Question 27

Compare and contrast the pharmacology of carbicarb, Sodium bicarbonate and THAM.

[Click here to toggle visibility of the answers]

College Answer

Carbicarb is an equimolar combination of sodium carbonate and sodium bicarbonate, generates a smaller rise in CO2 than sodabicarb. More consistently increases intracellular pH, inconsistent effects on hemodynamics, not commonly used clinically.

Sodabicarb: 8.4% or 4.2% solution. Hyperosmolar, generates high CO2, can cause paradoxical acidosis in the presence of a low output, cause hypokalemia, alkalosis and left shift of the curve. Phlebitis when given peripherally. On the other hand, frequently used to treat a metabolic acidosis if pH < 7.1, improves vasopressor responsiveness, may have a role in decreasing contrast nephropathy.

THAM: commercially available weak alkali. Buffers H+ ions. Buffering not associated with a CO2 rise. Side effects include hyperkalemia, hypoglycemia, extravasation related necrosis, and hepatic dysfunction.


Sodium bicarbonate pharmacology is discussed at length elsewhere. It is a dear and familiar product to most ICU trainees. The other two products are somewhat more exotic, and deserve a brief digression. For instance, carbicarb does not seem to be available in Australia.

As a table, the answer would look like this:

  Sodium bicarbonate Carbicarb THAM

An 8.4% (1mol/L) solution of NaHCO3 which offers 1000mmol/L of HCO3- and Na+ions.

An equimolar (300mmol/L) solution of Na2CO3 and NaHCO3which offers 666mmol/L of HCO3- ions, and 1000mmol/L of Na+ ions

An organic amine buffer, otherwise known as tris-hydroxymethyl-aminomethane, or tromethamine. The 3mol/L solution offers


Ideally IV, but can be given orally

IV only

IV only


Eliminated renally, as well as being converted to CO2 and exhaled (in process of buffering reactions). These two substances differ mainly in the amount of bicarbonate anion they add.

Rapidly eliminated by the kidney; 75% is excreted in the urine after 8 hours.

Adverse effects
  • Hypokalemia
  • Fluid overload
  • Hypercapnoea
  • Phlebitis
  • Hypokalemia
  • Fluid overload
  • Phlebitis
  • Fluid overload
  • Hypoglycaemia
  • Hyperkalemia
  • Phlebitis
  • Respiratory depression
  • Osmotic diuresis
Rationale for use

Sodium bicarbonate contributes HCO3which is a natural buffer, thus replenishing the buffer systems of the body in a state of acidosis.

The sodium carbonate component is supposed to act as a bicarbonae precursor, regenerating HCO3buffers without increasing the PaCO2.

THAM is a "third buffer" to complement the buffering capacity of endogenous HCO3and body protein.

At pH of 7.40, 30% of THAM is not ionized and therefore may penetrate cells and act as an intracellular buffer.

  • Metabolic acidosis with pH <7.10 and hemodynamic instability
  • Normal anion gap metabolic acidosis (esp. RTA)
  • Alkalinisation of urine to enhance the elimination of acidic drugs
  • Metabolic acidosis with hypercapnea
  • Viewed as an alternative to sodium bicarbonate for the treatment of metabolic acidosis


(or, situations in which it is known to be useless)

  • Hypokalemia
  • lactic aciosis
  • DKA
  • Hypokalemia
  • lactic aciosis
  • DKA
  • Uremia
  • Anuric renal failure

In neonates it is 
also contraindicated in chronic respiratory acidosis and salicylate intoxication.


The HOSPIRA booklet for THAM


Rhee, K. H., et al. "Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH." CHEST Journal 104.3 (1993): 913-918.


Schmidt, G. A. "Treatment of Acidosis: Sodium Bicarbonate and Other Drugs."Anaesthesia, Pain, Intensive Care and Emergency Medicine—APICE. Springer Milan, 2002. 681-693.


Filley, G. F., and N. B. Kindig. "Carbicarb, an alkalinizing ion-generating agent of possible clinical usefulness." Transactions of the American Clinical and Climatological Association 96 (1985): 141.