To Bicarb or Not to Bicarb?
Author: Amy Hembree, MD PGY-2
Peer Reviewers: Lauren Gruffi, MD PGY-2, Justine Sweeney, MD PGY-2
Faculty Editors: Mustafa Rasheed, MD
There comes a point in the resuscitation of most critically ill, acidotic patients where someone in the room asks: “Should we give bicarb?”
The answer to this question requires careful consideration, not only of the consequences of sodium bicarbonate administration, but also of the pathophysiology you are trying to treat. Here, we hope to give you a framework to think through your response, starting with how sodium bicarbonate actually works.
Pathophysiology:
The body regulates acid-base status through the carbonic acid-bicarbonate buffer system (seen in the figure below), renal bicarbonate handling, and respiratory CO₂ removal, typically making compensatory adjustments to serum pH over a 24-48 hour time period1,2.
Before deciding whether or not it’s appropriate to give sodium bicarbonate, it’s worth discussing what happens physiologically when we do. For our purposes, sodium bicarbonate has 5 primary effects, the significance of which we will discuss later:
Accepting a proton - Bicarbonate is a base, so by definition it is a proton acceptor, thereby increasing serum pH.
Producing CO₂ - As seen in the equation above, bicarbonate is metabolized by carbonic anhydrase to produce carbon dioxide and water. Without adequate ventilation, this rise in CO₂ can worsen both intracellular and systemic acidosis.
Shifting potassium intracellularly - Bicarbonate lowers serum potassium via multiple mechanisms, both through shifting potassium into skeletal muscles (by direct cotransport and by alkalinizing the serum and changing the gradient for H/K exchange) and by alkalinizing the urine to cause more efficient potassium excretion 3.
Shifting fluid intravascularly - Sodium bicarbonate is a hypertonic solution. 1 ampule of sodium bicarbonate has an osmolarity of 8.4%, roughly the equivalent of 6% normal saline2,4. This makes sodium bicarbonate twice as powerful an osmotic agent as one of our more commonly used hypertonic therapies (3% NS), and its administration can cause shifting of fluid out of cells through solute drag, increasing intravascular volume.
Alkalinizing the urine
Beyond these primary effects sodium bicarbonate is associated with hypocalcemia, hypernatremia, intracellular acidosis, paradoxical central nervous system (CNS) acidosis, decreased myocardial contractility, and increased lactate levels5–7.
Sodium bicarbonate has a wide range of consequences-–some rationalize our use of bicarbonate for clinical conditions, some are unintended side effects that should be carefully considered when weighing the pros and cons of giving sodium bicarb.
Cases Where Bicarb May Fix the Underlying issue:
Salicylate toxicity - In salicylate overdose, alkalinizing the urine with sodium bicarbonate will increase salicylate elimination by correcting acidemia, reducing tissue distribution, and improving urinary elimination8. Bicarbonate should be given to target a urine pH of 7.58.
Tricyclic Antidepressant (TCA) toxicity - The sodium in sodium bicarbonate helps to narrow the QRS (combatting the TCA induced sodium channel blockade). Additionally, the bicarbonate prevents dysrhythmias by facilitating a more alkaline pH, which favors the neutral (as opposed to active) form of TCA 8,9.
Non anion gap hyperchloremic metabolic acidosis - NAGMA typically results from bicarbonate loss (either through the GI tract or renally, such is the case with RTA), often with concurrent hyponatremia and hyperchloremia5. Logically, giving chloride-free sodium and replacing the missing bicarbonate would address the underlying cause of this acid-base abnormality. The evidence for bicarbonate use is strongest in patients with concurrent renal injury; the BICAR-ICU trial showed no overall difference in mortality between severely acidemic ICU patients who received bicarbonate and those who did not. However, it did show improved mortality in patients with concurrent AKI as well as a reduced need for dialysis by 17%10.
Cardiac Arrest - If you suspect cardiac arrest is due to metabolic acidosis, hyperkalemia, or TCA overdose, it is reasonable to give bicarbonate. In 2010, the American Heart Association removed bicarbonate from the undifferentiated cardiac arrest ACLS algorithm as there were no convincing studies showing benefit, and some showing worse outcomes. However, some argue that these worse outcomes are seen as physicians are more likely to give bicarbonate to more severely ill patients 5. There are no specific guidelines in regards to frequency of administration, and redosing should be guided by resuscitation2.
Cases Where Bicarb May (or May Not) Temporize the Situation:
Hyperkalemia - Mechanistically bicarbonate will drive potassium intracellularly (and to a small degree will increase renal elimination). However, the data has not proven that sodium bicarb should be used as monotherapy for hyperkalemia. If a patient has EKG changes consistent with hyperkalemia, sodium bicarbonate may help to shift potassium intracellularly and stabilize the cardiac membrane and should be used in conjunction with other agents11.
Pressor Refractory Shock - Vasopressor efficacy decreases in acidemic environments (specifically pH<7.15) due to impaired catecholamine signalling7. While sodium bicarbonate may improve metabolic acidosis and allow pressors to work more effectively, it has a wide array of adverse effects including: respiratory acidosis, increased lactate production, paradoxical intracellular acidosis and myocardial depression. Because these downstream effects may worsen the patient’s clinical picture, the etiology of acidosis should be considered before deploying sodium bicarbonate as a rescue therapy, and it should not be given indiscriminately to all acidemic patients on vasopressors7.
Cases Where Bicarb May Make Things Worse:
Respiratory acidosis - Bicarbonate increases serum CO2, which will worsen your problem. If you’re giving bicarbonate to a ventilated patient, adjust your respiratory rate accordingly to account for the increased CO2 you’ll be creating.
Anion Gap Metabolic Acidosis - Bicarbonate will not fix the underlying problem, and can worsen the clinical picture by causing fluid overload, hypokalemia, respiratory acidosis, hypernatremia, and increased lactate production among other complications1. There may be a role for bicarb in patients with lactic acidosis after initial resuscitation with pH<7.2 and concurrent AKI, though data is limited5.
DKA - Bicarb will worsen hypokalemia, which is usually the limiting factor in insulin administration to correct the underlying problem. Additionally, in pediatric patients bicarbonate administration is associated with cerebral edema12.
Severely hypocalcemic or hypernatremic patients should not receive bicarb as it may exacerbate these conditions2.
Administration Tips:
Bicarbonate can be given in its undiluted form as an ampule—50 mEq in a 50mL solution with an osmolarity of 8.4%13. It can also be administered in its diluted form, typically 150 mEq sodium bicarbonate in 1 L D5W with an osmolarity of 1.3%. Bicarb should be mixed with D5W as opposed to normal saline to avoid creating an increasingly hypertonic solution13. This "isotonic" form of bicarb allows for slower, controlled correction and is preferred over other diluents which can cause significant chloride load or hypertonicity. Often, 40 mEq of potassium chloride is mixed into the diluted solution as well to combat concurrent hypokalemia. Notably, bicarbonate cannot be co-administered with a number of medications, including epinephrine, dobutamine or any medications that contain magnesium or calcium. Therefore, additional IV access may need to be obtained to give sodium bicarbonate2,14.
Takeaway Points:
Sodium Bicarbonate use may temporize metabolic acidosis and alkalinize the urine, but it also causes increased CO2 production, hypokalemia, acts as an intravascular fluid bolus, hypernatremia, and hypocalcemia, among other adverse effects.
Sodium bicarbonate is most helpful for toxicologic indications, such as TCA or salicylate overdose.
In critically ill patients with non anion gap hyperchloremic metabolic acidosis, bicarbonate may be helpful, particularly for patients with concurrent acute kidney injury.
Bicarbonate should not routinely be given for cardiac arrest, and may only be helpful if there is reasonable suspicion that the arrest is secondary to hyperkalemia, TCA overdose, or metabolic acidosis.
In the treatment of hyperkalemia, sodium bicarbonate should not be used as a monotherapy, but may be helpful as an adjunct, particularly in patients with EKG changes.
In the case of pressor refractory shock with pH <7.15, consider the etiology of acidemia before administering bicarbonate.
Do not give sodium bicarbonate to patients with anion gap metabolic acidosis, respiratory acidosis, fluid overload, severe hypernatremia, or hypocalcemia.
References:
3. Farkas, Josh. Management of severe hyperkalemia in the post-Kayexalate era. emcrit.
7. Barola S, Shabbir N. Refractory Shock. In: StatPearls. StatPearls Publishing; 2023.
11. Pruitt J. The Beef with Bicarb! The Use of Sodium Bicarbonate in Hyperkalemia.
13. Farkas, Josh. Fluid Selection & pH guided fluid resuscitation. emcrit.
14.Pearlman J, Nickson C. Drugs for Cardiac Arrest. Life in the Fastlane.
