Question 27 | Deranged Physiology

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

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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.

Discussion

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
Properties	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
Administration	Ideally IV, but can be given orally	IV only	IV only
Pharmacokinetics	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 HCO₃^-which 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 HCO₃^-buffers without increasing the PaCO_2.	THAM is a "third buffer" to complement the buffering capacity of endogenous HCO₃^-and body protein. At pH of 7.40, 30% of THAM is not ionized and therefore may penetrate cells and act as an intracellular buffer.
Indications	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
Contraindications (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.

References

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.

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