Citation

Eastridge BJ, Salinas J, McManus JG, Blackburn L, Bugler EM, Cooke WH, Convertino VA, Concertino VA, Wade CE, Holcomb JB. J. Trauma 2007; 63(2): 291-7; discussion 297-9.

Affiliation

U.S. Army Institute for Surgical Research, Fort Sam Houston, Texas 78234-6315, USA. brian.eastridge@amedd.army.mil

Erratum On

J Trauma 2008;65(2):501.

Copyright

(Copyright © 2007, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0b013e31809ed924

PMID

17693826

Abstract

BACKGROUND: Clinicians routinely refer to hypotension as a systolic blood pressure (SBP) < or =90 mm Hg. However, few data exist to support the rigid adherence to this arbitrary cutoff. We hypothesized that the physiologic hypoperfusion and mortality outcomes classically associated with hypotension were manifest at higher SBPs.

METHODS: A total of 870,634 patient records from the National Trauma Data Bank with emergency department SBP and mortality data were analyzed. Patients (140,898) with severe head injuries, a Glasgow Coma Score < or =8, and base deficit (BD) <5, or missing data items were excluded from analysis. Admission BD, as a measure of metabolic hypoperfusion, was evaluated in 81,134 patients and mortality was plotted against SBP.

RESULTS: Baseline mortality was <2.5%. However, at 110 mm Hg, the slope of the mortality curve increased such that mortality was 4.8% greater for every 10-mm Hg decrement in SBP. This effect was consistent to a maximum of 26% mortality at a SBP of 60 mm Hg. Hypoperfusion (change in the slope of BD curve) began to increase above baseline of 4.5 at a SBP 118 mm Hg.

CONCLUSION: Taking the BD and mortality measurements together, this analysis shows that a SBP < or =110 mm Hg is a more clinically relevant definition of hypotension and hypoperfusion than is 90 mm Hg. This analysis will also be useful for developing appropriately powered studies of hemorrhagic shock.

Language: en