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Sodium bicarbonate

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Usual Diluents


Standard Dilutions   [Amount of drug] [Infusion volume] [Infusion rate]

50 meq/ 50 ml vial

May add ordered dose to empty viaflex bag or dilute in 50-1000ml.
[Infuse as directed]

Stability / Miscellaneous

EXP: 1 DAY (RT).

Monitor ABG's q2-3 hours to assess response. Administer IV either undiluted or diluted in other IV fluid (50-1000ml) depending on fluid status.

Osmolarity: 2Na + gluc/18 + BUN/2.8 (nml: 280-295).

pH [7.35-7.45],
pCO2 [35-45],
pO2 [75-100],
anion gap [12-14].
**Note: treat hypokalemia or hypocalcemia first if present.



In all cases, the primary goal in treating metabolic acidosis is to focus on reversal of the underlying process causing the acidosis.  Examples:  (1) Renal failure: dialysis if needed.
(2) Alcoholic ketoacidosis: fluids, electrolytes, thiamine, folic acid.  (3) Sepsis/shock: volume resuscitation, vasopressors, etc.  (4) Salicylate intoxication:  IV fluids, alkalinization of the urine, ....

If there is a severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) correct with sodium bicarbonate.    Sodium bicarb is also useful if the acidosis is due to inorganic acids (especially if renal disease is present).  However, when the acidosis results from organic acids (lactic acid, acetoacetic acid, etc) the role of bicarbonate is controversial.  In most cases of DKA or sever lactic acidosis the administration of sodium bicarbonate does not decrease mortality even when the acidosis is severe.  In sum, sodium bicarbonate should be reserved for severe cases of acidosis only (pH <7.2 and serum bicarbonate levels <10-12 meq/L).  This can be accomplished by adding 1 to 3 ampoules of sodium bicarb to D5W or 1/2NS.   IV-push administration should be reserved for cardiac life support and not metabolic acidosis.

Sodium bicarbonate administration: It is recommended that 50% of total deficit be given over 3 to 4 hours, and the remainder replaced over 8-24 hours. The usual initial target ((desired HCO3- concentration): 10 - 12 mEq/L, which should bring the blood pH to ~7.20. The subsequent goal is to increase the bicarbonate level to 15 meq/L over the next 24 hours.

Koda-Kimble et al:
Replace 50% over 3 to 4 hours and the reminder over 24 hours.  Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than 4 to 8 Eq/L over 6 to 12 hours to avoid the risks of over-alkalinization (paradoxical CNS acidosis; decreased affinity of hemoglobin for oxygen leading to tissue hypoxia and lactic acid production; sodium overload; and hypokalemia).

Format:  [Reference;  Recommendation.]


Kurtz I. Acid-Base Case Studies. 2nd Ed. Trafford Publishing (2004); 68:150.

"Following the acute administration of bicarbonate as a bolus, its effect on the systemic pH will be maximal. Over the subsequent hours, the bicarbonate which was originally administered will be taken up into cells. In addition, the elevation of systemic pH decreases the compensatory ventilatory response. These two effects will decrease the systemic pH from the maximum value that was obtained immediately following the administration of bicarbonate."  Effective volume of distribution of bicarbonate varies with the HCO3- concentration:

Bicarb Vd = (0.4 + 2.6/HCO3-) x Lean body weight.

Bicarbonate deficit = Bicarb Vd x (desired [HCO3-] - measured [HCO3-])

Lean body weight defined as usual IBW equations:
Estimated ideal body weight in (kg):
Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.

Important points:
1] Greater degree of metabolic acidosis --> Greater increases in bicarb Vd ---> Larger amounts of bicarb must be administered.

2] Following admin of bicarb (as a bolus), there is a time-dependent decrease in blood HCO3- conc. A portion of the  HCO3- which is initially distributed in the ECF space, subsequently enters the intracellular space.

3] As the blood HCO3- conc increases, the PCO2 increases as a results of a decrease in alveolar ventilation.


Ewald G, McKenzie C (editors). Manual of Medical Therapeutics, 28th edition. Little, Brown and Company. 1995. page 59 and 63.

Since the distribution of bicarbonate is about 50% of lean body weight, ... serum concentration to normal can be estimated as follows:

HCO3~ deficit (mEq) =  0.5 x lean body wt (kg) x (desired [HCO3-] - measured [HCO3-])

Lean body weight defined as usual IBW equations:
Estimated ideal body weight in (kg):
Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.



Ghosh A, Habermann TM. Mayo Clinic Internal Medicine Concise Textbook. CRC Press, 2007. p.599:914.

Bicarbonate deficit = 0.2 x weight (kg) x base deficit (mEq/L).



Kollef MH, Bedient TJ, Isakow W, Witt CA. The Washington Manual of Critical Care. Lippincott Williams & Wilkins, 2007; p185:583.

"Primary goal in treating metabolic acidosis is reversal of the underlying process. Administration of bicarbonate in controversial, as some clinical parameters may actually worsen... " "However, partial correction should be considered in the setting of life-threatening metabolic acidosis(pH<7.1) or when the serum bicarbonate is low enough (i.e., <10 to 12 mEq/L) that loss of effective respiratory compensation would result in life-threatening acidosis."

Bicarbonate deficit:  The amount of bicarbonate req'd to correct a metabolic acidosis can be estimated from the following formula:

Volume of distribution (Vd) = Total body weight (kg) x [0.4 + (2.4/[HCO3-])
 (Deficit) mEq of NaHCO3 = Vd x target change in [HCO3-]



Koda-Kimble M, Young LY, et al. Handbook of Applied Therapeutics. Lippincott Williams & Wilkins, 2006. P10.3(1104).

It is important to correct the underlying cause and to administer IV bicarbonate to maintain a pH >7.2-7.25.

Bicarbonate dose (mEq): 0.5 (L/kg) x Body weight (kg) x Desired increase in serum HCO3- (mEq/L)

Replace 50% over 3 to 4 hours and the reminder over 24 hours.  Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than4 to 8 mEq/L over 6 to 12 hours to
avoid the risks of over-alkalinization (paradoxical CNS acidosis; decreased affinity of hemoglobin for oxygen leading to tissue hypoxia and lactic acid production; sodium overload; and hypokalemia.

Risk of long-term HCO3- admin:
[1] Excess HCO3- converted to H2CO3-, then to CO2 gas, causing paradoxical metabolic acidosis with rapid penetration of CO2 gas into CNS.
[2] Decreased O2 release from hemoglobin.
[3] Arrhythmogenic.
[4] Increased serum osmolality.

In severe metabolic acidosis, bicarbonate may be given to correct the base deficit in the extracellular fluid within 24 hours. Parenteral bicarbonate therapy may be considered in patients when the pH is below 7.2 and should be discontinued once the pH reaches 7.2

==========PACKAGE INSERT DATA=========

Sodium Bicarbonate Injection, USP is a sterile, nonpyrogenic, hypertonic solution of sodium bicarbonate (NaHCO3) in water for injection for administration by the intravenous route as an electrolyte replenisher and systemic alkalizer. Solutions are offered in concentrations of 7.5% and 8.4%. Solutions in the Ansyr® II syringe have an approximate pH of 8.0 (7.5 to 8.5).

The solutions contain no bacteriostat, antimicrobial agent or added buffer and are intended only for use as a single-dose injection. When smaller doses are required, the unused portion should be discarded with the entire unit.
Sodium bicarbonate, 84 mg is equal to one milliequivalent each of Na+ and HCO3¯. Sodium Bicarbonate, USP is chemically designated NaHCO3, a white crystalline powder soluble in water.
Water for Injection, USP is chemically designated H2O.

The syringe is molded from a specially formulated polypropylene. Water permeates from inside the container at an extremely slow rate which will have an insignificant effect on solution concentration over the expected shelf life. Solutions in contact with the plastic container may leach out certain chemical components from the plastic in very small amounts; however, biological testing is supportive of the safety of the syringe material.


Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis.

Sodium bicarbonate in water dissociates to provide sodium (Na+) and bicarbonate (HCO3¯ ) ions. Sodium (Na+) is the principal cation of the extracellular fluid and plays a large part in the therapy of fluid and electrolyte disturbances. Bicarbonate (HCO3¯ ) is a normal constituent of body fluids and the normal plasma level ranges from 24 to 31 mEq/liter. Plasma concentration is regulated by the kidney through acidification of the urine when there is a deficit or by alkalinization of the urine when there is an excess. Bicarbonate anion is considered “labile” since at a proper concentration of hydrogen ion (H+) it may be converted to carbonic acid (H2CO3) and thence to its volatile form, carbon dioxide (CO2) excreted by the lung. Normally a ratio of 1:20 (carbonic acid; bicarbonate) is present in the extracellular fluid. In a healthy adult with normal kidney function, practically all the glomerular filtered bicarbonate ion is reabsorbed; less than 1% is excreted in the urine.


Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate.

Treatment of metabolic acidosis should, if possible, be superimposed on measures designed to control the basic cause of the acidosis - e.g., insulin in uncomplicated diabetes, blood volume restoration in shock. But since an appreciable time interval may elapse before all of the ancillary effects are brought about, bicarbonate therapy is indicated to minimize risks inherent to the acidosis itself.

Vigorous bicarbonate therapy is required in any form of metabolic acidosis where a rapid increase in plasma total CO2 content is crucial - e.g., cardiac arrest, circulatory insufficiency due to shock or severe dehydration, and in severe primary lactic acidosis or severe diabetic acidosis.

Sodium Bicarbonate Injection, USP is contraindicated in patients who are losing chloride by vomiting or from continuous gastrointestinal suction, and in patients receiving diuretics known to produce a hypochloremic alkalosis.

Solutions containing sodium ions should be used with great care, if at all, in patients with congestive heart failure, severe renal insufficiency and in clinical states in which there exists edema with sodium retention.
In patients with diminished renal function, administration of solutions containing sodium ions may result in sodium retention.
The intravenous administration of these solutions can cause fluid and/or solute overloading resulting in dilution of serum electrolyte concentrations, overhydration, congested states or pulmonary edema.
Extravascular infiltration should be avoided, see ADVERSE REACTIONS.

Overly aggressive therapy with Sodium Bicarbonate Injection, USP can result in metabolic alkalosis (associated with muscular twitchings, irritability, and tetany) and hypernatremia.

Inadvertent extravasation of intravenously administered hypertonic solutions of sodium bicarbonate have been reported to cause chemical cellulitis because of their alkalinity, with tissue necrosis, ulceration or sloughing at the site of infiltration. Prompt elevation of the part, warmth and local injection of lidocaine or hyaluronidase are recommended to reduce the likelihood of tissue sloughing from extravasated I.V. solutions.

Should alkalosis result, the bicarbonate should be stopped and the patient managed according to the degree of alkalosis present. 0.9% sodium chloride injection intravenous may be given; potassium chloride also may be indicated if there is hypokalemia. Severe alkalosis may be accompanied by hyperirritability or tetany and these symptoms may be controlled by calcium gluconate. An acidifying agent such as ammonium chloride may also be indicated in severe alkalosis.

Sodium Bicarbonate Injection, USP is administered by the intravenous route.

In cardiac arrest, a rapid intravenous dose of one to two 50 mL syringes (44.6 to 100 mEq) may be given initially and continued at a rate of 50 mL (44.6 to 50 mEq) every 5 to 10 minutes if necessary (as indicated by arterial pH and blood gas monitoring) to reverse the acidosis. Caution should be observed in emergencies where very rapid infusion of large quantities of bicarbonate is indicated. Bicarbonate solutions are hypertonic and may produce an undesirable rise in plasma sodium concentration in the process of correcting the metabolic acidosis. In cardiac arrest, however, the risks from acidosis exceed those of hypernatremia.

In less urgent forms of metabolic acidosis, Sodium Bicarbonate Injection, USP may be added to other intravenous fluids. The amount of bicarbonate to be given to older children and adults over a four-to-eight-hour period is approximately 2 to 5 mEq/kg of body weight - depending upon the severity of the acidosis as judged by the lowering of total CO2 content, blood pH and clinical condition of the patient. In metabolic acidosis associated with shock, therapy should be monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics and cardiac rhythm. Bicarbonate therapy should always be planned in a stepwise fashion since the degree of response from a given dose is not precisely predictable. Initially an infusion of 2 to 5 mEq/kg body weight over a period of 4 to 8 hours will produce a measurable improvement in the abnormal acid-base status of the blood. The next step of therapy is dependent upon the clinical response of the patient. If severe symptoms have abated, then the frequency of administration and the size of the dose may be reduced.

In general, it is unwise to attempt full correction of a low total CO2 content during the first 24 hours of therapy, since this may be accompanied by an unrecognized alkalosis because of a delay in the readjustment of ventilation to normal. Owing to this lag, the achievement of total CO2 content of about 20 mEq/liter at the end of the first day of therapy will usually be associated with a normal blood pH. Further modification of the acidosis to completely normal values usually occurs in the presence of normal kidney function when and if the cause of the acidosis can be controlled. Values for total CO2 which are brought to normal or above normal within the first day of therapy are very likely to be associated with grossly alkaline values for blood pH, with ensuing undesired side effects.

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.

Package insert: Rev: January, 2006. © Hospira 2006 EN-1105 Printed in USA. HOSPIRA, INC., LAKE FOREST, IL 60045 USA

Sodium Bicarbonate