Sodium Bicarbonate: Difference between revisions
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| pregnancy = Routine antacid and acidosis correction acceptable | | pregnancy = Routine antacid and acidosis correction acceptable | ||
| legal = [[USLegal:Prescription only|Rx-only]] for IV formulations; OTC for oral | | legal = [[USLegal:Prescription only|Rx-only]] for IV formulations; OTC for oral | ||
| mechanism = <vote slug="nahco3-mech-claim">Sodium bicarbonate raises serum pH directly via the carbonic acid / bicarbonate buffer system; in TCA overdose its benefit is partly pH-driven (reducing free | | mechanism = <vote slug="nahco3-mech-claim">Sodium bicarbonate raises serum pH directly via the carbonic acid / bicarbonate buffer system; in TCA overdose its benefit is partly pH-driven (reducing the free unbound fraction) and partly sodium-driven (overcoming TCA sodium-channel blockade), which is why hypertonic 8.4% is preferred over isotonic.</vote> Bicarbonate is not benign: high-volume use produces hypernatremia, metabolic alkalosis, hypokalemia, and (in arrest) paradoxical intracellular acidosis<ref name="nahco3-label" />. | ||
}} | }} | ||
== References == | == References == | ||
<references /> | <references /> | ||
Latest revision as of 04:44, 23 May 2026
Sodium bicarbonate is a systemic alkalinizing agent and antacid, used intravenously in severe metabolic acidosis, hyperkalemia with cardiotoxicity, tricyclic-antidepressant overdose with QRS widening, and (historically) cardiac arrest; orally as an antacid and urinary alkalinizer; and as the carrier base for many effervescent formulations[1]. Routine bicarbonate administration in cardiac arrest was removed from ACLS algorithms because it did not improve survival and worsened intracellular acidosis; the remaining strong indications are narrow and physiology-driven.
Sodium bicarbonate
Neut, many generic; OTC oral: Alka-Seltzer (with aspirin/citric acid), baking soda
Experience
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Summary
Classes
Common uses
Severe metabolic acidosis0, Hyperkalemia with ECG changes0, Tricyclic-antidepressant overdose with QRS widening0, Urinary alkalinization (salicylate or methotrexate toxicity, uric-acid stones)0, Symptomatic antacid (oral)0
Pharmacy
Starting dose
IV: 1 mEq/kg bolus in arrest indication, then titrated to ABG and clinical status; PO: 325-2000 mg up to QID as antacid
Preparations
4.2%, 7.5%, 8.4% IV (1 mEq/mL at 8.4%); 325, 650 mg oral tablets; bulk powder
US FDA Max
No fixed maximum; titrated to pH and bicarbonate level; chronic high oral doses cause metabolic alkalosis and volume overload
Pharmacology
Routes
IV, oral
Onset
Immediate (IV); within minutes (oral antacid)
Duration
IV: hours, dependent on ongoing acid load; oral antacid: ~30 minutes
Half-life
Not applicable (electrolyte and buffer)
Bioavailability
100% (IV); rapidly neutralized by gastric acid (oral)
Pregnancy
Routine antacid and acidosis correction acceptable
Legal status
Rx-only for IV formulations; OTC for oral
Purported mechanism
Sodium bicarbonate raises serum pH directly via the carbonic acid / bicarbonate buffer system; in TCA overdose its benefit is partly pH-driven (reducing the free unbound fraction) and partly sodium-driven (overcoming TCA sodium-channel blockade), which is why hypertonic 8.4% is preferred over isotonic.0 Bicarbonate is not benign: high-volume use produces hypernatremia, metabolic alkalosis, hypokalemia, and (in arrest) paradoxical intracellular acidosis[1].
References
- ↑ 1.0 1.1 FDA Prescribing Information, Sodium Bicarbonate Injection, Hospira, current revision. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/018802s022lbl.pdf