamethasone [DM]), using central hemodynamics (plasma volume [PV], cardiac output, oxygen consumption [VO2]), and survival as end-points. Septic shock was induced by intraperitoneal injection of live Escherichia coli bacteria. At 5 h in untreated septic rats, PV had dropped to 76%, cardiac output to 69%, and VO2 to 71% of preshock levels. Untreated septic animals had a mean survival time of 9.7 +/- 1.7 (SD) h, with none surviving 24 h. Regardless of therapy, cardiac output and VO2 at 10 h were predictors of survival time (p less than .01). Treatment was initiated at 5.5 h after bacterial injection, at a time when TS therapy alone had not improved the 24-h survival rate. Animals treated with DM, RL, and Alb, in this order, exhibited progressively improved central hemodynamics, and 24-h survival rate increased to 60% compared with 0 in untreated animals (p less than .001). The combination of DM and RL produced no further improvement. However, DM combined with 3% Alb restored VO2, cardiac output, and PV to 81%, 100%, and 125%, respectively, increasing the 24-h survival rate to 97% (29/30), significantly greater than that achieved by any other treatment modality (p less than .05).[1]References
- Oxygen consumption and central hemodynamics in septic shock treated with antibiotics, fluid infusions, and corticosteroids. Ottosson, J., Persson, T., Dawidson, I. Crit. Care Med. (1989) [Pubmed]
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