Normally, end-tidal CO2 is within 2 mm Hg of arterial PO2 (PaCO2). However, if dead space in the lungs increases owing to shock with poor lung perfusion, the arterial-end tidal PCO2 difference [P(a-ET)CO2] increases. We have found that in severely injured patients, P(a-ET)CO2 of less than 10 mm Hg is associated with survival and P(a-ET)CO2 of greater than 16 mm Hg is usually fatal. Our initial studies suggested that intravenously administered bicarbonate increases P(a-ET)CO2.
This retrospective therapeutic study evaluated the effects of intravenously administered bicarbonate in a cohort of 225 severely acidotic (arterial pH ≤ 7.10) trauma patients who underwent emergency surgery from 1989 through 2011. Patients were divided into groups: early deaths (<48 hours), deaths in the operating room, deaths within 48 hours, and survivors. Winter’s formula was defined as PaCO2 = (HCO3) (1.5) + 8 ± 4.
Of the 225 patients, the mean (SD) initial arterial pH was 6.92 (0.16) with HCO3 of 11.0 (3.5) mEq/L. According to the Winter’s formula, PaCO2 should have been 24 (4) mm Hg but actually was 50 (14) mm Hg. In 73 patients, the effect of an average of two to eight vials of bicarbonate increased HCO3 from 10.5 (3.1) mEq/L to 16.8 (4.0) mEq/L. In addition, PaCO2 increased from 44 (9) mm Hg to 51 (11) mm Hg and end-tidal CO2 stayed relatively constant (26  to 25 ). This resulted in a increase in P(a-ET)CO2 from 17 (9) mm Hg to 24 (13) mm Hg, affecting survival. In the final values after resuscitation, the P(a-ET)CO2 in the 75 patients who survived was 10 (6) mm Hg, while the 103 patients who died in the operating room or within 48 hours of surgery had a P(a-ET)CO2 of 23 (10) mm Hg (p < 0.001).
In severely acidotic, critically injured patients, reducing the PaCO2 to less than 40 mm Hg and decreasing the P(a-ET)CO2 to 10 (6) mm Hg should be attempted, using as little HCO3 therapy as possible. Bicarbonate should be given only if severe acidosis persists despite resuscitation and if PaCO2 levels near those which are appropriate can be obtained.
Therapeutic study, level IV.
From the Department of Surgery, Detroit Medical Center, Wayne State University School of Medicine, Detroit, Michigan.
Submitted: August 2, 2012, Revised: August 17, 2012, Accepted: August 28, 2012.
This study was presented at the 71st annual meeting of the American Association for the Surgery of Trauma, September 12–15, 2012, in Kauai, Hawaii.
Address for reprints: Robert F. Wilson, MD, Department of Surgery, Detroit Medical Center, Wayne State University School of Medicine, Detroit Receiving Hospital, 4201 St. Antoine, Suite 4S-13, Detroit, MI 48201; email: firstname.lastname@example.org.