The use of sodium bicarbonate in patients with Severe Lactic Acidosis

The use of Sodium Bicarbonate in emergency Situations

The utility of intravenous sodium bicarbonate in severe metabolic acidosis is to say the least controversial. Yet each time we are presented with a patient with severe acidosis it is almost irresistible to give the patient an ampule of sodium bicarbonate to “improve myocardial performance”, after all our endogenous catecholamines work better under more physiologic conditions, right? 

I made this review to help delineate the problems of treating acidosis with sodium bicarbonate in the patients with acute metabolic (specifically lactic) acidosis. This is not meant for patients with renal tubular acidosis or patients who have bicarbonate loss, in which bicarbonate therapy is generally accepted (usually oral replacement). Also this is not for toxicologic emergencies, or for use in treating hyponatremia.

When considering bicarbonate replacement we must first consider the following questions:

  •  What are the complications of metabolic acidosis?
  • Can bicarbonate raise the pH?
  • Are there any beneficial effects of sodium bicarbonate?
  • What are the deleterious effects of sodium bicarbonate therapy?


What are the untoward effects of metabolic acidosis?

Before you read on think out loud what in your mind are the detrimental effects of metabolic acidosis and we are not talking prognostically here. 

-Reduced myocardial performance and decreased sensitivity of the myocardium to catecholamines, probably due to a reduction in the number of beta-receptors on the myocardial cell surface. In multiple isolated animal studies this has not been confirmed. This is because serum acidosis does not always translate into worsened intracellular acidosis. Also acidosis improves oxygen unloading into metabolically active cells. 

-Arrythmogenic especially at a pH < 7.2. This makes resuscitation of individuals in ventricular fibrillation more difficult, and why bicarbonate therapy was adopted during cardiac arrest. Oh the rise and fall of medications during ACLS! 

On the other hand we know that most patients tolerate respiratory acidosis fairly well. Everyday we place patients on ventilator settings to optimize their PaO2, and allow the PCO2 to rise without significant untoward hemodynamic effects (permissive hypercapnia). At a pH < 7.0 this is less well characterized, since so few people allow patients to develop such acidemia. 

Also MANY patients in DKA are extremely acidemic and do quite well  (how many times have you seen a patient with DKA with a pH < 7.2 who walked out of the hospital in 2 days?)

Conclusion: Therefore the assumption that a low pH in it of itself is a precursor to hemodynamic collapse and requires treatment is false.  This does not mean you should not recognize the acidemia as a potentially poor prognostic sign, and a marker of severe disease.  


Can Bicarbonate raise the pH?

Bicarbonate itself is not the only determinant of blood pH, as everyone knows. 

If you follow the physiochemical method of acid base disorders the pH is determined by subtracting strong cations (Na, K, Ca and Mg) from strong anions (Cl- and SO4). The SID increases due to bicarbonate administration because of an increase in sodium (bicarbonate is not a strong ion at all). 

However, bicarbonate drives Le Chatelier’s principle of chemical equilibrium: (HCO3 + H+ <==> H20 + CO2) 

 which will drive CO2 production. Therefore if ventilation is fixed, or MAXED as in a patient with a Minute ventilation of 20L, excess CO2 production cannot be eliminated and a rise in CO2 negates any potentially beneficial effects of the bicarbonate itself.

IF that gave you a migraine let me say it in another way. 

Sodium bicarb does increase the serum pH but it also increases CO2 production (think about ETCO2 jumping during a code when giving bicarb if you do this) and if you cannot blow off the CO2 with increased ventilation it has no net effect on the serum pH.

*Another potentially MORE IMPORTANT problem with following the serum pH is that different compartments have different pH’s (i.e; inner mitochondrial membrane, blood brain barrier etc) and CO2 readily crosses many of these membranes whereas bicarbonate itself does not. Therefore are we making the central veins for sampling more alkalemic at the cost of worsening intracellular and cerebral acidemia? 

Multiple studies have demonstrated that sodium bicarbonate will worsen acidosis in the brain and CSF (LP sampling and spectroscopy MRI). Several animal studies have shown that intracellular pH drops in RBC’s, muscle, liver and lymphocytes. 

Conclusion: Yes bicarbonate can increase the serum pH, but its effects on intracellular pH are unknown, but likely worsen acidosis. 


What beneficial effects does sodium bicarb have, if any?

Few studies have addressed specifically if there is any beneficial effect of sodium bicarbonate in vivo. No RCT’s have shown improvements in mortality, there has however been conflicting results on its effect on arterial pH, and several studies have demonstrated untoward hemodynamic effects.  

In animals sodium bicarbonate was indistinguishable from saline bolus on hemodynamics (CO, MAP, and CVP)

In two human studies in patients with lactic acidosis, sodium bicarbonate raised serum pH and bicarb, but did not improve hemodynamics or catecholamine responsiveness (ScVO2, MAP, wedge pressure, CO unchanged when compared to saline). 

Bicarbonate is an excellent volume expander, since it is like giving hypertonic saline, so potentially it could be use for resuscitation. Also bicarbonate can be given as a bolus for patients with severe hyponatremia with neurologic findings (about the equivalent of 100 cc of 3% saline in one 50 meq ampule.) 

Conclusion: Bicarbonate infusion has not definitively shown beneficial effects in patient or surrogate outcomes like hemodynamics or amount of vasoactives being infused . In fact most studies suggest bicarb has no net effects other than volume expansion in the hemodynamically unstable.


The final question remains what are the potentially deleterious effects of administration of sodium bicarbonate?

The first time I brought up the utility of sodium bicarbonate in the cardiac ICU, I was met with 

“ DO you know how many times I have regretted giving sodium bicarbonate? That would be 0”.

Essentially clinicians believe it is a benign cheap medication, which has few adverse effects. Oh but so wrong you can be:


55 y/o M s/p crush injury who had recently come off CVVH and was now making more urine whose bicarbonate had continued to be low (15). He was on the vent, but because of his non-gap metabolic acidosis he was breathing significantly above the vent settings to drive his PCO2 down to compensate for this acidemia.  This was making weaning difficult, as the attending did not want to extubate a patient with a RR in the 30’s. 

The surgical intern on overnight thought he would order a sodium bicarbonate drip in order to improve his serum bicarbonate and pH to make him “ready” for extubation. 

The resident ordered a 50 meq/hr drip at 8pm and at 5am labs were sent. When I arrived for rounds a critical sodium value was 168 (increased from 132). His chloride was also 130 so we thought this was an error, unfortunately a stat ABG had a pH of 7.67 and a HCO3 of 52 from the excessive endogenous bicarbonate that was given. The resident had MEANT to order a bicarb drip (3 amps in a liter of D5W or sterile water) which has a total of 150 mEq in 1L, instead he ordered 50 mEq/hr! 

The patient was less arousable after stopping sedation and continuous EEG found the patient to be in non-convulsive status (which alkalemia predisposes you to). It was UGLY. 

Detrimental effects of bicarb:

  • Increased serum sodium
  • Increased serum osmolality
  • Hypocalcemia can be profound
  • May worsen lactic acidosis
  • Overshoot correction and metabolic alkalosis


Conclusion: Bicarbonate will raise the serum pH when used in patients with severe acidosis. However, it is more likely that bicarbonate infusion worsens intracellular pH and does not provide any beneficial hemodynamic effects. Therefore in patients with LACTIC acidosis (even at extremes of pH < 7.2) it is difficult to find any reason to recommend sodium bicarbonate therapy. 

You are better off attempting to divert more neurons to solving why they are so acidemic. So the next time your nephrologist calls and screams why they aren’t on a bicarb drip you can kindly explain that there literature the use of bicarbonate is at BEST controversial.