| Preparation of 0.1 N solution
[100 ml (100 meq ) of 1.0N HCL] [1000 ml] [Infusion rate: see bottom section]
Filter HCL with 0.22 micron filter before adding it to the IV bag .
Alternatively (Using 37% HCL stock bottle):
[8.3 ml of 37% HCL] [1000 ml NS or D5W]
Preparation of 0.15 N solution
[150 ml (150 meq) of 1.0 N HCL] [1000 ml]
| –This agent must be infused in glass or polyolefin container.
–Hydrochloric acid solution should be administered through a central venous line to prevent vein irritation, thrombophlebitis, or tissue necrosis. Do NOT infuse via a peripheral vein! Injection of HCl into a peripheral vein may cause extravasation and can produce severe tissue necrosis.
–Solutions for infusion should NOT exceed 0.2 N (increased risk of hemolysis and increased venous irritation). Concentrations >0.1 N have been reported to cause corrosive effects, even when administered through a central venous catheter.
–Serum electrolytes and blood gases should be measured every 4 hours.
–Solution should be filtered with a teflon 0.22 micron filter before adding to an IV bag. Sample filter: GE PTFE (Teflon®) Syringe Filters: Membrane compatible with most aggressive solutions. https://www.osmolabstore.com/OsmoLabPage.dll?BuildPage&1&1&1051
H+ ion deficit (mEq) = 0.3 X weight (kg) X (measured HCO3 – desired HCO3 [mEq/L])
Rate of H+ replacement: 0.1 – 0.2 mEq/kg/hour
For example, 0.1 N solution IV at 100 mL/h provides about 10 mEq/h
Stock bottle of 37% HCL.
Determination of molarity of 37% HCL V/V
37 ml of solute/100 ml of solution.
HCL – 37% v/v. Specific gravity: 1.19 g/ml
37ml/100 ml or 370 ml/1000 ml x 1.19 g/ml = 440.3 g/L
HCL Molecular weight = 36.5
440.3 grams /36.5 grams = 12.06 M or ~12M
Compounding 1 liter of 0.1N Solution
M1V1 = M2V2
(0.1)(1000) = (12) (x)
x = (0.1) (1000) / 12
x = 8.3 ml
Therefore add 8.3 ml of 37% HCL to 1 liter of D5W or NS to create a 0.1N HCL solution.
—OR —(Alternative calculation)
12M (37% HCL) = 12 moles/L = 12 x 36.5 = 438 g/L = 438 mg/ml.
Need 0.1 N = 0.1 M
0.1 M x 36.5 = 3.65 g/L = 3650 mg.
3650 mg / 438 mg = 8.33 ml*
| Stability/storage: 24 hr (RT)
Indication: treatment of severe or refractory metabolic alkalosis. IV HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when NaCl or KCl cannot be administered because of volume overload or advanced renal failure. May also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia or hepatic encephalopathy.)
|Base excess in blood (BE-B)
Base excess in blood (BE-B) is the number of mmol of strong acid that is needed to adjust to pH 7.4 a blood sample tested at pCO2 of 40 mm Hg and 37 C.It indicates the deviation in mmol/l of the buffer bases from the normal value.
BE – B = (1 – 0.014[Hb])([HCO3-] – 24 + (1.43[Hb] + 7.7)(pH – 7.4))
The BE requires the measurement of blood pH, hemoglobin, and HCO3.
|H+ deficit (mEq) = 0.3 x Wt(kg) x ([HCO3-] – 35)
|Rate of H+ replacement =0.1 to 0.2 meq/kg per hour.
The ‘Normality‘ of a solution is the ‘Molarity’ multiplied by the number of equivalents per mole. The ‘Molarity‘ of a solution is the number of moles of solute in one liter of solution. Source: https://www.uab.edu/clabsc/solution.htm
| Source: DRUGDEX®:
Storage and Stability:
HYDROCHLORIC ACID (0.1N) is stable and compatible in VIAFLEX(R) PLASTIC CONTAINERS over a 24 hour storage period (Pers Comm, 1987).
Most studies recommend a 0.1 to 0.15 Normal hydrochloric acid solution prepared in sterile water, 5% dextrose in water or normal saline (Wagner et al, 1980g; Williams & Lyons, 1980g). One group of clinicians prepared a 0.1 Normal hydrochloric acid solution by drawing 100 milliequivalents of concentrated hydrochloric acid into a syringe and filtering it through a disposable 0.22 micron filter as it was added to a liter of 5% dextrose in water or normal saline (Wagner et al, 1980g). Others prepared a 0.15 Normal hydrochloric acid solution by diluting 12.5 milliliters of concentrated hydrochloric acid (35% to 38%) to a total volume of 1 liter with sterile water (Williams & Lyons, 1980g).
INTRAVENOUS RATE OF ADMINISTRATION: The rate of infusion was 100 to 125 milliliters/hour of a 0.15 Normal hydrochloric acid solution in sterile water (Williams & Lyons, 1980g). One group of practitioners infuses a liter of 0.1 Normal hydrochloric acid in 5% dextrose and water or normal saline over 4 to 6 hours (Wagner et al, 1980g). Some clinicians have corrected severe metabolic alkalosis with prolonged infusion of hydrochloric acid (over a period of 17 days), administering 100 to 400 milliequivalents hydrochloric acid daily through a central venous catheter as 0.1 Normal hydrochloric acid (Reisman & Puri, 1982f).
The amount of hydrochloric acid (HCL) administered is based upon base excess (milliequivalent/liter), with an equivalent amount being administered. One report recommends the following formula (Wagner et al, 1980g): HCL (mEq) = Weight (kilogram) x 0.3 X base excess (mEq/liter).
The amount of hydrochloric acid administered to each of the 21 patients treated was based upon 1 of 3 equations: Bicarbonate Excess = (0.5 X Weight in kg) X (serum bicarbonate -24); OR Chloride Deficit = (0.2 X Weight in kg) X (103- serum chloride); OR Base Excess = (0.3 X Weight in kg) X (measured base excess). The pH of amino acid solutions containing added hydrochloric acid was significantly higher than that observed with hydrochloric acid added to normal saline. The addition of 100 milliequivalent/liter hydrochloric acid to normal saline produced a pH of approximately 1.5, whereas, addition of the same amount to a 3.5%, 5.5%, and 8.5% amino acid solution increased the pH to approximately 3, 4.5, and 5, respectively.
The infusion generally continues until the total base excess is between 0 and 50 milliequivalent (Williams & Lyons, 1980g).
Hydrochloric acid — If acetazolamide is ineffective, the metabolic alkalosis can be corrected directly by the intravenous infusion of HCl, which buffers the excess bicarbonate. HCl is usually given as an isotonic solution (150 meq per liter) over 8 to 24 h. It can be infused into a major vein (since HCl is very corrosive) or into a peripheral vein if the HCl is buffered in an amino acid solution and given with a fat emulsion.
The amount of HCl required (in meq) can be estimated from the space of distribution of bicarbonate in metabolic alkalosis (approximately equal to 50 percent of lean body weight [LBW] in kg) times the bicarbonate excess per liter:
HCO3 excess = 0.5 x LBW x (Plasma HCO3 – 24)
In a 60 kg woman with a plasma bicarbonate concentration of 38 meq/L, for example:
HCO3 excess = 0.5 x 60 x 14 = 420 meq
It is important to remember that this formula is only an estimate and that it does not take into account any continuing acid loss, as with nasogastric suction. Minimizing continuing acid loss in this setting with an H2-blocker also may be helpful.
| Source: Merck Manual:
Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.
Patients with Cl-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/h greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L and urinary pH normalizes after an initial rise from bicarbonaturia. Patients with Cl-unresponsive metabolic alkalosis rarely benefit from rehydration.
Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent correction of serum pH. Hemofiltration or hemodialysis is an option, particularly if volume overload is present. Acetazolamide 250 to 375 mg po or IV once/day or bid increases HCO3 − excretion but may also accelerate urinary losses of K+ and PO4 −; volume-overloaded patients with diuretic-induced metabolic alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.
Hydrochloric acid in a 0.1 to 0.2 normal solution IV is safe and effective but must be given through a central catheter because it is hyperosmotic and scleroses peripheral veins. Dose is 0.1 to 0.2 mmol/kg/h, with frequent monitoring of ABG and electrolytes.
| Alternatives (usage depends on patient specific conditions):
|– Ammonium chloride (NH4Cl) (Note: Hydrochloric acid is the drug of choice in patients with hepatic dysfunction who are unable to tolerate ammonium chloride.)
CLINICAL PHARMACOLOGY: The ammonium ion (NH4+) in the body plays an important role in the maintenance of acid-base balance. The kidney uses ammonium (NH4+) in place of sodium (Na+) to combine with fixed anions in maintaining acid-base balance, especially as a homeostatic compensatory mechanism in metabolic acidosis. When a loss of hydrogen ions (H+) occurs and serum chloride (Cl−) decreases, sodium is made available for combination with bicarbonate (HCO3−). This creates an excess of sodium bicarbonate (NaHCO3) which leads to a rise in blood pH and a state of metabolic alkalosis.
The therapeutic effects of ammonium chloride depend upon the ability of the kidney to utilize ammonia in the excretion of an excess of fixed anions and the conversion of ammonia to urea by the liver, thereby liberating hydrogen (H+) and chloride (Cl−) ions into the extracellular fluid.
Dosing: Ammonium Chloride Injection, USP is administered intravenously and must be diluted before use. Solutions for intravenous infusion should not exceed a concentration of 1% to 2% of ammonium chloride. Dosage is dependent upon the condition and tolerance of the patient. It is recommended that the contents of one to two vials (100 to 200 mEq) be added to 500 or 1000 mL of isotonic (0.9%) sodium chloride injection. The rate of intravenous infusion should not exceed 5 mL per minute in adults (approximately 3 hours for infusion of 1000 mL). Dosage should be monitored by repeated serum bicarbonate determinations.
100 mEq (5 mEq/mL) – 20 ml vial
For the treatment of hypochloremia or hypochloremic metabolic alkalosis in patients who cannot receive sodium chloride and who do not have end-stage hepatic disease: Intravenous dosage: Adults: Individualize dosage based on the patient’s carbon dioxide combining power. Each gram of ammonium chloride will reduce the carbon dioxide combining power of a 70-kg adult by about 1.1 volume %, or 16 mg/kg will lower the carbon dioxide combining power by 1 volume %. In the absence of edema or hyponatremia, the dosage may be calculated on the basis of the chloride deficit by the following formula: mEq of chloride ion (as ammonium chloride) = chloride deficit x 0.2 L/kg x weight (kg). The chloride deficit is 103 — serum Cl in mEq/L. One-half of the calculated value should be administered, the carbon dioxide combining power should be rechecked and the need for further treatment assessed. Do not exceed a concentration of 1—2% of ammonium chloride or an infusion rate greater than 5 ml/minute.
– Acetazolamide (Diamox): chloride-resistant metabolic alkalosis. Metabolic alkalosis (unlabeled use): I.V. 250 mg every 6 hours for 4 doses or 500 mg single dose; reassess need based upon acid-base status. Alternatively: 5-10 mg/kg/d PO/IV divided q6h. Carbonic anhydrase inhibitor that blocks HCO3 reabsorption in the proximal renal tubules.