Should I give Bicarbonate?
Should I give Bicarbonate?
ER SURVIVAL GUIDE/Should I give Bicarbonate?

Should I give Bicarbonate?

Sub Title
Separating indication from instinct
System
Misc
Published
Dec 22, 2025
Good posts start with good questions. Have an ER question? Send it here.
KEY
🔍- Deep Dive
📌- Clinical Application
🔸 - Weak Evidence
🔹 - Strong Evidence
📑 - Evidence summaries
✅ - Recommended treatment
⚠️ - Critical Information
This post exists because of a question someone asked me. It led to a lot of thinking and a lot of writing.
Thanks for asking , I enjoyed thinking this through.
Sodium bicarbonate is one of the most misused drugs in the emergency department ; perhaps because we subconsciously treat it as a magic fix for bad numbers.
Let’s slow down and examine whether that belief actually holds up.
We’ll start with a brief physiology refresher, because everything that follows makes more sense once the basics are clear.

Why pH matters

The human body tightly regulates blood pH between 7.35 and 7.45.
Even small deviations can significantly disrupt cellular function.
Because pH is logarithmic, seemingly minor changes reflect large shifts in hydrogen ion concentration. This is why even “mild” acidosis can be clinically important.

Bicarbonate: the primary extracellular buffer

A buffer is a solution that resists changes in pH when acids or bases are added.
Buffer systems consist of a weak acid and its conjugate base:
H⁺ + HCO₃⁻ ⇌ H₂CO₃ ⇌ H₂O + CO₂

How pH is regulated at the organ level

Lungs
  • Adjust minute ventilation to excrete or retain CO₂
Kidneys
  • Excrete hydrogen ions
  • Reabsorb or generate bicarbonate
  • Excrete excess bicarbonate
Hemoglobin
  • Buffers hydrogen ions
  • Facilitates CO₂ transport

What happens when pH drops despite these mechanisms?

Acidemia leads to:
  • ↓ Myocardial contractility
  • ↑ Risk of arrhythmias
  • ↓ Responsiveness to catecholamines
  • Peripheral vasodilation → hypotension
So yes — severe acidosis matters.
But does bicarbonate always help?
Not necessarily.

What actually happens when we give bicarbonate?

⚠️
Hypertonic sodium bicarbonate has a tonicity similar to 6% NaCl, making it roughly twice as hypertonic as 3% NaCl.
In most Indian emergency departments, the commonly used preparation is 7.5% sodium bicarbonate, 25 mL.
Approximate effects of one ampoule
  • 25 mL ≈ 22–23 mEq bicarbonate + 22–23 mEq sodium
  • Serum sodium increase: ~0.9–1 mEq/L
  • Osmotic sodium load → pulls ~55–60 mL of water into the intravascular space
  • Buffers hydrogen ions → generates CO₂ + H₂O
  • Excess bicarbonate is excreted by the kidneys
⚠️
Any benefit from bicarbonate depends entirely on the patient’s ability to exhale the generated CO₂.
If CO₂ cannot be eliminated, bicarbonate may fail to improve — and may even worsen — acidosis.

Why ventilation matters (especially in intubated patients)

After bicarbonate administration:
  • CO₂ production increases.
  • If minute ventilation cannot increase CO₂ accumulates.
This can:
  • Negate the pH benefit
  • Worsen intracellular acidosis
  • Increase PaCO₂ → increased work of breathing and cerebral blood flow
In effect, bicarbonate may simply exchange one acid (H⁺) for another (CO₂) - not always a net win.
⚠️
Be especially cautious when:
  • The patient is not intubated
  • Minute ventilation is fixed or limited
  • Severe hypercapnia is already present

What can go wrong with bicarbonate?

It’s worth addressing this early, because sodium bicarbonate is not a benign drug.
Potential adverse effects include:
  • Sodium and osmotic load (hypernatremia, hyperosmolality, volume overload)
  • Rebound (“overshoot”) alkalosis
  • Hypokalemia
  • Ionized hypocalcemia
  • Left shift of the oxyhemoglobin dissociation curve → impaired oxygen unloading
  • CO₂-related intracellular and CNS acidosis
  • Severe tissue necrosis with extravasation
  • Increased lactate production
  • Intracellular dehydration

What does the evidence say?

1. Cardiac arrest
AHA and ERC 2025 guidelines:
  • Routine sodium bicarbonate administration during cardiac arrest is not recommended
Exceptions to this are cardiac arrest due to:
  • Tricyclic antidepressant toxicity
  • Salicylate toxicity
📑
ICU-RESUS Trial (pediatric population)
  • Bicarbonate use during CPR was associated with:
    • Lower survival to hospital discharge
    • Worse neurological outcomes
Evidence for prolonged cardiac arrest remains conflicting, but routine use is not supported.
2. Hyperkalemia
AHA 2025
  • Effectiveness of bicarbonate in cardiac arrest due to hyperkalemia is not well established
ERC 2025
  • Recommends against routine bicarbonate use for hyperkalemia outside cardiac arrest
Why bicarbonate rarely helps
Theoretical benefits include:
  • Intracellular potassium shift
  • Increased renal potassium excretion
  • Dilution (as a non-chloride, non-acidic fluid)
These effects are clinically meaningful only in the presence of severe metabolic acidosis.
⚠️
Without significant acidosis, bicarbonate does very little for potassium.
Hypertonic vs isotonic bicarbonate
  • Hypertonic bicarbonate increases plasma tonicity → cellular dehydration → potassium exits cells (“solute drag”)
  • This may worsen hyperkalemia
In volume-depleted patients with metabolic acidosis, isotonic bicarbonate may be reasonable.
✅
Isotonic bicarbonate (1.3%)
  • Prepared by adding 150 mEq bicarbonate to 1 L of D5W
  • Bicarbonate deficit ≈ 0.5 × weight × desired ΔHCO₃⁻
  • Divide this by 150 to get the liters of isotonic bicarbonate required.
 
✅ Improves acidosis and may help hyperkalemia
❌ Watch carefully for volume overload
Otherwise, Ringer’s lactate is often the better fluid choice.
Despite containing 4 mEq/L of potassium, LR:
  • Does not meaningfully raise serum potassium
  • Avoids hyperchloremic acidosis, which shifts potassium out of cells
3. Acidosis: when (not) to give bicarbonate
Golden rule
👉 Treat the underlying cause - not the pH number.
That said, not all acidosis is the same.
Respiratory acidosis
  • Primary problem: CO₂ retention
  • Bicarbonate generates more CO₂
  • Do not worsen the physiology by giving Bicarbonate
Metabolic acidosis
High anion gap metabolic acidosis (HAGMA)
  • Caused by acid accumulation, not bicarbonate loss.
  • Management focuses on removing the acid.
  • Bicarbonate generally does not correct the underlying problem.
Important exceptions
  1. Methanol, ethylene glycol, salicylate toxicity
      • Urinary alkalinization improves toxin elimination
  1. Uremic acidosis
    1. AKIN stage 2–3
        • BICAR-ICU trial showed bicarbonate reduced need for RRT in selected patients
          • pH ≤ 7.20 AND serum HCO3- ≤ 20 mEq/L AND PaCO2 ≤ 45 mmHg AND moderate/severe AKI
        • Caveat: trial used 4.2% bicarbonate, not 7.5%
          • Isotonic bicarbonate may be preferable
        📑
        BICAR-ICU (2018)
        In critically ill patients with severe metabolic acidosis (pH ≤7.20), sodium bicarbonate did not improve overall mortality.
        In the AKI subgroup (AKIN 2–3), bicarbonate reduced the need for RRT and improved survival.
        BICAR-ICU 2 (2025)
        For critically ill patients with both severe metabolic acidosis and moderate to severe AKI, sodium bicarbonate therapy did not significantly decrease mortality
        🔸 SSC 2021: suggests bicarbonate in septic shock with severe metabolic acidemia and AKI
    2. CKD - Bicarbonate supplementation is a standard treatment in chronic kidney disease (CKD) to correct metabolic acidosis, which can slow the decline of kidney function.
  1. Lactic acidosis
      • Treat the cause
      🔸 SSC 2021 recommends against bicarbonate to improve hemodynamics or reduce vasopressors
  1. DKA
      • Acidosis resolves with adequate fluids and insulin
      • Routine bicarbonate is not recommended
        • When used the fluid of choice is isotonic bicarbonate.
      🔍
      Ketoacidosis in DKA is not merely a laboratory abnormality — it may represent a partly adaptive response.
      Acidemia shifts the oxyhemoglobin dissociation curve to the right, improving oxygen delivery to tissues. Blunting this response prematurely with bicarbonate may therefore be counterproductive.
      Excessive bicarbonate administration can also increase CO₂ generation. Because CO₂ freely crosses the blood–brain barrier, this may raise CSF PaCO₂, leading to paradoxical worsening of central nervous system acidosis, even as serum pH improves.
      In addition, bicarbonate therapy in DKA has been associated with:
      • Delayed clearance of ketones
      • Slower normalization of the lactate:pyruvate ratio
      • Increased risk of hypokalemia
      • Cerebral edema (particularly in pediatric patients)
      ✅
      Consider only in extreme acidosis (pH <7.0) with circulatory collapse, and with extreme caution (JBDS and ADA guidelines)
Non–anion gap metabolic acidosis (NAGMA)
Here, bicarbonate deficiency is the problem, so replacement makes physiologic sense.
  • Renal tubular acidosis → give bicarbonate
  • GI bicarbonate loss (diarrhea, fistulas, ureteral diversion) → give bicarbonate in severe cases
  • Hyperchloremic acidosis → consider bicarbonate to reduce renal injury and work of breathing
Fluid of choice: isotonic bicarbonate.
Decision tree to help guide bicarbonate choice
Decision tree to help guide bicarbonate choice

What Matters…

Before you give bicarbonate, answer these 3 questions
1️⃣ Can this patient eliminate CO₂?
Rising PaCO₂?
Fixed minute ventilation?
Exhausted or sedated patient?
👉 If NO → bicarbonate is contraindicated. Stop.
Fix that before considering bicarbonate.
2️⃣ What type of acidosis is this?
  • Respiratory → never bicarbonate
  • Metabolic
    • NAGMA → bicarbonate replaces a deficit
    • HAGMA → bicarbonate rarely helps
3️⃣ Is there a compelling indication that overrides the risks?
  • TCA or sodium channel blockade
  • Urine alkalinization for toxins
  • DKA with evere acidemia (pH ≤7.0) with cardiovascular collapse despite optimal support
  • Critically ill patient - AKIN 2 or 3 with pH<7.2
👉 If you can’t name one — don’t give it.

If you can’t explain why bicarbonate will help this patient, don’t give it.”
In the ER, less reflex and more physiology makes all the difference.

Want to Read More?

  1. Wigginton, Jane G., et al. "Part 9: adult advanced life support: 2025 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care." Circulation 152.16_suppl_2 (2025): S538-S577.
  1. Cao, Dazhe, et al. "Part 10: adult and pediatric special circumstances of resuscitation: 2025 American heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care." Circulation 152.16_suppl_2 (2025): S578-S672.
  1. Greif, Robert, et al. "European Resuscitation Council guidelines 2025 executive summary." Resuscitation 215 (2025): 110770.
  1. Jaber, Samir, et al. "Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial." The Lancet 392.10141 (2018): 31-40.
  1. Jung, Boris, et al. "Sodium Bicarbonate for Severe Metabolic Acidemia and Acute Kidney Injury." JAMA Cardiology (2025).
  1. O’Malley, Catherine M. N. FFARCSI*; Frumento, Robert J. MPH*; Hardy, Mark A. MD†; Benvenisty, Alan I. MD†; Brentjens, Tricia E. MD*; Mercer, John S. MD; Bennett-Guerrero, Elliott MD*. A Randomized, Double-Blind Comparison of Lactated Ringer’s Solution and 0.9% NaCl During Renal Transplantation. Anesthesia & Analgesia 100(5):p 1518-1524, May 2005. | DOI: 10.1213/01.ANE.0000150939.28904.81
  1. Sodium Bicarbonate Use During Pediatric Cardiopulmonary Resuscitation: A Secondary Analysis of the ICU-RESUScitation Project Trial. Pediatr Crit Care Med. 2022 Oct 1;23(10):784-792. doi: 10.1097/PCC.0000000000003045. Epub 2022 Jul 26. PMID: 35880872; PMCID: PMC9529841.
 
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