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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.
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).
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.
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:
Format: [Reference; Recommendation.]
Kurtz I. Acid-Base Case Studies. 2nd Ed. Trafford Publishing (2004); 68:150.
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:
Ghosh A, Habermann TM. Mayo Clinic Internal Medicine Concise Textbook. CRC Press, 2007. p.599:914.
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.”
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.
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
Risk of long-term HCO3- admin:
==========PACKAGE INSERT DATA=========
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.
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.
INDICATIONS AND USAGE
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.
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.
DOSAGE AND ADMINISTRATION
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.
The authors make no claims of the accuracy of the information contained herein; and these suggested doses are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this program shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user’s use of or reliance upon this material.PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. Read the disclaimer