Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study.
OBJECTIVE
To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis.


METHODS
Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized.


METHODS
Intensive care unit of a tertiary care hospital.


METHODS
Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines.


RESULTS
Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion.


CONCLUSIONS
Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.
Cooper
D J
DJ
St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
Walley
K R
KR
Wiggs
B R
BR
Russell
J A
JA
D000140:Acidosis, Lactic / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001639:Bicarbonates / Q000009:adverse effects / Q000627:therapeutic use*; D002118:Calcium / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D003627:Data Interpretation, Statistical; D004311:Double-Blind Method; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D016032:Randomized Controlled Trials as Topic; D012964:Sodium / Q000009:adverse effects / Q000627:therapeutic use*; D017693:Sodium Bicarbonate
D001639:Bicarbonates; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate; D012964:Sodium; D002118:Calcium