After reading some recent posts on emcrit.org and doing some research on quantitative acid-base analysis, I decided to write a simple post on a related subject: the controversy of administering sodium bicarbonate (or simply, “bicarb”) in the setting of lactic acidosis. With severe sepsis commonly causing lactic acidosis, it’s worth exploring. At first cursory glance, how could this not work? Bicarb is a base and the problem with lactic acidosis is acid. So, one would assume adding a base to an acid would neutralize things. However, adding NaHCO3 to a patient with lactic acidosis is not a good idea.
We are going to distill some review articles on the subject so us juniors can remember the basics and maybe learn a thing or two about current truth.
To simplify this presentation of complex ideas, I’ve organized this into two parts: the good and the bad. The good part will detail the intuitive and “advantageous” aspects of using NaHCO3 in lactic acidosis. The bad part will go into why it’s not so great or intuitive.
I. NaHCO3 will make solution more basic/raise the pH.
II. Despite raising arterial pH, NaHCO3 does not raise the intracellular pH nor the CSF pH.
III. NaHCO3 did not improve hemodynamics or catecholamine responsiveness.
IV. NaHCO3 may increase lactate.
Continue on for the more detailed explanations.
THE GOOD EXPLAINED:
I. NaHCO3 will make solution basic. Simply put, sodium bicarb will affect acid-base status towards alkalemia. But, not because of the bicarb. Rather, it is due to the sodium. NaHCO3‘s pH raising effects are from the Na+ strong cation. The HCO3– trivially affects pH because it gets blown off as CO2. This is crucial; if the minute ventilation cannot be increased (i.e. CO2 cannot be blown off), then the bicarb will not have a strong alkalinizing effect. Increased sodium increases the strong ion difference (SID). Increased SID = alkalosis. Decreased SID = acidosis. Just remember that for now; there’s more on that in quantitative acid-base texts, but we’ll settle for accepting that in the name of brevity. The determinant of blood pH is not HCO3–. HCO3– is a dependent factor that changes based on independent factors such as Na+, PCO2, and weak acids (like lactate).
THE BAD EXPLAINED:
II. NaHCO3 doesn’t raise the pH everywhere. It is widely held that NaHCO3 causes an intracellular acidosis. Animal studies have shown varying effects on pH. Most animal studies showed a drop in intracellular pH. Bicarb can’t cross the blood brain barrier, but it forms CO2 which readily can. Human studies also did not show a reliable intracellular response to NaHCO3.
III. NaHCO3 does not improve hemodynamics. Animal models have shown it causes a decrease in portal vein flow and worsens cardiac output.
IV. NaHCO3 may increase lactate. Though the mechanism is not entirely elucidated, animal and human studies have shown that bicarbonate infusion increases lactic acid production. Proposed mechanisms include a shift in the oxyhemoglobin dissociation curve or enhanced anaerobic glycolysis. Acidemia stalls glycolysis; exogenous NaHCO3 does the opposite thereby increasing lactic acid production.
Forsynthe et al. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000;117;260-267.
Gunnerson, K et al. (2013). Lactic acidosis. Medscape. http://emedicine.medscape.com/article/167027-overview
Weingart, SD. Podcast 96-Acid base in the critically ill-Part V-Enough with the bicarb already. Retrieved from emcrit.org.