Have you ever wondered: WHY do we reach for Sodium Bicarbonate in the ICU?

A History, A Physiology, A Philosophy

My apologies to this growing readership. After taking the summer of 2025 off from blogging, I’m back. I appreciate your patience 😀.

Let’s try a new take today— I’ll attempt to weave history, physiology, evidence, controversy, and philosophy into a practical piece.

Here is #3 of the Have You Ever Wondered…? 🧠 series- where we explore the why behind what we do at the ICU bedside.

Today’s question:

Why do we reach for sodium bicarbonate in the ICU?

🌙 👩‍⚕️🏥

Okay, let’s say it’s 3:00 a.m. in the ICU.

A patient lies before you: blood pressure collapsing, lactate rising, arterial blood gas pH of 6.9. The nurse asks: “Should we start a bicarb drip?”

Well, let’s just say, few questions in critical care stir more debate than this one. Sodium bicarbonate — one of the oldest drugs in our armamentarium — sits on the shelf, deceptively simple, almost alchemical: a white powder that promises to neutralize the acid of death itself. But behind that small vial lies more than a century of history, a web of physiology, and a philosophy of medicine that stretches back to antiquity.

Bicarbonate, first crystallized by French chemists in the 18th century, was not born as an ICU drug. Look up the Leblanc process (salt to soda ash, precursor process to making sodium bicarbonate) if you are interested. (Some web searches suggest ancient Egyptians first started with natron, a naturally occurring compound salt.)

Overall though, bicarb, as we call it, began in kitchens and factories as baking soda. In medicine, its journey started with treating “acid stomachs,” moved through resuscitation attempts in World War II field hospitals, and found its way into the ICU as a reflexive antidote to lactic acidosis in the 1960s and 70s.

But as modern physiology emerged, voices grew skeptical. By the 1980s, intensivist- and nephrologist-talking heads argued that bicarbonate was too blunt a tool — shifting carbon dioxide across cell membranes, perhaps worsening intracellular acidosis.

So, was it salvation, or illusion?

At its core, sodium bicarbonate (NaHCO₃) does one thing: it buffers hydrogen ions. It reacts with H⁺ to form H₂CO₃, which dissociates into water and CO₂.

Key physiological consequences:

• Immediate effect: rises in serum pH and HCO₃⁻, often stabilizing cardiac contractility and catecholamine responsiveness.
• Downside: the CO₂ ion produced diffuses rapidly into cells and across the blood–brain barrier, potentially worsening intracellular acidosis if ventilation cannot keep up.

In the lung 🫁, this means you must have a ventilation system ready to sweep away the exhaled CO₂. In the kidney 🫘, it means shifting sodium and water loads. In the brain, it means the possibility of paradoxical worsening — a cruel irony.

Pharmacokinetically, sodium bicarbonate distributes rapidly in extracellular fluid, with renal excretion dependent on GFR, and with sodium load implications for heart failure and volume-sensitive patients.

For decades, we had dogma, not data. Then came trials.

• No benefit in lactic acidosis: Studies since the 1980s onward showed that routine bicarbonate in sepsis, elevated lactic acid, and lactic acidosis did not improve mortality or hemodynamics (Cooper et al., 1990).

• The BICAR-ICU Trial (2018, JAMA): In 389 patients with severe metabolic acidosis (pH ≤7.20, HCO₃⁻ ≤20), sodium bicarbonate did not improve the primary composite outcome overall. (Mortality and organ failure.) But in the pre-specified subgroup of patients with acute kidney injury, bicarbonate reduced the need for dialysis and improved survival【PubMed ID: 29946726)].

BICAR-ICU

In critically ill patients with severe metabolic acidaemia (pH ≤7⋅20), does the infusion of sodium bicarbonate, compared with no infusion, to reach and maintain a targeted pH of 7⋅30 decrease the primary composite out­come of mortality by day 28 or the presence of at least one organ failure at day 7?

The Bottom Line A compendium of critical appraisals in Intensive Care Medicine research and related specialtiesSteve Mathieu

• Cardiac arrest: The AHA and European Resuscitation Council recommend against routine bicarbonate during CPR, reserving it for special circumstances (e.g., hyperkalemia, tricyclic antidepressant overdose, severe pre-existing metabolic acidosis).

• DKA: Guidelines emphasize insulin and fluids first; bicarbonate is only indicated if pH <6.9, reflecting the dangers of hypokalemia and paradoxical CNS acidosis. Some sources even argue that <7.05.

🌍 International guidelines today (SCCM, ESICM, KDIGO):

• Do not use bicarbonate routinely for lactic acidosis in sepsis.
• Consider it when pH <7.1, especially with concomitant AKI.
• Use it for specific toxicologic indications (TCA overdose, salicylate poisoning, hyperkalemia with ECG changes).
• NAGMA (Non-anion gap metabolic acidosis) with a serum bicarbonate level usually less than 18 mEq/L could be considered for exogenous bicarbonate administration.

Why So Much Controversy? 🗣️

I think we can say this because bicarb sits at the intersection of numbers and narrative.

3 P’s:

• On paper: It raises pH.
• In physiology: It can worsen intracellular acidosis.
• In practice: Sometimes it saves the crashing patient long enough for definitive therapy.

But it‘s a drug of temporality…it buys time— yet does not cure disease. Like a sorcerer’s stone, it can appear to transmute crisis into stability, but at a cost.

The controversy endures because clinicians are haunted by two fears:

1. Doing nothing while a patient acidifies into arrest.
2. Doing harm by chasing numbers with chemistry instead of physiology.

Philosophy at the Bedside

Marcus Aurelius: “What stands in the way becomes the way.”

Acidosis is not merely a lab value— it is a signal of failing cellular respiration, of mitochondria gasping under hypoxia, sepsis, or shock. To treat only the number is to miss the message.

Yet, philosophy also teaches pragmatism: when the patient’s heart is failing at pH 6.9, due to the extensive acidic milieu, even a temporary reprieve may give time for antibiotics, fluids, or dialysis to take hold. Bicarb, then, is less a cure and more a bridge — a plank laid across the torrent.

When to consider bicarb:

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• Severe metabolic acidosis (pH <7.1) with AKI or impending need for RRT/dialysis.
• Tricylic antidepressant (TCA) overdose
• Hyperkalemia
• Salicylate (aspirin) toxicity
• DKA with pH <6.9
• Specific peri-arrest scenarios, guided by ACLS: hyperkalemia, above

When to avoid bicarb:

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• Routine use in lactic acidosis from sepsis/shock.
• Isolated hyperchloremic metabolic acidosis without severe acidemia.
• Patients with volume overload, uncontrolled ventilation, or risk of hypernatremia.

Physician/APP Pearls:

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• Bolus (1–2 mEq/kg) for immediate rescue.
• Infusion (commonly 150 mEq in 1L D5W over several hours) for ongoing acidemia, guided by blood gases.
• Always consider to pair with adequate ventilation to eliminate excess pCO₂.
• Monitor electrolytes: potassium, calcium, sodium shifts.
• Monitor pH.

Nursing/RT Pearls:

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• Watch for peripheral IV extravasation— sodium bicarbonate is caustic.
• Auscultation for crackles— sodium bicarbonate can cause pulmonary edema.
• Track ABGs closely as not to overcorrect.
• Document hemodynamic response, urine output, neuro status/exam.

🤌🏼

Sodium bicarbonate is not a panacea. It is not the sorcerer’s stone. It is, rather, a reminder: that in critical care, numbers on a blood gas are both truth and illusion. The truth is acidemia kills. The illusion is that neutralizing the acid is the cure.

We reach for bicarbonate not because it solves the problem, but because sometimes it buys us time to solve the problem.

And in the ICU, time is often the most precious drug of all.

Maybe one day precision medicine will hit our Units. Mitochondrial dysfunction will be targeted in critical illness the way we are now targeting neoplastic cells by sophisticated immunotherapy.

REFERENCES

Jaber S, et al. Sodium Bicarbonate Therapy for Patients with Severe Metabolic Acidaemia in the Intensive Care Unit (BICAR-ICU). Lancet. 2018;392(10141):31-40). PMID: [29910040].

Kraut JA, Madias NE. Lactic Acidosis. N Engl J Med. 2014;371(24):2309–2319. PMID: [25494270].

Ghauri SK, et al. Bicarbonate therapy for critically ill patients with metabolic acidosis: a systematic review. Cureus. 2019 Mar 22;11(3):e4297. PMID: [31183278].

Perman SM, et al. 2023 American Heart Association Focused Update on Adult ACLS : Update to AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation.

Kitabchi AE, et al. Management of Diabetic Ketoacidosis. Diabetes Care. 2009;32(7):1335–1343. PMID: [19564476].

Wardi G, et al. A Review of Bicarbonate Use in Common Clinical Scenarios. J Emerg Med. 2023 August; 65(2):e71-e80.

Cooper DJ, et al. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med. 1990 Apr 1;112(7):492-8. PMID: [2156475].

Brooks, GA. Lactate as a fulcrum of metabolism. Redox Biology. 20-20 August, volume 35, 101454.