Correction of metabolic acidosis and for replacement therapy requiring the use of sodium bicarbonate.

Posology:
The quantity of Sodium Bicarbonate Intravenous Infusion BP to be infused is determined by the 
blood gas values. The following formula is a guide:
• Amount by ml of 8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP = negative base 
excess x body weight by kg x 0.3 (The factor 0.3 corresponds to the proportion of the extracellular 
fluid in relation to total body fluid).
Example:
If in a patient of 70 kg bodyweight the base deficit is 5mmol/l, then 5 x 70 x 0.3 = 105 ml of 8.4 % 
w/v Sodium Bicarbonate Intravenous Infusion BP are to be given.
 
Correction of metabolic acidosis should not be effected too rapidly. It is advisable to start 
administering only half of the calculated dose and adjust further doses according to the actual 
results of blood gas analysis.

Flow rate
Up to 1.5 mmol of sodium bicarbonate per kg body weight per hour, corresponding to 1.5 ml of 
8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP/kg bw/h.

Administration
Strictly intravenously. 8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP has an osmolarity 
of about 2000 mOsm/L and, when infused undiluted, it should be administered via a central 
venous catheter, preferably inserted into the vena cava.
Accidental intra-arterial administration may cause shock or may lead to the loss of an extremity.

Special warnings
8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP should not be administered in the 
following situations unless it has been established that its expected benefits clearly outweigh 
potential risks:
- Hypoventilation,
- Hypocalcaemia,
- increased serum osmolarity,
- Further in all situations where sodium intake must be restricted like cardiac insufficiency, 
oedema, hypertension, eclampsia, severe kidney insuffiency.
Administration of 8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP may lead to sodium 
and fluid overload.

Special precautions for use
Patient monitoring should include regular checks of the acid-base balance, the serum electrolyte 
concentrations and the water balance.
Hypokalaemia or hypocalcaemia should be corrected before beginning of the alkalinizing therapy.

Urine alkalinisation by sodium bicarbonate increases the elimination rates of acid drug substances,  e.g. acetylsalicylic acid, and decreases the elimination rates of basic drug substances.
Sodium bicarbonate may interact with gluco- and mineralocorticoids, androgens and diuretics increasing the potassium excretion.

As bicarbonate readily crosses the placental barrier, sodium bicarbonate solutions should only be given to pregnant women if clearly indicated. It should not be given in eclampsia, without careful consideration.
 

Not relevant.

Reactions which may occur because of the solution or the technique of administration include 
febrile response, infection at the site of injection, venous thrombosis or phlebitis extending from 
the site of injection, extravasation and hypervolemia.

Administration of 8.4 % w/v Sodium Bicarbonate Intravenous Infusion BP may lead to 
hypernatraemia, and serum hyperosmolarity.
Paravenous administration may lead to tissue necrosis.

Symptoms
Overdose may lead to alkalosis, hypernatraemia, and serum hyperosmolarity. When an acidosis is 
corrected too rapidly, especially in cases of concomitant respiratory disorders, the increased 
liberation of carbon dioxide may transiently aggravate cerebral acidosis.

Emergency treatment, antidotes
Therapy of alkalosis, depending on its severity: Infusion of physiological saline, correction of 
potassium; in marked alkalosis expert advice should be sought.

The pharmacological properties of sodium bicarbonate result from its physiological role in the 
HCO3 /CO2 buffer system.
Exogenously administered sodium bicarbonate rapidly absorbs hydrogen ions from the 
extracellular space and thus leads to a rise of the pH in the organism.
By this buffering process carbon dioxide is produced which is subsequently eliminated via the 
lungs. Therefore lung function should be unimpaired. Otherwise a marked rise of the pCO2 will 
cause an aggravation of intracellular acidosis.

In the kidneys, bicarbonate is filtered in the glomerula and the major proportion of it is re-absorbed 
in the tubules. Reabsorption is nearly complete at plasma bicarbonate concentrations of less than 
24 mmol/L. Renal bicarbonate reabsorption is reduced under therapy with diuretics of the thiazide 
group or those acting on Henle's loop.
The rise of the blood pH also affects the electrolyte balance.
The cellular potassium uptake is increased so hypokalaemia may be provoked or an existing 
hypokalaemia may be aggravated. The binding of calcium to plasma proteins is increased so 
hypocalcaemia may be provoked or an existing hypocalcaemia may be aggravated.
Bicarbonate readily passes across the placental barrier but it passes only slowly across the bloodbrain barrier.

There are no pre-clinical data of relevance to the prescriber which are additional to those already 
stated in other sections of the SPC.

Disodium edetate

Water for injections

Due to their alkaline pH, sodium bicarbonate solutions are incompatible with most medicaments. 
In particular, they must not be administered simultaneously with solutions containing calcium, 
magnesium or phosphate because of the possibility of precipitation.

Do not store above 25°C.

50 ml and 250 ml glass vials.

Before administration, the product should be visually inspected for any particulate matter and 
discoloration. 
For single use only. 
Any unused solution should be discarded.